(June 2014) (pdf) - Vermont Center for Integrative Herbalism

Integrative
Herbalism
Summer 2014
Journal of the Vermont Center for Integrative Herbalism
•
Materia Medica
Aralia nudicaulis
Centella asiatica
Acorus calamus and Acorus Americanus
Actaea racemosa as an alternative to hormone replacement therapy
Oplopanax horridus
Theobroma cacao as an antioxidant
Hypericum perforatum: potential interactions with testosterone replacement
Calendula officinalis in vulvovaginitis
The effect of Gossypium on the uterus
•
Therapeutics
Animal fats in pregnancy
Post induced abortion herbal therapeutics
Cross-sex hormone replacement therapy: herbal support for adverse events
Fibromyalgia syndrome
Hyperprolactinemia and premenstrual syndrome therapeutics
Diabetes mellitus: herbal, nutritional and lifestyle considerations
Generalized anxiety disorder: an integrative perspective
Kudzu in alcohol abuse
Post-myocardial-infarction ventricular remodeling and herbal therapeutics
Transforming trauma stored in the body: a holistic approach to PTSD
•
Case studies
Anxiety, stress management
Mood support, sleep latency, menstrual difficulties
Dermatographism, recurrent vaginosis
Lower leg edema, sugar cravings
•
General interest
Health Access issues
HPA Axis and Exogenous sex hormones
Some reflections on action-based classification of medicinal plants
A primer on leaky gut syndrome
Native plants for promoting beneficial insects in the garden
Pyrogenesis, Capsicum, and Zingiber
The use of animal fats in topical application
Volume 2, Number 1 (June 2014)
Welcome to another (much belated) issue of Integrative Herbalism. We are hoping
you will find much that is of interest in this volume, arranged by area of focus: articles on
botanicals, either comprehensive or focused on a specific area of applicability; detailed
papers on integrative therapeutics for a wide diversity of imbalances; comprehensive case
reports with follow-up data; and some fascinating pieces of general interest (including, for
example, a study of which medicinal species might be best suited to attracting beneficial
insects to your garden).
In this issue you will find that a good portion of the work has been dedicated to
exploring the effects of herbs on transgender people. For instance, articles explore potential
effects, side effects, and herbal interactions with exogenous hormones. I also recommend
the article on herbal therapeutics following induced abortion – a detailed, thorough, and
practical guide to navigating this difficult case.
We really feel that the caliber of work presented in this volume of Integrative
Herbalism is outstanding, and reflects the caliber of students with whom we have the honor
of working. As always, Integrative Herbalism is brought to you with full open access, in line
with our mission of supporting an open, diverse conversation about herbal medicine in the
twenty-first century.
For the plants!
Guido Masé, Director of Research
Vermont Center for Integrative Herbalism
Aralia nudicaulis
Jonathan Shapiro
Aralia nudicaulis is a common understory plant (McDonald) in the Araliaceae family whose
range stretches across most of the northern United States and Canada (USDA, NRCS). It is
a North American native (Felter and Lloyd 261) which likes to grow in rich, moist woods
(Harding 352). It has a long history of medical use by indigenous peoples and settlers in
North America (Horton 699). The Eclectics and others included it in their material medicae,
and several notable contemporary herbalists publish or speak about its properties.
A perennial plant, the aboveground parts of A. nudicaulis grow up two feet high (Foster and
Duke 63) although may be found as short as eight inches (Alpers and Murray 184). It sends
up a petiole and scape in early spring; the petiole at full growth has three divisions, each
bearing a compound leaf of three to five leaflets (Alpers and Murray 184). The plant flowers
in May through July (Cook 80) (Harding 353). “During the summer a dark purple, nearly
black, drupe develops about one-fourth of an inch in diameter. This fruit is probably a
welcome food for birds, as it disappears soon after ripening and can only seldom be found
on the ground under the leaves. It does not seem to serve for the propagation of the plant,
the creeping root-stock performing this function” (Alpers and Murray 184).
The root is the part used medicinally, and has variously been described as “perennial,
brown, yellowish, creeping, twisted, sometimes many feet long, the thickness of a finger”
(Howard 696); and “large, fleshy, horizontal, creeping, tortuous… very long, often many
feet in length, about six lines in diameter, and yellowish or brownish externally” (Felter and
Lloyd 261). Examples of the root up to 29 feet in length have been described (Alpers and
Murray 183). William Alpers records impressions of the root being more potent in the fall
(Alpers and Murray 189), and Jim McDonald recommends harvesting only the upright
portion of the root connecting to the horizontal rhizomes because it has a stronger taste
(McDonald).
A. nudicaulis has numerous common names, the most common of which are false
sarsaparilla, wild sarsaparilla, and spikenard (sometimes referred to as little spikenard).
(Alpers and Murray 183) (Cook 80) (Felter and Lloyd 261) (Foster and Duke 63) (Harding
352) (Howard 696) (McDonald) (Moore) (Rafinesque 53) (Sayre 252). Plants in the Aralia
genus tend to have either woody stems, acrid aromatics, and spines, or herbaceous annual
growth with somewhat succulent roots. The latter category often has a soothing balsamic
taste and is generally higher in aralosides, ginsenosides, and saponins. “The four Aralia that
can be loosely lumped together as ‘Spikenards’ are of this latter type.” (Moore).
The Eclectics and other 19th- and early 20th-century figures wrote about the plant’s uses and
indicated the plant for a wide range of acute and chronic complaints, but most mention its
alterative action and its effects on the pulmonary system in acute situations. Cook said it
“expend[s] its properties chiefly upon the skin and kidneys…. It is seldom employed in
pulmonary difficulties; yet is good whenever the lungs need a mild stimulant” (Cook 80).
Horton described it is a pectoral (Horton 80). Lloyd and Felter, in King’s American
Dispensatory, call it an alterative and mention its usefulness in pulmonary diseases (Lloyd
and Felter 262).
Sayre calls it an alterative (Sayre 252). Howard says that “all the
spikenards are popular medical plants throughout the United States” and that they are all
pectorals (Howard 699). Scudder includes it in his list of alteratives and notes that “it is
regarded by many as a valuable alterative agent” (Scudder 484).
Contemporary herbalists understand the plant’s effects in varying ways. Michael Moore
considers it a long-term tonic, writing that it has the “Ginseng-like effects of modifying
metabolic and emotional stresses” (Moore). Jim McDonald also views the plant as a
metabolic normalizer, but says the term adaptogen is “problematic” and categorizes A.
nudicaulis as an alterative with a specific action on the adrenal glands. McDonald elaborates
that it has a soothing, tonifying effect on the adrenals and can balance a person out when in
a state of sympathetic dominance, moving the body’s metabolism forward (McDonald).
At least one recent study has been performed on A. nudicaulis. A team of Canadian
researchers performed in vitro studies on hexane fractions of the root and fruit and noted
that they were cytotoxic against WiDr human colon adenocarcinoma cells, Molt human T-cell
leukemia, and HELA human cervix epitheloid carcinoma cells (Wang et al 2157).
Additionally, these two fractions were found to not differ significantly from the negative
control in minimum survival rates of non-cancer HUV-EC cells (Wang et al 2160).
Works cited:
Alpers, William C. and Benjamin L. Murray. “Aralia nudicaulis.” Proceedings of the American
Pharmaceutical Association, August, 1897. Baltimore, MD: American Pharmaceutical
Association, 1897. 183 – 190. Print.
Cook, William. The Physiomedical Dispensatory. Cincinnati: Wm. H. Cook, 1869. Print.
Felter, Harvey Wickes and John Uri Lloyd. King’s American Dispensatory. Cincinnati: The
Ohio Valley Company, 1909. Print.
Foster, Steven and James Duke. Eastern/Central Medicinal Plants and Herbs. New York,
Houghton Mifflin Company, 2000. Print.
Harding, A.R. Ginseng and Other Medicinal Plants. Columbus: A.R. Harding Publishing Co.,
1908. Print.
Horton, Howard. Howard’s Domestic Medicine. Philadelphia: Hubbard Brothers, 1879. Print.
“Herb TV jim mcdonald talks sarsaparilla.” Herb TV. YouTube. 2011. Web. 18 Feb. 2013
Moore, Michael. “Aralia (Spikenard) Folio.” Swsbm.com. Southwest School of Botanical
Medicine, 1997. Web. 18 Feb. 2013
Rafinesque, C.S. Medical Flora. Philadelphia: Atkinson & Alexander, 1828. Print
Scudder, John M. The American Eclectic Materia Medica and Therapeutics. Cincinnati: The
Scudder Brothers Company, 1898. Print.
Sayre, Lucius E. A Manual of Organic Materia Medica and Pharmacognosy. Philadelphia: P.
Blakiston’s Son & Co., 1905. Print.
USDA, NRCS. “The PLANTS Database.” Plants.usda.gov. National Plant Data Team, 2013.
Web. 18 Feb. 2013
Wang, Jennifer, Qiuzhu Li, Gerald Ivanochko, and Yaoge Huang. “Anticancer Effect of
Extracts from a North American Medicinal Plant – Wild Sarsaparilla.” Anticancer Research 26
(2006) 2157 – 2164. Print.
Gotu Kola
Elise Walsh
Botanical Nomenclature: Centella asiatica
(L.)
Family: Apiaceae
Common Names:
United
States:
i
Gotu
Kola,
Indian
pennywort
India: ii Brammi (Sanskrit)
Tamil: Vallarai.
Tel: Babassa, Mandukbrammi
Ben: Thulkurhi
Hindi: kula kudi
Mandukaparni (“frog-leaved”)
China: iii Ji xue cao
(“accumulation of snow herb”)
Japan: sekisetsuso
Korea: jeokseolcho
Part used/Definition: Fresh or dried aerial parts
Botanical Identification:
Gotu Kola is a perennial herb with a low, spreading habit. Leaves are reniform, 1-4.5 x 1.55 cm with a crenate margin, and born on 0.5-10 cm petioles. Surfaces are glaborous or
finely pubescent with 5-7 palmate veins.
iv
Inflorescence in a single umbel bearing 2-5 white
star shaped flowers attached directly to the base without a stalk. v Flowers are sessile with 2
or 3 brachts that bloom April to October.
(base of stem) is reddish in color.
vi
They produce small, 2-3mm long fruit. vii Stolon
Commercial Sources and Handling:
Gotu Kola is cultivated in India, Sri Lanka, and in the United States in Hawaii and Texas.
High quality material should be green in color
viii
and organically sourced whenever possible.
It is widely available as a dietary supplement under the Dietary Supplement Health
Education Act of 1944 (DSHEA). Adulteration of Centella is not common though it has
occurred due to a shared common name, Brahmi, which also refers to Bacopa monnieri. ix
Growing and harvesting information: Centella is distributed to nations in the southern
hemisphere including India, Sri Lanka, Africa, Madagascar, Australia, Cambodia, Thailand,
Lao, Vietnam, China, Indonesia, the Pacific Islands, Central and South America, and the
southern United States. x
Centella grows wild in moist, drainage areas, though it is amenable to cultivation. xi
Propagated most readily by root division, it grows as a perennial in tropical and sub-tropical
climates and as an annual in temperate climates. To cultivate in temperate climates it
should be transferred indoors to greenhouse during the cold season.
xii
Plant material should be dried in a dark ventilated space and stored immediately to maintain
potency. Gotu Kola should be stored in sealed container to protect from light, air and
moisture.
Taste/Odor: xiii
Rasa (taste): bitter, pungent,
Virya (action): cooling
Vipaka (post-digestive effect): pungent
Energetics: xiv Cooling to neutral and mildly astringent, balancing to all doshas.
Physiological Actions: xv
xvi
•
Nervine relaxant/ Anxiolytic
•
Connective tissue tonic
•
Veinous tonic
•
Vulnerary
•
Anti-inflammatory
•
Anti-oxidant
Specific Indications/patterns:
1. Wound healing and collagen modulation. xvii
2. Increases circulation to periphery, including both the brain and the extremities. xviii
Used in the Ayurvedic tradition to promote intellect, improve concentration, and
enhance meditative focus. xix
Doctrine of Signatures: leaf shape resembles the cerebellum, suggestive of its affinity for
cognition.
Channels entered: xx Liver, Spleen, Kidney
Tissue States: xxi depression, relaxation and atrophy
Clinical Use:
Nervous System:
Generalized Anxiety Disorder
Anxietous Depression
xxii xxiii
xxiv
To improve concentration, memory and alertness xxv
ADD/ADHD xxvi
o
Anti-aging tonic xxvii
Cognitive decline
xxviii xxix
(incl. dementia and Alzheimer’s disease) and memory loss
xxx
Epilepsy xxxi
Stroke xxxii
Integumentary:
Scleroderma xxxiii
Psoriasis and eczema
xxxiv xxxv xxxvi
Wounds, Scars, Burns xxxvii
xxxviii
Dry Skin Conditions xxxix (incl. Ichthyosis xl)
Cellulite
Keloid xlii
xli
Pre and Post Surgical healing
Ulcers
xlv xlvi
xliii xliv
(incl. oral surgery and cancer)
(internal and topical use)
o
diabetic ulcers
o
bed sores
o
syphilitic ulcers xlvii
Weak nails/ hair xlviii esp. in hypothyroidism
Leprosy
xlix l
Musculoskeletal:
Soft tissue injury to ligament or tendon
li lii
Osteoarthritis liii
Rheumatism liv
Joint injury and inflammation lv
Cardiovascular:
lvi
Varicose Veins lvii
Chronic venous insufficiency
Venous Hypertension
Stasis Ulcers (From varicose veins)
Many side affects of diabetes involving weakened micro-circulatory capillary flow:
o
Neurapthy
o
nephropathy
Gastrointestinal:
o
Hemorrhoids lviii
o
Inflammatory disease of bowel lix
lx
(including Ulcerative Colitis, Crohn’s
disease)
o
Gastric ulceration and inflammation lxi
o
GERD and other digestive tissue destruction to prevent scar tissue from
forming
o
Gingevitis, periodontal disease lxiii
Key Constituents:
•
lxiv lxv
Triterpene Saponins:
lxii
including Leaky gut
o
Asiatic acid, madecassic acid, centellic acid, centoic acid, asiaticentoic acid
o
Asiaticoside, madecassoside, centelloside , brahmoside, brahminoside,
thankuniside, iso-thankuniside, brahmic acid, isobrahmic acid
•
Glycosides: 3-glucosilquercetin, 3-glucosylkaempferol, 7-glucosylkaempferol
•
Flavonoids: quercetin, kaempferol
•
Volatile Oil:
o
Camphor, cineole
o
Sesquiterpenes: beta-caryophyllene, beta-farnesene, germacrene D
•
Alkaloid: hydrocotyline
•
Bitter principle: vellarine
•
Fatty acid: oleic acid, linoleic acid, palmitic acid, stearic acid and lignoceric acid.
•
Phytosterols: campesterol, sitosterol, and stigmasterol
•
Oligosaccharide: Centellose
•
Vitamin C
•
Beta-carotene lxvi
•
Potassium lxvii
•
Sodium
•
Amino acids
Pharmacology:
Centella’s primary constituents, the triterpene saponins (asiaticoside, madecassoside and
their aglycones asiatic acid, madecassic acid and others) have been most heavily researched
in isolation, are often administered at dose higher than what may be practical in human
subjects. Many of the plant actions are attributed to the Triterpene Fraction (TTF). Overall,
pharmacological research on whole and TTF extracts support Centella’s traditional uses for
venous pathologies, cognitive decline, anxiety, mood enhancement, epilepsy, cancer,
wounds and skin ailments.
Triterpenes are comprised of a 30-carbon skeleton with pentacyclic structure of 5-carbon
isoprene unit building blocks.
lxviii
Saponins are fat soluble, a portion of them are absorbed
into the small intestine while the remaining quantity will pass to the large intestine where
they are transformed by microbes into their aglycone, allowing them to be absorbed into the
blood stream. lxix
A pharmacokinetic examination by Grimaldi et al, found isolated asiaticoside underwent
conversion to asiatic acid in the digestive system. Blood plasma levels of asiatic acid (AA)
peaked five hours after administration (at 30 mg or 60mg dose) in healthy volunteers. Peak
plasma concentrations and half-life values were significantly higher after repeated
administration than those found following single dose. This study found that doses of 60mg
AA had a half-life of 3.40 hours following single dose, compared to 10.28 hours during
seven-day treatment. lxx
Cardiovascular Effects:
The Isolated triterpene saponins of Centella (or Total Triterpene Fraction (TTF)) have been
researched for their use in microangiopathy. Their activity within the vasculature involves
modulation of fluid balance and modulation of collagen synthesis. The triterpenes have been
found to be effective for relieving the signs and symptoms of venous hypertension and
venous insufficiency including edema, pain, cramping, heaviness in the lower extremities
and tiredness.
lxxi lxxii
In addition, TTF caused reversal of alterations in fluid movement, as
seen in the objective assessment of microcirculatory parameters such as capillary
permeability (using laser doppler flowmetry) and transcutaneous oxygen (PO2) and carbon
dioxide
(PCO2). lxxiii
lxxiv
Air
travel
can
cause
complications
for
individuals
with
microangiopahty due to high pressure and stasis, which may increase the risk of
thrombosis. TTF has been studied in subjects with venous diseases during air travel, where
it attenuated microcirculatory alterations and edema. lxxv
The secondary mechanism through which we see TTF working is to heal the lining of the
vasculature. TTF stimulates collagen synthesis and remodeling in and around the venous
wall, leading to stabilization of hypoechoic and low-density carotid plaques. lxxvi These
findings are relevant for reducing the risk of thrombosis and atherosclerosis, as well as for
improvement
of
microcirculatory
parameters
retinopathy, nephropathy and neuropathy).
in
diabetic
microangiopathy
(including
lxxvii lxxviii
Research involving whole plant extracts (alcoholic and aqueous) of Centella asiatica (CA)
was shown to prevent ischemic reperfusion injury following myocardial infarction in rats.
lxxix
Through preventing oxidation of lipids, protein and DNA, CA exerted a cardioprotective
effect in animal models. lxxx While administration was though oral route in these studies, it
exceed the dose ranges relevant for human consumption at 200mg/kg body weight of
aqueous extract and100-1000mg/kg alcoholic extract, respectively.
Nervous System Effects:
Research in animal models suggests whole CA extracts and dried leaf powder confer
neuroprotective
effects
through
modulation
of
neurotransmitter
status
(ie
GABA),
improvement in free radical scavenging activity and enhancement of neuronal branching.
Subsequent improvements in learning and memory are also seen.
Gamma-Aminobutyric acid (GABA) is an inhibitory neurotransmitter in the central nervous
system, increases in GABA availability bring about relaxation and reductions in anxiety. lxxxi
Whole plant extracts of Centella exhibit dose dependent increases in GABA levels in the rat
brain. lxxxii An invitro study found the mechanism by which brain GABA levels were affected
was though CA stimulating Glutamic Acid Decarboxylase (GAD), thereby increasing GABA
concentrations and neurotransmission. lxxxiii
Centella research has focused on possible mechanisms for attenuating age related
neurological changes. Aging causes progressive changes in the antioxidant defense system.
Oral administration of Centella extract to mice caused reductions in oxidative damage as
indicated by lower levels of lipid peroxidation and protein carbonyl oxidation. lxxxiv A 2008
study in animals found dried leaf powder of Centella administered to mice over a four-week
period caused significant reduction in malondialdehyde, reactive oxygen species and
hydroperoxide levels, as well as higher levels of anti-oxidant enzymes throughout the
brain. lxxxv
In addition to modulating neurochemical parameters aqueous CA extracts (dose of 200 and
300mg/kg) have been found to improve learning and memory as indicated by improvement
in proficiency at shuttle box, step through, step down and elevated plus maze paradigms.
lxxxvi
An Indian study found that fresh juice of Centella caused enhanced neuronal growth
(indicated by dendrite length and arborization) in the rat amygdala, as compared to
untreated cohorts, suggesting applicability for neurodegenerative disorders. The dosing
regime was 2,4 and 6mL/kg body weight of juice, this study serves to validate traditional
preparation methods of the plant despite high dose levels. lxxxvii
Neurodegenerative Conditions:
Alzheimer’s Disease (AD) is a neurodegenerative disease characterized by beta-amyloid (βamyloid) protein plaque accumulation, with numerous factors that may contribute to
pathogenesis. lxxxviii Given its traditional use to enhance cognitive function, Centella has been
examined in animal and invitro studies which suggest it relevance for this condition.
Preliminary research in this field has focused on animal and invitro examinations of the antioxidant defense system and β-amyloid plaque processing primarily, with a few studies
examining cholinergic system.
In animal models of Alzheimers Disease, administration of aqueous and powdered (2.5
g/kg/day) Centella extracts attenuate behavioral abnormalities associated with beta-amyloid
plaque, and improve learning. lxxxix
xc
In addition, post-mortem examinations demonstrated
reduction in oxidative stress parameters (glutathione and catalase levels) and significantly
reduced β-amyloid plaque levels.
xci xcii
Many of these actions can be attributed at least in
part to the TTF, which improved cognitive function and increased superoxide dismutase
(SOD) activity in the hippocampus and cortex when administered to animals orally. xciii
Isolated Asiatic acid applied invitro reduced production of β-amyloid protein, prevented
cellular apoptosis in tissue where high levels of beta-amyloid plaque were present, reduced
free radical concentrations and minimized glutamate-induced toxicity.
xciv xcv xcvi
Researchers
found a reduction in levels of β-secretase, which is involved in the production of β-amyloid
proteins and increased ADAM10 (an enzyme involved in processing β-amyloid protein),
suggesting this possible mechanism of action for these changes in brain chemistry. xcvii
Acetylcholinesterase (AcHE) inhibition is the mechanism of action for the majority of the
pharmaceuticals used to manage Alzheimer’s disease. This mechanism is not curative but
does help to manage cholinergic deficit, which is thought to contribute to the pathology.
Isolated triterpene fractions of Centella, (administered via Injection) demonstrated
inhibition of AcHE and improvements in learning and memory as indicated by passive
avoidance testing. xcviii Hydroalcoholic extracts of Centella applied invitro showed 50%
inhibition of AchE activity concentration of 100-150microg/mL, suggesting possible
relevance for managing nervous system changes in AD. xcix
Another mechanism by which Centella may be beneficial to neurodegenerative conditions is
by activity on cyclic AMP response element binding protein (CREB). CREB activity is relevant
to long term memory formation, and is the currently being researched as possible axis for
AD intervention. c Application of Centella extract invitro enhanced phosporylation of CREB in
both healthy cortical cells and neuroblastoma cell lines expressing β-amyloid. The study
suggests that increasing availability of CREB may be one mechanism of action by which
Centella extracts modulate cell signal transmission. ci
Epilepsy
Research in Epilepsy has been restricted to animal and invitro studies, further studies are
needed to determine the usefulness of Centella in seizure disorders at appropriate dose
ranges for human subjects. In rat models of epilepsy, animals treated with Centella orally
(at 200mg/kg and 300mg/kg body weight) showed increased levels of AcH and a reduction
in AcHesterase after the seizures compared to placebo. These studies suggest that AcH
sparing cholinergic modulation may contribute to the anti-convulsant activity of this plant,
supporting its use in minimizing cognitive damage caused by epileptic seizure. cii
ciii
Integumentary Effects:
Wounds, burns and keloids
Oral and topical applications of TTF of Centella (as cream) advance speed and quality of
wound healing and reduce both scaring and keloid formation. civ Centella’s wound healing
effects have been demonstrated in human subjects, a randomized placebo-controlled study
of diabetic wound patients (N=200) orally administered 100 mg asiaticoside three times per
day showed improved granulation tissue formation and reduced scaring. cv This activity is
attributed to isolated asiaticoside and madecassoside which stimulate Type I collagen
production in human cell cultures. cvi Animal research using Oral and topical administration
routes for whole Centella alcoholic extracts in both healthy and delayed healing (diabetic)
models saw faster rates of wound epithelialisation, wound contraction and increases in
tensile strength compared to controls.
cvii
cviii
Isolated TTF used in animal burn wounds
showed similar benefit with improvement of anti-oxidant activity, promotion of collagen
synthesis and angiogenesis. cix
cx
Finally, Centella has relevance for fibroproliferative
disorders such as keloid. An invitro study found it to prevent keloid formation through
inhibition of Transforming Growth Factor-β1 (TGF-β1) induced collagen synthesis and
Plasminogen activator inhibitor-1 (PAI-1) expression in keloid fibroblasts. cxi
Scleroderma
Isolated madecassol used orally and topically as ointment over 6 months reduced the
symptoms of scleroderma as indicated by reduction in hyperpigmentation, vascular trophic
disorder and number of lesions. cxii
Allergies and Pruritis
Animal modeling has shown high doses of CA extracts exhibit anti-allergic and anti-pruritic
activity to the skin. CA extracts (alcoholic and aqueous) inhibited mast cell degranulation,
reduced itching and exhibited anti-inflammatory activity comparable to ibuprophen.
Mechanisms are thought to involve the inhibition of enzymes such as protein kinase C,
protein tyrosine kinase and phospholipase A2, as well as lipoxogenase and cyclooxygenase,
which
contribute
biosynthesis.
to
pro-inflammatory
signaling
pathways
seen
in
prostaglandin
cxiii
Musculoskeletal Effects:
Animal models using TTF found benefit for degenerative joint conditions including
Rheumatoid and Osteoarthritis. cxiv One study demonstrated the inhibition of Nitric Oxide
(NO) production, and subsequent reduction in osteoarthritic cartilage degradation. cxv
Researchers have found modulation of both humoral and cellular-mediated immunity by
Madecassoside
to
contribute
to
this
anti-inflammatory
activity. cxvi
Madecassoside
administered orally to mice in arthritic model demonstrated reduced levels of infiltration of
inflammatory cells to the joint, reduced synovial hyperplasia, and lowered IgG levels,
thereby preventing joint destruction. cxvii
Immune System effects:
Preliminary research invitro and invivo has shown Centella extracts are anti-proliferative
and chemoprotective. Centella extracts demonstrate dose dependent inhibition of cancerous
human cell lines of the breast, colon and skin (melanoma).
cxviii cxix cxx
Modulation of certain
apoptosis regulating enzymes including Bax, Bcl-2 and caspase-3, as well as generation of
Reactive Oxygen Species are suggested mechanisms for these actions.
cxxi
In addition,
administration of CA extracts orally to animals exposed to radiation caused a reduction in
radiation-induced damage to DNA cxxii, suggesting further relevance of this plant during
radiation therapy.
Furthermore, invitro research has highlighted TTF’s anti-inflammatory activity through
chemical signaling. These isolated extracts inhibit production of nitric oxide (NO),
Prostaglandin E(2) (PGE(2)), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta
(IL-1beta) , IL-6 and cyclooxygenase-2 (COX-2). TTF inhibited activation of Nuclear FactorKappa B (NF-kappaB), and caused subsequent blocking of p65 protein translocation to the
cell nucleus. cxxiii These studies suggest its relevance for cancer therapy and to support
healthy tissue.
Clinical Trials:
This section includes research using whole plant extracts of Centella, excluding studies using
it in combination or using the isolated triterpene fraction (TTF). Clinical research using
whole Centella extracts are limited, and the available trials all have small sample size.
Research in human subjects involving cancer and venous pathologies has not been
performed, but given the usefulness of this plant in invitro and invivo applications, this area
should be explored.
Anxiolytic Effects:
Two small clinical trials support Centella’s use to attenuate anxiety. Given the positive
results from the research more large-scale studies are warranted. A small clinical trial of 33
subjects with Generalized Anxiety Disorder (GAD) were administered 500mg capsules
2x/day (of 70% hydro-ethanolic extract) of Centella asiatica (CA). They found significant
improvement in anxiety levels (indicated by standard questionnaires), as well as reductions
in stress and depression, and improved cognition. cxxiv
Centella’s anxiolytic activity was
examined in a double, blind placebo controlled study which assessed of forty healthy
subjects. Subjects received 12g/day of Gotu Kola daily and found reduced anxiety levels as
demonstrated by acoustic startle response compared to placebo. cxxv
Cognitive effects:
In a small, randomized double-blind, placebo controlled clinical trial, the effect of Centella
was examined on age-related decline in 28 health elderly subjects over the course of 2
months. Use of the highest doses of 750 mg Centella/day was found to be useful for both
improving working memory and improving mood. cxxvi
Cognitive effects in neurodegenerative models:
Clinical trials for use of CA in Alzheimer’s disease or other existing neurodegenerative
conditions are presently lacking. The only such study had a limited sample size of 6
individuals, ages 65 and above, with mild cognitive impairment (MCI). Subjects used
1000mg/day of Centella powder over a 6-month period and experienced improvement in
mental well-being, sleep quality, and reductions in depression. cxxvii
Safety Issues: cxxviii
Centella’s long held traditional use as a vegetable, and the current scientific literature both
attest to the safety of this herb.
cxxix cxxx cxxxi cxxxii
Side affects may include irritation topically
on open wounds or inflamed mucus membranes within the digestive system (ie. GERD). In
particular, topical application has the potential to cause rare cases of allergic contact
dermatitis in sensitive individuals, cxxxiii the reaction is believed to be due to Medecassol. cxxxiv
The isolated triterpene fraction is generally well tolerated, though it may cause skin
irritation or gastric upset.
cxxxvcxxxvi
High doses are well tolerated in animals, in mice
receiving 2.5g/kg dried plant orally showed no adverse affects.
cxxxvii
Centella is categorized by the FDA as Pregnancy Category B1, meaning limited applications
in women have shown no harmful effects on the fetus, and animal studies show similar
results. It is compatible with breastfeeding (Lactation Category C). Centella is considered
safe for use in children.
Preparation and Dosage:
Herbalist Todd Caldecott:
Fresh Juice (svarasa): 25mL BID-TID
Powder (Curna): 3-10g BID-TID
Tincture : fresh 1:2 95% ETOH; dry 1:3 50% ETOH
1-5mL BID-TID
Infusion (Phanta): 30-120mL BID-TID
Nasya oil: 2gtt for nervous system disorders
Herbalist Larken Bunce: cxxxviii
Tincture: Dry 1:2 30-35% ETOH
3-4mL of a 15mL Formula
For surgical healing, up to three-weeks pre and post-operatively: 7.5mL/day
Tea for soft injury of anxiety: 2-5g/day
Topical: Salve containing Centella infused oil or 3mL tincture in cream preparation
Herbalists Simon Mills and Kerry Bone: cxxxix
Tincture: 1:2, 30% ETOH , 3-6 mL/day
Tea Infusion: 1.8 g/day dried aerial parts
Triterpene Fraction (TTF):
60-180mg/day (approximately equivalent to 2.5-7 g/day of dried herb)
Herbalist Donald Yance:
cxl
Tincture: 1:1 fluid extract, 3-8mL/day
Tea infusion: 3-8g/day
Standardized Triterpene Extract: 150-1,000mg/day powder
KPS Khalsa and Michael Tierra: cxli
Fresh juice: 1-4 tsp, taken in the morning
Whole fresh herb cooked or raw in salad
Tea infusion:
For acute skin disease: 1-2 oz dried herb daily
For inflammatory skin disorders 1-3 oz dried herb daily
Capsule: 1 capsule/day as rejuvenating tonic
Nasya preparation with ghee:
For Nervous system disorders: 2 drops in each nostril several times daily
Chinese Herbal Medicine: Materia Medica: cxlii
Dried herb: 12-30 g
Combinations and Similar Herbs:
For eczema: viola, Oregon grape root and gotu kola. cxliii
For poorly healing wounds: calendula, echinacea and gotu kola.
For dry thinning hair with He Shou Wu. cxliv
Miscellaneous Facts:
First recorded writing about Centella was in the Divine Husbandman’s Classic Materia
Medica, the earliest Chinese pharmacopeia dated to 2698 BC. cxlv
i
Mills, Simon and Kerry Bone. The Essential Guide to Herbal Safety. Elsevier: St. Louis,
Missouri, 2005. 450-453.
ii
Nadkarni, KM (ed.) Indian Materia Medica, Volume One. Bombay: Popular Prakshan PVT.
LTD. (Twin Lakes, WI: Lotus Light Publications, 2006.)
iii
Bensky D, Clavey S, Stoger E, Gamble A. Chinese Herbal Medicine Materia Medica (3rd ed).
Eastland Press: Seattle, 2004.
iv
Flora of China. Volume 14 Page 18. Centella asiatica [Online Database]
http://www.efloras.org/florataxon.aspx?flora_id=2&taxon_id=200015478 Accessed
November 24, 2013.
v
Gleason HA and Cronquist A. Manual of Vascular Plants of Northeastern United States and
Adjacent Canada [2nd Ed]. New York Botanical Garden: New York, 1991.
vi
Flora of China. Volume 14 Page 18. Centella asiatica [Online Database]
http://www.efloras.org/florataxon.aspx?flora_id=2&taxon_id=200015478 Accessed
November 24, 2013.
vii
Flora of Pakistan Centella asiatica [Online Database]
http://www.efloras.org/florataxon.aspx?flora_id=2&taxon_id=200015478 Accessed
November 24, 2013.
viii
Bensky D, Clavey S, Stoger E, Gamble A. Chinese Herbal Medicine Materia Medica (3rd
edition). Seattle: Eastland press, 2004.
ix
Mills, Simon and Kerry Bone. The Essential Guide to Herbal Safety. Elsevier: St. Louis,
Missouri, 2005. 450-453
x
Herba Centellae. World Health Organization Mongraphs on selected medicinal plants
Volume 1. 1999. 295 pgs. [Online database]
http://apps.who.int/medicinedocs/en/d/Js2200e/10.html accessed November 24, 2013.
xi
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xii
Bunce, L. Gotu Kola Materia Medica Lecture October, 2012, Vermont Center for
Integrative Herbalism.
xiii
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xiv
Ibid
xv
Ibid
xvi
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
xvii
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xviii
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
xix
Van Loon, G (Ed.) Charaka Samhita Volume 1 (600-800AD). Chaukhambha Orientalia
Publishers, 2003.
xx
Bensky D, Clavey S, Stoger E, Gamble A. Chinese Herbal Medicine Materia Medica (3rd Ed)
Eastland Press: Seattle, 2004.
xxi
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
xxii
Jana U, Sur TK, Maity LN, Debnath PK, Bhattacharyya D. A clinical study of the
management of generalized anxiety disorder with Centella asiatica. Nepal Medical Coll J.
2010 Mar; 12(1): 8-11.
xxiii
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xxiv
Jana U, Sur TK, Maity LN, Debnath PK, Bhattacharyya D. A clinical study of the
management of generalized anxiety disorder with Centella asiatica. Nepal Medical Coll J.
2010 Mar; 12(1): 8-11.
xxv
Van Loon, G (Ed.) Charaka Samhita Volume 1 (600-800AD). Chaukhambha Orientalia
Publishers, 2003.
xxvi
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xxvii
Van Loon, G (Ed.) Charaka Samhita Volume 1 (600-800AD). Chaukhambha Orientalia
Publishers, 2003.
xxviii
xxix
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
Tiwari S, Singha S, Patwardhan K, Gehlot S, Gambhira IS. Effect of Centella asiatica on
Mild Congnitive Impairment (MCI) and other Common Age-related Clinical Problems. Digest
Journal of Nanomaterials and Biostructures 2008 Dec: 3(4) 215-220.
xxx
Wattanathorn J, Mator L, Muchimapura S, Tongun T, Pasuriwong O, PIyawatkul N, Yimtae
K, Sripanidkulchai B, Singkhoraard J. Positive modulation of cognition and mood in the
healthy elderly volunteer following the administration of Centella asiatica. Journal of
Ethnopharmacology. 2008 Mar 5; 116(2):325-32.
xxxi
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xxxii
Ibid
xxxiii
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
xxxiv
Khalsa KPS, Tierra M. The way of Ayurvedic Herbs: A Contemporary Introduction and
Useful Manual for the World’s Oldest Healing System. Lotus Press: Twin Lakes, WI, 2008.
xxxv
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xxxvi
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
xxxvii
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xxxviii
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
xxxix
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
xl
Grieve M and Leyel CF [Ed] A Modern Herbal. Tiger Books International: London, 1998.
xli
Pizzorno JE, Murray MT, Joiner-Bey H. The Clinician’s Handbook of Natural Medicine [2nd
ed]. Elsevier: St. Louis, MI, 2008.
xlii
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
xliii
Pizzorno JE, Murray MT, Joiner-Bey H. The Clinician’s Handbook of Natural Medicine [2nd
ed]. Elsevier: St. Louis, MI, 2008.
xliv
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
xlv
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
xlvi
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
xlvii
Grieve M and Leyel CF [Ed] A Modern Herbal. Tiger Books International: London, 1998.
xlviii
Khalsa KPS, Tierra M. The way of Ayurvedic Herbs: A Contemporary Introduction and
Useful Manual for the World’s Oldest Healing System. Lotus Press: Twin Lakes, WI, 2008.
xlix
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
l
Grieve M and Leyel CF [Ed]. A Modern Herbal. Tiger Books International: London, 1998.
li
Bensky D, Clavey S, Stoger E, Gamble A. Chinese Herbal Medicine Materia Medica [3rd ed].
Eastland press: Seattle, 2004.
lii
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
liii
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
liv
Grieve M and Leyel CF [Ed] A Modern Herbal. Tiger Books International: London, 1998.
lv
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
lvi
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
lvii
Wood, M. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants. North
Atlantic Books: Berkley, CA, 2008.
lviii
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
lix
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
lx
Grieve M and Leyel CF [Ed] A Modern Herbal. Tiger Books International: London, 1998.
lxi
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
lxii
Caldecott, T. Ayurveda: The Divine Science of Life. Elsevier: New York, 2006.
lxiii
Pizzorno JE, Murray MT, Joiner-Bey H. The Clinician’s Handbook of Natural Medicine [2nd
ed]. Elsevier: St. Louis, MI, 2008.
lxiv
Dr. James Duke’s Phytochemical and Ethnobotanical Databases. [Onilne Database]
http://www.ars-grin.gov/cgi-bin/duke/farmacy2.pl Accessed 20 November 2013.
lxv
Yance D. Adaptogens in Medical Herbalism. Healing Arts Press: Rochester, VT, 2013.
lxvi
Brinker F. Herb Contraindications and Drug interactions [3rd Ed]. Ecclectic Medical
Publications: Sandy, OR, 2001.
lxvii
Ibid
lxviii
Ganora, Lisa. Herbal Constituents: Foundations of Phytochemistry. Herbalchem Press:
Louisville, CO, 2009.
lxix
Mills, S and K. Bone. Principles and Practice of Phytotherapy: Modern Herbal Medicine.
Churchill Livingstone: New York, 2000. p24.
lxx
Grimaldi R, De Ponti F, D’Angelo L, Caravaggi M, Guidi G, Lecchini S, Frigo GM, Crema A.
Pharmacokinetics of the total triterpenic fraction of Centella asiatica after single and multiple
dose administrations to healthy volunteers. A new assay for Asiatic acid. J Ethnopharmacol.
1990 Feb; 28(2)235-41.
lxxi
Belcaro GV, Rulo A, Grimaldi R. Capillary filtration and ankle edema in patients with
venous hypertension treated with TTFCA. Angiology. 1990 Jan; 41(1):12-18.
lxxii
Pointel JP, Boccalon H, Cloarec M, Ledevahat C, Joubert M. Titrated extract of Centella
Asiatic (TECA) in the treatment of venous insufficiency of the lower limbs. Angiology. 1987
Jan;38(1 Pt 1):46-50.
lxxiii
Incandela L, Belcaro G, De Sanctis MT, Cesarone MR, Griffin M, Ippolito E, Bucci M
Cacchio M. Total triterpenic fraction of Centella asiatica in the treatment of venous
hypertension: a clinical, prospective, randomized trial using a combined microcirculatory
model. Angiology. 2001 Oct;52 Suppl 2:S61-7.
lxxiv
Belcaro GV, Grimaldi R, Guidi G. Improvement of Capillary permeability in patients with
venous hypertension after treatment with TTFCA. Angiology. 1990 Jul;41(7):533-40.
lxxv
Cesarone MR, Incandela L, De Sanctis MT, Belcaro G, Geroulakos G, Griffin M, Lennox A,
Di Renzo AD, Cacchio M, Bucci M. Flight microangiopathy in medium- to long-distance
flights: prevention of edema and microcirculation alterations with total triterpenic fraction of
Centella asiatica. Angiology. 2001 Oct;52 Suppl 2:S33-7.
lxxvi
Incandela L, Belcaro G, Nicolaides AN, Cessarone MR, De Sanctis MT, Corsi M, Bavera P,
Ippolito E, Griffin M, Geroulakos G, Sebetai M, Ramaswami G, Veller M. Modification of the
echogenicity of femoral plaques after treatment with total triterpenic fraction of Centella
asiatica: a prospective, randomized, placebo-controlled trial. Angiology. 2001 Oct;52 Suppl
2:S69-73.
lxxvii
Incandela L, Cesarone MR, Cacchio M, De Sanctic MT, Santavenere C, D’Auro MG, Bucci
M, Belcaro G. Total triterpenic fraction of Centella asiatica in chronic venous insufficiency
and in high-perfusion microangiopathy. Angiology. 2001 Oct;52 Suppl 2:S9-13.
lxxviii
Cesarone MR, Incandela L, De Sanctis MT, Belcaro G, Bavera P, Bucci M, Ippolito E.
Evaluation of treatment of diabetic microangiopathy with total triterpenic fraction of Centella
asiatica: a clinical prospective randomized trial with a microcirculatory model. Angiology.
2001 Oct;52 Suppl 2:S49-54.
lxxix
Pragada PR, Veeravalli KK, Chowdary KP, Routhu KV. Cardioprotective activity of
Hydrocotyle asiatica L. in ischemia-reperfusion induced myocardial infarction in rats. J
Ethnopharmacol. 2004 Jul;93(1):105-8.
lxxx
Gnanapragasam A, Yogeeta S, Subhashini R, Ebenezar KK, Sathish V, Devaki T.
Adriamycin induced myocardial failure in rats: protective role of Centella asiatica. Mol Cell
Biochem. 2007 Jan;294(1-2):55-63. Epub 2006 Jun 20.
lxxxi
Streeter C et al. Effects of Yoga Versus Walking on Mood, Anxiety, and Brain GABA
Levels: A Randomized Controlled MRS Study. J Altern Complement Med. 2010 November:
16(11):1145-1152.
lxxxii
Chatterjee TK, Chakraborty A, Pathak M, Sengupta GC. Effects of plant extract Centella
asiatica (Linn.) on cold restraint stress ulcer in rats. Indian Journal of Experimental Biology.
1992 Oct; 30(10):889-91.
lxxxiii
Awad R, Levac D, Cybulska P, Merali Z, Trudeau VL, Arnason JT. Effects of traditionally
used anxiolytic botanicals on enzymes of the gamma-aminobutyric acid (GABA) system.
Canadian Journal of Physiol Pharmacol. 2007 Sep; 85(9):933-42.
lxxxiv
Subathra M, Shila S, Devi MA, Panneerselvam C. Emerging role of Centella asiatica in
improving age-related neurological anti-oxidant status. Exp Gerontol. 2005 Aug-Sep; 40(89): 707-15.
lxxxv
Shinomol GK, Muralidhara. Effect of Centella asiatica leaf powder on oxidative markers
in brain regions of prepubertal mice in vivo and its in vitro efficacy to ameliorate 3-NPAinduced oxidative stress in mitochondria. Phytomedicine. 2008 Nov;15(11):971-84.
lxxxvi
Veerendra Kumar MH, Gupta YK. Effect of different extracts of Centella asiatica on
cognition and markers of oxidative stress in rats. Journal of Ethnopharmacology. 2002
Feb;79(2):253-60.
lxxxvii
Mohandas Rao KG, Muddanna Rao S, Gurumadhya Rao S. Enhancement of Amygdaloid
Neuronal Dendritic Arborization by Fresh Leaf Juice of Centella asiatica (Linn) During Growth
Spurt Period in Rats. Evid Based Complement Alternat Med. 2009 Jun;6(2):203-10.
lxxxviii
Patil SP, Maki S, Khedkar SA, Rigby AC, Chan C. Withanolide A and Asiatic acid
Modulate Multiple Targets Associated with Amyloid-beta precursor protein processing and
amyloid-beta protein clearance. J Nat Prod. 2010 Jul23:73(7):1196-202.
lxxxix
Soumyanath A, Zhong YP, Henson E, Wadsworth T, Bishop J, Gold BQ, Quinn JF.
Centella asiatica Extract Improves Behavioral Deficits in a Mouse Model of Alzheimer’s
Disease: Investigation of a Possible Mechanism of Action. Int J Alzheimers Dis. 2012:
2012:381974.
xc
Veerendra Kumar MH, Gupta YK. Effect of Centella asiatica on cognition and oxidative
stress in an intracerebroventricular streptozotocin model of Alzheimer’s disease in rats. Clin
Exp Pharmacol Physiol. 2003 May-Jun:30(5-6):336-42.
xci
Ibid
xcii
Dhanasekaran M, Holcomb LA, Hitt AR, Tharakan B, Porter JW, Young KA, Manyam BV.
Centella asiatica extract selectively decreases amyloid beta levels in hippocampus of
Alzheimer’s disease animal model. Phytotherapy research. 2009 Jan;23(1):14-9.
xciii
Xu MF, Xiong YY, Liu JK, Qian JJ, Zhu L. Asiatic acid, a Pentacyclic triterpene in Centella
asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y
cells. J Acta Pharmacol Sin. 2012 May; 33(5):578-87.
xciv
Mook-Jung I, Shin JE, Yun SH, Huh K, Koh JY, Park HK, Jew SS, Jung MW. Protective
effects of asiaticoside derivatives against beta-amyloid neurotoxicity. J Neurosci Res. 1999
Nov 1:58(3):417-25.
xcv
Lee MK, Kim SR, Sung SH, Lim D, Kim H, Choi H, Park HK, Je S, Ki YC. Asiatic acid
derivatives protect cultured cortical neurons from glutamate-induced excitotoxicity. Res
Commun Mol Pathol Pharmacol. 2000 Jul-Aug;108(1-2):75-86.
xcvi
Xu MF, Xiong YY, Liu JK, Qian JJ, Zhu L. Asiatic acid, a Pentacyclic triterpene in Centella
asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y
cells. J Acta Pharmacol Sin. 2012 May; 33(5):578-87.
xcvii
Patil SP, Maki S, Khedkar SA, Rigby AC, Chan C. Withanolide A and Asiatic acid Modulate
Multiple Targets Associated with Amyloid-beta precursor protein processing and amyloidbeta protein clearance. J Nat Prod. 2010 Jul23:73(7):1196-202.
xcviii
Nasir MN, Abdullah J, Habsah M, Ghani RI, Rammes G. Inihibitory effect of Asiatic acid
on acetylcholinesterase, excitatory post synaptic potential and locomotor activity. 2012 Feb
15; 19(3-4):311-6.
xcix
Mukherjee PK, Kumar V, Houghton PJ. Screening of Indian Medicinal Plants for
Acetylcholinesterase inhibitory activity. Phytoterapy Research 2007 Dec: 21(12):1142-5.
c
Silva J, Kogan J, Frankland P, Kida S. CREB and Memory. Annual Review of Neuroscience.
1998: 21: 127-148.
ci
Xu Y, Cao Z, Khan I, Luo Y. Gotu Kola (Centella Asiatica) extract enhances
phosphorylation of cyclic AMP response element binding protein in neuroblastoma cells
expressing amyloid beta peptide. J Alzhiemers Dis. 2008 Apr;13(3):341-9.
cii
Gupta YK, Veerendra Kumar MH, Srivastava AK. Effect of Centella asiatica on
pentylenetetrazole-induced kindling, cognition and oxidative stress in rats. 2003
Feb;74(3):579-85.
ciii
Visweswari G, Prasad KS, Chetan PS, Lokanatha V, Rajendra W. Evaluation of the
anticonvulsant effect of Centella asiatica (gotu kola) in pentylenetetrazol-induced seizures
with respect to cholinergic neurotransmission. Epilepsy Behav. 2010 Mar;17(3):332-5.
civ
Bosse JP, Papillon J, Frenette G, Dansereau J, Cadotte M, Le Lorier J. Clinical study of a
new antikeloid agent. Ann Plast Surg. 1979 Jul;3(1):13-21.
cv
Paocharoen V. The efficacy and side effects of oral Centella asiatica extract for wound
healing promotion in diabetic wound patients. J Med Assoc Thai. 2010 Dec;93 Suppl
7:S166-70.
cvi
Bonte R, Dumas M, Chaudagne C, Meybeck A. Comparative activity of asiaticoside and
madecassoside on type I and III collagen synthesis by cultured human fibroblasts. Ann
Pharm Fr. 1995;53(1):38-42.
cvii
Suguna L, Sivakumar P, Chandrakasan G. Effects of Centella asiatica extract on dermal
wound healing in rats. Indian J Exp Biol 1996;34:1208-1211.
cviii
Shukla A, Rasik AM, Jain GK, et al. In vitro and in vivo wound healing activity of
asiaticoside isolated from Centella asiatica. J Ethnopharmacol 1999;65:1-11.
cix
Wu F, Bian D, Zia Y, Gong Z, Tan Q, Chen J, Dai Y. Identification of Major Active
Ingredients Responsible for Burn Wound Healing of Centella asiatica Herbs. Evid Based
Complement Alternat Med. 2012;2012:848093
cx
Liu M, Dai Y, Li Y, Luo Y, Huang F, Gong Z, Meng Q. Madecassoside isolated from Centella
asiatica herbs facilitates burn wound healing in mice. Planta Med. 2008 Jun;74(8):809-15.
cxi
Bian D et al. Asiatic Acid Isolated from Centella Asiatica Inhibits TGF-β1-induced Collagen
Expression in Human Keloid Fibroblasts via PPAR-γ Activation. Int J Biol Sci. 2013 Oct
25;9(10):1032-42.
cxii
Guseva NG, Starovoitova MN, Mach ES. Madecassol treatment of systemic and localized
scleroderma. Ter Arkh 1998: 70(5):58-61.
cxiii
George M et al. Anti-allergic, Anti-Pruritic, and Anti-inflammatory Activities of Centella
Asiatica Extracts. Afr J Tradit Complementary Altern Med. 2009; 6(4):554-559.
cxiv
Yang CL et al. Scientific Basis of Botanical Medicine as Alternative Remedies for
Rheumatoid Arthritis. Clin Rev Allergy Immunol. 2013 Jun;44(3):284-300.
cxv
Hartog A, Smit HF, van der Kraan PM, Hoijer MA, Garssen J. In vitro and in vivo
modulation of cartilage degradation by a standardized Centella asiatica fraction. Exp Biol
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cxvi
Punturee K et al. Immunomadulatory activities of Centella asiatica and Rhinacanthus
nasutus extracts. Asian Pac J Cancer Prev. 2005 Jul-Sep;6(3):396-400.
cxvii
Liu M et al. Anti-rheumatoid arthritic effect of madecassoside on type II collagen-
induced arthritis in mice. Int Immunopharmacol. 2008 Nov;8(11):1561-6.
cxviii
Babykutty S et al. Apoptosis Induction of Centella Asiatica on Human Breast Cancer
Cells. Afr J Tradit Complement Altern Med. 2009; 6(1):9-16.
cxix
Bunpo P et al. Centella Asiatica Extract Induces Cell Cycle Arrest in Caco-2 Human Colon
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cxx
Park BC et al. Asiatic Acid Induces Apoptosis in SK-MEL-2 Human Melanoma cells. Cancer
Lett. 2005 Jan 31; 218(1):18-90.
cxxi
Ibid
cxxii
Joy J and Nair CK. Protection of DNA and Membranes from gamma-radiation induced
damages by Centella asiatica. J Pharm Pharmacol.2009 Jul;61(7):941-7.
cxxiii
Won J.H., Shin J.S., Park H.J., Jung H.J., Koh D.J., Jo B.G., Lee J.Y., Yun K., and Lee
K.T., 2010, Anti-inflammatory effects of madecassic acid via the suppression of NF-kappaB
pathway in LPS-induced RAW 264.7 macrophage cells. Planta Medica: 76, 251–257
cxxiv
Jana U, Sur TK, Maity LN, Debnath PK, Bhattacharyya D. A clinical study of the
management of generalized anxiety disorder with Centella asiatica. Nepal Medical Coll J.
2010 Mar; 12(1): 8-11.
cxxv
Bradwejn J, Zhou Y, Kzycki D, Shlik J. A double-blind, placebo-controlled study on the
effects of Gotu Kola (Centella asiatica) on acoustic startle response in healthy subjects.
Journal of Clinical Psychopharmacology 2000 Dec; 20 (6):680-4.
cxxvi
Wattanathorn J, Mator L, Muchimapura S, Tongun T, Pasuriwong O, PIyawatkul N,
Yimtae K, Sripanidkulchai B, Singkhoraard J. Positive modulation of cognition and mood in
the healthy elderly volunteer following the administration of Centella asiatica. Journal of
Ethnopharmacology. 2008 Mar 5; 116(2):325-32.
cxxvii
Tiwari S, Singha S, Patwardhan K, Gehlot S, Gambhira IS. Effect of Centella asiatica on
Mild Congnitive Impairment (MCI) and other Common Age-related Clinical Problems. Digest
Journal of Nanomaterials and Biostructures 2008 Dec: 3(4) 215-220.
cxxviii
Mills, Simon and Kerry Bone. The Essential Guide to Herbal Safety. Elsevier: St. Louis,
Missouri, 2005. p450-453.
cxxix
Van Loon, G (Ed.) Charaka Samhita Volume 1 (600-800AD). Chaukhambha Orientalia
Publishers, 2003.
cxxx
Khalsa KPS, Tierra M. The way of Ayurvedic Herbs: A Contemporary Introduction and
Useful Manual for the World’s Oldest Healing System. Lotus Press: Twin Lakes, WI, 2008
cxxxi
Jana U, Sur TK, Maity LN, Debnath PK, Bhattacharyya D. A clinical study of the
management of generalized anxiety disorder with Centella asiatica. Nepal Medical Coll J.
2010 Mar; 12(1): 8-11.
cxxxii
Wattanathorn J, Mator L, Muchimapura S, Tongun T, Pasuriwong O, PIyawatkul N,
Yimtae K, Sripanidkulchai B, Singkhoraard J. Positive modulation of cognition and mood in
the healthy elderly volunteer following the administration of Centella asiatica. Journal of
Ethnopharmacology. 2008 Mar 5; 116(2):325-32.
cxxxiii
Hausen BM. Centella asiatica (Indian pennywort), an effective therapeutic but a weak
sensitizer. Contact Dermatitis. 1993 Oct;29(4):175-9.
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Acorus calamus and Acorus americanus
Rebecca Dalgin
NOMENCLATURE
Botanical Nomenclature
Acorus calamus, Acorus americanus
Botanical Family
Acoraceae
Taxonomic
Distinctions
of
North
American
Population
Among botanists there has been debate as to
the taxonomical and botanical differentiation
among
Acorus
species
in
North
America.
Generally Acorus calamus (more specifically
differentiated as A. calamus var. americanus,
the diploid (2n) phenotype) or A. americanus have been used to refer to all Acorus species
in North America. While there is still confusion perpetuated in much of the literature, the
Flora of North America, published in 2000, is the first flora to clearly define two separate
morphologically distinct Acorus species: A. calamus, an introduced sterile triploid and A.
americanus, a native fertile diploid. Both species exist in North America (Thompson
2000:125).
Sub Species of A. Calamus
The species A. calamus is divided into phenotypes identified by the number of chromosomal
pairs contained in the DNA. Subspecies generally occur in different distribution areas. Much
of the literature refers to the diploid (2n) variety as A. calamus var. americanus. At present,
A. calamus var. americanus is often considered synonymous with A. americanus. The latter
is a distinctly diploid species (Thompson 2000:124) while A. calamus, found in North
America, Europe, temperate India and the Himalayan region, is triploid (Motley 1994). The
issues is further complicated as the A. calamus population in Asia does have a diploid
phenotype morphologically distinct from the North American diploid A. americanus
(Thompson 2000:124). This diploid is still classified as A. calamus. There is also a tetraploid
(4n) variety, A. calamus var. angustatus, found in Eastern and Tropical Southern Asia
(Motley 1994) as well as the hexaploid (6n) variety from the Kashmir area (Small and
Catling 1999:15). The differences among varieties are significant as they are associated
with different levels of chemical constituents resulting in variance of medicinal actions and
safety profile.
Species, Phenotype, and Distribution
Species
Phenotype
Sub Species Name
A. calamus
Diploid (2n)
Formerly
A.
calamus
Distribution
var. Asia
americanus
Triploid (3n)
A. calamus var. calamus
North
from
America
(introduced
Europe),
Europe,
temperate India, Himalayan
region
Tetraploid (4n)
A. calamus var. angustus
Eastern
and
tropical
Southern Asia
Hexaploid (6n)
A.
Diploid (2n)
americanus
Kashmir area
Formerly
A.
calamus
var. North
americanus
Common Names
English: Sweet Flag, Calamus
Cheyenne: wi'ukh is e'evo (bitter medicine)
Hudson Bay Cree: pow-e-men-arctic (fire or bitter pepper root)
Penobscot and Nanticoke: muskrat root
Pawnee: kahtsha itu (medicine lying in water)
Ayurvedic Tradition: Vacha
Chinese Medicine: shui chang pú (watery flourishing weed)
America
potentially Siberia
(native),
Definition/Part Used
Calamus consists of dried or fresh unpeeled rhizomes and roots of Acorus calamus or Acorus
americanus.
HABITAT
Habitat
Both A. calamus and A. americanus species grow in wet open areas, marshes, swales, and
along edges of quite water (Thompson 2000:126-127).
Companions and Role in Ecology
Calamus is often found growing among Blue Flag, Cattails and other wetland plants.
Muskrats are often found to be in the vicinity. It has even been speculated that the musk
scent they produce is due to the large quantities of Acorus they ingest. In her dissertation,
Thompson discusses the relationship between Acorus, muskrats, and humans. There seems
to be “a closely linked ecological relationship between Native Americans trapping muskrats
and using Acorus, muskrats eating Acorus, and Acorus. Muskrat feeding habits may in part
be responsible for the dispersal of Acorus, and Native American may have intentionally
planted Acorus both for their own medicinal use and to ensure food for the muskrat, which
was economically valuable to them (Morgan 1980). Thus, the many Native American names
for Acorus, which involve muskrat as a root word, may reflect an important economic and
ecological relationship among man, plants, and other wildlife” (Thompson 1995, 450).
Distribution and Range
There is some debate as to the origin of Acorus. Originally A. calamus was most likely native
to southern Asia spreading widely through the continent and then introduced and
naturalized in Europe and North America. Thompson proposes that A. americanus, the
distinctly fertile diploid species of North America, is related to A. calamus but has a long
portion of its history where it evolved separately (Thompson 1995; 385). The A. calamus
species in North America stem from a few initially introduced individuals (Thompson 1995;
414).
A. americanus range: Alta., B.C., Manitoba, N.B., Newfoundland, Labrador, N.W.T., N.S.,
Ontario, P.E.L., Quebec, Saskatchewan, Alaska, Connecticut, D.C., Idaho, Illinois, Indiana,
Iowa, Maine, Massachusetts, Michigan, Minnesota, Montana, Nebraska, New Hampshire,
New Jersey, New York, North Dakota, Ohio, Pennsylvania, Rhode Island, South Dakota,
Vermont, Virginia, Washington, Wisconsin, potentially central Siberia (Thompson 2000;
127).
A. calamus range: N.B., N.S., Ontario, Quebec, Alaska, Arkansas, California, Colorado,
Connecticut, Delaware, C.D., Georgia, Illinois, Indiana, Iowa, Kansas, Kentucky, Louisiana,
Maine, Maryland, Massachusetts, Michigan, Minnesota, Missouri, Nebraska, New Hampshire,
Hew Jersey, New York, North Carolina, Ohio, Oklahoma, Oregon, Pennsylvania, Rhode
Island, South Carolina, South Dakota, Tennessee, Texas, Vermont, Virginia, West Virginia,
Wisconsin, Europe, Asia, Africa, Indian Ocean Islands, Pacific Islands (Thompson 2000;
126).
BOTANICAL IDENTIFICATION
Botanical Identification: Shared Characteristics for A. calamus L. and A. americanus
General: Herbaceous, perennial, rhizomatous.
Leaves: Basal, not differentiated into petiole and blade, bases are sheathed, white and
colored with pink or red, remainder of leaf bright green, sword shaped, parallel venation.
Sympodial leaves (structure functioning as flower stem and bract [Haines 2000]):
sheathed base, develops inflorescence, sympodial leaf extends beyond inflorescence
Inflorescence: spadix, semi-erect, nearly cylindrical, tapering, obtuse apex
Flowers: arranged to cover the spadix in a diamond pattern, bisexual, six light brown
tepals, 6 stamen, yellow anthers, 1 green ovary (Thompson 2000: 124, 126; Hilty 2011).
Rhizome: stout, shallow branching, knobby with a brown exterior and white interior (Hilty
2011).
Morphological Differentiation Between A. calamus and A. americanus
Characteristic
Vegetative
Height
Leaf
Acorus calamus
Acorus americanus
up to 1.75m
up to 1.45m
Leaf Veins
1 prominent
Leaf Cross Section
rhomboid
2-6 prominent
swollen in center and gradually
tapering to ends
usually shorter than or equal to usually equal to or taller than
Sympodial Leaf
Leaf margin
vegetative leaves
vegetative leaves
often crisped or undulate
usually entire
usually
Spadix
4.9-8.9
cm
long
at usually
3.3-7.4
anthesis
anthesis
Flowers
3.0-4.0mm long
2.0-3.0 mm long
Pollen grains
not staining in aniline blue
Fruits
not produced
Seeds
not produced
cm
long
at
usually deeply staining in aniline
blue
obpyrimidal berries
tan narrowly oblong to obovate;
embedded in mucilage
While morphological differences appear to be quite clear, they are rather subtle and hard to
differentiate in the flesh. The difference in number of prominent veins is difficult to assess
as the prominence of the veins is relative to the mid-vein prominence. The secondary veins
of A. calamus are no more than .5 times the width of the mid vein while in A. americanus
one or more of the secondary veins is .75-1 times as wide as the mid-vein. The clearest
difference is seen in the formation of fruit. In late summer, A. calamus will appear to have a
shriveled
ovary
while
A.
americanus
will
show
swelling
ovaries
(Haines
2000).
Unfortunately, even though A. americanus does have the capability to flower and reproduce
sexually via berries and seeds, some sources conclude it rarely does so (Fara, 2005).
Table after Haines (2000) with additional information from Thompson (2000)
Botanical Identification: Differentiation Between Acorus and Other Species
While it has the potential to be confused with plants such as Iris or Cattail that often grow
alongside it and have similar sword shaped leaves, Acorus is differentiated by the unique
characteristic aromaticity of the bruised leaves or rhizomes. Additionally, Acorus leaves are
bright green/yellow green with a spadix borne midway up the sympodial leaf versus the
blue-green leaves and showy flower of Iris (Thompson 2000:125).
CULTIVATION AND HARVEST
Propagation and Cultivation
Propagation and cultivation is generally through root division in the spring. Calamus
particularly likes to grow on wetland edges, however it can be grown in a garden of field
with deep rich soil and daily watering (Babineau, 2000). Jim McDonald describes growing
the plants easily from root cuttings in a non-draining planter filled with wild soil. He
maintains high moisture in the planter, though routinely dumps of standing water to reduce
mosquito larvae growth.
Harvest
Pay particular attention as to the location from which it is harvested. Water should be clean
and not near contaminants as some consider the plant to take up pollutants (McDonald).
Harvest two to three year old roots and rhizomes in early Spring (once source specifies
June) or late autumn, ensuring they are not hollow. If harvesting from the wild, take only
part of the rootstock, replanting the rest to continue growing. Clean and dry whole or
tincture the unpeeled roots (Babineau 2000).
Endangered Status
According to the USDA plants database, A. americanus is considered endangered in
Pennsylvania (at the recommendation of Thompson). United Plant Savers recommends
judicious harvest. Thompson reports that both species are secure globally and A.
americanus is not at risk, but rare in regions at the edge of its range with seven political
regions having assigned unofficial conservation status to A. americanus. Four of these states
however are not in the natural range of A. americanus. More research is needed in the field
to refine conservation status (Thompson 1995;464). In India, A. calamus is considered
nearly endangered due to excessive wildcrafting (Verma et al., 2012).
COMERCIAL SOURCES AND HANDLING
Identify origin of plant and ploidy if possible to ascertain which constituents are present.
McDonald is skeptical of the legitimacy of differentiation between species commercially.
Dried root should not be kept for more than a year as it loses its aromaticity.
TRADITIONAL USE
First Nations of North America
As cataloged in Moerman's (1998) ethnobotanical dictionary, A. calamus is one of the top
ten plants with the greatest number of uses among first nation peoples. While referred to
almost exclusively as A. calamus in relation to use by indigenous peoples of North America,
it is most likely A. americanus that was/is actually used (Thompson 1995, 444). Though
extensive ethnobotanical reports of usage in indigenous North American cultures exist,
much information has been lost due to the history of oppression and exploitation. For this
reason, it is likely that there are
more subtleties in its traditional use by First Nations
peoples than documented in the literature.
Among different tribes, the plant has numerous names, indicators of its value and place in
their
medicine
and
culture.
Names
conveying
medicinal
action
or
taste
include
enausa'pokotikun(a simple penetrator) from the Menominee of Wisconsin, pow-e-men-artic
(fire root, bitter pepper root) from the Cree, wi'ukh is e'evo (bitter medicine) from the
Cheyenne of Montana and kahtsha itu (medicine lying in water) by the Pawnee. Other
names refer to the roots physical appearance; Ojibwa called it na'buguck (something flat),
Lenape named it pepachkana (place where it is broken again and again) and the
Caughnawaga of Quebec identified it as anon-no-ron ka-te-ra-ra-ken (with white roots).
Many other names refer to the plants faunal association with the muskrat-- the Micmac of
Atlantic Canada called it ig gig'wesukwul (muskrat root) and the Abenaki of Quebec called it
mokwaswaskw (muskrat plant) (Thompson 1995, 446).
In ethnobotanical literature, Sweet Flag is used for a vast variety of health concerns.
Following are the most widely used applications (as collated by Thompson, 1995) with the
number of tribes reported to consider Sweet Flag for that particular use:
Respiratory:
•
colds, flu, and sore throat (28 tribes)
•
anti-tussive (10 tribes)
General:
•
Prophylactic/tonic (13 tribes)
•
Panacea (13 tribes)
•
GI:
•
intestinal pain/colic (11 tribes)
•
carminative (9)
Nervous/Endocrine System:
•
“antifatigue”/stimulant (8 tribes)
•
diabetes (2 tribes; not widespread use for this purpose, however there is some
pharmacological data, anecdotal evidence and contemporary application; also type II
diabetes was not common before the arrival of industrialized food; account from
1950s of Dakotas using root successfully for diabetes Howard, 1953 p. 608-609 as
cited in Kindscher, 1992)
Other:
•
Toothache (12 tribes)
•
Analgesic for muscle/cramps/spasm/pain and contractions (8)
Spiritual:
•
amulet/protective charm (8)
•
ceremonial bundles or religious rituals (8)
For some tribes in particular, Sweet Flag was especially important. In the early 1900s, one
writer
reported
Sweet
Flag
as
“perhaps
the
most
important
herb
in
Penobscot
pharmacology” (Speck 1917; 305). To the Cheyenne, the plant was considered so sacred
that only qualified Sundance priests could collect it along with the making of offerings
(Thompson, 1995). Two stories, one from the Malecite and the other from the Penobscot
demonstrate the cultural and medicinal importance of Sweet Flag. Herbert Milton Sylvester
retells the Malecite tale:
“Long time ago a great sickness fell upon the tribe and many people died.
They died so fast
that those who were left could not make graves quickly
enough and many were put in one large hole. At last there appeared to one of
the men in a dream a strange being as of a man covered with joints of brass.
'I am, said he, Ke-wis-wask (sweet flag) and can make you well. Dig me up
and steep me in water and drink me and I will cure you. After saying this, he
disappeared. The next day the man did as he was told. He dug up the flag
root and steeped it and gave the water to the Indians and after drinking it,
they soon recovered.”
Frank Speck (1917; 305) recounts the Penobscot story:
“A plague of sickness was sweeping the Indians away. There was no one to
cure the people. One night a man was visited by a Muskrat in a dream. The
Muskrat told him that he was a root and where to find him. The man awoke,
sought the muskrat root, made a medicine of it, and cured the people of the
plague.”
A. americanus is still used in traditional ways. The Dakota traditionally wore a paste of the
plant on their faces during battle to instill fearlessness and provide stamina. It was thought
that since muskrats eat Acorus as a major food source it would make the warriors fearless
like the Muskrat. During the wars of the 20th century, Native American soldiers chewed on
Acorus rhizomes to promote stamina and endurance (Thompson, 1995).
Chinese Medicine
Other Acorus species, namely A. tatarinowii and A. graminaeus (both known as Acori
tatarinowii Rhizoma or shi chang pu), are more commonly used in Chinese medicine,
however A. calamus does have a place in the materia medica. Referred to as Acori calami
Rhizoma pharmaceutically, the Chinese name, shui chang
pú , translates literally into
“watery flourishing reed.”
Characterized as acrid, warm and bitter, shui chang pu enters through the channels of the
heart, liver and stomach. The rhizome is considered to transform phlegm, facilitate the
removal and elimination of dampness, open the orifices, strengthen the Stomach (refers to
Chinese concept of the Stomach), fortify the Spleen, kill parasites and stop itching.
As in nearly all of the traditional literature and cultures where A. calamus has been used for
a long time, shui chang pu is indicated for discomfort in the digestion specifically
characterized by dampness and turbidity obstructing the middle burner with epigastric pain,
abdominal distention, a poor appetite, and a greasy tongue coating. In this circumstance
shui chang pu acts to improve the movement of qi while strengthening the Stomach.
The other main indication for shui chang pu in the Chinese materia medica is tremors and
loss of consciousness or seizures originating from phlegm-heat (Bensky et al., 2004).
(Phlegm-heat arises from “external evils” binds the chest and congests and obstructs the
lungs [Wiseman and Ye 1998, 437]). Under these circumstances, Shui chang pu is useful by
extinguishing the wind, opening the orifices, and transforming the phlegm. (It is
recommended with specific other herbs for sudden loss of consciousness and for seizures).
Generally speaking the plant is used for epigastric distention due to damp stagnation,
diarrhea,
dysenteric
disorders,
wind-damp
painful
obstruction,
epileptic
seizures,
palpitations and forgetfulness. External applications are for sores and scabies. Of interesting
note is a statement in the Illustrated Classic of the Materia Medica from the eleventh
century that it should not be used for medicine. The Chinese Acorus is considered to have
up to 80% b-asarone and so use of the diploid A. calamus var. americanus (most likely
actually referring to A. americanus) is suggested. The aroma of A. calamus is considered to
be less intense than that of A. tatarinowii (Bensky and others 2004:958-959).
Ayurvedic
The name Vacha or Vaca for A. calamus in the Ayurvedic tradition means “voice” or
“speaking,” a name indicative of the intelligence or self-expression the plant is considered to
encourage (Frawley and Lad, 1989). Vacha is considered pungent, bitter, astringent/heating,
reducing to Vata and Kapha and increasing Pitta. The rhizome acts in a stimulant,
rejuvenative, expectorant, decongestant, nervine, antispasmodic, and/or emetic manner in
the nervous, respiratory, digestive, circulatory and reproductive systems. It is indicated for
colds, cough, asthma, sinus headaches, sinusitis, arthritis, epilepsy, shock, coma, loss of
memory, deafness, hysteria and neuralgia (Frawley and Lad, 1989). As in many other
cultures where it is used, its strength for digestion and its association with the
mind/clarity/nervous system seem most emphasized. Sometimes used on its own but most
often as part of formulas, the rhizome is used in dyspepsia, flatulence and diarrhea as a
stomachic and carminative (Caldecott 284; Dutt 1877, 251)
Considered sattvic, Vacha is “one of the best herbs” for the mind. In conditions where the
ability to speak is lost, as in apasmara (epilepsy), Vacha is considered to bring one back to
normal consciousness with its strong aromatic quality. Also in unmada, or psychosis, Vacha
is an important remedy. The applications for Vacha in Ayurveda are copious, however at a
basic level, the plant rejuvenates the brain and nervous system through purification and
revitalization while clearing out toxins and obstructions (Frawley and Lad, 1989).
European
Other than a mention in Dioscordes, the plant does not appear often in European literature.
Maude Grieves gives the lengthiest account. She discusses its use as a strewing herb on the
floors at church festivals and makes note of the peculiar ability of the spathe to give out
enough heat that the temperature around it rises noticeably. She explains that Acorus come
form the name given to the plant by Dioscordes, Acoron with Con meaning the pupil of the
eye. Grieves reports that in the time of Dioscordes it was used to address such issues. Like
all of the other accounts, Grieves classifies the plant as an aromatic bitter and carminative
used to increase appetite and benefit digestion. Chewing the dried root is useful for
dyspepsia. She notes the combination of calamus and Gentiana campestris in Stockton
bitters. Aside from digestion, Grieve also makes note of the dried root chewed to clear the
voice. For the immune system she discusses the root for ague, low fever, and as a mild
stimulant in typhoid cases. Grieve quotes Waller's British Herbal which consider the plant to
be “of great service in all nervous complaints” including vertigo, headache, and
hypochondria. Waller also consider it in the digestive system for dysentery, “chronic
catarrh,” and when mixed with some water and white wine, as a stomachic. In Grieves
account the powder is used as a substitute for ginger, cinnamon and nutmeg. In the British
Pharmaceutical codex, the plant is considered an aromatic bitter and carminative that works
by “removing the discomfort caused by flatulence and checking the growth of the bacteria
which give rise to it.” It is used, according to the codex, to increase appetite and improve
digestion (1911).
Eclectic
A. calamus does appear in the Eclectic literature, though, as Scudder (1898) notes, it is “but
little used by the profession.” It is generally considered carminative, aromatic, stimulating
and mildly tonic with use in flatulent colic, atonic dyspepsia, and general weakness of
digestions (Felter, 1922; Felter & Lloyd, 1898; Scudder,1898; Cook,1869). Cook writes it
“warms the stomach, aids the expulsion of flatus, and relieves cramps and colic.” It is
compared by Scudder to Angelica and Canella in its aromatic stimulant and mild tonic
activity. Also mentioned as a sialagogue (Felter, Scudder) and “breath perfume” (Felter).
Scudder elaborated on its use as a sialagogue considering it for rheumatic and paralytic
infections of the mouth. Externally King considered it a “valuable application” for indolent
ulcers. Felter & Lloyd (1898) and Scudder (1898) also consider it for “intermittents.”
Scudder recommends it as a substitute for tobacco.
Regulars
A. calamus was included in the Dispensatory of the United States of America. It was
classified as warm, “bitterish,” pungent and a “feeble aromatic.” Its main use was as an
adjuvant to preparations where a carminative was needed. The dispensatory comments the
plant may be “easily misused” if given too freely or in irritated stomach and bowel
conditions. One suggested preparation is boiled in milk with pimento or ginger.
SCIENTIFIC RESEARCH: CONSTIUENTS
Constituent Variety Among Chemotypes
Chemical constituents vary significantly among chemotypes. The variation is most clearly
documented for a and b-asarone, however other constituents are variable mostly in quantity
but also in content. Because studies generally come from India, or secondarily Europe, the
ploidy of the species is often not identified. However, due to the presence of b-asarone
content, an assumption is made that while the following constituents have application to A.
calamus and A. americanus, they are generally based on the former species.
Thompson notes in her dissertation on A. americanus that the essential oil profile of A.
americanus is significantly different than the triploid and tetraploid A. calamus as evidenced
by the work of Rost and Bos, 1979. Unfortunately this study is unavailable, but Thompson
does note the work of Rost and Bos for showing the presence of geranyl acetate, the main
constituent in the essential oil of the diploid North American species, a constituent absent in
the triploid and tetraploid populations of A. calamus.
Thompson summarizes “the confusion between two chemically-distinct, yet medicinallyimportant, species means that much of the literature on Acorus chemistry and use is
dubious in terms of species identification...With the realization that the name, A. calamus,
has been misapplied to another species, A. americanus, which is chemically-distinct from
true A. calamus, new studies to clarify the chemical composition and medicinal use of both
species are warranted” (Thompson 1995; 424).
Essential Oil Fraction (2-9%): Phenlypropanoids, Sesquiterpenes, and Monoterpenes
Phenylpropanoids: b, a, and g asarone, asarylaldehyde, acoradine, acoramone, coramone,
eugenol, methylisoeugenol, phenyl indene derivatives, and calamol (Raja 2009)
The phenlypropanoid fraction of the essential oil varies the most among chemotypes. The
Indian chemotype contains up to 80 % of its volatile oil fraction in phenlypropanoids while
the European is composed of 13% and the American has close to none (Wichtl 2004: 98).
The primary phenlypropanoid for which Calamus gains the most attention is b-asarone, also
called cis-isasarone. Levels of b-asarone found in the rhizome essential oil were not
detected in the diploid A. calamus var. americanus/A. americanus, but were found in the
triploid A. calamus var. calamus/ A. calamus var. vulgaris at levels of 9-19 % in fresh
and .3% in dried. Levels in A. calamus var. angustatus/ A. triqueter, the tetraploid variety,
were found at 85-95% in fresh rhizome and 4.4-8.3% in dried (European Medicines Agency
2005).
Sesquiterpenes:
Dried rhizomes yield about .62% sesquiterpenes and roots yield 2.5%
sesquiterpenes upon distillation. Sesquiterpenes include:
•
Monocyclic sesquiterpenes isolated from n-hexane extracted essential oil of
rhizome: shyobunone (forms from the heat sensitive acoragermacrone during steam
distillation), epishyobunone, and 2,6-diepishyobunone (Raja 2009; Wichtl 2004:98)
•
Bicyclic
sesquiterpenes
iscoalamendiaol (Raja
isolated
with
pet-ether-diethyl-ether
fraction:
2009)
•
Tricyclic sesquiterenes: calamenone (Wichtl 2004: 98)
•
Spirocyclic sesquiterpenes: acorone, isoacorone (Wichtl 2004:98)
•
Other sesquiterpenes: asulene (Meena 210), volatile/bitter sesquiterpene diketone
(Wichtl 2004:98), and dioxasarcogaiacol, recently
discovered
in
this
plant
(Zuag et al. 2011)
Monoterpenes: Isolated by steam distillation from the volatile oil include a and b-pinenes,
myrcene, Cymene-Para, Terpinen-a, Phellandrene-b, Terpinene-g, Terpinolene, Thujane and
Limonene (Wichtl 2004, Raja 2009, Meena 2010).
Non-Volatile Constituents:
Xanthone Glycosides
Bitter Glycosides: acorine and acoretin
Lignan: acoradin
Steroids: b-sitosterol
Flavones: Galangin
Triterpanoid saponins
Fatty Acids: myristic (1.3%), palmitic (18.2%), palmitoleic (16.4%), stearic (7.3%), oleic
(29.1%), linoleic (24.5%) and arachidonic (3.2%) (Asif 1984)
Sugars: maltose (0.2%), glucose (20.7%) and fructose (79.1%) (Asif 1984)
Inorganic Constituents: oxalate at 2% and calcium at .078% (Raja 2009)
Other: tannins (.6-1%), mucilage, choline and small grained starch (Raja; Wichtl)
Primary Constituents in Volatile Oil Fraction Among Varying Populations:
The following exemplifies the variety in primary volatile oil constituents. All of the plants
below were identified as A. calamus. Plant material origin if known is noted as is ploidy
where it is mentioned in the study.
Place
of Korea
China
Plant
(origin Finland
unclear)
Czech
Republic
Origin
Primary
41.5% methyl isoeugenol
74.6 % b-asarone
.75-1.87%
Constitue
21.3% cyclohexanone
22.2%
e.o.
nts of
6.87%
Essential
Oil
total 1.2-2.92% total
e.o.
IH-3A,7- methylisoeugenol
10.24%
b- 16.11%
methanoazulene
2.9% isoelemicin
asarone
asarone
4.94% bezenaminium
.3% methyleugenol 11.07%
18.65%
2.37%
cis-Asarone/
asarone
2.28% cyclohexanol
1.5%, calarene (1.5%)
1.29% a-gurjunene
b- n.d. a-asarone
n.d. elemecin
solavetivone
asarone
bg-
1.11%
2,
5-
cyclohexadiene
1.08% (+)-cuparene
ID
of “Korean A. calamus”
Plant
Part
“Rhizoma
Acori A. calamus
A. calamus
calami”/A. calamus
Part not specified; most Rhizome
Clean,
cut
and Cleaned,
likely rhizome however
dried rhizome
cut
and
dried
rhizome
Ploidy
Ploidy not specified
Ploidy not specified
Triploid
Study
Kim et al (2011)
Wichtl (2011; 783)
Dusek
Triploid
et
al Dusek
(2007)
et
(2007)
Comparison of Diploid and Triploid Alcoholic Extracts:
Data on the chemistry of A. calamus dipoloid species and A. americanus is scarce. The most
recent study that included a thorough examination of diploids A. calamus is elucidated
below. It is unclear whether the species being examined is indeed A. calamus of the diploid
varietal or actually A. americanus. The plants used in the study were grown in Botanical
Gardens at the University of Turin. As this is in Italy, it is unlikely that the plants are actually
A. americanus.
Comparison of Primary Constituents
Triploid Alcoholic Extract
Diploid Alcoholic Extract
11% beta-asarone
26.33% acorone
5.02% a-selinene
22.81 preiso calamendiaol
8.62% iso- shyobunone
3.28% E-b-ocimene
3.28% b-sesquiphellandrene
2.27% camphene
0% b-asarone.
2.00% s-cadinol
al
1.54% camphor
1.42% calarene
Data from Cinzia et al 2005
Full Comparison of Diploid and Triploid Chemical Constituents from Cinzia et al 2005:
Compound
KI
Diploid
Triploid
(%)
(%)
α-Thujenea
433 0.0
tr
α-Pinenea
440 tr
0.4
Camphenea
456 tr
2.3
Sabinenea
481 0.0
0.2
β-Pinenea
485 0.1
0.1
Myrcenea
499 tr
tr
γ-Terpinenea
531 0.0
tr
p-Cymenea
541 0.0
tr
Limonenea
547 tr
0.3
E-β-Ocimenea
559 0.0
3.3
Z-β-Ocimenea
572 0.0
0.3
γ-Terpinenea
588 0.0
tr
Terpinolenea
630 0.0
0.1
Linaloola
646 0.0
0.5
Camphora
715 0.0
1.5
Terpinene-4-ola
768 0.0
0.1
α-Terpineola
789 0.0
tr
Bornyl acetatea
948 0.2
0.1
Compound
KI
Diploid
Triploid
(%)
(%)
Nonanyl acetate
992 tr
0.0
α-Copaene
109 tr
tr
7
α-Funebrene
110 tr
0.1
5
α-Cedrene
110 0.2
0.0
6
β-Elemene
112 0.1
0.0
4
Dihydrocarveyl acetatea
112 0.1
0.0
9
α-Cedrene
113 tr
0.0
8
Z-Isoeugenola
114 tr
0.0
9
β-Funebrene
116 1.6
0.9
0
β-Cedrene
116 0.8
1.6
9
Calarenea
118 0.0
1.4
7
α-E-Bergamotenea
119 0.9
0.5
7
Prezizaene
121 0.7
0.4
0
Caryophyllenea
122 1.2
0.9
0
α-Humulenea
122 0.0
0.6
1
Z-β-Farnesene
123 1.7
1.2
Compound
KI
Diploid
Triploid
(%)
(%)
1
β-Copaene
123 0.6
0.0
8
β-Acoradienea
124 0.3
0.2
4
β-Curcumene
125 0.1
tr
2
α-Neocallitropsene
125 0.3
0.4
6
γ-Amorphene
126 0.3
0.9
6
ar-Curcumene
127 0.3
tr
1
β-Selinene
127 0.0
0.2
3
allo-Aromadendr-9-ene
127 0.2
0.4
7
α-Selinene
128 1.5
5.0
9
Bicyclogermacrenea
129 0.2
0.0
2
α-Muurolene
129 0.0
0.1
7
α-Amophene
129 0.1
0.0
8
Germacrene Aa
130 0.3
0.3
4
γ-Guaiene
130 0.0
0.4
8
iso-Shyobunone
132 8.6
6.9
Compound
KI
Diploid
Triploid
(%)
(%)
4
β-Sesquiphellandrene
133 3.3
2.7
6
E-Nerolidol
140 1.3
0.4
5
4-α-Hydroxygermacra-1(10),5-diol
141 1.6
1.8
5
Cedrola
143 0.5
0.5
1
Preisocalamendiola
147 22.8
7.8
0
β-Asaronea
148 0.0
11.2
8
Dehydroxy-isocalamendiola
149 0.3
0.0
7
τ-Cadinol
151 0.3
2.0
4
α-Cadinol
153 0.7
0.0
2
4-epi-Acorenone
156 0.4
0.2
2
Khusiol
157 0.1
5.9
3
Acorenonea
158 5.3
9.3
5
Torilenol
160 0.1
1.8
7
Acora-3,7(11)-dien-8-one
163 0.5
0.0
0
Squamulosone
168 0.1
0.0
Compound
KI
Diploid
Triploid
(%)
(%)
6
175 26.3
Acoronea
8.4
0
iso-Acorone
177 1.3
0.1
9
n-Hexadecanoic acid
195 0.2
0.0
4
Ethyl hexadecanoate
198 0.0
2.4
9
216 0.4
9,12-Octadecadienoic acid (Z Z)-
0.0
4
219 0.5
Methyl linoleatea
4.6
1
9.12.15-Octadecatrienoic
acid,
ethyl
ester. 219 0.1
(Z.Z.Z)-
7
γ-Sitosterola
326 0.1
0.8
2.6
9
Values are the mean of at least three injections. KI = Kovats Index.
a These compounds were identified by direct comparison with pure standards; tr = traces.
SCIENTIFIC RESEARCH: PHARMACOLOGY (Mukherjee, 2007 unless otherwise noted)
Constituent
Activity
Antispasmodic,
a-asarone
genotoxicity
and
mutagenicity,
sedative
and
hypnotic, CNS depressant, anticonvulsant, “behavioral changes,”
acetylcholinesterase
inhbitory/memory
enhancing
effect,
CV
actions, hypolipidemic effect
Essential oil
Antispasmodic, antibacterial, antifungal, anthelmintic, sedative and
hypnotic, CNS depressant, anticonvulsant, “behavioral changes,”
acetylcholinesterase
inhibitroy/memor
enhancing
effect,
anti-
inflammatory, CV actions
Asaraldehyde
Antifungal
Acoradin
Antifungal
b-asarone alcohol extract
Antifungal
Insecticidal, genotoxicity and mutagenicity, sedative and hypnotic,
b-assarone
CNS depressant, acetylcholinesterase inhibtory/memory enhancing
effect, CV actions
Acetone
Insecticidal
Lectins
Anti-cancer effect
Acorine
Bitter and orexogenic (Bunce, 2011)
SCIENTIFIC RESEARCH: SELECTED INVITRO AND INVIVO STDIES
Gastrointestinal System
Spasmolytic Activity: In vivo, the oil of Acorus calamus rhizome inhibited excessive
peristaltic movement of rabbit and dog intestines exhibiting an antispasmodic activity on
involuntary muscle tissue (Chopra 1954 as cited in Mukherjee 2007). Alcoholic extracts have
shown relaxation of isolated rat intestines (Agarwal et al. 1956), isolated guinea pig illeum
(Bhakuni 1988 as cited in Mukherjee) and isolated rabbit jejunum (Gilani 2006). a-Asarone
and the essential oil fraction to a lesser extent contribute to this spasmolytic activity
through direct musculotropic action (Das 1962 as cited in Mukherjee 2007). Gilani et al.
(2006) further elucidated the antispasmodic mechanism with the finding that the crude
extract inhibits both spontaneous and high K+ induced contractions. Based on this, Gilani et
al. hypothesis the spasmolytic activity is mediated through calcium channel blockade (CCB)
due to CCB-like constituents present particularly in the n-hexane fraction of the plant. Gilani
(2006) concludes this “provides a strong mechanistic base...for its traditional use in
gastrointestinal disorder such as colic pain and diarrhea.”
Antidiarrheal Activity: In addition to the in vitro study Gilani et al. performed
demonstrating a mechanistic explanation for antidiarrheal effects through anti-spasmodic
action, an in vivo experiment has also been conducted. In mice with castor-oil induced
diarrhea, both aqueous (at room temperature) and methanolic extracts of dry A. calamus
rhizome, harvested in India, were assessed for antidiarrheal properties. Extracts were
administered at doses of 3, 7.5 and 15mg thirty minutes prior to castor oil. A dose
dependent effect was seen for both extracts though to a greater extent with the methanolic
extract with which the induction time of diarrhea and total weight of the feces was reduced
significantly (Shoba and Thomas, 2001).
Antiulcerogenic Activity: The ability of A. calamus rhizome ethnolic extract to inhibit
gastric secretions and to protect gastroduodenal mucosa against injury from pylori ligation
and other ulcer inducing agents was examined in rats. A. calamus rhizomes used in this
study were “procured from the local market” presumably where the study took place in
Saudi Arabia. An oral dose containing 500mg of the plant per killogram of weight
administered thirty minutes prior to ulcer inducing agents showed significant antisecretory,
antiulcerogenic and cytoprotective activity in the rats. Volume and acidity of basal gastric
secretions were significantly decreased, as was severity of duodenal ulcers. Cytoprotectivity
against gastric lesions found in this study suggests a protective effect on gastric mucosa
potentially through “adaptive cytoprotection” wherein cytoprotective activity results from
prostaglandins generated via mild irritation. In A. calamus, this activity may be attributed to
sesquiterpenes (Rafatullah et al. 1994). a-Asarone may also be implicated as it has shone
antiulcer activity when
administered
intra-abdominally (at
310mg/kg)
or internally
(417.6mg/kg) to mice (Belova 1985). However, Belova's study involves a fairly high dose of
an isolated constituent applied in a manner not clinically applicable. Rafatullah et al (1994)
did conclude that their findings supported the traditional use of A. calamus for gastropathy,
however it should be noted the dose given in this study would be equivalent to a 55kg
person taking a 27.5g dose-an excessively large amount to consume.
Nervous System
Pharmacologically, A. calamus is considered to have significant effect on the central nervous
system as an anticonvulsant, sedative, hypnotic, and memory enhancer.
Anticonvulsant Activity: Hazra et al. (2007) concluded that Acorus calamus prevents the
development of ferric chloride induced epileptogenesis in rats by modulating antioxidant
enzymes. Results were based on pretreatment with 200mg/kg of A. calamus for 14 days
prior to induction along with diazepam.
In a 2009 mouse study (Yende et al) a hydro-alcoholic extract of A. calamus rhizome (most
likely procured in India) was studied along with antiepileptic pharmaceuticals (phenytoin
and phenobarbital) in induced seizures. 185mg/kg of the plant significantly potentiate the
anticonvulsant action of pharmaceuticals reducing the median effective dose of phenytoin
from 13.5mg/kg to 9.25mg/kg and phenobarbital from 8mg/kg to 5mg/kg. On its own, A.
calamus was mild to moderately effective at 250mg/kg and ineffective at 150mg/kg.
However, sub-effective doses of phenytoin (10 mg/kg) and phenobarbital (2mg/kg) had
significant effects even when administered with the ineffective 150mg/kg A. calamus dose.
The authors concluded that A. calamus shows synergistic anticonvulsant effects reducing
the dose of phenytoin and phenobarbital as well as the side effects. Based on a previous
study in which a-asarone prevented Metrazol-induced convulsions and electroshock seizures
(Dandiya, 1963) Yende et al. speculate a-asarone may also be responsible for the
anticonvulsant and synergistic effects with pharmaceutical anticonvulsants in their study.
Once again dosing in this study is rather excessive for practicality of human consumption.
More recently, Jayarman et al. (2010) studied a methanolic extract of A. calamus rhizomes
(procured from local market in India) administered orally to mice at 100 or 200mg/kg one
hour before injection of convulsion inducer PTZ. The extracts were accessed for constituents
and were found to contain saponins, alkaloids, tannins, sugars, gums and mucilage. The
extract increased the latency period and reduced seizure duration significantly in PTZ
induced seizures in a dose dependent manner. Because PTZ is hypothesized to induce
convulsions either through inhibiting the GABA pathway in the CNS or increasing central
noradrenergic activity, the authors suggest the extract is working through involvement in
these pathways either in a GABA-ergic or noradrenergic way (Jayarman 2010). While still on
the higher side, 5.5g for a 55kg person is a somewhat more realistic dose (100mg/kg).
A 2012 (Bhat et al.) study looked at the efficacy of two preparations of calamus on induced
seizures in rats as compared to control and the antiepileptic drug phenytoin sodium. Of the
two groups given calamus, one was given calamus that had undergone the traditional
shodhana (though not necessarily traditional for calamus) procedure of processing. During
this process, calamus was decocted successively in “Gomutra, Mundi kwatha (decoction
prepared from whole plant of Sphaeranthus indicus Linn.), Panchapallava kwatha (decoction
prepared from a group of five leaves), and Gandhodaka (decoction prepared from a group of
aromatic herbs)” followed by a 12 day drying period then ground into a powder. The
unprocessed calamus was dried and powdered in the same fashion. The rats received
powdered calamus mixed with water orally an hour before electroshock at a dose of
11mg/kg of body. This dose was extrapolated from the human dose of 120md/day dose
recommended by the Pharmacopoeia of India.
The study found that pretreatment of rats with both calamus preparations decreased
duration of tonic extensor phase with greater protection against induced seizures in the
shodhita (classically processed) group. Though not superior to phenytoin, which completely
mitigated the tonic extension phase, the study was concluded to confirm the anticonvulsant
activity of calamus, an effect enhanced by the shodhana process.
Neuroprotective: An investigation of a 1:1 ethanol water extract of A. calamus rhizome
(obtained in India) was preformed in rats experiencing neurotoxicity from acrylamide. The
A. calamus extract was dosed at 25mg/kg for ten days. In rats treated with the plants, hind
limb paralysis was significantly reduced. Glutathione levels also increased significantly, but
there was no effect on dopamine receptors. The explanation for this is not yet understood,
however the increased glutathione levels may explain the overall neuroprotective effect
observed. The authors concluded that “neurobehavioral changes produced by ACR
(acrylamide) may be prevented following treatment with Acorus calamus rhizomes” (Shukla
et al. 2002).
In another study (Shukla et al. 2006), the neuroprotective potential of a 1:1 ethanol water
extract of A. calamus rhizome in rats with middle cerebral artery occlusion induced ischemia
was
examined.
Treatment
with
the
extract
significantly
improve
neurobehavioral
performance, decreased malonaldialdehyde levels in the cortex, increased reduced levels of
glutathione and SOD activity, and improved neurologic function score.
In a 2013 review (Schroder et al.), calamus was one of several individual plant and
traditional formulas investigated for ability to regenerate or protect neurons, specifically in
treating chemotherapy-induced peripheral neuropathy. The review found three studies
carried about by the same scientists in which rats were inflicted with neuropathy causing
events (chronic constriction injury of sciatic nerve, tibial and sural nerve transection, and
vincristine induced) and then treated with Acorus calamus, which attenuated nerve pain in
all three trials (Muthurman & Sing, 2011a; Muthurman, Sing & Jaggi, 2011, Muthurman &
Sing, 2011b).
Antidepressant Activity: In an animal model of depression, behavior and 5-HT receptor
involvement were evaluated before and after the administration of A. calamus (from India)
dosed orally at 18mg/kg over four weeks. Behavioral deficit was prevented, however the
plant did not elicit significant change in 5-HT1A receptors. The authors concluded the plant
has a clear antidepressant action, but because there was no significant change in 5-HT1A
receptor sensitivity, an anxiolytic effect was not marked (Tripathi and Singh 2010).
Sedative/Relaxant Activity Activity: Both European and Indian A. calamus have been
shown to potentiate sedative action of pentobarbitone (Dandiya 1959) and the steam
volatile fractions have prolonged sleep time in mice treated with pentobarbital and
hexobarbital with the highest sedation activity in the volatile fraction of the petroleum ether
extract (Dandiya and Cullumbine 1959). Malhotra et al. (1962) speculate the potentiation
effect may be mediated through serotonin and catecholamines. A direct sedative
tranquilizing effect was found in rats, mice, cats and dogs (Dhall and Bhattacharya, 1968).
Isolated b-asarone has been shown to sedate rats (Bose et al. 1960). Unfortunately, details
and dosing on the studies was unavailable.
In a more recent study (Hazra and Guha, 2002), the effect of an ethanolic extract of A.
calamus on rat brains was examined. In rats administered the extract at 200mg/kg and
300mg/kg for 14 days, electrographic recording showed an increase in activity and
norepinephrine levels in the cerebral cortex but a decrease in the midbrain and cerebellum.
Seretonin increased in the cerebral cortex but decreased in the midbrain. Dopamine
increased in the caudate nuclea and midbrain but decreased in the cerebellum. The authors
concluded A. calamus exerted a CNS depressive action by changing electrical activity and
altering brain monamine level in various brain regions.
In 2011 Zuagg et al. further clarified the GABA-ergic properties of A. calamus. A petroleum
ether extract of the rhizome (obtained in Switzerland) were screened on Cenous oocytes
that transiently expresses GABA A receptors of the subunit combination a1, b2, and g 25.
The extract was found to enhance GABA, the major inhibitory CNS neurotransmitter.
Individual constituent activity was measured as well. b-Asarone, (+)-dioxasarcogaiacol (a
sesquiterpene
previously
unidentified
in
A.
calamus),
(+)-shyobunone,
and
(+)-
preisocalmendiol were the four most active principles in inducing GABA. Isoshyobunone and
acorenone exhibited weak GABA modulating properties. All constituents enhanced GABA in a
concentration dependent manner. Because b-asarone induced highest potentiation of GABA
the authors of the study speculate that the sedative and tranquilizing activities of the
essential oil may be due to this constituent.
Acetylcholinesterase Inhibiton: In vitro tests seem to demonstrate acetylcholinesterase
(AchE) inhibiton (Oh 2004, Houghton 2006, Mukherjee 2007). Hydroalcoholic extracts and
essential oil of A. calamus rhizomes showed effectivity as a methanol extract (Oh et al
2004), hydroalcoholic extract, and essential oil fraction. Greater inhibition was seen using
the essential oil than the hydroalcoholic extract (Houghton et al. 2006 as cited by
Mukherjee). Of the constituents found in A. calamus, b-asarone is a more active inhibitor of
AchE than a-asarone and is considered to be the constituent responsible for this activity
(Mukherjee 2007).
Antimicrobial Activity
A. calamus was tested in vitro against methicillin-resistant Staphylococcus. Extractions of
A. calamus using ethyl acetate, acetone, and methanol demonstrated antibacterial activity
as well as synergistic antibiotic activity with antibiotic pharmaceuticals. Flavanoids and
phenols were considered to be the major active constituents in the plants antimicrobial
activity (Agil 2006). A study specifically of Korean A. calamus showed the essential oil,
hexane extract, and isolated methyl isoeugenol (the primary constituent in the rhizomes
used) had strong antimicrobial activity as per the following table:
Antimicrobial Activities of the Essential Oil, Hexane Extract, and Major Components from
Rhizome of Korean A. calamus (copied from Kim et al. 2011)
Kim et al. note specifically the anti-microbial property of the extract and essential oil against
the bacteria, Propionibacterieum acne, involved in
acne vulgaris and suggest its use in
topical acne vulgaris remedies (Kim et al. 2011). While this study attribute antibacterial
activity to isoeugenol, this property has also been attributed to alpha and beta asarone
(Ganjewala 2011).
Wound Healing
A 2014 study (Shi et. al) assessed A. calamus in vitro for its anti-inflammatory effects and
in vivo for its ability to heal wounds. In vitro, they found that applied to RAW 264.7 cells, A.
calamus inhibited mRNA expression of inflammatory mediators. They found aqueous
extracts applied topically to animal wounds BID to TID “enhanced significantly the rate of
skin wound-healing.”
Respiratory System
Bronchodilatory: In an examination of the crude extract of A. calamus applied to guinea
pig tracheal segments, a relaxing effect on high K+ contractions was observed. The nhexane fraction was equally potent against both carbachol and K+ contractions while the
ethylacetate fraction was more potent against carbachol precontractions and was only
negligible in its dilatory effects against K+ contractions. The authors concluded that the
crude extract of A. calamus exhibits a papaverine-like dual inhibition of calcium channels
and phosphodiesterase in their n-hexane fraction demonstrating pharmacological basis for
the use of the plant in airway disorders (Shah and Gilani, 2010).
Use in Diabetes
Increase of Insulin Excretion and Decrease in Carbohydrate Break Down: The ethyl
acetate fraction of A. calamus was found to increase insulin secretion in HIT-T15 cells and
inhibited a-glucosidase activity in vitro. (In type II Diabetes, a-glucosidase inhibitors are
used pharmaceutically to prevent digestion of carbohydrates into sugars absorbable through
the intestine thus reducing a potential spike in blood sugar). In vivo, doses of A. calamus
(rhizome harvested
in
Indonesia)
ethyl
acetate
fraction
(200,400
and
800mg/kg)
significantly decreased fasting serum glucose and reduced the increase of blood glucose
levels after loading with amylum (starch). The authors of the study concluded the ethyl
acetate fraction of A. calamus may have hypoglycemic activity by promoting release of
insulin while inhibiting a-glucosidase effectively improving postprandial hyperglycemia. The
control of postprandial hyperglycemia is considered especially crucial in maintaining
cardiovascular health in those with diabetes (Si et al. 2010).
Decrease in Serum Glucose and Increase in Adiponectin: An earlier study found that
A. calamus ethyl acetate fraction in vitro increased glucose consumption mediated by insulin
in L6 cells. In vivo, the fraction administered to mice at a dose of 100mg/kg reduced
significantly serum glucose, triglyceride, and free fatty acid levels while increasing
adiponectin levels. (Adiponectin is an insulin sensitizing hormone secreted by adipocytes.
Low levels of adiponectin are often found prior to development of type II diabetes ([Linh et
al., 2005]). Serum insulin was not significantly decreased. Whereas the insulin sensitizing
diabetes drug, rosiglitazone increases body weight, A. calamus decreased overall intake of
food and water and did not result in any weight gain. The authors concluded that due to its
insulin sensitizing ability, A. calamus has potential uses in diabetes and associated
cardiovascular complications (Wu, 2009).
Activation of PPAR Receptors: A third study analyzed a variety of plants in their relation
to the peroxisome proliferator-activated receptors (PPAR) which are considered central in
metazoan lipid and glucose homeostasis. In dislipidemia, fibrate drugs are used to
synthetically activate PPAR-a (thus lowering cholesterol) while in diabetes glitazones are
used to activate PPAR-g
( t h u s in c r e a
extracts studied, Acorus calamus (most likely sourced from Germany) was among the most
active in terms of PPAR activation providing, as the study
concludes, additional
pharmacological support for traditional use of A. calamus in diabetes (Rau et al. 2006).
Clinical Trials:
Premedicant Prior to Anesthesia: Forty healthy patients were divided into two groups.
Group I (control) received injected Glycopyrrolate (a pre-anesthetic that acts as an
anticholinergic to reduce salivation, bronchial secretions and minimize bradycardia; it is also
used to reduce GI secretions in ulcer treatment) and Phenergan (CNS depressant
potentiator). Group II (Trial) were premedicated with Glycopyrrolate and 100mg of A.
calamus (most likely sourced in India) orally ninety minutes prior to anesthesia. A. calamus
was found to raise body temperature and produce good sedation reducing anesthesia
induction time and
reducing the post operative recovery time from anesthesia.. No
cardiovascular or respiratory depression was produced. The authors concluded that A.
calamus was useful in ensuring quick and smooth anesthetic induction. They found it
preferable to Phenergan for allaying apprehension and reducing complications during
anesthesia (Pande and Mishra, 2009).
Anxiety Disorder: A clinical trail with thirty-three participants was undertaken to
determine the effects of A. calamus in generalized anxiety disorder. A. calamus was given
as a 70% hydro-ethnolic extract inside gelatin capsules at a dose of 500mg two times a day
after meals. The regimen was undergone for sixty days with assessment at days 0, 30 and
60. A. calamus (most likely obtained from West Bengal area) was found to significantly
attenuate anxiety related disorders, reduced stress phenomenon as well as correlated
depression and improve significantly the willingness for adjustment. Patients did not report
any adverse events nor were there any observed by physicians. Self-perceive stress
improved by 23.3%, depression scale by 22.5%, and adjustment score by 22.8%. All were
considered statistically significant. In summary the authors of the study considered A.
calamus to reduces stress, attenuate anxiety, negate depression, and enhance adjustment,
attention and ability to cope with mental overwork (Bhattacharyya et al. 2011).
MODERN THERAPEUTIC USE
The following section takes into account contemporary use and traditional modalities,
pharmacological research, and the experience of modern herbal practitioners to summarize
the use of A. calamus and A. americanus in current clinical applications. Note that chemical
differences between species and ploidys does effect their medicinal application.
Note that Ayurvedic uses and Chinese uses are most likely referring to 3n, 4n, or 6n
phenotypes (though there is a 2n phenotype in Asia). Traditional uses from indigenous
peoples of North America may be referring to either species (A. americanus or A. calamus
3n). McDonald is most in depth about A. americanus specifically.
Energetics:
•
warm, dry, astringent
•
Ayurveda (Frawley and Lad, 1986): astringent/heating/pungent; decreases Vata
and Kapha, increases Pitta
•
Chinese Medicine (Benseky et al., 1994):
◦
Enters heart, liver and stomach meridians
◦
Transforms phlegm, facilitates removal and elimination of dampness
◦
Opens the orifices
◦
Strengthens the stomach
◦
Fortifies the spleen
Taste: bitter, pungent, acrid, aromatic, astringent, resinous (Wood, 2009; Frawley and Lad,
1986; Bensky et al., 1994)
Taste Differentiations Among Phenotypes: Following from different chemistries, species
and phenotypes vary in taste. McDonald (2012) describes the higher volatile oil strains (A.
calamus 3n &4n) as heavy, oily and aromatic while he writes the native North American
variety (A. americanus) is more well rounded in its action and has a taste profile that is
more bitter, spicy and “zingy.”
Summary of Actions (Skenderi, 2003 ;Tierra, 2008; McDonald ,2012; Frawley and Lad,
1986; Benskey et al., 2004):
•
Antispasmodic (particularly smooth muscle)
•
Anticatarrhal
•
Carminative
•
Orexigenic
•
Aromatic Bitter
•
Anti-bacterial
•
Insecticidal
•
Fungicidal
•
Emetic (in higher doses)
•
Expectorant
•
Nervine
•
Opens Orifices
•
Transforms phlegm and removes dampness
•
Stimulant/Energizer/Relaxant
•
Mental Rejuvinative
Actions Separated Out According to Eclectic, Traditional, and Modern Herbalists:
Attributed actions vary depending on source. For the most part, everyone agrees calamus
works on the digestive tract, use as a nervine and expectorant is less uniform.
•
PDR for Herbal Medicines 4th Ed (Thomson Healthcare, 2007): stomachic,
carminative, digestant, sedative, rubefacient, neurotherapeutic
•
Skenderi (2003): aromatic, bitter tonic, demulcent, antispasmodic, carminative,
astringent, mild neurocirculatory stimulant
•
Tierra (2008): stimulant, carminative, expectorant, emetic
•
Smith (1999)aromatic bitter, carminative, tonic to mm of membrane of mouth and
throat
•
Ayurveda:
stimulant,
rejuvenative,
expectorant,
decongestant,
nervine,
antispasmodic, emetic (Frawley and Lad, 1986); energizer, antispasmodic, nervine
(Khalsa & Tierra, 2008)
•
Culbreth (1927): Stimulant, carminative, tonic bitter, aromatic; dyspepsia, colic,
flatulency, coughs
Action Differentials Among Species: McDonald (2012) writes Indian Acorus (A. calamus) was
favored among the eclectics after a passage in King's American Dispensatory reading
"Persian and East Indian calamus is said to be of better quality than that of other parts of
the world". This species, McDonald writes, acts more strongly on the digestion containing
higher volatile oil content. While the eclectics preferred A. calamus, McDonald prefers A.
americanus, which he describes as “more balanced” in action. Depending on what activity
or qualities one is looking for, they both have their place, though they are slightly different
places.
Summary of Uses: (Wood, 2009; Smith,1999; Hoffman, 2003; Skenderi,2003; Frawley and
Lad, Bensky et al., 2004; McDonald, 2012)
Gastrointestinal:
atonic
dyspepsia/unease
in
stomach/bowels,
putrid
flatulence,
hypertonic digestion (Snow as cited by Bunce, 2011), deficient or excessive digestive
secretions (Treben; Cabreara as cited in Tierra & Khalsa, 2008, p. 113), increases
peristalsis, spastic gastrointestinal tract, loss of appetite, anorexia due to convalescence,
anorexia due to stomach cancer, minor diarrhea, constipation, gastric ulcers, colicky pain,
digestive discomfort with bacterial involvement, dysentery, bad breath
Gastrointestinal/Nervous System: IBS, reflux if also scattered, anorexia nervosa
Nervous System: failing
memory
due
to
old
age/drug
abuse,
improves
mental
focus/sharpens memory, lack of comprehension, inability to grasp words, impaired
consciousness, restore power of speech after stroke, comma, shock, insanity, depression,
anxiety, neuralgia, headache, anxiety from tobaccos cessation, epilepsy, neuropathy
•
Added to baths to reduce nerves and offer a “state of tranquility” (Tierra, 1998,
p.108).
•
Aid to quit smoking tobacco or marijuana (Tierra,1998; Treben)—Tierra cites its
ability to help with lack of mental focus for its use as an antidote for marijuana;
Tierra also writes that chewing calamus root and then smoking creates a “mild
feeling of nausea” p.108
Respiratory: spastic/irritable dry coughs, spastic bronchitis, tracheitis, chest cold, common
cold, asthma, chronic catarrh, sinus headache, toothache, inflammation of mouth and
throat, throat cold, head cold, rhinitis with reduced thinking, catarrh in head, congested
sinuses, laryngitis/horse voice worse from over use/sing in atmosphere with tobacco smoke,
toothache
•
McDonald (2012) writes calamus “excels in addressing throat colds, sore throats,
irritable coughs, chest colds, and head colds,” particularly he goes on to explain,
when one has the feeling of head congestion, a completely stuffy nose along with a
“hazy dullness.” Also “strongly antimicrobial,” McDonald chews Calamus when been
exposed to contagions.
•
Oil nasya: an “exceptionally decongestant” (McDonald, 2012) preparation for using
calamus to clear up stuffy sinuses and a stuffy mind. (See preparation and dose for
recipe.)
Musketal Skeletal: rheumatic pains, arthritis, cold achy joints
Endocrine: increased energy, allays hunger, relaxant despite stimulant qualities, potentially
useful in diabetes
Reproductive: Henriette Kress (2012) writes of chewing on calamus root for endometriosis
and of using it for menstrual cramps.
Cardiovascular/Circulatory:
•
Treben uses warm calamus baths for chilblains by steeping roots overnight in water,
bringing to a boil the next day, infusing for five minutes, then soaking the area
affected in the preperation; also uses for cold hands and feet
Specific Indications:
Gastro-Intestinal
•
Atonic dyspepsia-slow, sluggish, deficient digestion (Bunce, 2011; McDonald, 2012)
especially associated “with tension, and perhaps infection or purification” (McDonald,
2012), flatulent digestions
•
Hypertonic digestion (Snow as cited by Bunce, 2011))-clamped down, spasmodic,
cramping digestion
•
Digestive discomfort from dampness and turbidity causing epigastric pain, abdominal
distention, poor appetite and a greasy tongue (Bensky et al., 2004)
•
Dizziness and nausea, McDonald considers a “primary indication” (2012)
•
GERD, especially if scattered and anxious (McDonald, 2012)
•
First choice her for nausea associated with panic attacks (McDonald, 2012)
Nervous System
•
Anxiety
◦
Of anxiety and calamus, McDonald writes, “it is of this virtue of the plant that has
really stood out to me, and set it wholly apart from any other remedy I might
consider to ease anxiety” (2012). He describes its action as “unscattering energy.”
◦
“Invaluable”
for
anorexia
nervosa
because
of
bitter/anxiolytic
combination
(McDonald, 2012)
◦
•
Nausea associated with panic attack (McDonald, 2012)
Trauma: post trauma that was handled well in the moment but flashback result in
nausea/dizzyness-Acorus brings back to reality (McDonald, 2012)
Epilepsy
•
◦
Tremors and loss of consciousness or seizures originating from phlegm-heat
(Bensky et al., 1994)
Mental Clarity
•
◦
Satvic, considered one of the best herbs for the mind and congested thinking
◦
Lack of mental focus—Ayurvedic traditional use, Tierra speculates coming out of its
ability for “focusing the digestive power” (Tierra.1998; p.108)
Other:
•
Laryngitis caused/aggravated by speaking, yelling and/or singing (McDonald)
Stimulating and Relaxing
Calamus is considered both simulating and relaxing. While this may vary some with phenotype
and species, both qualities do come up across the board. McDonald (2012) explains this
seeming contradiction well:
“"Stimulant" and "relaxant" shouldn't be seen a contradictory uses occupying opposite
ends of a polarity: stimulating herbs increase the expression of the vital force, while
relaxants relax resistance to that expression. They work together in a complimentary
fashion to achieve the same end: better flow of energy and vitality. Calamus isn't a
sedative (it won't put you to sleep), but can be incredibly effective in treating
anxiety. Incredibly effective”
Calamus and the Voice: Cross-culturally, calamus has a traditional association with the voice.
Herbalist Joyce Wardwell explains, as quoted by McDonald (2012), the use of Calamus during
the Inipi Ceremony. During hours of singing on end at a Pow-Wow, singers may chew on a bit
of calamus root to help numb the vocal chords and continue singing. Wardwell reports that
calamus “increase(s) saliva, increase(s) range…and center(s) ones energy.” In Ayurveda,
calamus is called vacha, meaning “to speak” or “speech.” Khalsa writes this “refers to its
action on the fifth chakra and its propensity to help you speak from your highest
consciousness” explaining that it is considered “to stimulate the power of self-expression.” On
a more literal level, Khalsa (2009) discusses the use of Vacha with autistic clients to promote
self-expression connecting the brain and the mouth, promoting verbalization, communication,
articulation,
speech and self expression. Wood (2009) points out the rhizome looks very
much like the trachea.
Calamus and Autism: Khalsa (2009) discusses the use of calamus in autism as both a plant to
promote self-expression and for its use in epilepsy, a condition often occurring in conjunction
with autism.
Calamus as “Teacher Plant:”
This section affords a whole other write up about calamus but I would feel remiss in not
including some mention of it. Those who have a relationship with calamus, and in many of the
traditional uses, calamus is considered a sacred plant. Jim McDonald has a very deep
relationship with this plant, considering calamus a “Teacher Plant.” He writes (2012):
“ Calamus is best understood as a plant whose spirit teaches those who make
relationship with it how to live in a good way upon the Earth; to live gently, lucidly,
perceptively.
She is subtle, and teaches a subtlety of perception, a subtlety of
awareness”
SAFETY PROFILE
Concerns: There is a broad range of suggestions regarding the safety of calamus ranging
from not fit for human consumption to safe. The concern is due mainly to one constituent,
b-asarone. The concern stems mostly from numerous studies where rats were fed large
quantities of b-asarone. A document published by the Belgian Scientific Committee on Food
(2002) details the numerous experiments (many of which are unpublished) done. The
document can be accessed hear in full for a thorough review of the studies:
Despite long standing traditional use even of the high b-asarone content containing
phenotypes, based on these studies, it is generally recommended that these varieties only
be used short term or that varieties and species with lower b-asarone content are used
instead. The FDA prohibits use of calamus, calamus oil, or extract of oil in food (2013). Mills
and Bone (2005) suggest use only of Acorus with low levels of b-asarone and that the
isolated volatile oil not be ingested. In their more recent edition of their book (2012), Mills
and Bone still list A. calamus in an appendix of “toxic or potentially toxic herbs” that should
not be taken during pregnancy or lactation and that are “not recommended for internal use
under any circumstances” (p.968). The Herbal PDR 4th ed, summarizes that with proper
dosage, there are no known health hazards or side effects but to avoid long term use. The
AHP gives calamus a safety rating of 1, meaning “herbs that can safely be consumed
appropriately” (1043). In an earlier publication, McGuffin writes, “the potential hazard of low
doses of… b-asarone…is very minimal” (2007,134). However, he goes on to write that long
term use of b-asarone containing herbs is not advisable. In accordance with the caution to
avoid large dose (which would result in emesis) or long term use, calamus was traditionally
used in some cultures only in small amounts and for shorter periods of time (Bensky et al.,
1994; Thompson 1995).
Other herbalists (McDonald) do not feel the concern over the use of the rhizome (versus
large isolated quantities of b-asarone) is warranted writing he does not “worry at all” about
the use of the whole plant as potentially carcinogenic (2012). Indeed, in every experiment
with negative effect cited in the Belgian Scientific Committee on Food Publication (2002),
doses of b-asarone where far higher than suggested doses of the whole plant in terms of
mg/kg of body weight.
Additionally, many of the studies deeming b-asarone problematic in that publication were
done in the 1960s and 70s. More recent studies (Muthuraman and Singh, 2012; Shah et al.
2012) challenge the conclusions made by previous studies regarding the safety of Acorus.
Of additional consideration, is the effect various preparations of A. calamus may have on the
presence of b-asarone (see section in dose and prep below).
A. americanus and the 2n phenotype of A. calamus are considered safe as they do not
contain b-asarone as long as they are positively identified (tricky to do both in commerce
and in the field).
Pregnancy and Lactation:
Herbs containing b-asarone should be avoided in pregnancy and lactation. McDonald,
though not concerned with the b-asarone content, still advises against using calamus during
pregnancy feeling it is more “overtly medicinal plant” than is advisable to use during
pregnancy.
Other Concerns:
•
Emetic in high doses
•
More suited to Vata and Kapha then Pitta
•
Not in deficient yin (Bunce, 2011)
•
Antagonizes ephedra (Bunce, 2011)
•
“It can easily be misused by giving it too freely, or in irritable conditions of the
stomach and bowels “ (Cook, 1869). Use gently if going to use in a condition like
IBS.
Interactions:
•
No clinical trials or case reports of drug interactions.
•
Animal studies show potentiation of sleep time induced by pento-barbitone (Gardner,
2013).
•
Moderate CYP450 interaction potential (Pandit et al, 2010)
DOSAGE AND PREPERATION
Notes on Preparation and b-asarone:
A 2009 study (Chen et. al) concluded decoction of the root, as is done in Chinese Medicine,
reduces the b-asarone. (This preparation is most likely lacking in other essential oils
attributed to the carminative, antispasmodic effect of Acorus).
Two studies out of India, one published in 2013 (Gholkare et al.) and in 2012 (Bhat et al.),
discuss and evaluate the traditional process of Shodhana or sodhana prakriya (Gholkare et
al, 203), translated as
“purificatory procedures” (Baht et al, 2012) or “detoxification
process” (Ghokare, 2013) or just simply defined as “processing” (Ilanchezhian et al., 2006).
Bhat et al. (2012) explains shodhana is designed “to overcome the undesired effects from
various poisonous and nonpoisonous drugs.” Oddly, this particular study does not once
mention b-asarone, explaining the reason for shodhana of calamus is not elucidated in any
of the Ayurvedic texts the study refres to, but speculating the reason it is to mitigate the
emetic effects of calamus.
The later study (Gholkare et al., 2013),however is specifically geared at assessing the
effects of shodhana on b-asarone. While shodhana prakriya is a traditional way of
processing certain plants, it not entirely clear in either of the studies, nor with further
research, if shodhana prakriya for calamus specifically is a traditional preparation. It seems,
that most likely, this is a modern use of a traditional process. Gholkare et al. explain that it
is due to the presence of b-asarone that calamus undergoes shodhana in the Ayurvedic
system. According to Bhat (2012), the Ayurvedic pharmacopoeia of India as recommending
sodhana be applied specifically to calamus. (Bhat, 2012).
Various versions of sodhana were carried out in both studies essentially involving three
three hour session of boiling in various substances, including water in some of the trial,
drying, washing, and then drying again. Sodhana also may involve steaming.
Gohlkar et. al. concluded that b-asarone was reduced in the three different shodhana
process tried (one traditional, the other two modified), attributing the decrease of b-asarone
to volatilization. Additionally, other substances used during the shodhana process may
contribute to decrease in b-asarone content (Laddha et al., 2009).
While I did not come across any mention of calamus being prepared traditionally in this
way, decoction in milk (Tierra and Khalsa, 2008; Frawley and Ladd, 1986) or water (Frawley
and Ladd) does appear to be traditional. This would also serve to volatize some of the
essential oils (though not as much as nine hours of boiling done in the shodhana processes).
Summary of Dosage and Preparation Recommendations:
Tincture Prep:
•
British Herbal Pharmacopeia: 1:5 60% alcohol (3n variety)
•
Galen’s Way Herb Company: 1: 1.5 40-45% alcohol
Ayurvedic Tradition (Frawley and Ladd, 1986):
•
250-500mg of powder decocted in either milk or water or made into a paste
•
Paste applied externally to forehead for headaches or on painful arthritis joints
•
Nasal herb “perhaps the best” for administration in nasal congestion and nasal
polyps
Chinese Tradition: (Bensky et al., 2004): 3-6g QD
Culbreth (1927): 1-4g dried rhizome
Smith (1999): 30-40 drops BID-QID
Tierra (2008):
•
3-9g in infusion
•
tincture: 10-30 drops
•
1tsp dried root infused
McDonald (2012): Is a big advocate of simply chewing on the dried rhizome, 1-2 tbsp.
While this is his preferred method, if one is to take an aqueous extract, he prefers a cold
infusion steeped overnight. Maria Treben concurs writing “the calamus root tea is only
prepared as a cold infusion” at a dose of 1tsp per ¼ litre of cold water. Treben suggest cold
infusing overnight then lightly warming with a waterbath in the morning.
British Herbal Pharmacopoeia (1983):
•
1-3g dried herb (3n variety) or 1-3g in infusion TID
•
2-4ml of 1:5 tincture as a dose
Candied: Historically, the root was often candied.
Topical Preparations:
•
Ayurveda-Paste applied exteranlly to forehead for headches or on painful arthritis
joints (Frawley and Ladd, 1986):
•
Ayurveda-Nasal herb “perhaps the best” for administration in nasal congestion and
nasal polyps (Frawley and Ladd, 1986)
•
Oil Nasya for Decongesting Sinuses and a “Foggy Mind” (McDonald):
1. Infuse root in oil and water over a double boiler, heating until all water
evaporates.
2. Strain root.
3. Laying down, with head tilted back to prevent dripping, apply a little oil to nostril
and snuff into the sinuses.
•
Calamus Bath: “About 200 gm. of Calamus roots are soaked in 5 litres of cold water
overnight, brought to the boil the next day, allowed to infuse and added to the bath
water” (Treben).
•
Poultice (Bunce, 2011)
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Black Cohosh (Cimicifuga racemosa) as
an Alternative to Hormone Replacement
Therapy for Menopausal Symptom
Control
Leilani Courtney
Menopause is a change that occurs during the
fourth and fifth decades of a woman’s life,
when
natural
ovarian
senescence
occurs,
resulting in the gradually change of hormonal
levels of estrogens and androgens. Sometimes,
this process is induced by surgical menopause
or
ovarian
treatment
failure
as
(Al-Azzawi,
a
cause
2009).
of
cancer
Under
all
circumstances, the declining, and often widely
fluctuating, levels of estrogen and androgens
can produce a variety of symptoms in many
tissues of the body.
The signs of this change
can include vasomotor symptoms, (hot flashes,
night
sweats),
decreased
bone
density,
changes in mood and energy (psychological
problems,
insomnia,
poor
concentration
&
cognition, depression), loss of pubic hair and changes in the genital tissues (vaginal
atrophy, vaginal dryness, endometrium), and sexual desires and functions (Laakmann,
2012).
All women at some point will go through this change, and as there is an estimated 50
million women in the United States (80% showing symptoms) that have reached
menopause to date (“Menopause,” 2013). It is no wonder that treating these symptoms is a
primary concern for health care practitioners and women alike.
Hormone replacement
therapy (HRT) use synthetic hormones, that may or may not be identical to those made in
the human body, but are believed to act similarly enough in order to relieve moderate to
severe symptoms (Hendrix, 2007).
HRT has also shown some beneficial effects on bone
health and osteoporosis (Low Dog, 2003), although as more women undergo this treatment,
many are finding that the risks are outweighing the benefits – showing a recent decline of
50% in hormone replacement therapy (Ross, 2012). Since this synthetic form of therapy
was initiated before there was sufficient understanding of the molecular mechanisms of
estrogen (and their similar looking synthetic replicas), several years of this on-going
therapy has resulted in known side effects of bloating, breast tenderness, cramping,
irritability, depression, breakthrough bleeding, or a return to monthly periods (Low Dog,
2003). More potentially serious side effects include increased risk of endometrial, ovarian
and breast cancers (Rossouw, 2002) from hormone induced estrogen receptor-positive cell
proliferation (Low Dog, 2003). The risks for these serious health concerns, in particular the
cancers associated with HRT, are higher in women over the age of 55 years and for those
that have used HRT for more than 5 years (Lieberman, 1998). What was once believed to
be a healthy alternative, the Women’s Health Initiative found enough associated risks with
HRT that in 2002, the US Preventative Services Task Force voiced a published
recommendation against the routine use of HRT for prevention of chronic conditions of
menopause (“Menopausal hormone, et al,” 2012).
For women that do not wish to experience the symptoms of menopause, but also do not
wish to undergo HRT, there are natural and effective alternative therapies that have long
traditional specifications for treatment of these symptoms. There is a general skepticism of
the efficacy and safety of medicinal herbs that have not undergone clinical testing, and now
with the ever-growing interest in natural medicine, this field is gaining the interest of many
scientific evaluations. Although there are many herbs that aid in the menopause treatment,
the rhizome of black cohosh (Cimicifuga racemosa) is the most widely studied (Lieberman,
1998).
Black cohosh has a long history of clinical use and has been used in Europe for almost 50
years to manage menopausal symptoms (Low Dog, 2003). This herb was previously
described as a phytoestrogen, but with recent evidence, it is indicated that black cohosh
may act more like estrogen in only a few parts of the body. The estrogenic effects of this
plant are understood to reduce hot flashes via the brain, potentially help to prevent or treat
osteoporosis in the bones, and possibly alleviate dryness and thinning of the vagina
(Seidlová-Wuttke, 2003).
Interestingly though, unlike current estrogens in HRT, that act
non selectively as an agonist in all tissues that contain estrogen receptors, it does not
appear to act like estrogen in the breast or the uterus, and therefore reduces the
possibilities for estrogenic cancer to form in those tissues (Bodiet, 2002). Another proposed
mechanism of action for black cohosh is through serotonergic pathways.
This was
suggested after it was discovered that women on anti depressants experienced less hot
flashes and night sweats, therefore it is possible that black cohosh works by also inhibiting
the reuptake of serotonin (Oktem, 2007).
Although it is recognized that a large, long-term study using rigorous methodology is
needed to fully understand the mechanisms of treatment and effects, after reviewing much
of the data regarding safety and efficacy of black cohosh, it should be reassured to be a safe
option for women who wish to take it for relief of menopausal symptoms.
Even if not
immediately as effective as HRT, there are considerably less side effects, and seen to be as
effective over time as hormone replacement therapy (Low Dog, 2003).
REFERENCES
Al-Azzawi, Farook, and Santiago Palacios. "Hormonal changes during menopause." Maturitas
63.2 (2009): 135-137.
Bodinet, Cornelia, and Johannes Freudenstein. "Influence of Cimicifuga racemosa on the
proliferation of estrogen receptor-positive human breast cancer cells." Breast cancer
research and treatment 76.1 (2002): 1-10.
Dog, Tieraona Low, Kara L. Powell, and Steven M. Weisman. "Critical evaluation of the
safety of Cimicifuga racemosa in menopause symptom relief." Menopause 10.4 (2003):
299-313.
Hendrix, Susan L. "Menopause: Merck Manual Home Edition." Menopause: Merck Manual
Home Edition. Merck Sharp & Dohme Corp., a Subsidiary of Merck & Co., Inc, June 2007.
Web. 17 Feb. 2013.
Laakmann, Elena, et al. "Efficacy of Cimicifuga racemosa, Hypericum perforatum and Agnus
castus in the treatment of climacteric complaints: a systematic review." Gynecological
Endocrinology 28.9 (2012): 703-709.
LIEBERMAN, SHARI. "A review of the effectiveness of Cimicifuga racemosa (black cohosh)
for the symptoms of menopause." Journal of Women's Health 7.5 (1998): 525-529.
"Menopause." University of Maryland Medical Center. N.p., n.d. Web. 17 Feb. 2013.
"Menopausal Hormone Therapy for the Primary Prevention of Chronic Conditions." : U.S.
Preventive Services Task Force Recommendation Statement. AHRQ Publication, Oct. 2012.
Web. 17 Feb. 2013.
Oktem, Mesut, et al. "Black cohosh and fluoxetine in the treatment of postmenopausal
symptoms: a prospective, randomized trial." Advances in therapy 24.2 (2007): 448-461.
Osmers R, Friede M, Liske E, et al. Efficacy and safety of isopropanolic black cohosh extract
for climacteric symptoms. Obstet Gynecol. 2005;105:1074-1083.
Ross, Stephanie Maxine. "Menopause: a standardized isopropanolic black cohosh extract
(remifemin) is found to be safe and effective for menopausal symptoms." Holistic Nursing
Practice 26.1 (2012): 58.
Rossouw, J. E., et al. "Writing Group for the Women’s Health Initiative Investigators. Risks
and benefits of estrogen plus progestin in healthy postmenopausal women: principal results
from the Women’s Health Initiative randomized controlled trial." Jama 288.3 (2002): 32133.
Seidlová-Wuttke, Dana, et al. "Evidence for selective estrogen receptor modulator activity in
a black cohosh (Cimicifuga racemosa) extract: comparison with estradiol-17beta." European
journal of endocrinology 149.4 (2003): 351-362.
Ethnobotanical Uses of Oplopanax horridus
Suzyanna Mapachi
From the Cascades and north
along the Pacific coast grows
Oplopanax, an important
medicinal plant that is still used
by various indigenous groups of
the region in which it grows.
Oplopanax is an unmistakable
spiny shrub that can grow up to
ten feet tall in the right
conditions. (2) I encountered
Oplopanax growing in the
temperate rainforests of the
Olympic Peninsula, where its quite moist year round with a shady forest canopy. The leaves are
maple-shaped and large to be able to catch the bits of sunshine that make its way through the
canopy of sitka spruce, western hemlock and douglas fir. The most striking feature of this plant to
me are the spines that cover the entirety of its stem. Its been used extensively as a physical
medicine and as a spiritual medicine, and these two types of medicine often overlap in traditional
coastal cultures. (3)
Oplopanax horridus's common name is devil's club – most likely due to its diabolical-seeming
spiky stems. There are 13-15 known etymons for Oplopanax in over 25 different languages. (2)
While there is very little pharmacological research, we can gain some insight into its medicinal
uses from the traditional cultures that have a relationship with Oplopanax.
The first ethnographic record of the use of devil's club is from 1843, when the chief physician
for the Russian American company, Eduardo Blaschke, reported the use of devils club ash as a
treatment used by the Tlingit for sores. (1) Listed in the following paragraphs are specific uses by
different tribes of people.
The Tlinget, of southern Alaska and coastal British Columbia, used seal fat to infuse the inner
bark and this preparation was drunk as an emetic and cathartic. The inner bark was chewed and
poulticed onto wounds to relieve pain as an emergency analgesic. The infusion of the bark and
root were drunk for general strength, colds, chest pains, arthritis, ulcers, constipation and
tuberculosis. It was mixed with pine pitch for skin wounds and abrasions. The dried inner bark
was laid on cavities for pain relief. (3)
The Tanaina, of southern Alaska, made a decoction of the stem for fever, used the inner bark
decoction for tuberculosis, stomach upset, coughs, cold, swollen glands, boils and sore throats
and other infections. (3)
The Haida, of northern British Columbia, used the decoction of the inner bark in a sea water
solution that was drunk for 9 days for rheumatism and arthritis. The stems were also used like a
whip as a counter-irritant for arthritis. The bark was chewed and the juice swallowed for colds.
The berries were used on childrens heads to treat lice and dandruff. (3)
The Gitksan, of the Skeena river in British Columbia, used a decoction of Oplopanax stems as a
purgative in treating gonorrhoea, and with Viburnam as a diuretic. The bark was also used
mashed with Abies bark, Pinus gum and Lysichitum root and applied warm to boils, ulcers and
rheumatism. (3)
Oplopanax has documented use as an appetite stimulant, for arthritis and rheumatism, as birth
control, as a blood purifier, for broken bones, for cancer, during childbirth and menstruation, as an
emetic and purgative, for fever, flu, gall stones, haemorrhaging and blood disorders, for heart
disease, for internal and external infections, as a laxative, for lice and dandruff, for measles, as an
analgesia, for pneumonia, various respiratory ailments, for coughs, colds, as a skin wash, for
various sores, stomach trouble, as a tonic, for venereal disease and vision problems. The most
widespread traditional uses has been for the treatment of external and internal infections, from
cuts and scrapes to tuberculosis. The most common preparation is a decoction of the stem bark.
(1)
There are many ethnographic accounts of spiritual applications of Oplopanax. It was used by
many tribes as a protective plant. Various groups used the bark and stems as an amulet, bathed
in the infusion for protection, and the ash was used in protective face paint for ceremonial dancers
who were vulnerable to evil influences during rituals. (1) The Straits Salish and the Ditidaht
combined devils club charcoal with bear grease for making a blue tattoo ink. Devils club was used
in homes as a wash to purify the space after a sickness or death, and placed in the home to
protect against bad influences. (1)
Devils club has also been used in everyday utilitarian life. The woody stems were carved into fish
lures, since the wood is light weight. The Hesquit scraped the spines off the bark and boiled them
down with Vaccinium and Lonicera berries to make a paint and basket dye. (4)
Acknowledging that ethnobotanical research is often a form of colonization is important to say in
this paper. I believe that the only real primary sources on Oplopanax are the people indigenous to
the region it grows, and have a long history of co-existence with this plant.
1.
Lantz, Trevor C., Swerhun, Kristina, Turner, Nacy J. - Devil's Club (Oplopanax horridus): An
Ethnobotanical Review (HerbalGram 2004) Issue 62 pages 33-48 http://cms.herbalgram.org/herbalgram/issue62/article2697.html
2.
Moore, Michael – Medicinal Plants of the Pacific West (Santa Fe: Red Crane Books, 1993)
pg. 125-128
3.
Turner, Nancy J. – Traditional use of devil's-club (Oplopanax horridus; Araliaceae) by native
peoples in western North America (Journal of Ethnobotany, 1982) pg. 17-38
4.
Pojar, Jim; MacKinnon, Andy - Plants of the Pacific Northwest Coast : Washington, Oregon,
British Columbia and Alaska (Lone Pine Publishing, 1994) pg. 82
Chocolate and its Antioxidant Content
Rachel Davey
The health benefits gained from
consuming
chocolate
significant
come
from
antioxidant
its
content.
Procyanidins, an antioxidant in cacao, is
found in higher concentrations in cacao
than
2002)
cranberries
When
and
blueberries.(Gu
compared
to
other
chocolate products it was determined
that the amount of cocoa solids has a
direct correlation to the amount of procyanidins and the therefor the amount of antioxidant
capacity. (Gu 2006, Figure 3 & 5)
The antioxidants found in cacao are responsible for
suppressing low-density lipoproteins (LDL) oxidation and the formation of atherosclerosis
(Kurosawa, 2005); inducing vasodilation and reducing hypertension in men (Fisher, 2003);
increasing insulin sensitivity (Grassi, 2005); and inhibiting the growth of breast cancer cells
(Ramljak, 2005).
In response to studies indicating that dark chocolate had a significant antioxidant content,
(Miller, 2006) more and more “dark chocolate” products began showing up on shelves.
A
chocolate bar with a cocoa solid content of 40-100% is now referred to as “dark chocolate”.
Attempts to test the antioxidant content of cocoa or chocolate and its subsequent products have
illuminated many variables (McShea, 2008) which make it difficult to assess: genetic variability,
processing, product recipes and bioavailability of the antioxidant constituents.
High
variability
of
polyphenol
content
in
different
cacao
varieties;
epicatechin
concentrations among freshly harvested seeds of verified genetic origin ranged from 21.89 –
43.27mg/g.
(Richelle,1999; Thomas-Berberan, 2007) Similar variation has been found between
batches and growing regions. While cacao has remarkable health benefits it is safe to say that a
majority
of
chocolate
consumers
today
do
not
eat,
raw,
unfermented,
cacao
as
the
Olmec/Mayan/Aztec people did nearly 1000 years ago. The processing of the cacao takes place
to remove the bitterness and astringency lent by theobromine, caffeine, l-leucine, procyanidins,
and catechin flavonoids.(Stark, 2006), therefore removing the bitters will inevitably involve the
breakdown or removal of some of these constituents.
Processing on the simplest level involves, fermentation of the fresh seeds, drying &
roasting and finally winnowing. Fermentation involves spontaneous inoculation of the seeds over
the course of seven days, primarily from yeasts and later bacteria. Fermentation occurs unevenly
within a batch allowing for much variety in the outcome. It is during this first step that some of
the bitter antioxidants are destroyed. This may be because of the temperature reached during
fermentation 50oC (122oF) or exposure to the by products of fermentation: lactic acid, ethanol
and acetic acid.
Under-fermented cacao seeds contain more antioxidant than fully fermented
seeds; a technique utilized by producers interested in a “raw” product. The seeds are then dried
until much of the moisture is removed. The seeds are washed off and then roasted. Roasting
serves to loosen the husk from the fermented cotyledon as well as to bring out the favorable
flavors of the chocolate.
Temperatures at this point reach as high as 150oC (302oF).
While
catechins have been proven to be fairly stable at high temperature (Wang, R, 2006) epichatechins
may require the stabilizing influence of other present molecules to remain intact.
Winnowing removes the woody husk of the cacao seed by shaking it violently; during this
process the cotyledon is broken into 2-mm fragments called nibs.
Sometimes the nibs are
roasted again to further enhance the flavor. The nibs, which are comprised of 50% fat (cocoa
butter) can be melted down into liquor or they can then be pressed to separate the cocoa butter
from the cocoa solids, which are then ground into a fine cocoa powder. Cocoa powder contains
approximately 87% cocoa solids and is where the antioxidants are found. (Gu 2006)
Processing of the chocolate until it reaches the stores follows a series of steps that involve
secret “tricks of the trade” that are largely unknown to people outside the industry. Pressing and
grinding further expose the cocoa to high temperatures. Conching is a multi-day heat treatment
step, which applies gentle grinding to improve the flavor characteristics and reduce the
concentration of free acids and other volatile by-products from the cacao bean. (McShea, 2008).
“Dutching” is an alternative process to conching and utilizes a mild base to neutralize the free
acids.
Antioxidants are significantly reduced during the Dutching process, making this process
undesirable for maintaining the antioxidant activity in chocolate products. (Miller, 2006)
The next step is typically to add, dairy fats, sweeteners and emulsifiers, whose purpose is
to improve on the flavor or mask remaining bitterness. The addition of fats, sugars, emulsifiers
etc. present their own risks as well as further dilute the overall presence of cocoa solids and
therefore antioxidants in the resulting product. When does chocolate cease to be chocolate?
The U.S.D.A has established reference amounts for commonly eaten cocoa and chocolate
products: natural/Dutched powders: 5g, baking chips and unsweetened chocolate: 15 g and milk/
dark chocolate: 40 g. A serving, based on the reference amount, of milk chocolate, dark
chocolate, or unsweetened chocolate would provide on average 108, 517, and 312 mg of
procyanidins; and 3200, 9100, and 6950 Trolox equivalents (TE) of antioxidant capacity (AOC),
respectively.
These amounts exceed those in most foods on a per-serving basis. The
consumption of one serving of these chocolates would provide more procyanidins and antioxidant
capacity than the average daily amount consumed in the United States (Gu 2004, Wu 2004).
The bio-availability and net benefit of the resulting antioxidants when combined with the
added ingredients of the chocolate product being consumed needs to be properly weighed. Are
the health risks of consuming sugar and fats offset by the presence of antioxidants? Current data
on bioavailability suggests that the presence of other ingredients does not seem to prevent the
uptake of epicatechin. (Keough, 2007; Roura, 2007)
In the end I believe that chocolate in its darkest and or rawest forms can truly be a benefit
to someone’s health as long as the goal is to ingest antioxidants and not dessert. You have to
separate the chocolate from the bar.
Sources
Fisher, N. D.; Hughes, M.; Gerhard-Herman, M.; Hollenberg, N. K. Flavanol-rich cocoa
induces nitric-oxide-dependent va- sodilation in healthy humans. J. Hypertens. 2003, 21,
2281- 2286.
Grassi, D.; Lippi, C.; Necozione, S.; Desideri, G.; Ferri, C. Short- term administration of
dark chocolate is followed by a significant increase in insulin sensitivity and a decrease in
blood pressure in healthy persons. Am. J. Clin. Nutr. 2005, 81, 611-614.
Gu, L., House, S.E., Wu, X., Ou, B., and Prior, R. L. Procyanidin and Catechin Contents and
Antioxidant Capacity of Cocoa and Chocolate Products.
J. Agric. Food Chem. 2006, 54,
4057−4061
Gu, L.; Kelm, M. A.; Hammerstone, J. F.; Beecher, G.; Holden, J.; Haytowitz, D.; Gebhardt,
S.; Prior, R. L. Concentrations of proanthocyanidins in common foods and estimations of
normal consumption. J. Nutr. 2004, 134, 613-617.
Gu, L.; Kelm, M.; Hammerstone, J. F.; Beecher, G.; Cunning- ham, D.; Vannozzi, S.; Prior,
R. L. Fractionation of polymeric procyanidins from lowbush blueberry and quantification of
procyanidins in selected foods with an optimized normal-phase HPLC-MS fluorescent
detection method. J. Agric. Food Chem. 2002, 50, 4852-4860.
Katz DL, Doughty K, Ali A.
Cocoa and chocolate in human health and disease.
Antioxid
Redox Signal. 2011 Nov 15;15(10):2779-811.
Keogh JB, McInerney J, Clifton PM. The effect of milk protein on the bioavailability of cocoa
polyphenols. J Food Sci. 2007;72(Suppl):S230–S233.
Kurosawa, T.; Itoh, F.; Nozaki, A.; Nakano, Y.; Katsuda, S.; Osakabe, N.; Tsubone, H.;
Kondo, K.; Itakura, H. Suppressive effects of cacao liquor polyphenols (CLP) on LDL
oxidation
and
the
development
of
atherosclerosis
in
Kurosawa
and
Ku-
sanagi-
hypercholesterolemic rabbits. Atherosclerosis 2005, 179, 237-246.
McShea, A et. al Clinical benefit and preservation of flavanols in dark chocolate
manufacturing. Nutrition Reviews 2008;66(1):630-641.
Miller KB, Stuart DA, Smith NL, et al. Antioxidant activity and polyphenol and procyanidin
contents of selected commer- cially available cocoa-containing and chocolate products in the
United States. J Agric Food Chem. 2006;54:4062–4068.
Ramljak, D.; Romanczyk, L. J.; Metheny-Barlow, L. J.; Thomp- son, N.; Knezevic, V.;
Galperin, M.; Ramesh, A.; Dickson, R. B. Pentameric procyanidin from Theobroma cacao
selectively inhibits growth of human breast cancer cells. Mol. Cancer Ther. 2005, 4, 537546.
Richelle M, Tivazzi I, Enslen M, Offord EA. Plasma kinetics in man of epicatechin from black
chocolate. Eur J Clinical Nutr 1999;53:22-6
Roura E, Andres-Lacueva C, Estruch R, et al. Milk does not affect the bioavailability of cocoa
powder flavonoid in healthy human. Ann Nutr Metab.
2007;51:493–498.
Stark T, Bareuther S, Hofmann T. Molecular definition of the taste of roasted cocoa nibs
(Theobroma cacao) by means of quantitative studies and sensory experiments. J Agric Food
Chem. 2006;54:5530-5539.
Tomas-Barberan F, Cienfuegos-Jovellanos E, Marin A, Muguerza B, Gil- Izquierdo A, Cerda
B, et al. A new process to develop a cocoa powder with higher flavonoid monomer content
and enhanced bio-availability in healthy humans. J Agric Food Chem 2007;55:3926–35.
Wang, R., et al. Kinetic study of the thermal stability of tea catechins in aqueous systems
usinf microwave reactor. J Agric Food Chem. 2006;54:5924-593
Wu, X.; Beecher, G. R.; Holden, J. M.; Haytowitz, D. B.; Gebhardt, S. E.; Prior, R. L.
Lipophilic and hydrophilic anti- oxidant capacities of common foods in the United States. J.
Agric. Food Chem. 2004, 52, 4026-4037.
Hypericum
and
HRT
Testosterone’s
Interactions with CYP450 System
Danielle Rissin- Rosenfeld
I decided to do my research paper
on
the
ways
perforatum
in
which
(St.
Hypericum
John’s
Testosterone
used
Replacement
Therapy
wort)
in
and
Hormone
(HRT)
are
metabolized, in order to determine whether
or not they are contraindicated.
There
evaluation
has
of
not been
risks
administration
for
of
thorough
testosterone
Female
to
Male
transgendered people, this includes a lack
of studies on
with
other
its effects and interactions
drugs
and
Therefore this paper is
the
research I
herbs.
[8,14]
a comparison of
have
found on both
subjects and in particular attempts to
evaluate
whether
contraindicated
Hypericum
alongside
is
Testosterone
administration.
Hypericum has been popularly used for depression. [5,6,12] Because of its wide use
for depression many studies have evaluated drug-herb interactions of Hypericum and
pharmaceutical drugs. [12]. Paul Bergner talks about the metabolism of Hypericum in Phase
I detoxification in the liver and the intestinal and kidney cells. [1] He says, “Many drugs are
mainly metabolized by the CYP3A enzymes, as are many fat soluble hormones, including
estrogens and cortisol and testosterone.” [1]
A study based on the interactions between Hypericum and oral contraceptives found
that
“Hypericum is a potent inducer of the hepatic cytochrome P450 (CYP) 3A4 enzyme
and the P-glycoprotein drug transporter, both of which can result in lower blood
concentrations of drugs that are substrates for these pathways.” [12] Another review also
stated that Hypericum “has been implicated in lowering serum concentrations and the
efficacy of several drugs, including oral contraceptives. Several reports have also
documented breakthrough bleeding and unwanted pregnancies with concomitant use of
Hypericum and oral contraceptives.” [13]
Oral
metabolized
contraceptives
by
CYP3A.)[11,14]
the
and
other
Cytochrome
The enzyme that
steroid
P-450
converts
hormones
enzyme
including
system
testosterone
in
the
testosterone
liver
are
(specifically
to a 5a- dihydrotestosterone
(DHT) is mainly found in androgen responsive tissue: brain, pituitary, skin, bone and liver.
After testosterone is metabolized in the liver 90% is excreted in the urine. [11] CYP2C19
was also found to oxidize testosterone enzymes and in human liver microsomes.[15]
HRT testosterone is often
taken
by
Female
to
Male (F to M)
transgendered
people, as well as people of many different genders, to develop characteristics such as
increased body hair, deepened voice, cessation of menses, clitoral growth, and increased
muscle mass. [8, 13] Testosterone is administered by either injectable or transdermal
preparations. Injectable formulations are most commonly used. [4,8,13].
The research of a transgendered male MD Nick Morton and Jamie Booth found that:
“There are numerous drugs that increase or decrease the activity of this enzyme. This
change in P-450 activity may cause increased or decreased levels of sex steroids as well as
other drugs metabolized by this system. Cytochrome P-450 Inducers may cause decreased
levels of testosterone.”[1, 12]
In an ex vivo study based on Hypericum’s induction of hepatic drug metabolism
through activation of the pregnane X receptor, a 48 hour isolation study took place. The
CYP3A4 enzymes were induced with crude ethanol extracts of St. John's wort, rifampicin (10
μM), or hyperforin (1 μM) and were added to the culture medium as 1,000× stocks in either
ethanol or dimethyl sulfoxide. This resulted in the binding of PXR which switched the
enzymes. [9] The study concluded that Hypericum activates the orphan nuclear receptor
PXR and consequently induced the expression of CYP3A4, meaning that Hypericum is likely
to interact with the many drugs that are metabolized by CYP3A4. [9]
CYP3A4 is shown to be one of the major P450 forms involved in catalyzing
Testosterone.[15] The most common form of interaction is when a foreign chemical (i.e.
Hypericum) acts as an inhibitor or inducer for the CYP enzyme metabolizing a drug. This
can result in slow or fast clearance of the drug and therefore reduce its effects.[13] Paul
Bergner says that, “Depending on whether the drugs are metabolized to their active form or
inactive forms by the enzymes, simultaneous consumption of Hypericum extracts may
either increase or decrease blood levels. Consequences could range from innocuous to fatal
depending on the nature of the drug and how critical the drug dose is to the patient's
health.” [1]
In conclusion
pharmaceutical
Hypericum
has been
found
to
be contraindicated
drugs, including HRT Testosterone.[1]
with many
Both Hypericum and
HRT
Testosterone are processed through the CYP450 pathway and specifically by CYP3A4.
[9,11, 13, 15]. Since Hypericum has been shown to be an inducer of CYP3A4, it may
decrease the desired effect of HRT Testosterone. [9,13,15] It may also result in other
side effects [1], but
there
has
been little
research
to determine
what
results may
occur.[8,14] Based upon my research I believe people receiving HRT Testosterone should
be cautious or avoid taking Hypericum concurrently. Taking HRT testosterone and
Hypericum at the same time may decrease the desired effects of testosterone, by speeding
up its metabolism through Hypericum’s inducing effects on the CYP450 pathway.
Unfortunately in reviewing the literature no case reports were found.
Bibliography
1.
(Bergner, P. Hypericum, drug interactions, and liver effects. Medical Herbalism
(2000)11(2):16)
2.
de Maat, Monique MR, et al. "Drug interaction between St John's wort and
nevirapine." Aids 15.3 (2001): 420.
3.
Ellingwood, 1919. The American Materia Medica. Digital image. Henriette's Herbal
Homepage. N.p., 2001-2013. Web. 15 Feb. 2013.
4.
Gooren, Louis J., Erik J. Giltay, and Mathijs C. Bunck. "Long-term treatment of
transsexuals with cross-sex hormones: extensive personal experience." Journal of
Clinical Endocrinology & Metabolism 93.1 (2008): 19-25.
5.
King's American Dispensatory, 1898. Digital image. Henriette's Herbal Homepage. N.p.,
1999. Web. 15 Feb. 2013.
6.
Komoroski, Bernard J., et al. "Induction and inhibition of cytochromes P450 by the St.
John's wort constituent hyperforin in human hepatocyte cultures." Drug metabolism and
disposition 32.5 (2004): 512-518.
7.
Maréchal, J‐D., et al. "Insights into drug metabolism by cytochromes P450 from
modelling studies of CYP2D6‐drug interactions." British journal of pharmacology153.S1
(2009): S82-S89.
8.
Moore, Eva, Amy Wisniewski, and Adrian Dobs. "Endocrine treatment of transsexual
people: a review of treatment regimens, outcomes, and adverse effects." Journal of
Clinical Endocrinology & Metabolism 88.8 (2003): 3467-3473.
9.
Moore, Linda B., et al. "St. John's wort induces hepatic drug metabolism through
activation of the pregnane X receptor.” Proceedings of the National Academy of
Sciences 97.13 (2000): 7500-7502.X receptor."
10.
Wentworth, J. M., et al. "St John's wort, a herbal antidepressant, activates the steroid X
receptor." Journal of endocrinology 166.3 (2000): R11-R16.
11.
Morton, R. Nick, MD, and Jamie Booth, MD. "Medical Therapy and Health Maintenance
for Transgender Men: A Guide For Health Care Providers." Medical Therapy and Health
Maintenance for Transgender Men: A Guide For Health Care Providers(2005): 1-98.
Web.
12.
Sarino, Lord V., et al. "Drug interaction between oral contraceptives and St. John's
wort: appropriateness of advice received from community pharmacists and health food
store clerks." Journal of the American Pharmacists Association47.1 (2007): 42-47
13.
Saxena, Akansha, et al. "Pharmacovigilance: Effects of herbal components on human
drugs interactions involving Cytochrome P450." Bioinformation 3.5 (2008): 198.
14.
Sherbourne
Health
Centre.
"Sherbourne
Report." Guidelines
and
Protocols
for
Comprehensive Primary Health Care for Trans Clients, Sherbourne Health Center(2009):
1-63. Web. 14 Feb. 2013. <http://www.sherbourne.on.ca/PDFs/Trans-Protocols.pdf>.
15.
Yamazaki,
Hiroshi,
hydroxylation
by
and
Tsutomu
cytochromes
P450
Shimada.
2C19,
"Progesterone
2C9,
and
3A4
and
in
microsomes." Archives of biochemistry and biophysics 346.1 (1997): 161.
testosterone
human
liver
Treating Vaginitis with Calendula
Emily Peters
Vaginitis or vulvovaginitis includes various
inflammatory conditions in the vagina, usually
accompanied by an infection, itching, irritation,
and
abnormal
vaginitis
vaginal
symptoms
are
discharge.
caused
Almost
by
all
bacterial
vaginosis, vulvovaginal candidiasis (VVC or a
yeast infection), and trichomoniasis. This report
will focus on treatment for VVC or undiagnosed
vulvovaginitis. VVC is usually caused by an overgrowth of Candida albicans, but can also be
caused by C. tropicalis and C. glabrata. Many women self diagnose and treat themselves for
vulvovaginal candidiasis without having a microscopically confirmed diagnosis. VVC is
especially difficult to diagnose because 50% of all women have Candida organisms as a part
of their normal vaginal flora. Specific symptoms of VVC include mild to severe vaginal
itching and irritation, possibly with a characteristic white curd-like vaginal discharge with a
mild yeast-like odor. The vulva can be inflamed, swollen, red and raw (Romm 256-259). The
Merck Manual calls VVC Candidal vaginitis. Specific symptoms they include are vulvar
burning or irritation, pruritus, dyspareunia (pain during vaginal penetration), dysuria
(painful or uncomfortable urination), and a white cottage cheese-like discharge that adheres
to the vaginal walls. Symptoms may increase the week before menses. A healthy vaginal
flora is kept in balance by Lactobacillus spp, preventing overgrowth of pathogenic bacteria
(Merck). Eclectic herbal physicians Harvey Wickes Felter and John Uri Lloyd did not use
distinct terms for different types of infection; they used the term leucorrhoea or vaginitis for
any white discharges of the vagina (Felter, Felter and Lloyd ).
In treating these infections, our goal is to both find the root cause and to relieve the
symptoms. Possible causes include: fungi or bacterial pathogen overgrowth, intestinal
microorganism imbalance, pregnancy, change in pH, hygiene products, allergies, antibiotic
use, antifungal treatments, oral contraceptives, hormonal replacement therapy, hormonal
imbalances, spermicide, lubricants, latex, frequent intercourse, multiple sexual partners,
sexual transmission, stress, diabetes, hyperglycemia, and immunosuppression such as
HIV/AIDS (Romm 258). Aviva Romm suggests that one common cause of chronic vaginitis
could be intestinal dysbiosis and permeability (leaky gut syndrome)(265). It is important for
a person who has symptoms of VVC to explore their own risk factors and seek assistance in
treating the possible root cause if the symptoms persist for a long time or are recurring.
Using Calendula
Eclectic physicians Felter and Lloyd pronounce that “in vaginitis, endometritis, all
uterine and vaginal abrasions, and non-malignant ulcerations, leucorrhoea, and as an intrauterine wash, calendula has received strong endorsement.” (Felter and Lloyd). It is a nonirritating, non-poisonous vulnerary that promotes the healing of wounds and stimulates
healthy tissue regeneration (Felter, Romm 263). A wash of calendula flowers was used for
vaginitis, cervicitis, endometritis, vaginal abrasions, gonorrhea and leucorrhea. It has also
been effective to reduce discharges (Felter). It is recommended to be used internally to aid
the local action (Felter and Lloyd).
The essential oil of calendula flowers have shown anti-bacterial and anti-fungal
activity in-vitro specifically against Candida albicans (Jannsen). Matthew Wood connects the
immune tonic properties of calendula to its lymphatic action, as the lymphatics are a
location of much immune activity. Wood also states that “calendula is used for conditions
where there is dampness in the wound or in the tissues: thrush, swollen lymphatics, and
vaginal discharge” (Wood 1997, 181-184). He explains an antiseptic action of calendula as
due to stimulating the body, and sending impurities to the surface. He indicated it as an
immune tonic, for use on all wounds, abrasions, and infections. He describes calendula as
being suited for people with a history of candida and depression, as well as specifically for
leucorrhea and a dry, irritated vaginal wall. calendula's bright yellow flowers are indicated
for “places where the sun doesn't shine” including the groin (Wood 2008, 154-158).
Calendula as a vulnerary is soothing to digestive mucosa and other mucous membranes
(Wood 2004, 243-244). David Winston describes calendula as an antifungal, antibacterial,
styptic for conditions including bacterial vaginosis (Winston 68).
Aviva Romm indicates calendula as an important ingredient in topical vulvovaginitis
preparations, as an antimicrobial vulnerary that promotes tissue regeneration (263). Topical
treatments she recommends for vulvovaginitis are a sitz bath or a peri-rinse. A sitz bath
involves making a strong tea diluted with water, putting it in a basin and sitting in it for 5-20
minutes. To make a peri-rinse you take the same tea and wash the area as needed, using a
squeeze water bottle if preferred. The tea is anti-microbial and anti-inflammatory. A
recommended combination is: calendula, thyme, lavender and uva-ursi in equal parts. As an
anti-microbial, calendula can directly reduce infections. As a vulnerary, calendula heals and
strengthens the sensitive epithelial tissues of the vagina and vulva, and tones the mucous
membrane in the gastrointestinal tract (263-264). If one cause of VVC is intestinal
permeability as Romm suggested, an important aspect of recovery is to improve the
integrity of the intestinal mucosa and restore healthy gut flora. The former can be reduced
by taking herbs internally similar as we use externally: vulnerary, anti-microbial, antiinflammatory herbs including calendula. The balancing of intestinal flora can be helped with
probiotic foods or supplements (265). The Eclectics also point out the importance of using
calendula internally to aid the local action (Felter, Felter and Lloyd). Although they don't
specify the mechanism of action internally, we can expect that the effectiveness is due to its
actions as an anti-microbial, vulnerary and anti-inflammatory, and that these actions are
exerted in the GI tract.
Calendula's long history of use for different kinds of vaginitis should encourage us to
try it. I began writing this article while having persistent low-grade symptoms of a yeast
infection for 2 weeks. I had a diagnosis of VVC in the past, though not recently. I decided to
try using calendula in the ways suggested through the texts. I made a tea with calendula,
lavender and oregano, and used it as an external wash 3 x/day, with a tincture of calendula
taken internally 3-5x/day. My symptoms cleared completely within 2 days, I continued the
treatment for one more day, and I haven't had any recurring symptoms since.
Many women suffer from vaginitis and either don't go to a clinic for a diagnosis, or
are not properly diagnosed because of difficulties in establishing the cause (Romm 256259). Calendula is a safe herb to use internally and externally with no known toxicity or
contraindications except for people with known allergies to members of the Asteraceae
(Hoffman 534-535). Its wide range of therapeutic actions and safety suggests that
calendula is an excellent remedy for vulvovaginal candidiasis and for undiagnosed
symptoms of vaginitis. It helps bring symptomatic relief, heal the tissues, and potentially
provide support in treating underlying causes especially if consumed internally as Felter and
Lloyd suggest.
Bibliography
Felter, Harvey Wickes. “Felter, 1922: the Eclectic Materia Medica. - Calendula officinalis,
marigold” Henriette's Herbal Homepage. Michael Moore, 2001-2013. Web. 16 February
2013.
Felter, Harvey Wickes and Lloyd, John Uri. “King's American Dispensatory, 1898- Calendula
(U.S.P.). Henriette's Herbal Homepage. Henriette Kress. 1999-2013. Web. 16 February
2013.
Hoffmann, David. Medical Herbalism: The Science and Practice of Herbal Medicine. Inner
Traditions/Bear & Co, 2003.
Janssen, A. M., et al. "Screening for antimicrobial activity of some essential oils by the agar
overlay technique." Pharmacy World & Science 8.6 (1986): 289-292.
Romm, Aviva Jill. Botanical Medicine for Women's Health. Churchill Livingstone/Elsevier,
2010.
Soper, David E. “Vaginitis.” The Merck Manual for Healthcare Professionals. Merck Sharp &
Dohme Corp. February 2012. Web. 16 February 2013.
Winston, David. Herbal Therapeutics: Specific Indications for Herbs & Herbal Formulas.
Herbal Therapeutics Research Library, 2003.
Wood, Matthew. The Book of Herbal Wisdom: Using Plants as Medicines. North Atlantic
Books, 1997.
Wood, Matthew. The Earthwise Herbal: A Complete Guide to Old World Medicinal Plants.
North Atlantic Books, 2008.
Wood, Matthew. The Practice of Traditional Western Herbalism: Basic Doctrine, Energetics,
and Classification. North Atlantic Books, 2004.
The effect of Gossypium sp. on the
Uterus
Allison Dellner
Gossypium species have an ethnobotanical history of use as an abortificatient,
emmenagouge, and parturient 1. A decoction of the fresh inner root bark of Gossypium was
used by African American slaves in the cotton districts of the southern United States
particularly to abort early pregnancies 2 . Eclectic doctors corroborate this use; saying
Gossypium herbaceum was known to “procure abortion without injury to general health”,
noting its relative non-toxicity in the context of abortifacient herbs, but had little confidence
in the efficacy of Gossypium to act on the uterus 3 . This paper attempts to find more a
specific action for Gossypium and to substantiate or disprove its claims as an abortifacient.
William Cook says that although it is claimed to be abortifacient, he did not think it
exerted any powerful influence on the uterus, but that its action was “rather good”. Cook
thought of Gossypium as a “feeble medicine” to be used as a relaxant, a mild uterine tonic
when the nervous system is irritable in labor, and to slowly promote menstruation in
“nervous persons”. In over ten years experience, Cook “did not get a strong article in
experiments“. 4
Harvey Felter blamed the freshness of the bark, saying that the “old root is valuless
as medicine”, noting that the fresh root was not available to many. In his materia medica,
Felter echoed Cooks experience, using Gossypium root as an emmenagouge in late
menstruation, and claiming it was not as effective in improving uterine inertia during labor
as it was touted. Felter also noted that Gossypium root was “non-toxic” 5.
In present day, Gossypium species are still used by women and midwives as an
abortifacient and emmenagouge 6. The language used to describe it’s action has changed to
describe the synergystic effect it has with oxytocin. “Cotton root” does not contain or mimic
1
Ellingwood, Finley M.D. The American Materia Medica, Therapeutics and Pharmacognosy (1919)
Wood, George B. "A Treatise On Therapeutics, And Pharmacology Or Materia Medica Vol2". (1867)
3
Cook, William. "The Physiomedical Dispensatory." Online version http://www. ibiblio.
org/herbmed/eclectic/cook/ (1869)
4
Cook, William. "The Physiomedical Dispensatory." Online version http://www. ibiblio.
org/herbmed/eclectic/cook/ (1869)
5
Felter, Harvey Wickes, M.D. The Eclectic Materia Medica, Pharmacology and Therapeutics (1922)
6
Shelton, Mary "Endangered Midwifery Allies." Midwifery 33 (2004).
2
oxytocin, but only will potentiate the effects of oxytocin already present in the body 7 .
Michael Moore has some opinions on this plant, having used the species of cotton native to
Mexico and parts of the southwest, Gossypium thurberi. Moore uses this plant as a “reliable
oxytocin synergist” that increases the tone and contractability of the uterus, and also of the
seminal vessicles, prostate and the myoendothelial tissues of the breast. He points to the
interest in research that Gossypium periodically receives, and then claims that researchers
find nothing “patentable” in the plant and then moves on 8.
It is interesting to me that the modern uses Moore describes for Gossypium are
related to male reproductive anatomy because there are many studies concerned with an
isolated constituent called gossypol, which causes a decrease in sperm density and motility
and eventually sterility in men 9. The other body of research on Gossypium is done on cows
and lambs. One cow study focused on the effects that eating cottonseed products had on
the reproductive quality and ability of ruminant animals. The outcome was largely that the
amount of gossypol is dangerously high in cotton seed and negatively affects the ovulation,
pregnancies and fertility of the cows 10.
Another interesting animal study was done on a patent that was being created for a
blend of herbs to help with encouragement of the “let down” reflex of milch animals such as
sheep and cows. The animals were being treated with synthetic oxytocin to ease in the let
down. The trial blends contained
varying amounts of Asparagus Racemosa, Gossypium
arboreum, Foeniculum vulgare, Lepidium sativum, Cholophytum boivilianum, Ipomoea
digitata, Withania somnerifa, and Leptadenia reticulata. The outcome of using this formula
was that the animals had an easier time in “letting down” their milk, and also the quantity
of milk that they produced was greater, even up to 3 days after administration of herbs. The
use of the herbal formula also had none of the same side effects that farmers were
accustomed to noticing from the oxytocin shots.
A “synergystic effect” was reported to
occur when these herbs were used in combination with each other.
11
Although this study
was done on ruminants, I find it interesting that Gossypium is used in this formula as a
substitute for oxytocin. It somewhat substantiates the claim that Gossypium is an oxytocin
potentiator. The body of research I did find on modern Gossypium actions and constituents
7
Moore, Michael http://www.hrbmoore.rt66.com (1995) from Henriette’s Herbal Homepage
Moore, Michael “Herbal Tinctures in Medical Practice” (1996) from www.swsbm.com
9
Gu ZP “Low Dose Gossypol for Male Contraception” Asian J Androl. 2(4):283-7 (2000 Dec)
10
Randel RD “Effects of gossypol and cottonseed products on reproduction of mammals.”J Anim Sci.
1992 May;70(5):1628-38.
11
Patil, Prasnt Neminath. “Herbal compositions imhaproving lactation of farmed livestock.” U.S. Patent
Application. 13/501,574
8
merely underscored the fact that it is under-researched in the female population and there
is much more we could know about its use as an emmenagouge 12.
It was my personal
experience with a deficit of information on Gossypium that led me to ask what it actually
does and what its mechanisms were.
All of the reading have done now on Gossypium informs my own personal experience
with using the root bark tincture. Knowing the actions of this herb and learning about the
reputation it had to be safe with little side effects, I tried using Gossypium as an
abortifacient in the second and third weeks of pregnancy. After doing this paper, I decided
my dose of 10 drops every 2 hours was too low, as this is a very high dose plant. Now I also
can understand why my combination was unsuccessful. There was probably not sufficient
levels of oxytocin in my body to work together with the herbs to potentiate an abortion.
12
Gruber, Christian W., and Margaret O’Brien. "Uterotonic plants and their bioactive constituents." Planta
medica 77.3 (2011): 207.
Fats in the Prenatal Diet:
Healthy,
Hazardous,
or
Just
Plain
Confusing?
Kate Westdijk
My mother recently disclosed that, when she was pregnant with me, she would try to be
“good” and make it through her full time work day on a diet of carrot sticks, raisins, and
saltine crackers. Then, at the end of her work day- and her guilt as she admitted this was
palpable- she would scramble to the nearest convenience store, buy a pint of Ben & Jerry’s
vanilla ice cream, pull off the top, and lick it as she drove home.
Clearly, she was
experiencing some confusion about what she was “supposed to” eat, and what her body was
craving.
Dietary fat plays a key role in the development of healthy tissue and function during
pregnancy and in the growing fetus (Larque, E., 2012; Jordan, R. G., 2010; Innis, S. M.,
1993). Recent reviews of the scientific literature do not substantiate historical claims that a
diet high in fat will lead to cardiovascular disease and obesity (Ajala, O. et al., 2013; Hite,
A. H., 2011; Siri-Tarino, P. W., et al., 2010). Despite these facts, concerns about dietary
fat intake are held by, and conveyed to, pregnant women (BabyCenter, 2013; USDA, 2013;
Kleinman, R. E., 2009; Root, R., & Browner, C., 2001), and common prenatal nutrition
resources are quick to warn of the danger of excessive weight gain in pregnancy (Murkoff,
H. & Mazel, S., 2008; Brewer, G. S., & Brewer, T. H., 1983). However, sufficient fat intake
is essential for a safe pregnancy and delivery (Jordan, R. G., 2010; Odent, M., 2006;
Brewer, G. S., & Brewer, T. H., 1983), as well as healthy fetal development (Larque, E.,
2012; Kleinman, R. E., 2009).
There is general agreement in the medical community that the “good fats” - such as
the omega-3 alpha linolenic acid- are important as part of a prenatal diet (BabyCenter,
2013; USDA, 2013; Kleinman, R. E., 2009). Other less mainstream nutrition sources also
include saturated fatty acids as an important component of the human diet (Gedgaudas, N.,
2011; Enig, M. G., & Fallon, S., 2006; Schmid, R. F., 1997).
However, discriminating
between “good fats” and “bad fats” is a confusing challenge for the average citizen (Taubes,
G., 2008), and approximately three thousand women per year in the United States (5%)
receive inadequate to no prenatal care in order to receive information on healthy dietary
choices (Child Trends Data Bank, 2012; US Census Bureau, 2012). Prenatal nutrition advice
impacts women’s dietary behavior while pregnant (Sweeney, C. et al., 1985), but women
receiving this advice have reported that is often contradictory or vague (Root, R., &
Browner, C., 2001). The Pediatric Nutrition handbook even goes so far as to suggest that
any fat besides essential fatty acids could be eliminated from the diet and replaced by
carbohydrates (Kleinman, R.E., 2009), but emerging evidence suggest that this would not
be wise because of the connections between high carbohydrate diets and obesity (Hite, A.
H., 2011). If a pregnant woman is able to access adequate prenatal care in the first place,
and then persevere through conflicting societal and medical concerns about fats and links to
obesity (not to mention their own body messages and cravings), the recommended sources
and quality of the fats they consume may not be sufficient for delivering the types of fatty
acids necessary for a healthy pregnancy (BabyCenter, 2013; Kleinman, R. E., 2009; Brewer,
G. S., & Brewer, T. H., 1983).
Which Fats are Important for a Healthy Pregnancy?
Polyunsaturated Fatty Acids
There are two polyunsaturated fatty acids (PUFAs) recognized as essential dietary nutrients:
linoleic acid (LA) and alpha linolenic acid (ALA).
They are called “essential fatty acids”
because they must be derived from the diet (Kleinman, R. E., 2009). Linoleic (an omega 6
fatty acid) and α-linolenic acid (omega 3) act as precursors for the synthesis of longer
chained PUFAs (Simonpoulis, et al., 2000).
Modern agriculture, due to its emphasis on
production and not nutrition, has reduced the omega 3 fatty acid content in many foods
(Simopoulos, A., 2002). Excess omega 6 and deficient omega 3 leads to an imbalanced
immune response from inflammation as well as increased risk of cardiovascular disease
(Fontani, G. et al., 2005) and poor bone growth and metabolism (Watkins, B. A. & Seifert,
M. F., 1996).
Long Chain Polyunsaturated Fatty Acids (LCPUFAs) make up the majority of human
brain tissue and the retina (Innis, S. M., 1993).
The long chain fatty acids DHA and EPA,
from fish oil, have been correlated with key pregnancy outcomes for both the mother and
the developing fetus. Benefits to both may include reduced risk of eclampsia (Odent, M.,
2006; Velzig-Aarts, F. V. et al., 1999; Imhoff-Kunsch, B., et al., 1991) and increased
gestation length (Jordan, R. G., 2010). LCPUFAs consumed in pregnancy have been linked
to improved cognitive development and reduced allergies postpartum (Larque, E., 2012).
DHA supplementation during pregnancy decreased the duration of infant illnesses and the
occurrence of colds in children (Imhoff-Kunsch, B. et al., 2011).
The commonly recommended sources of PUFAs often include vegetable oils, fortified
eggs, or dairy products (due to concerns about mercury contamination of marine sources)
(BabyCenter, 2013; USDA, 2013; Kleinman, R. E., 2009), but these sources are likely to
supply oxidized or rancid oils which do not impart the sought health benefits (Enig, M. G., &
Fallon, S., 2006; Gallobart, J. et al., 2001). Instead, they are correlated with a variety of
other problems such as cardiovascular disease or bone weakness (Gedgaudas, N., 2011;
Ravnskov & McCully, 2009; Gallobart, J. et al., 2001; Parhami, F. et al., 1997). Whole food
sources of PUFAs, such as sardines or avocados, typically contain natural antioxidants that
protect fragile fatty acids in both the food and the tissue of the consumer. Sardines are also
a low-mercury fish that would be an excellent choice for pregnant women (Abehlson, A. et
al., 2011).
Saturated Fatty Acids
Saturated fat in the human diet is controversial and conventional nutrition sources generally
associate it with increased risk for obesity and cardiovascular disease (Kleinman, R. E.,
2009; Lees, R.S., 1990). However, a recent review of 21 studies, published in the American
Journal of Clinical Nutrition, determined that there is no scientific basis for the widely held
(and practiced) claim that saturated fats contribute to cardiovascular disease (Siri-Tarino, P.
W., et al., 2010). Another recent review of high fat, low carbohydrate diets indicate that
healthy levels of fat in the diet can actually prevent excessive weight gain by contributing to
feelings of satiety and reducing cravings for sweets (Hite, A. H., 2011).
There is simply
insufficient evidence to justify restriction of saturated fats from our diets (Ajala, O., 2013).
Conversely, proponents of traditional diets recognize that saturated fats from natural
sources (as opposed to hydrogenated in a lab) are safe and even necessary in the human
diet, especially in pregnancy, for several reasons (Gedgaudas, N., 2011; Enig, M. G., &
Fallon, S., 2006). Saturated fats are important for the growth and maintenance of healthy
bones (Watkins, B. A. & Seifert, M. F., 1996). They are the only stable fats to cook with
because they are inherently resistant to oxidation, and, when consumed with essential fatty
acids for example, they protect these fragile lipids from oxidation (also known as rancidity)
so they can be used for healthy processes in the body (Enig, M. G., & Fallon, S., 2006;
Feher, J. et al., 2007).
Saturated fats are required for absorption and use of essential fatty
acids (Garg et al, 1988) as well as essential vitamins such as A, D, and E (Romm, A. J.,
2011).
In sum, saturated fats provide many benefits, and there is insufficient scientific
evidence to suggest that they be restricted from our diets.
Ironically, my mother still lovingly blames me, not the ice cream, for the weight gain she
experienced in her pregnancy.
Perhaps if she had been encouraged to nourish her body
with high quality fats and proteins throughout her day, her experience may have been less
frustrating and confusing.
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Herbal Therapeutics Post-Induced
Abortion
Lisa Weiss
Approximately one in four recognized pregnancies in the United States ends in an
induced abortion (Rock and Jones 2008).
According to the American Congress of
Obstetricians and Gynecologists, more than 1.2 million abortions occur each year and one
third of all women will have had either a medical or a surgical abortion by the age of 45
(ACOG 2010). Surgical abortions are the most common type performed in the U.S (ACOG
2011) –only 6% of all induced abortions are medical (Finer and Henshaw 2000). There are
risks associated with both medical and surgical abortion, and women concerned about these
risks or experiencing side effects from either procedure may consult an herbalist.
This
paper only considers the therapeutics post-legally performed abortion; those performed by
an untrained practitioner, common in countries where abortions are illegal, come with
additional risks (Faundes 2010).
During a typical medical abortion, two pharmaceuticals are given: Mifepristone and
Misoprostol.
Mifespristone binds to progesterone receptors but does not activate them,
acting as an anti-progesterone (ACOG 2005). Without progesterone, the lining of the uterus
thins, preventing the embryo from remaining implanted, and the cervix softens (ACOG
2011). Misoprostol, a prostaglandin E analogue, is administered either orally or vaginally 48
hours after administration of Mifespristone (ACOG 2005). Misoprostol causes the uterus to
contract and expel the embryo (ACOG 2011). There is typically a follow up 14 days postadministration to confirm expulsion. After a medical abortion, bleeding is much heaver than
from menses and cramping may be severe, though some degree of bleeding and uterine
cramping is necessary for the abortion to complete (ACOG 2005).
It is advised to seek
emergency care if two full-sized sanitary napkins per hour for two hours in a row are
saturated with blood (Creinin and Aubeny 1999).
However, less than 1% of women will
need emergent curettage because of excessive blood loss (Schaff et al. 1999).
Over the
counter pain medications are recommended after medical abortion for pain from uterine
cramping (ACOG 2005).
Five deaths have been reported associated with medical abortion
and in three of five cases, the cause was infection with Clostridium sordellii, an anaerobic,
gram-positive bacteria (CDCP 2005).
The most common type of surgical abortion is suction/vacuum curretage. Before the
procedure, local anesthesia is applied to the cervix and general anesthesia or sedatives may
or may not be given. A speculum is inserted to hold the vagina open and a dilator is then
inserted into the cervix to stretch the opening. After the cervix is dilated, a small tube is
inserted into the uterus.
pregnancy.
The tube is attached to a vacuum pump, which removes the
Antibiotics are given post-operatively to prevent infection.
Soreness or
cramping may occur for up to two weeks after the procedure. Bleeding may last up to six
weeks, but is rarely heavy enough to require a blood transfusion (ACOG 2011). In cases of
hemorrhage, most often due to uterine atony, uterotonic agents, such as Methergrine
(Planned Parenthood 2005), are given along with manual compression of the uterus (Rock
and Jones 2008).
Practitioners working with clients post-abortion should be aware of the symptoms
that indicate necessary emergency care.
Acute hematometra (post-abortal-syndrome)
occurs in 1.1 per 100 abortions and the cause is unknown.
Symptoms include a large,
tender uterus; severe cramping; and less blood then expected within two hours after the
procedure.
Women with these symptoms should immediately return to their doctor or to
the emergency room. Treatment is a repeat of the curretage followed by uterotonic agents.
Retained tissue is also possible, occurring in 1 in 100 surgical abortions. Symptoms include
fever, cramping, and excessive bleeding.
Antibiotics and a second curretage may be
needed—clients with these symptoms should be referred back to their doctor (Rock and
Jones 2008). Gestational age is one of the key factors determining the likelihood of serious
complications
post-abortion;
complications
increase
progressively
with
advancing
gestational age (Rock and Jones 2008).
Lahteenmaki and Luukkainen (1978) studied the first menstrual cycle after an
induced abortion in 18 women. They found that the plasma concentration of estradiol and
progesterone declined rapidly, and was followed, in most women, by an increase in plasma
estradiol levels from the seventh post-abortal day onward.
The authors also report that
progesterone was lower than normal during the luteal phase of the cycle, and that ovulation
returned during the first cycle in 14 of the 18 women.
Feelings of relief, sadness, elation, or depression are common post-abortion and may
be strong because of hormonal changes (Planned Parenthood 2005). In a mega-analysis of
22 peer reviewed studies, Coleman (2011) reports that women who have had an abortion
experience 81% higher risk of mental health problems compared to women who have not,
including alcohol misuse, anxiety, depression, and suicide.
shown to be attributable to abortion.
Nearly 10% of the 81% was
Suliman et al. (2007) report that of 133 women
choosing to have a surgical abortion, 18.2% had symptoms of PTSD at three months post-
procedure.
Pre-procedural cortisol levels were correlated with these PTSD symptoms,
indicating that women experiencing a stress response to the procedure were more likely to
experience PTSD later.
Likewise, Fergusson et al. (2009) demonstrate that the risks of
developing mental health problems are dependent on the extent of distress or guilt reported
by a woman pre-procedure.
Other than a handful of trials on Chinese herbal formulas for post-abortion
hemorrhage, no pharmacological research or clinical trials have been conducted specifically
on herbal therapeutics post-abortion. Below is a collection of plants used by both modern
and historical herbalists/doctors for post-abortion recovery and some extrapolation from
research conducted on related or more general subjects.
For a woman that connects her anxiety, depression, and/or PTSD to an abortion,
nervines, anti-depressants, and adaptogens may be indicated, most likely as adjuvants to
counseling with a mental health professional.
Some of the following plants could also
benefit the male partner, who may also be affected by the abortion.
Because similar
hormonal changes occur after pregnancy as after abortion (low estrogen and progesterone
levels (Lahteenmaki and Luukkainen 1978)), herbs typically used in postpartum depression
such as Hypericum perforatum, Artemesia vulgaris (Hoffmann 2003), Rosmarinus officinalis
(Wood 2004), and Melissa officinalis (Weed 1986) may be useful. Not only have multiple
clinical trials demonstrated the use of H. perforatum as an anti-depressant, it also has
antimicrobial,
nervine,
and
astringent/vulnerary
properties
(Mills
and
Bone
2000).
Artemisia vulgaris, which Matthew Wood recommends for women who have been through
abortions or other “harshness” in the uterus, is a mild nervine and anti-depressant (Wood
2009).
The antispasmodic (Khan 2009) and antibacterial (Chen 1989) properties of A.
vulgaris also make it useful post-abortion.
R. officinalis, a nervine and antispasmodic
(Hoffmann 2003), was demonstrated by Machado et al. (2009) to have an anti-depressant
effect in mice through an interaction with the monoaminergic system. M. officinalis has mild
antidepressant properties, is useful for spasm and anxiety, and is possibly trophorestorative
(Hoffmann 2003). In a double-blind placebo-controlled study conducted by Kennedy et al.
(2003) mood was assessed in 20 healthy individuals given one capsule with 1000 or 1600
mg of powdered, dried M. officinalis. With either dose there was a significant increase in
“calmness” compared to placebo. Another plant to consider is Lavandula officinalis, which
Culpeper describes as having “...special good use for all the griefs of the head...” (Culpeper
1995) and which is indicated when there is grief around loss of a connection with someone
or something (Bunce personal communication 2011). Not only does L. angustifolia have a
history surrounding grief, a common emotion felt by women post-abortion, it is also a
nervine (Hoffmann 2003) and anti-depressant. Akhondzadah et al. (2003) investigated L.
angustifolia alone (dose of 3mL of a 1:5 tincture), imipramine alone, and a combination of
the two in the treatment of mild to moderate depression in a random, double-blind study.
All three treatment groups showed significant improvement in depression scores. Leonurus
cardiaca may also be indicated for its nervine and antispasmodic properties as well as for its
potential to regulate the menstrual cycle (Hoffmann 2003).
Adaptogens may be useful post-abortion because of the increase in cortisol levels
reported in some women pre- and post-procedure (Suliman et al. 2007).
adaptogens useful post-abortion include Withania somnifera,
Specific
Rehmannia glutinosa,
Glycorrhiza glabra, and Asparagus racemosus. W. somnifera is not only an adaptogen but
also an immune stimulant (Yamada et al. 2007), a calming nervine, an antispasmodic, and
contains Iron (Mills and Bone 2000). Bhattacharya et al. (2000) found support for the use
of W. somnifera as a mood stabilizer in clinical anxiety and depression. R. glutinosa is an
adrenal trophorestorative, has anti-hemorrhagic properties, is rich in iron, and balances
hormones/regulates menstruation (Mills and Bone 2000). G. glabra inhibits glucocorticoid
hepatic metabolism, slowing down the rate that cortisol is broken down by the body and
thus sparing the adrenals from having to produce more (Whorwood 1993). Phytoestrogens
present in G. glabra inhibit seratonin re-uptake (Ofir et al. 2003) as well as balance sex
hormones by inhibiting progesterone dehydrogenases (Mills and Bone 2000). In addition,
G. glabra, along with several other herbs, is part of a chinese formula called “Free and Easy
Wanderer Plus” that is reported to be useful for PTSD (Wang et al. 2009). A. racemosus is
a nourishing adaptogen and rejuvenating tonic that has been demonstrated to reduce
corticosterone levels produced by stress (Kanwar 2010).
The saponins in A. racemosus
modulate levels of estrogen in the body (Rao 1981) and the plant is also reported to act as
an antidepressant (Singh 2009), an immune stimulant (Sharma 2011), and an antibacterial
against gram-positive bacteria (Mandal 2000).
Though the research demonstrates that in many women, hormone levels return to
“normal” within the first menstrual cycle post-abortion, a percentage of women will still
experience low levels of sex hormones, especially progesterone (Lahteenmaki and
Luukkainen 1978).
In such women, there are several herbal agents, other than the
hormone modulating adaptogens mentions above, that may be useful.
William LeSassier
recommends, for both balancing the hormones and toning sexual organs and glands, equal
parts Smilax officinalis, Cnicus benedictus, Mitchella repens, Viburnum prunifolium, and
Glycyrrhiza glabra as a tea. He suggests drinking 4-5 cups a day during the first week after
an abortion, 2-3 cups in the second week, 1-3 cups in the third, and tapering off to one cup
in the fourth week (Parvati 1978). Gail Edwards recommends Vitex agnus-castus after an
abortion to restore hormone balance, normalize reproductive function, and act as an antiinflammatory on the endometrium (Edwards 2000). Bergmann et al (2000) report that V.
agnus-castus increases progesterone secretion in the luteal phase.
If sex hormones are
having trouble returning to normal, liver function should be examined. In addition, because
Vitamin E protects pituitary and adrenal hormones from oxidation (follicle stimulating
hormone, luteinizing hormone, etc.), supplementation or recommending more whole grains
in the diet is a good idea (Haas 2006).
If a woman experiences unusually heavy bleeding after an abortion but not enough
to warrant emergency care, uterine astringents should be employed to act as antihemorrhagic agents on the uterus. Many of the plants listed below will be of benefit postabortion even if excess bleeding is not a concern because they also act as uterine tonics—
strengthening and nourishing the tissue and function of the reproductive system.
Astragalus membranaceus together with Leonurus artemisia have been extensively studied
in China for prolonged bleeding after medical abortion (Qin 2005, Zha 2008).
Matthew
Wood recommends Alchemilla vulgaris not only for uterine hemorrhage but also for gently
balancing the menstrual cycle after abortion. Elisabeth Brooke uses it when there is trauma
to the uterus from abortion to “maintain feminine organs and psychological security” (Wood
1997).
Rubus spp. have long been used to strengthen and tone the uterus as have
Viburnum spp., which improve nutrition, circulation, and enervation to the uterus, as well as
act as astringent tonics for hemorrhage and pain (Hoffmann 2003). The eclectic physicians
had a few favorite plants for uterine hemorrhage.
Fyfe (1908) recommends Capsella
bursa-pastoris as a specific for hemorrhage after spontaneous abortion and writes that
Cinnamomum zeylandicum “is one of the most certain remedies we have for uterine
hemorrhage.” Caulophyllum thalictroides was also employed after spontaneous abortion to
relieve irritability of the reproductive system and prevent hemorrhage (Stephens 1930), as
well as for its nervine property (Stephens 1936). C. thalictroides (Weed 1986) as well as
Achillea millefolium (Tilgner 1999) tonify atonic uterine tissue and relax spastic uterine
muscles, making them both useful in the case of uterine cramps as well. Scudder (1898)
wrote that Mitchella repens “exerts a direct influence upon the reproductive apparatus of the
female, giving tone and improving functional activity.
It has been extensively used as a
uterine tonic...”. M. repens has the added benefit of being a moderately stimulating tonic
nervine (Lyle 1932). More recently, Shipochliev (1981) tested the water extracts of several
herbs and reported that Matricaria recutitia, Calendula officinalis, Plantago sp., Symphytum
officinalis, and Capsella bursa-pastoris have a uterotonic effect on rabbit and guinea pig
uteri.
If uterine cramping is an issue post-abortion,
antispasmodics are indicated.
Dioscorea villosa, Matricaria recutita, Zingiber officinale, Valeriana officinalis, and/or
Viburnum spp. all work to ameliorate pain from spasm in the uterus, specifically (Hoffmann
2003). After an abortion, the pituitary releases oxytocin, causing the uterus to clamp down
(cramp) so that the uterus can return to its original size (Rock and Jones 2008). Plants that
synergize with oxytocin, such as Gossypium spp. root bark, Caulophyllum thalictroides, and
Capsella bursa-pastoris (Moore 1995) may help speed the process along, lessening the
duration of cramps as well as preventing excessive blood loss.
To prevent post-abortion infection, immune stimulant or antibacterial herbs may be
useful, particularly if a woman elects not to take the recommended 7-day round of
antibiotics. Ellingwood (1919) recommends Echinacea sp. for sepsis after a badly conducted
abortion, but it may be useful even after a safely conducted one.
Baptisia tinctoria is
recommended in King's American Dyspensitory (Felter and Lloyd 1898) for septicemia
following retained fragments of placenta after abortion. Wagner et al (1985) found immune
stimulating polysaccharides in Echinacea purpurea, E. angustifolia, Calendula officinalis,
Matricaria recutita, and Eleutherococcus senticosus, all of which are useful post-abortion for
their other properties. Hydrastis canadense is indicated both for its antibiotic and uterine
tonic properties (Hoffmann 2003).
A well-strained sitz bath may be a good use of H.
canadense post-abortion. Both Aristolochia paucinensis (Gadhi et al. 1999) and Capsaicin
fructans (Cichewicz and Thorpe 1996) are reported to have antibacterial properties
specifically against Clostridium spp. If a woman chooses to take conventional antibiotics,
pre and probiotics should be recommended (Haas 2006).
If bleeding is heavy post-abortion, consider supplementing with Iron rich herbs such
as Urtica dioica, Rumex Crispus, Rehmannia glutinosa, and Taraxacum officinalis.
Also,
recommend dietary sources of Iron such as liver, leafy greens, molasses, beef, and apricots
(Hoffmann 2003).
Plants indicated after any operation also apply post-surgical abortion. This includes
Arnica montanum to lessen trauma after surgery (Karow 2008) and Centealla asiatica to aid
in wound healing (Shukla 1999).
Other supportive strategies post-abortion include
counseling about birth control/fertility and encouraging self-care (sleep, good diet) for
rebuilding.
Planned Parenthood recommends deep uterine massage, heating pads, warm
liquids, and rest for both cramping and heavy bleeding. They also recommend not doing
the following for two weeks post-abortion: sex; strenuous exercise; placing anything in the
vagina; douching; or using perfumes, bubbles, or oils in bath water (Planned Parenthood
2011).
Below are potential formulas for women of different constitutions (for simplicity's
sake, they are formulated as tinctures, but some of the plants could be combined into lovely
teas/decoctions.):
Post-abortion Formula for Vata Woman 10 ml (5ml BID)
Rosmarinus officinalis – antidepressant, antispasmodic, nervine, synergist (1 ml)
Glycyrrhiza glabra – adaptogen, antidepressant, hormone modulator (3 ml)
Rubus spp. (leaf) – uterotonic, iron rich (2 ml)
Asparagus racemosus – adaptogen, antibacterial, antidepressant, hormone modulator,
immune stimulant (2 ml)
Matricaria recutita – antispasmodic, nervine, immune stimulant, uterotonic (2 ml)
Post-abortion Formula for Pitta Woman 10 ml (5 ml BID)
Lavandula angustifolia – antidepressant, antimicrobial, nervine, synergist (1 ml)
Caulophyllum thalictroides or Viburnum spp. – antispasmodic, nervine, uterotonic (2 ml)
Rehmannia glutinosa – adaptogen, anti-hemorrhage, hormone modulator, iron rich (3 ml)
Leonurus cardiaca – antispasmodic, nervine, menstrual cycle regulator (2 ml)
Matricaria recutita – antispasmodic, nervine, immune stimulant, uterotonic (2 ml)
Post-abortion Formula for Kapha Woman 15 ml (5 ml TID)
Artemisia vulgaris – antibacterial, antidepressant, antispasmodic, nervine (1 ml)
Calendula officinalis – antiseptic, antispasmodic, mild immune stimulant, uterotonic (1 ml)
Vitex agnus-castus – hormone modulator (4 ml)
Withania somnifera – adaptogen, antispasmodic, nervine, iron rich, immune stimulant (3
ml)
Alchemilla vulgaris – mild hormone modulator, uterotonic (2 ml)
Hypericum perforatum – antidepressant, antimicrobial, astringent, vulnerary (4 ml)
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Adverse Effects of Cross-sex Hormone
Replacement Therapy
Linden de Voil
This paper explores potential side effects of long term cross sex hormone therapy in
transsexual individuals, with focus on delineating which risks have been clinically
observed and which are potential concerns that have not been seen in vivo. Although
there is some potential to use herbs with feminizing or masculinizing effects as a
substitute or adjunct to hormone therapy, my interest in this research is on supporting
the organs and systems which may be negatively impacted by CSHRT. Hormone
treatment is often accompanied by various surgical interventions, which involve a
separate set of risk considerations not covered here. For the sake of brevity I have not
outlined the positive/desired effects of hormones, which are covered extensively in many
guides focused on gender transition; I have listed some excellent online resources with
my references.
Worldwide incidence of transsexualism (defined as gender identity disorder) as
estimated by the American Psychological Association DSM-IV at 1 in 100,000 female to
male (FM) and 1 in 30,000 male to female (MF). However, as there have been no formal
epidemiological studies, these numbers are based on indirect evidence of patients who
have presented for referral to hormone therapy and surgeries, which they are presumably
able to afford. There is likely a much higher incidence of transsexualism and, more
broadly, gender dysphoria, with some estimates as high as
1:750 for MF and 1:1400 for FM (Horton 2008).
CSHRT is widely used and generally accepted as part of a standard protocol for
individuals who want their external gender presentation to align more closely with their
perceived gender. In MF transwomen, therapy usually consists of an anti-androgen
(commonly spironolactone, sometimes flutamide or cyproterone acetate) alongside some
form of estrogen, which may be taken orally, transdermally, or by injection. Estrogen is
taken in high dose, three to five time the dose for a natal female undergoing hormone
replacement therapy, in order to produce feminization of secondary sex characteristics and
to assist in suppression of testosterone. Progesterone may be included, although it is not a
standard measure, and clinical evidence for efficacy is lacking. Transmen typically take
only testosterone, in a dose sufficient to suppress menses and produce masculinization of
physical characteristics, up to the standard
dose for hypogonadal natal men (Hembree et al 1994, Gorton 2005).
Various hormone preparations and administration routes have their own risks, which
are outlined here in relation to the specific systems impacted. The greatest concern is use
of ethinylestradiol in particular, and oral estrogens generally, which carry greater health
risks
than
other
estrogen
preparations,
including
significantly
increased
risk
of
thromboembolism in the first year of treatment (Toorians 2003, van Kesteren
1997), greater prevalence of hepatotoxicity and increased markers of inflammation
(Goodman 2012, Wilson 2009).
Sex hormones have well documented slow acting gene-mediated effects through
activation of nuclear receptors; more recently estrogen and testosterone have been
shown to inducerapid effects through cell membrane receptors, which are found in the
brain, reproductive organs, and cardiovascular tissues. In vitro, they appear to have
some activity at neurotransmitter receptors, although this has not yet been shown to have
clinical relevance (Falkenstein 2000).
Main sites affected or potentially affected by CSHRT include the breast tissue,
ovaries and uterus, bone, liver, pituitary gland, adrenals, heart and vasculature.
Research specific to trans populations is necessarily limited, with many studies
comprising a very small population; in many cases, research remains inconclusive.
Cardiovascular health and inflammation:
While the effects of testosterone administration on transmen are not always the same
as for natal males, some relevant research is worth noting. A 2013 review suggests that
although evidence is conflicting, in hypogonadal natal males testosterone is primarily
protective and anti-atherogenic, resulting in increased coronary artery flow, overall
vasodilation and calcium-channel blocking effect; most negative effects result from its use
in the frail elderly or in supraphysiological doses, which are not recommended for the
purposes of gender transition (Kelly 2013).
Sodium retention and mild edema are considered typical side effects of treatment
with anabolic steroids, whether oral or injected; research on hypogonadal natal men also
shows an increase in extracellular fluid volume under the influence of exogenous
testosterone, without any corresponding changes in aldosterone, ANP, or blood pressure
(Bassil 2009, Johansson 2005).
Overall, most FM trans-specific studies show changes in inflammatory markers,
including increase of the vasoconstrictive protein endothelin-1, C-reactive protein, and
homocysteine, with decreased HDL, increased triglycerides and lipid oxidation, and an
increase in visceral fat deposition (Elamin 2009, Gooren 2008). There is an increased risk of
polycythemia, which increases further with age; if severe, this includes increased risk of
venous and arterial thrombosis (Gorton 2005).
However, multiple studies conclude there is generally no change in relative
cardiovascular morbidity outcomes or increase in significant adverse events following
CSHRT; a 2008 multi-study review (n=712) showed no increase in blood pressure, insulin
sensitivity, clotting factors or arterial stiffness (Giltay 1998, Gooren 2008, Elamin
2009). The exception is administration of testosterone undecanoate, which was linked to
increased blood pressure in 4 out of 35 users, with two cases of severe hypertension
(Mueller 2007).
For MF transwomen, use of oral estrogens resulted in increased inflammatory markers
associated with CV risk; however, transdermal estrogen does not produce the same result.
(Transdermal applications are significantly more expensive than oral estrogens, and may
not be covered by health insurance.) Risk increases dramatically when compounded by
additional factors, particularly smoking. (Wilson 2009).
Compared
to
control
groups,
transwomen
show
increased
rates
of
venous
thromboembolism and cerebrovascular disease, with rates of heart attack comparable
to those of natal men. In the same study, transmen showed no increase in any negative
CV outcomes, but did have increased rates of type-2 diabetes (Wiercx 2013).
Changes in the Th1/Th2 ratio (as expressed by interferon gamma/interleukin 4) can be
seen in both MF and FM, with a relative increase in Th1 resulting from androgen
administration and decreased Th1 from estrogen (Giltay 2000). This shift toward Th2
phenotype could be an influential factor, considering that although some CV risk
markers appear to increase for transmen, actual adverse outcomes are increased only in
transwomen.
Bone density
Because estrogen plays a significant role in maintenance of bone density, there is
some concern about risk of osteopenia/osteoporosis following hormone replacement,
especially in the case of oophorectomized transmen. The most relevant study shows that
estrogen use in MF transwomen is linked to maintenance or increase in bone density.
Although there should be some estrogen created from aromatization of testosterone in
FM, this may not be adequate to prevent bone mineral loss after removal of the ovaries
(van Kesteren 1996, 1998). It is suggested that postoophorectomy transmen may want to supplement calcium, and possibly vitamin D, as a
post-menopausal natal female would do (Gorton 2005).
Hepatic function
Multiple mortality and morbidity studies have shown no increase in hepatic
pathologies in connection with CSHRT, other than higher rates of infectious hepatitis
among transwomen (Asschman, van Kesteren, Gooren).
Alterations in hepatic function are considered a standard associated risk with use of
testosterone replacement therapy.
However, cholestasis, hepatotoxicity and hepatic
tumors have only been documented in connection with oral forms of C-17 alkylated
testosterone, generally in supraphysiological dose range; liver pathology has not been
linked to use of transdermal or injectable unmodified testosterone within dose ranges used
for HRT in either trans or natal men (Bassil 2009, Gorton 2005).
It is recommended that transmen be screened regularly (1-2 times per year) for
changes in liver function. Unexplained elevated enzyme levels are found in 15% of
transmen on hormone therapy (van Kesteren 1997). Although it is unclear if such changes
are linked to overt pathology, reductions in dose may be recommended by the prescribing
physician if this occurs (Gorten 2005, Hembree 2009).
In transwomen, use of anti-androgenic drugs other than spironalactone or finasteride,
including leuprolide, flutamide, ketoconazole, and cyproterone acetate, has significant risk
of hepatotoxicity, usually appearing as hepatitis with jaundice (Thole
2004). Cyproterone, leuprolide and flutamide are most commonly used in treatment of
prostate cancer; the effective dose to induce desired feminization is much higher, and
consequently carries greater risk of side effects.
Both testosterone and estrogen are primarily metabolized in the liver, through various
CYP pathways; testosterone is a 3A4, 2C9, and 2C19 substrate (Choi 2005); estrogen is a
1A2 and 3A4 substrate (Tsuchiya 2005). Oral ethinylestradiol is often not recommended
for CSHRT, due to the high dose required and increased risk for thromboembolism and
changes in hepatic protein synthesis, but in some instances it is used. Ethinylestradiol
persists for longer in the blood, with greater effect on the liver, than injectable or
transdermal estradiol (Kapp 2009).
Evidence does not show increased hepatic risk for trans people using CSHRT,
relative to same-sex HRT; however, it should be considered in the same light as longterm use of any hepatically-metabolized pharmaceutical drug.
Breast health and cancer
There is a theoretical concern for increased risk of breast cancer for transwomen;
recent research on natal women shows an increase in breast cancer rates among
recipients of estrogen and progestin combination therapy, which in some cases is also
used for transwomen. (Chlebowski 2009).
However, a study of 816 MF transwomen found zero cases of breast cancer (van
Kesteren 1997) and a recent study showed that both transmen and transwomen fall into the
normal range of occurrence of breast cancer in natal men (Gooren 2013).
Many, though not all, transmen undergo a type of mastectomy that leaves some
breast tissue in place. In a study of transmen following at least 6 months of hormone
therapy, post-mastectomy histology showed atrophic reduction of glandular tissue,
increase in fibrous connective tissue, and no atypical hyperplasia or carcinoma.
(Grynberg 2010).
Another 2013 morbidity study showed equal rates of all cancers in both MF and FM
transsexuals when compared with control groups of natal men and women (Wiercx
2013).
Based on the most recent research, there appears to be no increased risk for breast or
other cancers.
Ovaries, uterus and prostate
Because of limited amounts of research and clinical evidence, there has been
concern about the effects of long term use of androgens on the ovaries and uterus of
transmen, and particularly for the potential risk of cancer. Bilateral oophorectomysalpingectomy and hysterectomy are generally recommended within five years of
starting hormone treatment. This is based on a risk-prevention strategy, the ability to
subsequently decrease dose of testosterone, and on the idea that transmen are likely to
have some degree of discomfort or trauma surrounding gynecological exam, and therefore
are less likely to seek out the annual preventative screenings recommended if the organs
are retained. (Gorton 2005, Hembree 2009).
No increase in cervical or uterine cancers has been reported. Three cases of ovarian
cancer have been reported in transmen, although it is unclear if this represents an actual
increase in rate of occurrence (Moore, Asscheman, Hembree). However, there is a
demonstrated upregulation of androgen receptors in the ovaries following CSHRT, and
some in vitro evidence links increased ovarian androgen receptor activity with growth of
cancer cells. (Ahonen 2000, Sheach 2009).
Some research has pointed to potential connection between cross-sex androgen
therapy and increased incidence of PCOS. However, this is complicated by the evidence
that transsexuals have a higher incidence of pre-existing PCOS, compared to cisgender
natal females, before beginning hormone therapy. (Bosinski 1997).
Research published in 1991 showed changes in the ovaries of FM transsexuals after
androgen therapy, judged to be consistent with changes caused by PCOS (Pache
1991). Additionally, some associated markers for PCOS appear to increase in transmen
after hormone therapy; in FMs, androgen therapy increases both ADMA and
endothelin-1 levels, which have been shown to have positive correlation with incidence of
PCOS; however, causation is unclear (Polderman 1993, Bunck 2009, Charitidou
2008).
A 2007 study in Japan found that although 58% of FM patients had PCOS ovarian
characteristics, there were no corresponding increases in insulin resistance, which was
linked only to obesity and not to PCOS morphology. (Baba 2007). Another study showed
that although there was an increase in antral follicles consistent with PCOS in
79% of FM patients, 45% of patients also showed significant endometrial atrophy
(Grynberg 2010). A third study showed universal atrophy similar to that found in postmenopausal women (Perrone 2009). This year a surprising new study out of Japan
reported that although androgen therapy does induce some hyperplasia within the
ovaries, there is no change to antral follicles, and the changes present are not consistent
with PCOS (Ikeda and Baba 2013).
Within the last five years, research has begun to show that although there are
morphological changes to the ovaries after androgen therapy, these changes do not
necessarily mimic PCOS, nor is there evidence of increased rates of endometrial cancer or of
metabolic changes similar to those linked with PCOS. Given that fertility is never reliably
preserved after CSHRT, and that amenorrhea is a desired effect, the main relevant effect of
PCOS in FMTs is metabolic disregulation and increased risk of cancer due to endometrial
hyperplasia. Evidence appears to be mounting that neither of these is, in fact, increasing in
occurrence following CSHRT.
While concerns regarding PCOS in transmen may perhaps be allayed, there is not
enough evidence to come to a clear conclusion on risks for ovarian cancer. There is
little research into the possible need for estrogen in transmen using CSHRT, other than
reducing risks for osteoporosis. However, the lack of research does not assure us of
benefit. The choice to undergo or refrain from oophorectomy and/or hysterectomy is
individual and must involve weighing of risks of surgery, potential future health risks,
and individual ability and desire to monitor gynecological health.
Effects on original gonads are generally, though not always, less relevant for
transwomen, who are much more likely to undergo reassignment surgery that includes
orchiectomy, as it dramatically increases feminization results while reducing the required
dose of hormones. Although the prostate is not removed as part of GRS, it generally
atrophies without the influence of testosterone; however, this is not always the case,
and there have been reports of BPH significant enough to warrant surgical intervention, in
one instance after 25 years on CSHRT (Casella 2005). Similarly, reported cases of prostate
cancer in transwomen are extremely rare, and incidence is certainly not increased by
CSHRT; risk results from lack of preventative screening or non-treatment. (Asscheman,
van Kesteren 1997).
HPA/cortisol
Given that "close crosstalk exists between sex hormones and glucocorticoids at
both neuroendocrine and peripheral levels, with different specificities according to
sex," (Pasquali 2012), and that both estrogen and testosterone modulate HPA activity
(Handa 1994, Rubinow 2005), we can reasonably expect that CSHRT may cause
alterations to corticoids and other elements of the endocrine system. Trans-specific
research in this area is extremely limited, and relevant primarily to transmen; to some
extent we can extrapolate from other research, but more information is needed to draw
any firm conclusions.
Introduction of exogenous testosterone into healthy natal men resulted in an increase
of ACTH but an inhibition of cortisol; the ACTH:cortisol ratio was lower, suggesting
decreased adrenal sensitivity, mediated by the adrenal gland itself, not the pituitary.
(Rubinow 2005). In transmen, testosterone has been shown to result in increased
adrenal androgen output by up to 70% (Polderman 1994) as well as overall higher levels
of cortisol, DHEA, and androstenedione (Polderman 1995). Although inconclusive, this
suggests that CSHRT in transmen could be linked with alterations in HPA function at the
adrenal level.
In addition to physiological changes to adrenal function, cortisol production may be
impacted by the well-documented increase in social stressors encountered by transgender
and transsexual individuals (Israel 1997, Haas 2011.) A recent study explored transitionspecific sets of stressors in FMTs, perceived levels of stress and correlated rise in cortisol,
along with increased C-reactive protein and diminished decline in nocturnal blood pressure.
The researcher linked these markers to acute stress caused by the transition process,
which generally declined by the third year after beginning hormone therapy (du Bois,
2012). Interestingly, another study found that a.m. cortisol levels, which were already
elevated in pre-CSHRT trans individuals, declined in the year following commencement of
therapy, which was attributed to reductions in stress linked to transition (Colizzi 2013).
What both of these studies have in common is the existence of elevated cortisol and
perceived stress levels among trans individuals, regardless of causation.
There is also a reported correlation between use of testosterone and worsening or
unmasking of obstructive sleep apnea; in addition to other health risks, sleep apnea can
induce intermittent nocturnal cortisol spikes and correlative HPA disregulation. However,
this connection is not solidly documented; although there have been a
number of case reports, a recent meta-review suggests that there is not enough reliable
evidence to posit a link between TRT and OSA (Hanafy 2007).
Conclusions
Endocrinologist Dr. Louis Gooren, who has co-authored many of the studies on
transsexual health, summarized his perspective after two decades clinical experience and
research: "It is clear now that sex reassignment of transsexuals benefits their well- being,
although suicide rates remain high. Cross-sex hormone administration to transsexuals is
acceptably safe in the short and medium term. However, potentially adverse effects in the
longer term are presently unknown. The data, although limited, of surrogate markers of
cardiovascular disease and the reports of cancer in transsexuals leave room for cautious
optimism" (Gooren 2008).
When weighing risks of treatment, it is important to remember that transgender/
transsexual individuals are at an increased risk of suicide or self harm, with actual suicide
attempts perhaps as high as 1:3 (Haas 2011). Risk of suicide is reduced from
20% when gender dysphoria is untreated to 1% after treatment; such a significant
reduction may be considered to mitigate potential detrimental effects of hormone
treatment (Levy 2009, Gorton 2005).
CSHRT is, for many individuals, a lifelong treatment plan that may begin as early as
adolescence. In most areas, its risks are not greater than those associated with same- sex
HRT, and are amenable to intervention, including preventative screening and supportive
lifestyle choices.
Resources for more detailed info about CSHRT treatment, protocol and effects:
R. Nick Gorton, Medical Therapy and Health Maintenance for Transgender Men:
A
Guide
For
Health
Care
Providers.
(Free
online
version
available
from nickgorton.org)
Transgender Health Care Info Archive: transgendercare.com. (Extensive info about MF
hormone protocol and surgeries)
Hudson's guide to transition: ftmguide.org. (Excellent resource for FM hormone,
surgical, and lifestyle transition)
The Center of Excellence for Transgender Health: transhealth.ucsf.edu.
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Fibromyalgia: Patterns, Pathology and
Strategies for Herbal Support
Emily Peters
Introduction
Fibromyalgia (FM) is a syndrome characterized by widespread musculoskeletal pain,
physical and mental fatigue, efort intolerance, non-restorative sleep and mood disturbance
(Van Houdenhove 2006). Herbalist Chanchal Cabrera describes the clinical features of FM:
“Symptoms generally begin as diffuse aching and stiffness which slowly worsen over a
period of weeks or even months. Eventually the muscle stifness and pain become chronic
and constant, and there are frequently 'trigger points' in the muscles. These are exquisitely
tender nodules that are palpable. Symptoms also include local muscle spasm and low grade
inflammation. … Frequently there will be poor sleep, overwhelming fatigue, irritability,
anxiety, bladder and urethral irritation, irritable bowel symptoms, and general malaise.”
(Cabrera).
There doesn't appear to be a clear cause of FM, but rather it is clinically associated with high
levels of stress, depression, post-traumatic stress disorder (PTSD), childhood and adult
abuse,
and
hypothalamus-pituitary-adrenal
(HPA)
dysfunction
(Walker,
Peres,
Van
Houdenhove 2006). Stress activates the sympathetic nervous system's fright, fight or freeze
response, and long term stress can have great impacts on the HPA axis and overall
neuroendocrine function (Van Houdenhove 2004). In this paper, I will describe the
symptoms and patterns of FM, outline the relationship between FM and stress, and explain
pathogenic mechanisms though which FM syndrome could arise. Ten I will briefy explore
strategies for herbal support that take into account the person's constitution, energetics and
symptom presentation.
Symptoms and Patterns
FM is far more common in women (Cabrera, Van Houdenhove 2005) and affects between 2
and 10% of people in industrialized countries. The criteria for diagnosis of FM is chronic
widespread pain in all four quadrants of the body and in the axial skeleton, tender points in
11 out of 18 designated areas, and is generally accompanied by an increased sensitivity to
pain throughout the entire body (Clauw). FM is characterized by generalized allodynia, or
pain elicited from stimuli that are not usually painful, and by hyperalgesia, or increased
intensity and prolonged duration of pain caused by stimuli. Karl Henriksson states that “FM
should be suspected in any chronic musculoskeletal pain condition when localised or
regional pain spreads to several sites, when temporary or intermitted pain becomes more or
less continuous, when pain on movement becomes pain at rest, or when segemental
allodynia/hyperalgeia becomes generalised.” In one study comparing 191 patients with FM,
80% reported that localized pain gradually developed into widespread pain (Henriksson).
Overlap of symptoms as well as frequent comorbidity is found between FM and other
unexplained symptoms, including: chronic fatigue syndrome, PTSD, low back pain, anorexia,
insomnia, irritable bowel syndrome, headaches, migraines, multiple chemical sensitivity,
joint disorders, major depression, anxiety, and panic attacks (Masé, Peres, Clauw, Mills &
Bone pg 311). A general personality pattern common to people with FM includes low selfesteem, anxiety, depression, lack of emotional openness, excessive striving for achievement
and recognition, aggression inhibition, and harm avoidance (Van Houdenhove 2004).
Clinical observation suggests that FM often occurs in the aftermath of a long period of
physical or emotional stress, often associated with depression. Additionally, FM seems to be
precipitated by an additional triggering physical or emotional event such as an injury,
infection, toxic exposure, or emotional trauma (Vertolli, Masé, Van Houdenhove 2006).
Other possible triggering factors include Epstein-barr viral infection, hormone alterations,
hypothyroidism, lyme disease, parvovirus infection, physical trauma and Q fever (Clauw). In
the experience of Chanchal Cabrera, primary FM is the most likely to occur in healthy young
women who tend to be stressed, tense, depressed, anxious, and striving, while men are
more likely to develop FM from a particular physical strain (Cabrera).
A Close Relationship with Trauma and Stress
In a 1997 study comparing patients with rheumatoid arthritis (RA) and FM, patients with FM
had significantly higher lifetime prevalence rates of all forms of abuse and greater severity
of childhood trauma. In this study, Edward Walker states that “physical assault in adulthood
[is] found to have a strong relationship with unexplained pain. Trauma severity was
correlated significantly with measures of physical disability, psychiatric distress, illness
adjustment, personality, and quality of sleep in patients with fibromyalgia … ” Nearly all FM
patients had experienced some form of trauma. In this study, associations were also found
between trauma and pain intensity, number of pains, perceived stress, neuroticism and
illness coping. Walker states that “... there is a high correlation between victimization
history and the number of medically unexplained physical symptoms the patient has
experienced ... Tis high correlation suggests that early experiences of victimization for which
there were no timely interventions may be expressed over time through the appearance of
medically unexplained physical symptoms. Te original trauma might actually gradually
transform into physical symptom manifestations …” (Walker).
Walker speaks to research that suggests people can store trauma in our bodies, and this
can manifest physically. Tis 'theory' that modern medicine is (finally) giving a voice to is a
timeless lived experience that many, many people know in their bodies to be undoubtedly
true. Nonetheless, this research is a signifcant step towards validating 'unexplained' physical
illness, particularly for survivors of abuse and trauma.
A 2009 study explores the link between PTSD and FM. PTSD is characterized by the
emergence of symptoms after a person experiences one or several/recurring traumatic
event(s). Symptoms of PTSD include: re-experiencing the trauma via nightmares, memories
or
intrusive
thoughts;
emotional
avoidance
or
numbness;
and
hyperstimulation
characterized by insomnia, hyperarousal and irritability. Women with high disability pain
have been found to be more likely to have experienced child abuse, adult sexual assault,
more severe spousal abuse, lifetime abuse-related injuries and PTSD symptoms (Peres).
Many FM patients' symptoms resemble PTSD; individuals with PTSD often present with
chronic pain and vice versa; both conditions involve similar pathways through with the
symptoms can escalate. FM patients with PTSD reported significantly higher levels of
avoidance, hyperarousal, re-experiencing, anxiety and depression than FM patients without
high levels of PTSD. The prevalence of PTSD amongst FM patients was found to be much
higher than the general population and women with FM reported more traumatic events
than their male counterparts. Both disorders seem to be induced by relatively short term
stress followed by chronic pathology, suggesting that the stress may induce a selfperpetuating vicious cycle. Clinical experience suggests that clients with PTSD and FM,
especially with high levels of dissociation, will present with worse symptoms in response to
exposure to traumatic triggers (Peres). It is also possible that early life stress and trauma
can alter the set point of the stress response system, contributing to an increased
susceptibility towards stress-related disorders and stress in general later in life. (Van
Houdenhove 2004)
The clinical relationship between pain and depression is well recognized; FM and depression
are both stress-related conditions and lifetime depression is a risk factor for FM. Te
relationship between stress, depression and FM exists in a recursive pattern that traps the
patient in a vicious cycle (Van Houdenhove 2006). Pain in FM should not be considered
merely an expression of depression, as the stress of the illness may lead to depression,
contributing to further symptoms such as sleep problems, less adaptive coping, physical and
mental dysfunction and decreased quality of life. Anxiety also plays a perpetuating role in
FM by increasing arousal, irritability, muscle tension, hyperventilation and avoidance
behavior, resulting in higher pain intensity, more tender points, increased functional
limitations and increased fatigue (Van Houdenhove 2004). Constant pain is both a physical
and emotional stressor, often leading to psychological distress including depression
(Henriksson). A high correlation has been found between the number of tender points
reported by a patient and measures of anxiety, distress and depression (Clauw). FM
patients tend to had a difficult time dealing with emotional stressors, which could partially
explain the role of stress in the onset of the condition; their symptoms, particularly chronic
pain, lead to increased stress, contributing to a vicious cycle that is self-perpetuating. (Van
Houdenhove 2005).
Pathogenic Mechanisms
FM is thought to arise from acute stress, medical illness and various pain conditions in
conjunction with a variety of neurotransmitter and neuroendocrine imbalances, including
HPA dysregulation, excessive pronociceptive input, and defcient modulatory signaling via
noradrenergeic and seratonergic pathways (Peres). A study found that those who had
chronic widespread pain were three times more likely to have signifcantly lower levels of
saliva cortisol and higher levels of post-stressor serum cortisol than the control group,
demonstrating an HPA axis dysregulation (McBeth). FM is characterized by HPA axis
hyporeactivity to physical and mental stressors. Tis altered neuroendocrine responsiveness
could be described as a 'loss of resilience' of the stress response system. “Te available
evidence seems to confrm … that the stress response system of patients with chronic pain
and fatigue may be impaired after a period of overburdening by physical and/or emotional
stressors, Tis may imply a biologic 'switch' from hyperactivity to hypoactivity of the system,
associated with function or even structural receptor changes, and followed by a cascade of
disturbances in immunologic, neurotransmitter, and central pain processing mechanisms”
(Van Houdenhove 2005).
It is important to understand how the stress response can lead one to hypoactivity of the
stress response system, which is a presentation of HPA dysregulation, hypocortisolism and
adrenal exhaustion. Te hypothalamus and/or amygdala perceive and judge danger, which is
impacted by past experiences and emotional memory. When a threat or stressor is
identifed, the hypothalamus stimulates three pathways: the alarm reaction via sympathetic
nervous system, stimulating the locus ceruleus; intermediate reaction via sympathetic
nervous system, stimulating the adrenal medulla; and the adaptation or resistance reaction,
via hypothalamic corticotropin releasing factor (CRF) to pituitary, then ACTH to stimulate
the adrenal cortex to secrete cortisol (Bunce July 2013).
Cortisol impacts virtually every tissue in the body. It stimulates muscle protein breakdown,
liberating arachidonic acid to be used by the liver in gluconeogenesis leading to elevated
blood sugar. It increases resistance to trauma, infection, hemorrhage and exertion in the
short term, while decreasing immune competence in the long term. It down-regulates
macrophages, stimulates T lymphocytes, and suppresses serotonin, histamine, and
eicosanoids (prostaglandins and leukotrienes). It decreases levels of GnRH, LH/FSH,
progesterone and testosterone, decreases delta wave (deep) sleep patterns, increases
prolactin, and stimulates morning wakefulness (Bunce July 2013).
Te amygdala can bypass the frontal cortex when a stressor is perceived as an emergency,
even when there is no real danger. Te amygdala becomes hyper-aroused, stimulating the
hypothalamus and amygdala to both release CRF. Trauma can be reactivated, anchoring us
in old learned emotional patterns via the amygdala; this is where emotions become
physiology. Chronic exposure of HPA to corticoids can down-regulate sensitivity, interrupting
negative feedback loops. Arousal can be maintained because of this positive feedback from
repeated
amygdala
stimulation. Tis shifts one's perception
of 'reality' to become
hypervigilant. Te cycle continues, as continued perception of stress maintains the stress
response.
Over
time,
this
cycle
will
eventually
lead
to
adrenal
exhaustion
and
hypocortisolism (also called the allostatic load). Tis chronic long term exposure to stress
response causes symptoms that overlap signifcantly with FM including: reduced immune
response, anxiety/depression, fatigue and sleep disruption, cognitive defcit, and muscle
weakness. Insulin-resistance, hypothyroid function, sex hormone dysregulation, PCOS,
osteoporosis and hypertension can also be a part of a HPA dysregulation picture (Bunce July
2013).
In FM, the HPA axis and the sympathetic nervous system are both dysregulated. Tis causes
changes in neurotransmitter function, immune function and central pain mechanisms.
Dysregulated immune activity includes the release of pro-infammatory cytokines that can
promote lethargy, fu-like symptoms, social withdrawal, concentration difculties, mood
lowering and pain-threshold lowering, which all can ft the symptom picture of FM. Changes
in central pain processing has been confrmed by brain imaging studies in FM patients, linked
to the inadequate descending pain inhibition and a dysfunction of endogenous opioid and
low CRF (Van Houdenhove 2006). A study found that 80% of FM had elevated levels of
Substance P in the CSF, which has been linked to the release by neurons in the CNS. Te
constant pain hypersensitivity could be due to changes in the function of sensory neurons
and how they send information to the CNS in response to noxious stimuli (Henriksson).
Stress-induced pro­infammatory cytokines such as IL-1, IL-6, and TNF-alpha also may
contribute to the pathogenesis of pain. Research suggests that prostaglandins, leukotrienes,
pro-infammatory cytokines, and nitric oxide could also play a role in the pathophysiology of
FM (Van Houdenhove 2004).
Traumatic experiences may increase vulnerability to FM by psychosocial mechanisms, such
as hypertension of muscles, sleep problems, HPA axis dysfunction, and inadequate stress
coping from low self-esteem, depression and abuse. Perpetuating stressors can decrease
quality of life and likelihood of recovery, such as: not accepting the condition and thus not
adjusting lifestyle accordingly, a lack of social support, and not being accepted as sufering
from a legitimate illness. (Van Houdenhove 2006).
An Herbalist Approach to FM
In caring for a person with FM, it is very important to understand people's stories. Listening
and giving emotional support can help to understand how their condition is afecting them. If
appropriate, we could help people shape their views diferently (Bunce Dec. 2013).
Conceptualizing FM as a stress disorder may help with client-practitioner rapport and
encourage patients to address psychosocial issues (Van Houdenhove 2004). It is important
to evaluate a client's diet, nutrition and lifestyle factors and help them to envision healthy
changes and assess whether there is gut infammation that is complicating symptoms
(Bunce Dec 2013, Cabrera). Toxic exposure has also been found to be a precursor to FM; in
assessing a client's history it is important to consider this as a possible causative factor and
formulate accordingly (Bunce Dec 2013, Vertolli).
Looking through the lens of the Ayurvedic doshas, we can see how FM can arise in diferent
constitutional picture. In the cold and dry Vata, we are likely to fnd a client with little to no
resources, gone through adrenal fatigue to exhaustion with anxiety. A Kapha will likely be
stagnant, depressed and prone to worry about others. A Pitta will likely exhibit the
infammatory picture of autoimmunity and hypersensitivity with FM as a secondary complaint
(Bunce Dec 2013). Matthew Wood considers FM to be an expression of the damp
stagnation, torpid tissue state. He explains that a build-up of unneeded fuids, precipitating
into thick phlegm, prevents tissues from getting enough nutrition so they become fabby and
weak and this causes pain in the muscles, with accompanied symptoms of skin lesions,
backed up digestive and liver function, lymphatic stagnation, and in some cases
hypothyroidism. He indicates that blood purifers or alteratives are the most appropriate
herbal remedy (Wood 2004). Tis seems to best ft the Kapha picture that Bunce describes.
Michael Vertolli views the typical constitutional pattern as autoimmune and infammatory,
following emotional or toxic stress (Vertolli), ftting the Pitta pattern the most clearly. In any
person, of course we fnd many overlapping energetic patterns and there usually is not a
perfectly clear constitutional picture – people are complex and we should tailer their specifc
herbal protocols based on their unique presentation.
Herbal goals for support include: pain management, decrease substance P, improve
detoxifcation, bufer stress perception and anxiety, improve circulation, improve sleep,
normalize immune function, regulate HPA axis and modulate infammation (Bunce Dec 2013,
Cabrera, Masé, Vertolli). Tere are many dozens of herbs that can meet these goals; I am
going to give examples of herbs that seem to be the most specifc for FM based on my
research. An herbalist can choose other plants based on the person's set of symptoms, for
issues such as GI infammation, insomnia, acute pain, anxiety, hypothyroidism, etc.
Anti-infammatory and nervine herbs help to relieve symptoms of pain and improve mood.
Hypericum perforatum, St John's wort, is useful for depression, as an anodyne and a nerve
tonic, if the medication list allows (Masé, Cabrera, Mills & Bone). Actaea racemosa, black
cohosh, is used as an anti­infammatory for the muscles and for someone with a dark and
brooding mind, signs of congestion, and with shifting, sharp, spasmodic pain especially in
the back and neck (Cabrera; Wood 1997); it is also indicated for a person with a history of
sexual abuse, alcoholism or drug abuse; with heavy, aching pain, muscular tension and
rheumatic pain made worse with activity (Alfs pg 35). Uncaria tomentosa, cat's claw root
bark, is immunomodulant and anti-infammatory for joint pain, rheumatism and FM (Bunce
Dec 2013, Alfs pg 43). Curcuma longa, turmeric, is a useful warming anti-infammatory
(Cabrera, Mills & Bone). A cognitive stimulant and brain tonic would be useful, such as
Rosmarinus of., rosemary; Centella asiatica, gotu kola; Avena sativa, milky oats; or Ginkgo
biloba, ginkgo (Cabrera, Alfs pg 62, Mills & Bone).
Alterative, circulatory stimulant herbs can help support elimination and detoxifcation.
Arctium lappa, burdock, and Apium graveolens, celery seed, are useful alteratives with a
specifc afnity for the musculoskeletal system (Cabrera, Mills & Bone, Wood 2004). Te bitter
nervine Verbena spp., vervain, has a tonic efect on the glands of the body (Cabrera). Urtica
dioica, nettle, can be indicated for FM as a nutritive tonic. Juglans nigra, black walnut hulls,
and Fucus vesiculosus, kelp, are both useful when hypothyroidism accompanies FM
(Cabrera, Wood 2009). Zanthoxylum, prickly ash bark, is a useful circulatory stimulant
specifcally for encouraging blood fow to the muscles (Bunce Dec 2013, Cabrera). For
stagnation of fuids and to help eliminate toxins, a lymphatic such as Phytolacca decandra,
poke; or Galium aparine, cleavers, would be useful (Cabrera, Wood 2004). For supporting
the immune system, Echinacea spp., has been found useful (Cabrera, Mills & Bone).
Adaptogenic herbs have an important role to play in supporting the adrenals, normalizing
the HPA axis, and generally improving one's stress response. Adaptogens that have been
used for FM include: Eleutherococcus senticosis, eleuthero, as an adrenal tonic and energy
enhancer; Glycyrrhiza glabra, licorice, as an adrenal-restorative and anti-infammatory; and
Ganoderma lucidum, reishi, for disturbed Shen, to modulate immunity, for pain and joint
weakness, insomnia, and especially for a pro-infammatory, hypersensitive person (Bunce
Dec 2013, Mills & Bone, Cabrera, Alfs pg 92). Any adaptogens would be useful here as well,
chosen based on the person's constitution and specifc presentation, and are most useful for
long-term support (Bunce Dec 2013).
Complementary Strategies
Strategies to reduce pain and stress, improve sleep, reduce anxiety and depression,
detoxify, modulate immunity and regulate the HPA axis should be complemented by body
work and therapy. When FM overlaps with a history of trauma, it is very important that
treatment focus on both physical and emotional dimensions. Te role of evaluating
someone's traumatic history and helping them process it should be taken on carefully by
someone trained to do so – a therapist or psychologist who understands the process of
uncovering and healing from trauma; for many people it can be very painful and difcult to
look at and reconstruct these memories (Peres). Careful low-intensity aerobic exercise,
tailored to the person's abilities can also be useful (Van Houdenhove 2004). Herbalists have
found it helpful to refer clients to massage therapy, craniosacral therapy, counseling, and
spiritual/awareness type practices (Masé, Vertolli).
Cognitive behavioral therapy is particularly helpful to optimize coping, implement adaptive
lifestyle changes and encourage long-term self-care (Van Houdenhove 2004). Cognitive
therapy is a structured, directive form of psychotherapy where the goal is to help the
patient identify maladaptive cognitions and change them. Te approach of mindfulness
meditation has been found to be efective in the treatment of patients with chronic pain. It is
a system of self-inquiry that stems from Buddhist philosophy and leads to increased
awareness of one's thoughts, sensations, feelings, consciousness and the nature of one's
mental processes. A study found that a mindfulness meditation based stress reduction
program signifcantly improved the symptoms of patients with FM (Kaplan).
Conclusion
Conventional medicine has not established strategies to cure FM. Tey can use medications
for sleep, IBS, pain management, depression and anxiety, as well as recommending
cognitive behavioral therapy and aerobic exercise (Clauw). HPA axis dysregulation is not
recognized as being curable . With a holistic mindset, we are able to step back and evaluate
the root causes of imbalances that can cause debilitating syndromes such as FM. Te
research suggests that HPA axis dysregulation, usually stemming from long-term trauma,
toxicity, or another physical/mental stressor, seems to be a likely cause of FM. In our herbal
strategy we can assess the person's energetic constitution and explore what stressors may
have led to this imbalance for them. Along with referrals to therapy and body work, we can
formulate herbal remedies with alteratives, anti-infammatories, nervines, and adaptogens to
help relieve symptoms and support the body, particularly the stress response, to come into
balance.
References
Alfs, Matthew. 300 Herbs, Their Indications & Contraindications. Old Theology Book House,
2003.
Bunce, Larken. Personal Interview. 5 Dec. 2013.
Bunce,
Larken.
"Adrenal
Cortex
and
Adrenal
Medulla
Dysfunction;
Stress
&
HPA
Dysfunction." VCIH, Montpelier. 25 July 2013. Lecture.
Cabrera, Chanchal. “Musculoskeletal – Fibromyalgia.” Med Herb. Paul Bergner, 2001. Web. 9
Dec. 2013.
Clauw, Daniel J. "Elusive syndromes: treating the biologic basis of fibromyalgia and related
syndromes." Cleveland Clinic Journal of Medicine 68.10 (2001): 830-830.
Henriksson, Karl G. "Fibromyalgia-From syndrome to disease. Overview of pathogenetic
mechanisms." Journal of Rehabilitation Medicine-Supplements 41 (2003): 89-93.
Kaplan, Kenneth H., Don L. Goldenberg, and Maureen Galvin-Nadeau. "The impact of a
meditation based stress reduction program on fibromyalgia." General Hospital Psychiatry
15.5 (1993): 284-289.
Masé, Guido. “Re: Researching fibromyalgia.” Message to Emily Peters. 2 Dec. 2013. Email.
McBeth,
John,
et
al.
"Hypothalamic-pituitary-adrenal
stress
axis
function
and
the
relationship with chronic widespread pain and its antecedents." Arthritis Research & Therapy
7.5 (2005): R992.
Mills, Simon, and Kerry Bone. Principles and Practice of Phytotherapy. Modern Herbal
Medicine. Churchill Livingstone, 2000. Pg. 311.
Peres, Julio FP, Andre Leite Gonçalves, and Mario FP Peres. "Psychological trauma in chronic
pain: implications of PTSD for fibromyalgia and headache disorders." Current Pain and
Headache Reports 13.5 (2009): 350-357.
Van Houdenhove, Boudewijn, and Ulrich T. Egle. "Fibromyalgia: A stress disorder?."
Psychotherapy and Psychosomatics 73.5 (2004): 267-275.
Van Houdenhove, Boudewijn M. D., and Ulrich Egle. "The role of life stress in fibromyalgia."
Current Rheumatology Reports 7.5 (2005): 365-370.
Van Houdenhove, Boudewijn, and Patrick Luyten. "Stress, depression and fibromyalgia."
Acta Neurologica Belgica 106.4 (2006): 149.
Vertolli, Michael. “Re: Researching fibromyalgia.” Message to Emily Peters. 3 Dec. 2013.
Email.
Walker, Edward A., et al. "Psychosocial factors in fibromyalgia compared with rheumatoid
arthritis: II. Sexual, physical, and emotional abuse and neglect." Psychosomatic Medicine
59.6 (1997): 572-577.
Wood, Matthew. The Book of Herbal Wisdom: Using Plants as Medicines. North Atlantic
Books, 1997. Pg. 221-222.
Wood, Matthew. The Practice of Traditional Western Herbalism: Basic Doctrine, Energetics,
and Classification. North Atlantic Books, 2004. Pg. 221-222.
Wood, Matthew. The Earthwise Herbal: A Complete Guide to New World Medicinal
Plants.North Atlantic Books, 2009. Pp. 208-209.
Herbal
Therapeutics
for
physiological
hyperprolactinemia concurrent with PMS
symptoms
Angie Barger
Hyperprolactinemia is characterized by higher than normal blood levels of PRL.
Elevated PRL levels can be physiological or pathological. 10 Pregnancy, lactation, nipple
stimulation, and stress can physiologically induce hyperprolactinemia. 10 The most common
pathological causes of hyperprolactinemia are prolactinomas (PRL producing tumor),
hypothyroidism, drugs, renal failure and cirrhosis of the liver. 10 This paper will address the
physiology,
pathophysiology
and
herbal
therapeutics
for
lactation-induced
hyperprolactinemia concurrent with PMS.
In lactation, PRL secretion inhibits dopamine. 9 PRL is a peptide hormone from the
anterior pituitary that controls milk production in the breast, and appears to play a role in
regulation of the immune system.
9 Dopamine is an amine Central Nervous System
neurotransmitter associated with sensing pleasure. 9 PRL is primarily controlled by an
inhibiting hormone from the hypothalamus, Prolactin inhibiting hormonr (PIH). 9 There is
good evidence to suggest that PIH is actually dopamine.10
Pre-menstrual syndrome (PMS) is defined by psychological, behavioral and physical
symptoms which occur in the luteal phase of the menstrual cycle.10
collection of possible symptoms.
A syndrome is a
In PMS, there are estimated to be 150 collective
symptoms. This paper focuses on those included in PMS-A: tension, irritability, insomnia,
depression, anxiety, etc. and PMS-D: low estrogen levels with overlapping PMS-A symptoms
and PMS-H.
These specific PMS groups have been linked to excess PRL in the bloodstream.
10 PMS theory currently supports an abnormal tissue response to the normal changes of
the menstrual cycle. 4 Fluctuating estrogen and progesterone levels may be implicated, but
serotonin, endorphins, androgens and/or other neurotransmitters and hormones can be part
of the physiological picture. 8 The menstrual cycle is a transformative cycle, generated by
the interplay of secretory sites, the hypothalamus, the anterior pituitary and the ovaries,
and of the hormones they produce. 10
Relevant anatomy in a woman's body actually
changes throughout the month, characterizing the female reproductive system's mobility
and changeability. 10
PMS-A, PMS-D and PMS-H are linked to elevated levels of PRL in the bloodstream. 11
With improved liver function, hormones will be processed more efficiently, leading to less
PMS symptoms – and specifically less PMS-A, D and H resulting from excess PRL. 11 Excess
PRL, in addition to stress, inversely affects dopamine levels, leading directly to depression
or anxiety.
Elevated PRL levels are also indicated in the following PMS categories and
symptoms:
•
PMS-A : nervousness, tension, irritability, mood changes and anxiety. 10
•
PMS-D : depression, forgetfulness, crying, confusion, and insomnia. 10
•
PMS-H : fluid retention, weight gain, swelling of extremities, breast tenderness and
abdominal bloating. 10
The combination of these female sex hormones secreted into the bloodstream
simultaneously demands a healthy metabolic center: the liver. The liver metabolizes female
sex hormones that control the menstrual cycle: Follicle stimulating hormone (FSH),
Lutenizing hormone (LH), Gonadotropin releasing hormone (GnRH), Estrogen, Progesterone
and Inhibin. In PMS, the liver's processing speed can be improved with herbal therapeutics.
9
While menstrual female sex hormones are spiking in the bloodstream PRL is steadily
secreted to produce breastmilk.11
When the liver has a low level of function, sex
hormones recirculate in the bloodstream instead of being metabolized efficiently. 10
If the
tissue's capacity to regenerate new cells is compromised by disease, the body's entire
metabolism will be affected.
This results in elevated blood serum levels of PRL, inducing
hyperprolactinemia. Regardless of our lifestyle, the liver is heavily taxed simply living a daily
life in the 21st century which includes 16,000 chemicals which did not even exist one
hundred years ago. The liver should be herbally supported to increase optimal performance,
especially in the concurrent case of hyperprolactinemia and PMS. 15
Pathophysiology
In PMS dysfunction, treatment should support the return to underlying functional
rhythms. Conventional medicine treats menstrual cycle rhythm dysregulation with the birth
control pill - . After a two to three month cycle, the pill is withdrawn, upon which time the
body seems to “reboot” itself and the medication can be withdrawn after regulation.10 The
most widely used birth control pill contains either two hormones: estrogen and progestin, or
sometimes just progestin.1 When released in a timely manner throughout the menstrual
cycle, progestin will prevent ovulation.1
Just prior to menstruation, levels of progesterone and estrogen, as well as Calcium
(Ca), and Magnesium (Mg) – which allows dopamine in the brain – drop. This may influence
pain, insomnia, muscle cramping and stress reactions. 9, 6 Dopamine is a Central Nervous
System (CNS) Neurotransmitter connected with sensing pleasure. 9 A dopamine deficiency
is indicated in PMS, anger and irritability alike.
As hormones drop, so do endorphins, which can result in insomnia, anxiety and
irritability. Immune response also drops, leading to flare-ups of chronic issues like herpes.
These physiologies are interconnected and linked to an abnormal tissue response to the
normal changes of the menstrual cycle 11,10
Further study is needed to determine which factors effect milk output in
breastfeeding mothers. 6 Further study is also warranted to determine if breastfeeding
mothers with a large output tend more towards the pathologies associated with elevated
levels of prolactin in the blood. An elevated state of hyperprolactinemia in the situation of a
prolactinoma appears different in the body than elevated levels of prolactin in a
breastfeeding woman.7
During lactation, the pituitary down regulates the mRNA gene
receptor expression of prolactin receptors, but not in the case of a prolactinoma .7
Therefore, elevated levels of prolactin will continue to circulate in the bloodstream for longer
in a breastfeeding mother but not necessarily in a person with a prolactinoma. 7 PRL inhibits
the activity of aromatase which plays an important role in biosynthesizing steroid hormones
and is present throughout the body, including the liver and fatty tissue, further leading to
decreased liver function during high PRL production. 10
Some strategies for decreasing PRL levels can result in decreased milk production,
and so should be monitored if a mother intends to continue breastfeeding while using herbs
like Vitex agnus-castus to deal with pathologies attributed to low levels of dopamine.6
Focus should instead be on supporting the liver to most efficiently process the sex hormones
in her bloodstream. Further research is warranted to determine if breastfeeding mothers
with high output of breastmilk can utilize strategies for decreasing prolactin levels and still
successfully breastfeed with a lower output and possibly reduced hyperprolactenemia.
Research does not currently show whether women with high output of breastmilk have high
levels of PRL as opposed to women with low breastmilk output.
Therapeutics
PMS-A (anxiety), is characterized by a HOT and dry tissue state, nervous tension,
anxiety, irritability, mood changes and insomnia.
PMS-A is associated with high estrogen
and low progesterone, either from corpus luteum deficiency or the liver’s inability to break
down excess estrogen/sex hormones. PMS-A also may result from
increased CNS
stimulation, stimulating effects of estrogen, high environmental exogenous estrogens:
animal products/plastics, etc. 10 PMS-D (depression), is characterized by a COLD and moist
tissue state, depression, forgetfulness, crying, confusion, insomnia, and/or withdrawal.
PMS-D is associated with excess progesterone, which causes CNS depression, lowered
serotonin. 10 PMS-H (hyper hydration) is characterized by a COLD, stagnant tissue state
and reveals itself as bloating, breast tenderness, abdominal bloating and weight gain. 10
These three conditions are linked to excess prolactin in the bloodstream. 10
Herbal Therapeutics Goals, Actions and Herbs
Herbally, we aim to address the following goals:
- Correct any hormonal imbalance through the
HPA axis.10
Hormonal
normalizers are used when the endocrinology (not the liver) is indicated in excess
hormone levels.
Paeonia lactiflora contains paeoniflorin, a monoterpene glycoside which
contributes to its effectiveness
in the treatment of PMS and hyperprolactenemia among
other gynecological conditions. 20 A low dose of Vitex agnus-castus lowers PRL levels wile
improving the secretion of breastmilk as a galactogogue.23 Dosage for Vitex agnus-castus
is 1:2 or 1:3, 60-75% EtOH, 1 ml TID of fluid extract for three to nine months. 9
- Correct Essential Fatty Acid (EFA) status, responsible for the normal function and
development of most tissues including the liver and blood vessels. 8 Mills and Bone suggest
a supplement of Evening primrose Oil at 3000 – 4000 mg per day.10 EFA status can also
be remedied with Flaxseed Oil, as suggested by Ruth Trickey in Women, Hormones and the
Menstrual Cycle, at 1-2 tablespoons/day (T/d), oily fish 12-20 oz/week, or Cod Liver Oil
supplements at 1-2 T/d. 8
-Treat the main physical symptoms as they occur.
Circulatory stimulants
like
Zingiber officinale and Ginko biloba aid the body in detoxifying by moving the blood to
muscles and joints. Zingiber officinale is dosed at 0.7-2 mL daily of 1:2, 1.5-5 ml per day of
1:5.10 In China, Zingiber is mainly used to promote sweating and as an expectorant for
colds and chills.
Western herbalists also regard it as a good circulatory stimulant. 27
Diuretics are used for fluid retention in PMS-H: Taraxacum officinale leaf decoction can be
drunk to "purify the blood", and for nervousness. 31 Galium aparine is traditionally used for
cystitis, indicating it as a diuretic by Michael Howard in. Traditional Folk Remedies. 26
Dosage for Galium aparine is 3.5-7 ml at 40% EtOH of 1:2 liquid extract daily.
Urtica dioica
is appropriate as tincture or tea. Urtica dioica is suggested at 2-6 ml at 40% EtOH of 1:2
liquid extract or 2-3 T/quart infused per day. 28 Urtica is energetically dry and may not be
appropriate for vatas with PMS-A. Analgesics address aches & pains in PMS-H: Zingiber
officinale contains pungent qualities which produce analgesic effects. 22 Corydalis cava is
fast and the strongest pain remedy when pain comes from stasis in the abdomen.
It is
usually paired 4:1 with Eschscholtzia californica, inducing a powerful anti-inflammatory
action as well.
Viburnum opulus, or Crampbark, attends to spasms within 10 minutes. 29
Crampbark, also an antispasmodic nervine, has a liquid extract dosage of 1:2.5, 40%
alcohol, 10% glycerin (to get tannins), 3-4 mL TID/QID;favor frequency over larger dose.
29
-Treat emotional disturbances : tonics for depression, sedatives for anxiety.10
Nervine relaxants are indicated for anxiety in PMS-A, Valeriana officinalis, or Valerian root,
referred to as “Nature's Tranquilizer in Penelope Ody's Complete Guide to Medicinal
Herbs,calms the nerves with chemicals called valepotriates that seem to depress the
nervous system, especially potent in a fresh plant extract.27 Valerian is dosed at 2-6 ml of
1:2 liquid extract daily at 60% EtOH to capture the volatile oils.10
Piper methisticum, or
Kava kava, is known for its kava lactones which have potencies similar to cocaine and
procaine as local anasthetics.30 Kava also reputes anti-anxiety effect without sedation or
hypnotic effects. 31 Dosage for Piper methisticum is 3-6 ml daily of 1:2 liquid extract at
60% with coconut milk fat to extract kava lactones.
Leonorus cardiaca, or Motherwort, was
once described by Mrs. Maude Grieve as “especially valuable in female weakness and
disorders, allaying nervous irritability and inducing quiet and passivity of the whole nervous
system”.32 It is a safe nervine relaxant at doses of 2-4 mL TID 1:2, 50% alcohol, or 1mL
as needed for immediate anxiety relief.33
Nervine tonics are indicated for anxiety in PMS-A, depression in PMS-D.
particularly noted
formula is Schisandra
chinensis
in
combination
with
A
Hypericum
perforatum and Withania somnifera. 8 Vitamin B complex may help with PMS-A symptoms
relating to stress. 24
-Compensate for adverse effects of stress on the body with adaptogens. 10
Adaptogens are indicated to transform the perception of stress and balance the
Hypothalamic-Pituitary Axis. Eleutherococcus senticosus, Siberian Ginseng, is noted to have
similar properties to Panax Ginseng, both worthy of mention as “the king of tonics”.34
Eleuthero will help a person get
through the stress, but Ginseng will help them recover
from having been stressed out – on your nerves, vasculature, entire physiology - starting
with endocrine system.35
Dosing of Eleuthero is 1:4 at 50% EtOH, 2-8 ml daily.30
Withania somnifera, or Ashwagandha, is indicated as a substitution for psychotropic drugs in
Premenstrual Dysphoric Disorder (PMDD), a PMS serious mood disorder.8
Ruth Trickey
suggests the choice herb Hypericum perforatum formulated with Withania somnifera, an
anxiolytic such as Lavandula officinalis, and a hormone-modulating herb such as Vitex
agnus-castus.8 This combination would also be appropriate especially for PMS-A or PMS-D.
Withania somnifera is taken in large doses, and is a food like herb. Suggested dose of the
fluid extract is 35-90 ml per week of a 1:2 fluid extract at 40% EtOH to preserve the
steroidal withanolides, believed to be responsible for many of the adaptogenic qualities.8,
10
Schisandra
chinensis
is
the
key
player
in
our
team
of
herbs:
adaptogen,
hepatoprotectant, hepatic anti-inflammatory, anti-oxidant, cholagogue and nervine – it is
indicated in every tissue state of hyperprolactinemia concurrent with PMS where the liver is
to blame. Dosage is 1-1.5 ml, 1:3 at 60-70% (to preserve lignans) EtOH TID.10
-Balance hepatic metabolism (Stage 1 and Stage 2). Hepatoprotectant herbs are
indicated to protect the liver from further damage and secondarily efficientize hormone
metabolism. The main indications for Schisandra chinensis is the primary hepatoprotectant
due to its anti-oxidant activity and production of hepatic glutathione levels.18, 19
Silybum
marianum, Milk Thistle, or isolated Silymarin, also a galactagogue and a cholagogue,
protect the liver by producing an anti-oxidant effect on liver tissues and enhancing the
metabolism of some drugs (phytochemicals) via enzyme pathways in the liver.12,13 The
standard dosage of Milk Thistle is 200 mg 2 to 3 times a day of an extract standardized to
contain 70% silymarin.37 Taraxacum officinale root can be used generally as a liver tonic
by increasing bile production and secretion.14 Tincture the fresh root 1:2, 35%, 5-10 mL
TID. 25 Mills and Bone suggest the following formula as hepatoprotectant when a taking
the contraceptive pill: Taraxacum officinale 1:2, 35 ml, Silybum marianum 1:1, 35 ml and
Schisandra chinensis 1:2, 35ml for a 100 ml formula, dose 5-10 mL TID.10
Cynara
scolymus works as a cholagogue, choleretic antioxidant and promotes regeneration of the
liver cells. 16, 17 Cynara is dosed at 3-8 ml of 1:2 liquid exract per day.
10
-Treat the liver if signs of sluggishness are apparent with bitters, cholagogues,
choleretics ; reduce oxidative damage, remove offending substances. Anti-inflammatory
herbs can decrease the initial site of inflammation in the liver; Anti-oxidants improve liver
function and avoid further damage. Schisandra chinensis and Circumin extract, from
Curcuma longa, are excellent liver anti-inflammatory herbs with anti-oxidant properties.21
Circumin extract is dosed at 500 mg, 1.755 g/day.36,37 Cholagogues release more bile
from the liver into the bloodstream as fat metabolizes enhancing liver metabolism. Bitter
qualities of Schisandra chinensis, Taraxacum officinale Root and Cynara scolymus,
mentioned also as hepatoprotectants, serve as cholagogues at the same dosage
mentioned.8
Because of the individual nature of PMS, conventional treatment is primarily
symptomatic and non-pharmacologic. Stress management, counseling, conflict
resolution, biofeedback and guided imagery are all recommended. Exercise,
supplements and dietary changes are also suggested. If improvement is still
needed, medications are prescribed and can include birth control pills, Selective
Serotonin Reuptake Inhibitors (SSRIs), Non-steroidal anti-inflammatory drugs
(NSAIDs) or progesterone which is clinically shown ineffective for mood and
behavior symptoms of PMS/Premenstrual Dysphoria (PMDD), and sertonergic
antidepressants. 11, 2
Non-herbal
supportive
strategies
hyperprolactinemia concurrent with PMS.
are
of
utmost
important
when
balancing
Exercise increases dehydroepiandrosterone
(DHEA), a precursor to female sex hormones, and balances the impacts of cortisol. Cortisol,
an anti-inflammatory agent of stress reactions, exits the bloodstream system when one
exercises. 10 Otherwise it is involved in a negative feedback loop when in regulation. If
cortisol exits the body, the HPA axis will become more sensitive to it, thus the body will not
have to produce it in continuous high amounts if it perceives a stressor.
As with any
sensitization in the body, less of the neurotransmitter or hormone is needed if more
receptors are available to receive the signal.9 A woman's awareness of the timing of her
cycle could establish compassion for oneself.
Beer should be avoided, which further
increases prolactin levels.8
In conclusion, an abnormal tissue state is currently the scientific explanation for PMS.
From an herbal perspective, tissue state will aid the selection of herbal treatment. When
hyperprolactinemia accompanies PMS, elevated prolactin levels can be attributed to
physiological conditions if a woman is lactating. High levels of hormones in the bloodstream
in addition to the myriad of chemicals in the daily environment are taxing to even a slightly
damaged liver. Extreme care is given first to her liver and then to balance hormones if the
liver therapeutics are ineffective. Prolactin-inhibiting/ Dopaminergic herbs may be indicated
if the woman has high output of breastmilk, without threatening her breastfeeding
relationship with her baby. This theory is currently unsupported by research and deserves a
bit of attention.
Herbs are the best supportive strategy to improve liver health and
subsequently decrease symptoms of physiological hyperprolactinemia concurrent with PMS
through efficient hormone metabolism.
References
1.
Planned
Parenthood
Informative
website.
Accessed
at
-
http://www.plannedparenthood.org/health-topics/birth-control/birth-controlpill-4228.htm
2.
Freeman, W. Treatment of depression associated with the menstrual cycle:
premenstrual dysphoria, postpartum depression, and the perimenopause. Dialogues Clin
Neurosci. 2002 Jun;4(2):177-91.
3.
Cotterill, S. Department of Child Health, University of NewCastle upon Tyne.
Accessed at - http://www.cancerindex.org/medterm/medtm12.htm
4.
Selye, Hans (1974). Stress without distress. Philadelphia: Lippincott
5.
Fukusima, M. and Ota, . 1988. 'Endocrinological effects of Shakuyaku-kanxo-to (TJ-
68) and Toki-shakuyaku-san (TJ-23) in sulpiride-induced hyperprolactinemic rats', Recent
Advances in the Pharmacology of Kanpo (Japanese Herbal) Medicines, eds E. Hosoya and Y.
Yamamura, Excerpta Medica, Amsterdam. pp. 155-62.
6.
Hill PD, Aldag JC, Demirtas H, Zinaman M, Chatterton RT. J Hum Lact. 2006
Aug;22(3):305-14.
7.
Tokai J Exp Clin Med. 2010 Jul 20;35(2):62-5.
Maeda H, Izumi S, Kato Y, Cai LY,
Kato T, Suzuki T, Nakamura E, Sugiyama T, Fuda T, Takahashi K, Kondo A, Matsumoto T,
Ishimoto H.
8.
Trickey, R.
Women, Hormones and the Menstrual Cycle: Herbal and medical
solutions from adolesence to menopause. 1998: Allen & Unwin. pp. 116-119, 274-282, 371,
454, 481,
9.
Silverthorn, D.
3rd ed. Human Physiology: An Integrated Approach. Benjamin
Cummings. San Francisco, CA. 2004. pp. 826, 869.
10.
Mills, S., Bone, K. Principles and Practice of Phytotherapy. 2000: Churchill Livingstone.
p. 195, 239, 241.
11.
Bancroft, B.
Lecture on Pathology of PMS and Female Reproductive System.
Vermont Center for Integrative Herbalism. 2011.
12.
Batakov, E.A.
2001.
'Effect of Silybum marianum oil and legalon on lipid
peroxidation and liver antioxidant systems in rats intoxicated wit carbon tetracloride', Eksp
Klin Farmakol 64(4), pp. 53-5.
13.
Beckmann-Knopp, S.Rietbrock, S. Weyenmeyer, R. et al. 2000. 'Inibitory effects of
silibinin on cytochrome P-450 enzymes in human liver microsomes', Pharmacol Toxicol
86(6), p. 250-6.
14.
Willun,
G.
1993.
'Taraxaci
radix
cum
herba',
in
Herbal
Drugs
and
Phytopharmaceuticals, ed. N.G. Bisset. CRC Press, Boca Raton.
15.
Resnick, C.
1995. Nutritional Regulation of Detoxification, American Association of
Naturopathic Physicians, Tree Farm Cassettes (audio tape).
16.
Kiso, Y., et al., Nat Prod 1983; 46 (6): 841-847.
17.
Camaras, J. et al., Med Sci Res 1987; 15: 91-92.
18.
Liu, GT.
Pharmacological actions and clinical use of fructus schizandrae.
Chinese
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Ota, H. and Fukisima, M. 1988.
'Stimulation by Kanpo prescriptions of aromatase
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A. Mahesh, R. Jeyachandran, L. Cindrella, D. Thangadurai, V. P. Veerapur, D.
Muralidhara Rao (2010). Hepatocurative potential of sesquiterpene lactones of Taraxacum
officinale on carbon tetrachloride induced liver toxicity in mice. Acta Biologica Hungarica
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Diabetes Mellitus: Herbal, Nutritional and
Life Style Therapeutics
Aisling Badger
Pathophysiology:
Diabetes is a life long illness where there are continual high levels of glucose in the
blood. An endocrine system failure can also result when the beta cells produce insulin but
the cells are unable to use it properly- leading to insulin resistance( Kumar, et al 1189).
Through my research I have discovered that herbs can play a supportive role in decreasing
blood sugar levels while increasing insulin production, specifically in type II. A healthy well
educated diet is also crucial in treating diabetes, and seems to be one of the leading
problems in the development of this disease.
Most commonly we see Type I, II and
Gestational Diabetes. Type I is an auto immune destruction of the beta cells where over
time the pancreas loses the ability to produce insulin, making us dependent on daily
injections. The cause is unknown but may be linked to a genetic component, and is often
developed at a young age. Type 2 or
“ adult onset” is a non insulin dependent diabetes, which is the most common among
adults. In type II, the cells are not able to respond to the insulin that is present, causing
insulin resistance. As a result blood glucose cannot get into cells to be stored for energy,
leading to
high levels of sugar in the blood, creating what we know as Hyperglycemia.
Insulin resistance can also often become apparent in people 10- 20 years before the onset
of diabetes type II ( Kumar, et al,1194+).
Gestational Diabetes is high blood sugar levels that develop during pregnancy. It usually
disappears after delivery, although the mother becomes more at risk for type 2 diabetes
later in life. (University of Maryland Medical Center, alternative medicine index) According to
the American Diabetes Association, all women should be screened for diabetes in their third
trimester.
The endocrine system is composed of glands that are responsible for secreting
hormones directly into the bloodstream.
All of the glands can have an inter-relational
connection to each other and the diseases that arise from endocrine system disfunction,
such as Diabetes( Kumar,1156). Insulin; a hormone secreted by the pancreas, is produced
by beta cells to control blood sugar in our body. After eating, our body starts the process of
breaking down sugars and starches into glucose which enters the blood stream and our cells
take up as energy. Resistance to insulin accompanied with high levels of sugar in the blood
leaves our liver, body fat and muscle cells to inappropriately respond to the insulin that is
present(Kumar). If left untreated complications that arise from insulin deficiency and high
levels of sugar in the blood, can cause an array of vascular and oxidative diseases especially
in the retina, kidney, and blood vessels, thus effecting other organs(University of Maryland
Medical Center), Some research has linked an increase of Diabetes to obesity levels, the
growing rate of poverty, sedentary life styles and poor diet(Adam Drewnowski,Journal of
Clinical Nutrition). Development of diabetes may also stem from genetic heritage, certain
infections, and other chronic illnesses( University of Maryland Medical Center). Inflammation
is also a key role for those with type II Diabetes. Inflammatory markers such as cortisol
induce insulin resistance in the liver. Certain inflammatory markers and stress hormones
have been found to be increased in those with type II diabetes( University of Maryland
Medical Center). Diabetes effects 16 million people in the US, half of whom have never been
diagnosed, Each year 800,000 people in the US develop diabetes and 54,000 die from the
complications related to diabetes. It is currently the leading cause of end stage kidney
failure, onset blindness, and lower limb amputations( American Association of Diabetes,
Statistics).
THERAPEUTICS:
While alongside conventional therapy, there are many herbs that have been well
researched as ways to improve insulin resistance, and its production from the pancreas, as
well as support the body to lower blood sugar levels.
Bitter melon ( Momordica charantia ) an ayurvedic herb, is widely used for diabetes. It
seems to stimulate insulin sensitivity, by increasing the rate that cells bring in sugar and
decreasing the rate of sugar production by the liver. Studies have shown that compounds
extracted from bitter melon were similar to that of the enzyme AMPK (activated protein
kinase)which controls the movement of glucose transporters to the cell surface- important
for the uptake of glucose from the blood stream. (Garven Institute of Medical Research,
2008). One study looked at the effect of bitter melon on non insulin dependent, and non
diabetic rats and found that the fruit extract significantly reduced blood glucose during the
50 g oral glucose tolerance test. (Leatherdale BA, Et al. 1981)
Gymnema ( Gymnema sylvestre ) is known as “the sugar destroyer”. It interferes with the
taste receptors on the tongue so that that taste of sweetness cannot be perceived at the
moment. It has been shown in several clinical trials to help reduce blood glucose, blood
lipids , body weight and
suppress appetite. It showed ability in vitro to stimulate insulin
release from the pancreas. This may be a good herb for people who are slightly over-weight
with metabolic syndrome, or for those who really need to get past the sugar cravings.
(Shanmugasundaram ER, et al, 1990)
Fenugreek ( Trigonella foenum-graecum) has been highly researched and shown in several
studies to have consistent ability to reduce blood glucose, cholesterol and triglycerides in
people with elevated glucose levels. In a 2-month study of 25 people with type 2 diabetes,
fenugreek (1 g daily of a standardized extract) significantly improved levels of blood sugar
and insulin response while their triglyceride levels decreased and HDL cholesterol levels
increased compared to those on the placebo(Gupta A,et al 2001).
Cinnamon (Cinnamomum zeylanicum) is used as an effective treatment for those with type
II diabetes accompanied with high cholesterol. A study in Pakistan conducted a 40 day
study with 60 people who all had type 2 diabetes. Daily they were given doses of either 1, 3
or 6 Gm of powdered cinnamon. The results showed cinnamon to improved blood glucose
levels by 18-29 %, and cholesterol levels by 12-26%. They indicated that cinnamon used by
folks with diabetes could help reduce the risk factors associated with diabetes(Khan A, et al.
2003). Another trail using 3 g daily also found that cinnamon improved blood sugar levels(
Mang B et al. 2006). While another showed that daily HbA1c (a measurement of blood sugar
levels over a period of time) levels were reduced when cinnamon was taken daily (Akilen R,
et al. 2010).
While certain herbs are used for their effectiveness of controlling blood sugar and
insulin, its important to mention the role that Supportive Herbs play in a disease like
diabetes.
Adaptogens – herbs which help us adapt to stressful situations by normalizing our stress
response and the inflammation it caused.
They are particularly helpful for blood sugar
imbalances because of their effects on cortisol and glucose metabolism. They directly effect
our adrenals which are responsible for mediating stress in the body. If our adrenals are
deficient then we cannot properly respond to stress. Our blood sugar levels can fall on the
low side and leave us hypoglycemic and fatigued, which temporarily can be remedied by
sugar to boost energy levels. The adrenals also secrete the hormone nor-epinephrine when
our blood sugar levels fall. By supporting our adrenals, adaptogens can help to normalize
balanced blood sugar, maintain our stress response and reduce the symptoms of
hypoglycemia (Hoffman 483).
American Ginseng ( Panax quinquefolius) is
supportive to digestion, the absorption of
nutrients and good for those who are truly exhausted. In a study performed on American
Ginseng, it appeared to improve blood sugar control ( Vuksan V, Sievenpiper JL, 2000)
while another study found benefits with ginseng and its ability to improve the mood and
energy of patients( Sotaniemi EA,et al 1995).
Eleuthero( Elutherococus senticoscus) is supportive in the assimilation of nutrients, helpful
for improving energy levels, and normalizing immune function. Often given to those who are
truly depleted. Eleuthero would be helpful for those with immune impairment and severe
fatigue. (Tierra)
Medicinal mushrooms all seem to help with blood sugar balance especially Reishi
(Ganoderma Lucidum) and Agaricus blazei, or subrufescens. Both offer rejuvenation effects
by effecting the liver and making it more sensitive to insulin. They mediate inflammation
while providing a rich antioxidant and free radical scavenging effect to the body. Reishi is
known for its anti inflammatory calming effect on our Shen, while supporting the body to
build its strength. It is a wonderful adaptogen, and useful for long term use ( Tierra, 115).
A study on agaricus blazei murill extract improved insulin resistance in type 2 diabetes. The
placebo trial used 536 type II patients all of whom had been taking Glcazide and metformin
for more than 6 months. Patients were given 1500 mg Algaricus blazei Murill (AMB) extract
or the placebo daily for 12 weeks. The Homeostasis model assessment for insulin resistance
( HOMA-IR) was used to measure the effects and outcome of the study. After, it was
reported that the patients that received the supplement of ABM had a significantly lower
HOMA-IR index than those in the placebo group. It was concluded that extract of ABM
improves insulin resistance among people with type 2 diabetes. ( Hsu CH, et al 2007)
Milk thistle ( Silybum marianum)
has been used extensively for protecting the liver
against various strains of hepatitis, poisoning, cirrhosis, or from liver toxic medications. A
small but well conducted study found that milk thistle extract silymarin, could be useful in
improving blood sugar levels. One group received a silymarin (200 mg) tablet 3 times along
side conventional therapy.
The second group received the placebo. The patients were
monitored monthly and at the end of the trial the results showed a significant decrease in
cholesterol, and LDL levels in group who was given the silymarin. It was reported that
silymarin treatment in type II diabetic patients for has potentail to improve the glycemic
index (Huseini HF, Larijani B et al 2006).
Bitters are stimulating to the appetite and
support the absorption and assimilation of
nutrients, as well as enhancing liver function. Most tend to also have a balancing effect on
blood sugar by helping to regulate the secretions of pancreatic hormones ( Hoffman, 498).
Dandelion root (Taraxacum officinale)helps to slows transit time which increases insulin. It
is a hepatic antioxidant, and is helpful in hypoglycemia, and a wonderful herb especially if
the diet it low in soluble fiber ( Hoffman, 587).
Schisandra ( Schisandra chinensis) has a strong liver effect which also effects sex hormone
imbalance. It has been used to regulate blood sugar and improve the digestion of fats. Its
sour taste gives it a cholegogue effect that stimulates bile and excretion, which stabilizes
imbalances within the body( Tierra, 118).
Nervines are supportive to the nervous system, and are beneficial because of the calming,
relaxing effect which can be helpful to reduce anxiety. They are grounding, nourishing and
strengthening, and are often used to reduce irritability and mood swings that accompany
intense cravings (Hoffman, 517).
Oats ( Avena sativa) are rebuilding and deeply regenerative to the nervous system,useful
for people who feel depleted and weak. They have been specifically used for people who
have anxiety and and exhaustion that is also associated with depression(Hoffman, 532).
Hawthorn ( Crataegus laevigata) is rich in flavonoids and
is a herb for the heart, both
emotionally and physically. Its tonic, anti-inflammatory and circulatory effect helps to
reduce anxiety and gives a sense of protection and connection to the heart while physically
reducing the risk for cardiovascular disease and other heart related problems (Hoffman,
542).
Linden ( Tilia europea) a relaxing herb that also has an affinity to the heart, has been used
specifically for the prevention of atherosclerosis, and high blood pressure; common side
effects of diabetes. It has a tonic like action to the nervous system, and combined with
hawthorne makes an fantastic circulatory tonic (Hoffman, 589).
Stevia ( Stevia rebaudiana) could also be helpful for people in diabetes because of its
slower absorption time of sugar into the body. It has also been shown to be useful in weight
management( Anton SD, et al, 2010).
NUTRITIONAL APPROACHES:
Diet playa a key role in the prevention and management of diabetes. It is important to learn
how to Nourish ourselves. Refined sugar and carbohydrates do not sustain or nourish us in
the way our body truly wants. They provide a quick rise and fall of blood sugar, while
temporarily relieving the cravings for sugar, or in the case of taste: sweetness. In most
traditional systems of healing, sweet tasting foods are considered to be those that are
building and nourishing to our bodies. Full sweets would include foods such as whole grains,
legumes, nuts and seeds, dairy, fruits, and colorful root vegetables( Pitchford, 189-190).
Paul Pitchford, Author of Healing with Whole Foods says that “ the obvious remedy is to
consume less of the foods that are stressful to the liver and weaken the spleen and
pancreas”. This would include foods that greasy and fatty foods; such as red meats, eggs,
seeds, excess oils, and foods that have been denatured or refined; sugar, white flours,
synthetic fats etc, and excessively sweet, salty or spicy foods.
These foods increase inflammation, hypersensitivity, and an increase of sugar into the diet.
Small frequent meals rich in protein and good fat are helpful to stimulate insulin production,
while stabilizing and balancing our blood sugar(371-372). Common deficiencies within a
diabetics diet should be looked at closely.
Protein is often lacking a person’s diet who regularly consumes food rich in sugar and
carbohydrates, especially true to those who eat a vegan or vegetarian diet that is not well
prepared or balanced. It provides the overall energy that stabilizes our blood sugar levels
longer. Providing a protein source at every meal could be especially helpful for those with
diabetes( Hass,60).
Fat is crucial because it lubricates our bodies, feeds the nervous system and allows the
break down process to happen over a longer period of time thus delaying the absorption of
sugar into the blood. Consuming a good oil source such as olive, flax or pasture raised
butter will help to stabilize the breakdown and prevent rapid blood sugar spikes. Fat is also
a source of energy and can supply the body with a fuel that can be used when needed(
Hass, 73).
Fiber which is a naturally occurring source of sugar, provides a steady drip of glucose into
the blood stream rather than all at once. Rich fiber containing foods leave less of an impact
on blood sugar levels, which can be determined by what we know as the glycemic index of
food( Hass, 37-38).
Supportive Strategies:
Exercise is crucial for the management and prevention of diabetes. It improves the bodies
use of insulin by lowering blood glucose levels and properly using sugar within our muscles
to produce energy. Beneficial in cardiovascular health exercise improves the flow of blood
throughout our body and increasing the heart's pumping ability. It helps promote weight
loss by supporting the decrease of excess body fat, improving insulin sensitivity and
lowering blood pressure. Studies have also shown that people with type 1 diabetes who get
regular exercise reduce the need for insulin injections( University of Maryland Medical
Center).
Learn to Relax. It is important to be aware about the relaxing effects that sugar and the
typical american diet has on the brain. The physiological action beyond this is that sugar
creates a temporary increase of dopamine and opioid levels, as well as the effect of our
seratonin levels. Under stress the adrenals secrete adrenaline, which raises blood sugar
levels and sends the body into a "fight or flight" mode. Continual stress results in a steady
release of adrenaline which leads to an overstimulation of glucagon to keep blood sugar
high. The body tries to counter act this is by pushing the pancreas to secretes more insulin
in order to bring the high levels of blood sugar down. Relaxations strategies such as deep
breathing, yoga, walks, baths or a hot cup of tea can help reduce anxiety, and tension and
increase circulation of the blood( Thomas Cowan, Weston A Price Foundation).
It is important to recognize that over the years within our society, cases of diabetes
have been rapidly increasing. This is partially due to the fact that as we have evolved, sugar
has become more readily available to us, and partially due to the lack of education on how
to nourish and care for our bodies. Perhaps there is a lack of purpose or desire to care for
ourselves, or nourishment missing on a deeper level that makes us live the way we do.
While the search for a cure to diabetes continues along all medical fronts, research proves
that by educating ourselves on ways to live healthier lives, we may be able to support and
manage a disease that can be so life threatening.
References:
Akilen, R., A. Tsiami, D. Devendra, and N. Robinson. "Glycated Haemoglobin and Blood
Pressure-lowering Effect of Cinnamon in Multi-ethnic Type 2 Diabetic Patients in the
UK: a Randomized, Placebo-controlled, Double-blind Clinical Trial." Diabetic Medicine
27.10 (2010): 1159-167. Print.
Anton SD, Martin CK, Han H, Coulon S, Cefalu WT, Geiselman P, Williamson DA. "Effects of
Stevia, Aspartame, and Sucrose on Food Intake, Satiety, and Postprandial Glucose
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Baskaran,
K.,
B.Kizar
Ahamath,
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Drewnowski, Adam, and SE Specter. "Poverty and Obesity: the Role of Energy Density and
Energy Costs." American Journal of Clinical Nutrition 79.1 (2004): 6-16. Web. 04
Dec. 2011.
Gupta A, Gupta R. "Effect of Trigonella Foenum-graecum (fenugreek) Seeds on Glycaemic
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Haas, Elson M., and Buck Levin. Staying Healthy with Nutrition: the Complete Guide to Diet
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Hoffmann, David. Medical Herbalism: the Science and Practice of Herbal Medicine.
Rochester, VT: Healing Arts, 2003. 483+. Print.
Huseini, H. Fallah, B. Larijani, R. Heshmat, H. Fakhrzadeh, B. Radjabipour, T. Toliat, and
Mohsin Raza. "The Efficacy OfSilybum Marianum (L.) Gaertn. (silymarin) in the
Treatment of Type II Diabetes: a Randomized, Double-blind, Placebo-controlled,
Clinical Trial." Phytotherapy Research 20.12 (2006): 1036-039. Print.
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Leatherdale, B. A., R. K. Panesar, G. Singh, T. W. Atkins, C. J. Bailey, and A. H. Bignell.
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Understanding the Diagnosis and
Treatment for Generalized Anxiety
Disorder from an Integrative
Perspective
Leilani Courtney
Anxiety is a normal and even beneficial emotion to experience at times. It is part of
our hard wiring for safety and survival, giving us the internal cue to gear up for “fight
or flight” when sensing potential harm or dis-ease. Anxiety from health issues,
financial concerns or troubled relationships are ordinary responses to stressful
situations. When these worrisome emotions become excessive, unrealistic, persistent,
and interfere with normal daily activities, this may be a form of mental illness
(ADAA). Anxiety disorders are pathological presentations of arousal, tenseness, and
increased autonomic activity, such as heart rate, blood pressure and respiration
(Bunce, APA).
For people with anxiety disorders, the constant and overwhelming
worry can be crippling. This paper will engage in a discussion about the causes of
anxiety and the current modalities of therapy, with a specific focus on generalized
anxiety disorder.
Understanding Anxiety Disorders:
Anxiety disorders are the most common psychiatric illness in the United States, with
each year an estimated 18% (40 million) adults in America affected and 8% of
teenagers (NIMH “Anxiety disorder”). There are several categories of anxiety
disorders, including panic disorder (PD), obsessive-compulsive disorder (OCD), posttraumatic stress disorder (PTSD), social anxieties, specific phobias, and general
anxiety disorder (GAD).
Although the varieties of anxiety disorders each specify unique characteristics, all
have common feelings of excessive and irrational fears and dread (NIMH “Anxiety
disorder”).
The overwhelming percentage of Americans with anxiety disorders is all together
heartbreaking and concerning. If the evolutionary purpose of anxiety is to
foreshadow danger ahead, what does this say about the population of our country?
Anxiety is not
only a serious psychological disorder; it is also a ‘canary in the coal-mine’ for
underlying
health concerns. Compared to the general population, clients with anxiety disorders
are more likely to develop a medical illness (Rogers), as well as prolong the duration
of a medical illness (Shader). Conversely, patients with a chronic medical illness are
more likely to be diagnosed with an anxiety disorder (Wells). Certain medical
conditions have higher comorbidity with anxiety, including Grave’s disease, anorexia
nervosa,
Alzheimer’s
disease,
mitral
valve
prolapse,
heart
arrhythmias,
hypertension, chronic obstructive pulmonary disease, irritable bowel syndrome, and
diabetes (NIMH “Generalized anxiety disorder (GAD),” Winston, Masé). Overall,
patients with anxiety disorders have higher rates of mortality from all causes
(Gliatto). Although there have been incredible advances in western medicine’s
understanding of the body and brain chemistry, it appears the deeper researchers
look, the more difficult it is to separate what is an emotional or physical ailment
(Winston).
Tendency towards chronic anxiety may be a behavior that is learned, inherited,
triggered or chemically imbalanced (Faustino, “Natural medicines database”). From
an integrative perspective, it is important to understand the root cause of the
disorder in order to effectively treat the person. Much like depression, growing up in
a household with an anxious parent increases the chances of an anxious child
(Baldwin, Sarris and Panossian, Winston). There is also evidence that a genetic
component is at hand (Kendler), making the idea of coming from “a long line of
worriers” much more genetically plausible! Emotional triggers may induce anxiety for
any number of reasons, such as with depression, trauma, illness, financial concerns,
family issues, abuse, divorce, and other major life changes. Chemical triggers that
may exacerbate anxiety are long-term alcohol (Carguilo), nicotine (Morisette), and
caffeine use (Bruce, Wise); as well as medications like benzodiazepines (Ashton),
steroids, over the counter sympathomimetics, selective serotonin reuptake inhibitors
(SSRIs), digoxin, thyroxine, theophylline, and antihistamines (“Natural medicines
database”, Wise). Environmental triggers may also be an overlooked cause for
increasing anxiety in the US and around the world (Bunce, Winston). Life today may
not have the same primitive fears of survival it once had, but it may be argued that it
is more stressful, complicated and confusing than ever before. The social expectation
for the standard of a “happy” life has become nearly unachievable. As a culture, we
have shifted away from being a reflection of nature and rocketed into a technological
craze of consumerism and perpetual dissatisfaction. When expectations of security
are unrealistic and excessive, it is no wonder that anxiety will follow this same
pattern.
The pathophysiology of anxiety disorders is still being unraveled, although current
evidence hypothesizes some degree of imbalance of serotonin, noradrenaline,
glutamine, and GABA neurotransmitter levels and transmissions (Sarris and
Panossian). Neurotransmitters are an infinitely complicated orchestra of chemical
messengers that help move information from nerve cell to nerve cell, and without the
proper
levels,
messages
cannot
be
communicated
properly.
This
break
in
communication will then alter the brain’s reaction and initiating stress responses
(NIMH “Anxiety disorder”). The understanding of the “neurotransmitter imbalance”
theory is based on the observable mood improvements that occur when taking
selective serotonin reuptake inhibitors (SSRIs), selective serotonin and noradrenalin
reuptake inhibitors (SNRIs), and benzodiazepines (Mukherjee, Sarris and Panossian).
Whether the stressors stems from physical or emotional root, the body is equipped to
respond in the same defense through the Hypothalamus-Pituitary-Adrenal axis (HPA
axis) (Bunce). The HPA axis is a major part of the neuroendocrine system that
controls reactions to stress and regulates many body processes, including mood and
emotions, digestion, immune system, sexuality and energy storage / expenditure
(Bunce,
Pariante).
HPA
exhaustions
involves
the
suppression
of
dehydroepiandrosterone (DHEA), testosterone and estrogen synthesis, all hormones
which work to improve mood (Bunce). Low estrogen is associated with decreased
serotonin
correlation
production, while
between
both
progesterone
sex
hormones
acts
on
GABA
deficiencies
and
receptors,
increased
showing
anxiety
(Antonijevic, Bunce). This is also evident pre-menstrually and peri- menopause,
when estrogen levels decline and there is a distinct change in mood, specifically
anxiety (Antonijevic, Bunce).
Generalized Anxiety Disorder:
Many anxieties can remain on-going, debilitating and “beyond the control” of the
client, ultimately adversely affect their daily life (APA). The diagnosis can be difficult
since many anxiety disorders share common symptoms, but for now I will highlight
the most common diagnosed anxiety, Generalized Anxiety Disorder (GAD).
GAD
affects 3.1% of US adult population (6.8 million US adults) and twice as many women
as men (NIMH “Anxiety disorder”). There has been some refining of the definition of
GAD over time, as originally there was little distinction between panic disorder and
GAD. Panic disorders are now better understood to be intense, brief, acute anxiety,
with variable periods of remission and relapses (“Natural medicine database”). GAD
on the other hand, is not associated with these intense physical attacks, but as
defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) it is a
“chronic state of apprehensive expectation and uncontrollable worry concerning
multiple daily life events or activities and accompanied common manifestations of
psychic or motor tension for more than half the time of at least 6 months” (APA,
Boulenger).
Symptoms and behaviors associated with GAD fall under 3 categories
(APA): (1) Excessive physiological arousal
Muscle tension, irritability, fatigue, restlessness, insomnia
(2) Distorted cognitive processes:
Poor concentration, unrealistic assessment of problems, worries
(3) Poor coping strategies:
Avoidance, procrastination, poor problem-solving skills
Understanding the client’s medical and mental history is the first step to an initial
assessment, as well as gathering an understanding of family relationships, career,
spiritual connection, acute and chronic stressors, and somatic ailments (Bunce,
Winston). Client’s symptoms can present in a wide range and degree of severity.
Many complaints may be the result of anxiety without the client aware of their
connection, just as other seemingly unrelated factors may be triggering anxiety
(Schweizer). It is important to differentiate the anxiety between “Acute” (brief or
intermittent episodes lasting hours to weeks, often preceded by stressors) and
“Chronic” (persistent or unremitting lasting months to years, can even be seen as a
personality trait) in order to better understand if the anxiety tends more towards
panic attacks or depression (Schweizer). This will help differentiate the most effective
therapeutic path to recommend.
There is also a well established trifecta between anxiety, depression and sleep
disorders, with nearly 50% of adults with depression also diagnosed with an anxiety
disorder (Gliatto), 65-90% of adults with depression experience a sleep disorder,
and 50% of adults with sleep disorders experience generalized anxiety (“Sleep and
mental health”).
Although this connection and intertwining of ailments is not the focus of this paper, I
feel it is critical to point out how closely symptoms of imbalance will perpetuate each
other, and therefore how important it is to address sleep, depression, anxiety, and
underlying health concerns together.
Therapeutics for Generalized Anxiety Disorder:
Psychological Therapies Non-pharmacologic modalities should be the first line intervention for clients with
GAD symptoms and behaviors. There are a variety of therapy options, each focusing
on different ways to discover what anxiety triggers and how to lessen and even reset
them. Psychotherapy involves talking with a trained mental health professional to
discover different ways of thinking, behaving and reacting to situations (NIMH
“Generalized anxiety disorder (GAD)”). Some of its methods include relaxing and
breathing techniques, and finding new ways to support a balance in the patient’s life.
Psychotherapy practitioners listen and offer objective feedback, while helping clients
examine stressors in life and find better ways of coping or eliminating them
(Grohol).
Cognitive-behavioral therapy (CBT) works with people to change thinking and
behavioral patterns when reacting to anxiety-provoking situations (NIHM “Anxiety
disorder”). Through psych education, relaxation training, cognitive restructuring
and behavioral aspects, fears can be confronted and desensitized (Sarris and
Moylan). Mindfulness-based cognitive therapy is clinically effective at relieving
anxiety and depressive symptoms in clients with generalized anxiety disorder
(Kim), although only when the client is ready to confront their fears (Sarris and
Moylan).
Pharmacological medication:
For clients whose anxiety is significantly impairing their daily function and quality of
life, pharmaceutical medications are very often prescribed. However, it is important
to note these medications do not cure or address the root of the anxiety, they simply
control the symptoms (Andreatini and Lacerda). Starting with the very first dose,
pharmacological drugs work by altering brain chemistry, although full effect requires
a series of changes to occur which sometimes takes several weeks (NIMH “Anxiety
disorder”). A variety of drugs have proven effective in generalized anxiety disorder
management, although each drug has its benefits and drawbacks that need to be
carefully considered for each individual (Andreatini and Lacerda, Faustino). There are
many cases that prescription medication is specific and warranted, such as anxiety
that is unresponsive to therapy, herbal, dietary and lifestyle modifications or for
severe
disorders
while
other
therapeutic support
is
in
progress.
However,
prescription drugs are most often the primary action for addressing anxiety, with
11% of middle-aged women and 5.7% of middle-aged men using anti-anxiety
medications, and 11% of the entire US on anti- depressants (Pratt).
Antidepressants
Antidepressants were developed to treat depression but are also effective for anxiety
disorders, although generally take 4 to 6 weeks before taking full effect (NIHM
“Anxiety disorder”). Antidepressents such as venlafaxine (Effexor®), paroxetine
(Paxil®) and imipramine (Tofranil®), have a high incidence of non-adherence to
treatment (NIMH “Anxiety disorder”), and side effects of cholinergic symptoms,
sexual dysfunction, insomnia, and withdrawal issues (Adreatini and Lacerda, Sarris
and Panossian)
SSRIs
Some of the newest antidepressents are called selective serotonin reuptake
inhibitors, or SSRIs (Faustino). These work to alter levels of serotonin in the brain,
which, like other neurotransmitters, help brain cells communicate with one eachother
(Faustino). SSRIs must be started at low doses and gradually increase until they
reach the beneficial effect over several weeks (Sarris and Moylan). Popular SSRIs to
anxiety disorders are fluoxetine (Prozac®), sertraline (Zoloft®), escitalopram
(Lexapro®), paroxetine (Paxil®), and citalopram (Celexa®). Venlafaxine (Effexor®)
is closely related to SSRIs and is often used to treat GAD (NIMH “Anxiety disorder”).
SSRIs have fewer side effects than older antidepressants, but still can cause an initial
increase in anxiety in early stages (problematic for patient compliance), nausea,
headaches, sleep difficulties or sexual dysfunction in over 50% of users in the long
term (Sarris and Moylan).
Anti-Anxiety Drugs
High potent benzodiazepines are the most commonly prescribed anxiolytic and act on
gamma-amino-butyrc-acid (GABA)
/
Benzodiazepine receptors (NIMH
“Anxiety
disorder”). They have established efficacy for quick relief of many anxiety disorders
but do not actually decrease worrying (Sarris and Moylan). They act to lower anxiety
by decreasing vigilance and by eliminating somatic symptoms (ex. Muscle tension).
Some popular benzodiazepines are diazepam (Valium®) for anxiety, clonazepam
(Klonopin®) for social phobia and GAD, lorazepam (Activan®) for panic disorder, and
alprazolam (Xanax®) for panic disorder and GAD (NIMH “Anxiety disorder”).
Benzodiazepines are quick acting, but not without limitations and side effects. They
are not suitable for long term because of concerns of dependency and tolerance
development. Benzodiazepines risk sedation, amnesia, potential abuse and/or
dependency, withdrawal syndrome, and possible long-term cognitive effects from
interactions with depressants of the central nervous system (Andreatini and Lacerdo,
Faustino, Sarris and Moylan, Shader).
Buspirone (Buspar®)
Buspirone is a newer anti-anxiety medication for GAD (NIMH “Anxiety disorder”). It
is similar in the mechanism of action to a benzodiazepine, but take at least 2 week for
effectiveness and without the concern for tolerance and dependency. Possible side
effects include dizziness, headaches, and nausea (NIMH “Anxiety disorder”). Also,
despite the potential interest of many new pharmacological treatments of GAD, recent
years have shown that the development of new anxiolytic drugs often appear limited
by high-rates of placebo response in numerous clinical trials (Boulenger).
Herbal Medicine:
In the human body, there are infinite molecular processes involved in the stress
response mediated by the central nervous system (CNS). Many of these compounds
are active against a wide range of targets, and may cause numerous effects and
changes (Sarris and Panossian). Considering the complexity of mental disorders, the
modulation of a single neurotransmitter target may not necessarily treat the patient
as successfully as approaching multiple targets of the neuro/endocrine systems
(Sarris and Panossian,). Supporting this theory is the ever-increasing validity of
traditional herbal medicine to treat anxiety (Sarris and Panossian, Ernst 2007,
Faustino). Unlike synthetic drugs made in a laboratory, plants are influenced by a
phytochemical profile that is as different as the soil it was grown in, resulting in
overall biological effects that rely on synergistic interactions between plant
constituents
(Faustino,
Kennedy
and
Wightman,
Sarris
and
Panossian). Furthermore, anxiety disorders are more both under-treated and over
prescribed, motivating patients of all kinds to seek non-conventional treatment
(Sarris and Moylan). In a recent US cross sectional and longitudinal survey (2012),
43%
of
individuals diagnosed
with
an
anxiety
disorder
use
a
variety
of
complementary therapies (Sarris and Moylan). With the rising cost of prescription
medications and their unwanted side effects, patients are exploring herbal and other
natural remedies (Lakhan).
The main goal for supporting a client with GAD is to help reduce their perception of
stress. This may be regulated through supporting the HPA axis, the CNS function
via neurotransmitters, and sometimes sedating or supporting cognition function
(Bunce, Faustino). Secondary goals may be to improve digestion and nourishment
since the mind-gut connection is so tightly connected, and address inflammation
exacerbated by chronic stressors (Bunce). When supporting someone with GAD,
the herbal actions may include antidepressant, anxiolytic (relaxing nervine),
adaptogen, bitters digestives, nootropic (cognitive enhancing), sedative, hypnotic,
anti-inflammatory, and analgesic effects (Bunce).
Herbal medicines work in similar mechanisms as pharmacological drugs, which
makes sense since it is estimated that 25% of all drugs on the market today contain
compounds that are directly or indirectly derived from plants (Faustino, Koehn).
Some plants modulate anxiety disorders through the modulation of neuronal
communication and through the alteration of neurotransmitter synthesis (Sarris and
Panossian). Anxiolytic herbs may have effects on the GABA system, either via
inducing ionic channel transmission by voltage-gated blockage, through alterations
of membrane structures, GABA transaminase or glutamic acid decarboxylase
inhibition, or less commonly via biding with benzodiazepine receptor sites (e.g.
GABA-A) (Sarris and Panossian). Other actions may involve stimulating or sedating
CNS activity, and regulating or supporting the healthy function of the endocrine
system and HPA-axis (Gliatto).
A comprehensive review of plant-based medicines that have clinical evidence of
anxiolytic activity (as of 2012) revealed 21 human clinical trials (Faustino). Efficacy
was found for several herbs for treating a range of anxiety disorders (Sarris and
McIntyre). Specifically for reducing generalized anxiety with herbal preparations, the
most promising evidence supports the use of Kava (Piper methysticum) (Ernst and
Pittler, Sarris and Laporte). Additional research points towards a beneficial effect from
Ginkgo (Ginkgo biloba) (Woelk), Passion flower (Passiflora incarnata) (Akhondzadeh,
Aslanargun, Movafegh), Chamomile (Matricara recutita) (Amsterdam, Wong), Scullcap
(Scutellaria lateriflora) (Wolfson), Lemon balm (Melissa officinalis) (Kennedy and
Scholey, Kennedy and Little), Bacopa (Bacopa monniera) (Pase), Rhodiola (Rhodiola
rosea) (Bystritsky), Hawthorne (Crataegus oxyacantha) (Hanus), California poppy
(Eschscholtzia californica) (Hanus), and Ashwagandha (Withania somnifera) (Cooley)
(Sarris and Panossian). There is currently little evidence supporting the use of St.
John’s Wort (Hypericum perforatum) for anxiety disorders, while there is strong
evidence for its use in depression (Sarris and Panossian, Schüle, Singer). Many of
these anxiolytic herbs have the potential for additional applications to support
secondary goals often paired with anxiety, such as improving mood (Chamomile,
Kava, Lemonbalm, St. John’s Wort), support for insomnia (Passion flower, Scullcap),
enhancing cognition via nootropic activities (Bacopa, Ginkgo), and adaptogenic tonics
to combat chronic stress (Ashwagandha) (Sarris and Panossian, Mills).
Diet and Lifestyle:
The connection of diet and physical activity to mood regulation is clearly linked
(Bunce). There is much research in this area of study, but for brevity I will just skim
the surface.
To start, anxiety levels are greatly decreased by walking for 60 minutes, or running
20-30 minutes, for at least four days per week (Gliatto). Other modalities of exercise
that show beneficial results in modulating stress and anxiety are mindfulness, yoga
and tai chi (Sarris and Moylan). Diet and nutrition are gaining evidence everyday
about their close relationship with anxiety and mental disorders. With strong
evidence for the prevention and treatment of psych disorders with Omega-3 fatty
acids, which have shown specific support in mood disorders and depression
(Freeman).
Conclusion:
It is clear that anxiety disorders are a destructive pandemic that is affecting nearly 1
in 5 adults in the US.
Anxiety is too easily becoming a way of life and accepted
state of mind. Without fully understanding where these mood disorders are
stemming from, they will continue to perpetuate a blurring memory of how it feels to
be truly content.
Prescription drugs may be effective at masking the symptoms, but not without the
cost
The
to
topic
health
is
not
and
whether
our
right
for
pure,
non-medicated
happiness.
synthetic drugs or natural methods are better, as this is as
complicated as the individuals and compounds in question, but simply that complime
ntary therapies can
being
support
each other while the
root of the
anxiety
disorders are
addressed. Through herbs, nutrition, lifestyle, therapy, and pharmacological
medications, there is great potential to increase the efficacy of not simply repressing
the symptoms of anxiety, but serving to better understand and overcome them.
"Worry is a thin stream of fear trickling through the mind. If encouraged,
it cuts a channel into which all other thoughts are
drained."
—
Arthur
1883-1935.
Somers
Roche,
American
journalist,
writer,
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Kudzu in alcohol abuse
Beracah Sullivan
I grew up in a home where drugs
and alcohol weren’t consumed but were
discussed a great deal.
My mother is a
recovering alcoholic and my stepfather is a
recovering drug addict. My stepfather ran
a drug treatment center for many years
before he went on to work for NY State to
put
together
protocol
for
policies,
drug
procedures
treatment
and
facilities.
There are as many factors that go into the
development of ones dependency and addiction as there are in treating it.
Often addicts
are given prescription drugs in order to help them through withdrawal symptoms and detox
from alcohol and narcotics. Some of which can be just as addictive as the substances they
are looking to stop using.
Though we haven’t formally touched on the subject herbal
medicine to help break the pattern of addiction yet in our studies, there have been brief
mentions of it here and there during class discussion.
What plants have been traditional
used in the treatment of alcohol and drug addiction and in what ways can they assist in
breaking the cycle of dependency.
I was able to find more abstract then full text studies on Kudzu (Pueraria lobata), a
Chinese Medicinal herb that has a long history of being used to treat alcohol addiction. A
study published last year involving 17 men ages 21-33 years old, looking to reduce their
alcohol consumption in a non-treatment environment.
For a period of 8 weeks, (2 weeks to
set a base line, 4 weeks of treatment and then 2 weeks follow) the participants were given
a standardized Kudzu extract of 250 mg isoflavones t.i.d or a matched placebo on a daily
basis.
They reported their alcohol consumption and desire to use alcohol via a wrist
actigraphy device and had laboratory visits twice a week so that medication adherence
could be monitored as well as any adverse effects. The study found that patient compliance
was very good and that there were no adverse changes to vital signs, blood chemistry and
renal or liver function. While the patients reported no change in their desire and craving for
alcohol, they did see a reduction in the amount of alcohol drinks consumed within the week
by about 34-57%, there was a reduction in the amount of heavy drinking days and there
were longer periods of abstaining from alcohol consumption (1). While this particular study
mentioned the fact that they used isflavones of the Kudzu plant they didn’t specify which
ones specifically or if it was a combination of a few that were given.
The next abstract I found identified the isoflavones present in Kudzu that are
believed to be responsible for the reduction of alcohol consumption in animals and humans,
daidzin, daidzein and puerarin, though it admitted that it was unsure as to how exactly it
suppressed alcohol consumption.
It speculated that extracts of Kudzu may work by
antagonizing the opioid receptors. This is similar to the action that naltrexone has on those
same opioid receptors (2).
The one full text study I was able to find focused on the kudzu isoflavone puerarin as
the constituent that reduces alcohol consumption. The authors weren’t completely clear as
to how or why puerarin worked with in the body, but the suggested that it may be due to
it’s ability to alter ALDH2 or that it might be working on the monoamine oxidiseacetaldehyde pathways (4). 10 adults participant who had reported having an average of
9-17 drinks per week took 2 capsules of 300mg of purified puerarin two times a day. There
was a placebo week that was administered in order to create a base line and then
participants were a placed in a relatively realistic setting in order to track and observe their
drinking. The study found that the participants had a reduction in the amount of beer they
consumed, the time it took and the number of sips that it took to finish those beers where
increased. Daily diaries showed that participants drank slightly less during the treatment
week vs the placebo week.
While it is a pilot study, the results seem to suggest that
puerarin and kudzu root could help in the reduction of alcohol consumption as well as alter
their drinking patterns (3).
While I was a little disappointed that I couldn’t find any studies about other
herbs/herb combinations that I have seen or heard mentioned in class discussions, it is
good to know that there are some studies on the topic. I think that realistically a single
isoflavonoid, or a single herb for that matter, isn’t going to be the end to alcohol abuse, but
I think that it should be seriously considered as part of the creation of a support system that
is built in around people who are looking to start making healthier choices for themselves
and their lives.
Because addiction is such a layered issues I believe plants, with their
multiple constituents and secondary metabolites and layers of ways in which they can reach
us and heal us, could be really key in helping to support and nourish people through the
process of getting and staying clean.
1.
A
standardized
kudzu
extract
(NPI-031)
reduces
alcohol
consumption
in
nontreatment-seeking male heavy drinkers.
Lukas SE, Penetar D, Su Z, Geaghan T, Maywalt M, Tracy M, Rodolico J, Palmer C, Ma Z, Lee
DY.
Psychopharmacology (Berl). 2013 Mar;226(1):65-73. doi: 10.1007/s00213-012-2884-9.
Epub 2012 Oct 16.
2.
[Medicinal plants in the phytotherapy of alcohol or nicotine addiction. Implication for
plants in vitro cultures].
Ozarowski M, Mikołajczak PŁ, Thiem B.
Przegl Lek. 2013;70(10):869-74. Polish.
3)
The isoflavone puerarin reduces alcohol intake in heavy drinkers: a pilot study.
Penetar DM, Toto LH, Farmer SL, Lee DY, Ma Z, Liu Y, Lukas SE.
Drug Alcohol Depend. 2012 Nov 1;126(1-2):251-6. doi: 10.1016/j.drugalcdep.2012.04.012.
Epub 2012 May 10.
4) Keung WM. Preclinical Studies of Kudzu (Pueraria lobata) as a Treatment for Alcohol
Abuse. In: Keung WM, editor. Pueraria: The genus Pueraria. Taylor & Francis; New York:
2002. pp. 144–158
This is the info regarding the study that I had mentioned in the class discussion about
Declinol that I passed on using because I found follow up articles regarding a federal lawsuit
against them.
Declinol, a Complex Containing Kudzu, Bitter Herbs (Gentian, Tangerine Peel) and
Bupleurum, Significantly Reduced Alcohol Use Disorders Identification Test (AUDIT) Scores
in Moderate to Heavy Drinkers: A Pilot Study.
Kushner S, Han D, Oscar-Berman M, William Downs B, Madigan MA, Giordano J, Beley T,
Jones S, Barh D, Simpatico T, Dushaj K, Lohmann R, Braverman ER, Schoenthaler S, Ellison
D, Blum K.
J Addict Res Ther. 2013 Jul 2;4(3). pii: 153.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835486/
Interestingly enough, If I had taken the time to read the whole study I would have seen
that it incorporated some of my original questions about bitter herbs and alcohol
consumption.
Lesson learned here- read the study all the way through!
In addition, when I went back and read more into the link about Declinol, the lawsuit was
more of a trademark and copyright infringement.
http://www.prweb.com/releases/declinol/10/prweb11269894.htm
Here is an editorial article that addresses some of the concerns I’ve heard within the drug
treatment community about the fine line that treatment facilities must walk in transitioning
patients from one addiction to possibly another with a pharmaceutical.
http://www.psychologytoday.com/blog/ending-addiction-good/201304/facing-the-rootcauses-addiction
I think that this article out lines some key points that play into what I was going for in my
research project. It is important to keep in mind that 1) herbalism should be considered as
a partner in the transition of Detox and that in many cases medical supervision is a must. 2)
Taking herbs without some other kind of support system to help a patient address the root
issues of alcohol and drug abuse is probably going to lead to a false sense of security, which
may eventually lead to relapse.
Pathophysiology
and
Therapeutics
Post-Myocardial
Infarction
of
Ventricular
Remodeling
Steve Byers
INTRODUCTION:
Cardiac remodeling refers to changes that take place in the architectural shape, size,
and physiological function of the heart, after an injury to the myocardium. There are many
complex mechanical and biochemical processes that result in cardiac remodeling and many
different diseases or dysfunctions (such as in the heart valves), which may lead to
remodeling of the myocardium. Generally, most of the remodeling takes place in the left
ventricle in post-myocardial infarction (MI) patients. Yet globally, the heart is vulnerable to
remodeling in all areas, especially where there has been damage. The focus of this paper
will be primarily on post-MI ventricular remodeling.
Mild cardiac remodeling is a “normal process” that occurs throughout our lifetime as
a result of normal aging. i Various researchers apart of Framingham study have found that
the most common form of remodeling is of the left ventricle (LV) which occurs concentrically
where the LV thickness slowly increases and the LV cavity decreases in size when observing
preserved or increasing ejection fractions. ii LV thickness occurs more predominantly in
women, especially older women, than men across all ages, which is perhaps due to reduced
cardiomyocyte dropout and slightly higher cardiomyocyte turnover displayed in aging
women. iii Despite this evidence, there is still no clear correlation between age-related
concentric thickening and heart disease.
iv
That said, considering the effects of obesity,
hypertension, and diabetes, LV wall thickness does increases yet LV cavity size does not
decrease proportionately with age which is perhaps indicative of an inability to compensate
for increased wall stress from increased blood pressure.
v
Other factors such as family
history with heart disease has become a predictor of increased risk of developing eccentric
LV geometry in offspring who do not have heart failure. vi
MYOCARDIAL INFARCTIONS
According to recent Center for Disease Control statistics vii, every 1 in 4 deaths in
America are caused by heart disease. Of those 600,000 deaths, 385,000 deaths are from
coronary heart disease. On average, 715,000 Americans have a heart attack every year and
of those, 525,000 are a first heart attack (about 75% of those people). It is estimated that
coronary heart disease expenses (health care services, medications, and lost productivity)
collectively cost $108.9 billion each year. Identifying and supporting areas of prevention is
critical to reducing the prevalence of this epidemic in America. Risk factors for having a MI
include diabetes mellitus, hyperlipidemia, smoking, obesity, hypertension, male gender
(higher incidence in men of all ages but difference between men and women narrows with
age), and family history. viii
A myocardial infarction occurs when a coronary artery is occluded beyond the critical
point that its normal cellular function and homeostasis are maintained. When a thrombus
forms on an ulcerated or unstable atherosclerotic plaque, coronary arteries can be occluded
beyond their critical threshold (>75%) to move blood. ix A thrombus large enough will
occlude the artery and cause a MI resulting from ischemia of the myocardial tissue and
eventually necrosis of myocardial tissue down stream from the thrombus. This occlusion
causes a decrease in oxygen, glucose, and nutrients to the myocardium through the
coronary arteries and leads to ischemia of those cells.
A MI can also be triggered by increased myocardial metabolic demand where the
heart is unable to compensate for the demand (i.e. the out of shape man with hypertension
shoveling the driveway after a big snow storm and has a heart attack). Other forms of
increased myocardial metabolic demand include severe hypertension, severe aortic stenosis,
cardiac valvular pathologies, and low cardiac output states associated with a decreased
mean aortic pressure necessary for coronary perfusion. x
The more the artery is occluded and the longer amount of time that it is occluded,
will contribute to increased amounts of ischemic damage. Two types of ischemia have been
defined for MIs. Ischemia that spreads fully through the heart muscle from the endocardium
through the myocardium to the epicardium is called a transmural MI. If only partial muscle
death occurs through the muscle, it is referred to as a sub-endocardial or non-transmural
MI. Emergency medical services often use a protocol of thromolytic medications referred to
as “clot busters” and now even more commonly use catheterization with a metal stent in
order to clear the blockage as soon as possible. Stents did not exist until 1978, when the
death rate of myocardial infarction patients was 25% and now after 35 years of improved
medical protocols, that number has dropped to 5% in hospitals with catheterization labs. xi
The sooner the clot is removed, the less ischemic damage will occur and the better the
outcome of survival and quality of life post-MI.
Another consequence of MI damage is the repair process (discussed more below)
involving fibrosis, which is initially integral in providing structural integrity with scar tissue in
the areas of necrosis of myocardial tissue. Yet in the long run, post-MI fibrosis becomes one
of the causes of continuous LV remodeling leading to progressive ventricular dilation,
diminished cardiac performance, and ultimately chronic heart failure. xii Research has shown
that it is possible to predict morbidity and mortality based on the extent of remodeling. xiii
PHASES OF LEFT VENTRICULAR REMODELING
Three phases of adverse left ventricular (LV) post-infarction remodeling have been
defined to outline the physiological effects of the infarction and the proceeding myocardial
remodeling. Vanhouette et al. (2006) xiv describes the phases in detail which will be the main
reference for the following phases described below unless otherwise noted (see Figure 1 for
a overall schematic of the pathophysiology of ventricular remodeling):
Phase 1- Early Wound Healing Phase (0-7 days post-MI):
The death of myocytes induces a cascade of mechanical and biochemical responses
that help balance cardiac output as well as initiate necrotic myocyte clean up and
compensation for fewer functioning myocytes. Reduced cardiac output leads to activation of
the Renin Angiotensin Aldosterone System (RAAS) as well as signaling of the adrenal
medulla and sympathetic nerve terminals to release Norepinephrine (NE) and to block its
reuptake. Both responses to reduced cardiac output cause vasodilation and signal the
release of Angiotensin II (ANG2). NE and ANG2 stimulate endothelin (ET-1), which is a
stimulus for myocyete hypertrophy and signals the secretion of Ventricullar Natriuretic
Peptide (VNP) and Atrial Natriuretic Peptide (ANP), an inhibitor of catecholamine, ANG2, ET1, and aldosterone. Both ANP and VNP are powerful vasodilators, and are released in the
atrium and ventricles, respectively, in response to increased ventricular stretch. They both
increase cardiac output by reducing systemic blood volume through naturesis and therefore
reduce blood pressure and also reduce vascular resistance.
During this phase, depending on the severity of the ischemia, the infarction zone
expands throughout the heart tissue as a result of serine protease degradation of
intermyocete collagen struts and neutrophil release of metalloproteinases (MMPs). xv An
imbalance between MMPs and Tissue Inhibitor of metalloproeinases (TIMPs), allows MMPs to
degrade the extra-cellular matrix (ECM) surrounding the myocardial tissue by signalling
inflammatory cytokines, neutrophils, macrophages, growth factors, and angiogenic factors
to clean up and remove necrotic myocytes as well as initiate tissue regrowth. This is the
beginning of a process that leads to the laying down of collagen and hypertrophy.
Within hours of infarction, myocardium wall thinning and ventricular dilation results
and leads to an insidious cycle of higher blood pressure which places more stress on the
walls of the LV. In response to an increase in macrophages, fibroblasts, and wall stretch,
ANG2 and ET-1 are released and initiate hypertrophy of the cardiomyocytes. xvi Noninfarcted myocardial tissue also takes on the burden of extra work to keep the heart
functioning normally and becomes stretched, consequentially adding to further hypertrophy
of myocytes.
Phase 2 - Granulation and Early Remodeling Phase (7-21 days post-MI):
This phase is largely distinguished by a process of removing the necrotic tissue and
initial rebuilding of tissue. Macrophages continue to phagocytose necrotic myocetes while
myofibroblasts increase activity as they proliferate into the infracted area. A mixture of
collagens, proteoglycans, and matricellular proteins (such as osteopontin, thrombospondin1 and -2, and fibronectin) is deposited by fibroblasts to make granulation tissue. Dead
myocardial tissue, which normally looks like thin, strait columns under a microscope when it
is healthy, is replaced by scar tissue that is much wider and disorganized in comparison.
Later, granulation cells apoptose and are replaced by new collagen laid down by
myofibroblasts who leave a thin hypocellular scar. Also during this phase, the non-infarcted
myocetes experience hypertrophy from stretch and an expanding infarction zone. Several
animals studies measuring MMP and TIMP levels during this phase show a rising and falling
of levels of various MMPs as well as a rise in TIMP levels but not until day 14. This evidence
demonstrates a heavy signaling of MMPs during this phase, which is responsible for
increased LV remodeling.
Phase 3 - Late Remodeling Phase (21 days post-MI):
LV regional remodeling takes place for weeks, months, and years after a MI. Animal studies
suggest a continually fluctuating level of MMPs and TIMPs, which contribute to the process
of chronic inflammation and collagen formation leading to chronic LV remodeling.
BIOMARKERS OF HEART HEALTH
Several biomarkers have been identified in association with LV hypertrophy. Creactive proteins, biomarkers of inflammation as well as fibrinogen and plasminogen
activator inhibitor-1 (PAI-1) have been found to be indicators of altered LV geometrical
changes xvii and collagen biomarkers such as collagen types I and III xviii. Homocysteine has
also been used as a marker for predicting risk of heart failure, though when levels are
reduced to “normal levels” when they were once high, the risk of heart failure is still
prevalent. xix The most reliable biomarker for predicting remodeling has been aldosterone to
renin ratio (ARR) which has been clearly associated with eccentric and concentric ventricular
hypertrophy.
xx
This is significant since it is clear that activation of the RAAS and ANG 2
levels have already clearly been associated with LV remodeling as mentioned above.
THERAPEUTICS
Despite the polypharmacy of drugs used to prevent post-MI remodeling, heart failure can
still occur. There are several approaches, which can be considered to inhibit and prevent the
processes involved in cardiac remodeling which may incorporate both pharmaceuticals and
herbal medicine where appropriate:
•
Preventing ischemic damage
•
Lowering high blood pressure
o
•
Regulating RAAS and ANG2 expression
Reducing fibrosis and collagen formation
o
Down regulating TGF-beta1
•
Inhibiting MMP activity
•
Inhibiting Endothelin formation
•
Reducing excessive aldosterone levels
•
Addressing secondary factors such as insulin resistance, which contributes to myocardial
hypertrophy xxi. Improve insulin sensitivity.
•
Reducing overall inflammation
•
Address compounding factors contributing to further heart damage such as
o
Reduce stress, anger, tension
o
Improve circulation
o
Prevent atherosclerosis progression
o
Make necessary lifestyle/diet changes to reduce risk of another MI and improve
overall health perhaps with the guidance of Cardiac Rehabilitation Services. 1
In the process of considering potential medicinal plants for use in post-MI scenarios,
a combination of traditional uses will be mixed with modern scientific studies that have
created interest in several plants and their actions on reducing remodeling and hypertrophy.
While many studies focus on isolated constituents used in animal studies, they will still be
included for the sake of potential extrapolation for indicated actions in congruence with
traditional use.
The general energetic picture of the post-MI patient is somewhat dependent on their
overall constitution and the phase of remodeling they are in. Generally, the overall energetic
picture of someone in a post-MI condition will be cool and deficient lacking vitality and Qi. In
general, the herbal strategies will be to warm and rebuild the deficient person.
ACTIONS:
Primary:
Cardioprotective
Secondary: Diaphoretic
Anti-inflammatory
Nervine
Anti-fibrotic
Anti-cholesteremic
Circulatory Enhancement
Lymphatic
Vasodilator
Adaptogen/Endocrine Modulator
HERBS:
Hawthorn- Cratageus oxycanthoides:
Anti-inflammatory, Anti-oxidant, Nervine, Vasodilator, Cardiac Trophorestorative
Hawthorn is a well known and highly researched cardio trophorestorative that
improves conditions such as mild congestive heart failure, mitral valve prolapse,
myocarditis, arrhythmias, atrial fibrillation, palpitations, angina, improved recovery from
MIs, preventing atherosclerosis, mildly lowering high blood pressure, and preventing or
improving ischemic heart disease conditions. xxii
Tea (Infusion): 1-2 tsp. dried berries, 8 oz. hot water, steep for 1 hour, take 3
1
This component of healing from a MI is critical to determining the quality of life and reduction of post-MI
remodeling. While it is essential to discuss diet and exercise, the limits to the length of this paper have left me with
no other option than to put the thought into a footnote and encourage further reading for those interested. Also, it
would be a great loss not to mention the emotion influences, such as anger, grief, heart break, and anxiety as well as
the benefits of spiritual practices such as prayer, meditation, and positive thinking.
cups/day
Tincture (1:5), 30-35% ETOH, 10% Vegetable Glycerin Dose: 3-5 ml (60-100 gtt.)
QID
Capsules: 2 (00) capsules TID
Solid extract - 1/4 - 1/2 tsp. 2x/day
Rosemary Rosmarinus officinalis:
Anti-inflammatory, Anti-oxidant, Diaphoretic, Nervine
In an animal study using a diterpene phenol extract of Rosemary, pulmonary fibrosis was
inhibited through the mechanism of inhibiting up-regulation of TGF-beta1 and inhibiting
excessive collagen deposition, especially collagen-I formation. xxiii
Tea (Infusion): 1/2 tsp. powdered herb, 8 oz. hot water, steep covered for 15-20
minutes, take 2-3 cups/day
Tincture (1:5) 65% ETOH Dose: 1-2 ml (20-40 gtt.) TID/QID
Night Blooming Cereus - Selenicereus grandiflorus:
Cardiotonic, nervine, and diuretic
This plant was used by the Eclectics for “Athlete’s heart” and more recently has been
used by David Winston for lowering blood pressure in people, especially those with insulin
resistance and blood pressure and cholesterol levels that have been creeping up every year
starting at age 30 xxiv.
He has also used it for heart disease with an irregular, feeble
heartbeat and pulse accompanied with anxiety, dyspnea, or depression. Winston also finds
it effective for mild to moderate congestive heart failure with angina, decompensation of the
heart due to nicotine use, and for mitral valve prolapse.
Tincture (1:2), 40% ETOH Dose: .5-1.5 ml (10-30 gtt.) TID
Boswellia Boswellia serrata:
Anti-Inflammatory, Analgesic, Circulatory Stimulant.
In an animal study, a primary constituent of its resin, incensole acetate, was shown
to inhibit TNF-α, IL-1β and TGF-β1 expression, as well as NF-κB activation following head
trauma and had a therapeutic window of treatment up to 6 hours xxv following the ischemic
injury. It is a very effective anti-inflammatory and analgesic especially in cases of congealed
or stagnant blood where there is pain and trauma.
Tea (Decoction): 1/2-1 tsp. dried resin, 12 oz. water, decoct 15-20 minutes, steep
covered 45 minutes take 4 oz. 3x/day
Tincture (1:5), 70-80% ETOH Dose: 1.5-2.5 ml (30-50 gtt.) TID
Capsules-Standardized to 25-37% Boswellic acids: 300-400 mg TID
Gotu Kola – Centella asiatica
Adaptogen (mild), anti-inflammatory, anti-oxidant, circulatory stimulant, anti-ulcerogenic,
nervine, vulnerary.
Gotu Kola is used for any degenerative disorder pertaining to the muscles or fascia.
It is a useful adjunct in a protocol for mitral valve prolapse, endocarditis, cardiomyopathy,
and ischemic heart disease and for inhibiting scar tissue formation. xxvi In an animal study
with rats subjected to a myocardial infarction and were given an extracted constituent from
Gotu Kola called madecassoside, which was shown to reduce c-reactive protein and superoxide dismutase levels as well as reducing ischemia reperfusion injury. xxvii
Tea (Infusion): 1-2 tsp. dried herb, 8 oz. water, steep covered 45 minutes, take 4
oz. 3x/day Tincture (1:2), 30% ETOH Dose: 1.5-2 ml (30-40 gtt.) TID
Capsule: 200 mg standardized extract (40% asiaticosides): BID/TID
Red Sage – Salvia miltiorrhiza- Dan Shen (TCM)
Analgesic, anti-coagulant, anti-inflammatory, anti-oxidant, cardioprotective, peripheral
vasodilator
Dan shen is useful for angina pain, reducing blood pressure in hypertension, reducing
cholesterol and trigylceride levels, reducing palpitations, improving cardiac circulation, and
for preventing the development of atherosclerosis. xxviii In TCM it is used for conditions of
blood stasis in the chest (including the heart) and abdomen as well as for symptoms of
“disturbed Shen.” There are several animal studies validating the use the constituent
salvianolic acid B for reducing cardiomyopathy and remodeling by inhibiting TGF-beta1,
MMP-2 and MMP-9 expression. xxix
xxx xxxi
Tea (Decoction): 1-2 tsp. dried root, 8 oz. water, decoct 10-15 minutes, steep 1
hour, take 2-3 cups/day.
Tincture (1:4 or 1:5), 45-50% ETOH Dose: 1.5-3 ml (30-60 gtt.) TID/QID
Chinese Figwort - Scrophularia ningpoensis
Anti-inflammatory, cardiotonic, hypotensive, vasodilator, lymphatic
An animal study conducted on rats subject to a myocardial infarction were given an extract
of Scrophularia ningpoensis for 4 weeks. Rats given the figwort showed a decrease in the
left ventricular weight index, heart weight index, a decrease in ANG2, hydroxyproline, and
reduce collagen deposition as well as down regulate TNF-alpha andTGF-beta1 in the
myocardium when compared to the control group. xxxii It has a mild positive inotropic effect
on strengthening the heart and can be used along with stronger remedies for mild cardiac
edema. xxxiii
Tea (Decoction): 1 tsp. dried, powdered, root, 8 oz. water, decoct 10 minutes, steep
1 hour, take 2 cups/day
Tincture (1:4-1:5), 50% ETOH Dose: 1-2 ml (20-40 gtt.) TID
Corydalis - Corydalis yanhusuo
Anti-inflammatory, analgesis, anti-arrythmic, anti-spasmodic, anti-ulcerogenic
An animal study found it to attenuate myocardial hypertrophy and reduce levels of
collagen formation in rats that were fed 200mg/day of corydalis extract starting 2 weeks
after being induced with myocardial pressure overload. xxxiv In one animal study with cats, it
was shown to decrease resistance of blood flow and increase blood perfusion to coronary
arteries by improving the contractile function of the heart and reducing the consumption of
oxygen by the heart muscle. xxxv In TCM, pain is associated with stagnation. Corydalis has
been used to move stagnant Qi and stagnant blood especially where there is chest pain,
angina, arrythmia, and coronary artery disease. xxxvi It can also be used for preventing
myocardial ischemia.
Tea (Decoction): 1 tsp. dried rhizome, 10 oz. water, decoct 15 minutes, steep 1
hour, take 2-4 oz. 3-4x/day.
Tincture (1:4 or 1:5), 50-60% ETOH Dose: 1-2 ml (20-40 gtt.) QID
Asian Ginseng – Panax ginseng
Adaptogen, anti-inflammatory, anti-oxidant, cardioprotective, nervine, immune amphoteric
It is used in TCM for total depletion of upright qi with yang collapse where the person
is experiencing SOB, shock, a cold sweat, shallow respiration, and had a feeble pulse. xxxvii
Several animal studies on ginsenosides from Panax ginseng have shown them to have an
ability to reduce adverse post-MI remodeling xxxviii and reduce myocardial ischemia and
reperfusion injury.
xxxix
Tea (Decoction): 1-2 tsp. dried root, 12 oz. water, decoct 30 minutes, steep 1 hour,
take 2 cups/day
Tincture (1:5), 50% ETOH Dose: 1-2 ml. (20-40 gtt.) TID
Reishi - Ganoderma lucidum:
Adaptogen, anti-cholesteremic, Anti-inflammatoy, Anti-oxidant, Cardiotonic, Nervine
Reishi helps prevent atherosclerosis, lowers blood pressure, inhibits platlet aggregation,
reduces triglyceride levels, and cholesterol.
xl
It is also used for symptoms of disturbed
Shen.
Tea (Decoction): 1-2 oz. dried mushroom, 32 oz. water, decoct 2-4 hours, take 3-4
cups/day
Tincture (1:5), 25% ETOH Dose: 4-5 ml (80-100 gtt.) 4-5x/day
Capsules (mycelia extract): three 500-1000 mg capsules, 3x/day.
Turmeric - Curcuma longa:
Anti-inflammatory, anti-oxidant, anti-cholesteremic
In a study with rats induced with a MI, curcumin was found to reduce the size of
infarction by protecting against myocardial ischemia and reperfusion injury after 30 minutes
of occlusion of the left anterior descending coronary artery. xli Curcumin may thin the blood
and is used for preventing abnormal cell signaling. Turmeric can reduce C-Reactive protein
levels and prevents atherosclerosis and lipid oxidation. xlii
Tincture (1:2 or 1:4), 60% ETOH Dose: 2-4 ml (40-80 gtt.) TID/QID
Curcumin Capsules - Standardized 80-90% Curcumin: 500 mg TID
Barberry - Berberis vulgaris:
It helps rebalance heart rhythm, is an endothelial fibrosis inhibitor, and stabalizes
plaque. xliii It may also inhibit MMP activity in patients with congestive heart failure. xliv
The berries have been found to be hypotensive and vasodilating in rats with
hypertension. xlv
Tea (Decoction): 1 tsp. dried root bark, 8 oz. water, decoct for 10 minutes, steep 45
minutes to 1 hour, take 4 oz. 3 -4x/day
Tincture (1:5), 60% ETOH Dose: 1.5-3 ml (30-50 gtt.) TID/QID
Capsule: 1000-2000mg QD- 15-20+ g of barberry root a day at a 5-6% berberine
content.
Rhodiola – Rhodiola rosea
Adaptogen, antioxidant, cardio-protective
Rhodiola
has
been
used
for
lowering
c-reactive
protein
levels,
preventing
atherosclerosis, preventing myocardial infarctions, and reducing symptoms of angina and
mild congestive heart failure. xlvi It is also used in TCM for relieving heart blood stagnation
and heart yang deficiency.
Tea (Decoction): 1-2 tsp. dried root, 10 oz. water, decoct 15 minutes, steep covered
for 45 minutes take 1-2 cups/day
Tincture (1:5), 30% ETOH Dose: 4-6 ml (80-120 gtt.) TID
APPENDIX
Figure 1: Pathophysiology of Ventricular Remodeling
Diagrammatic representation of the many factors involved in the pathophysiology of
ventricular remodeling. ECM indicates extracellular matrix; RAAS, renin-angiotensinaldosterone system; CO, cardiac output; SVR, systemic vascular resistance; LV, left
ventricular; and AII, angiotensin II.
G S J , and Sharpe N Circulation 2000;101:2981-2988
REFERENCES:
i
Cheng S, Vasan RS. 2011. Advances in the epidemiology of heart failure and left
ventricular remodeling. Circulation. Nov 15;124(20):e516-9.
ii
Ibid.
iii
Ibid.
iv
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Center for Disease Control and Prevention. 2013. “Heart Disease Facts”. Accessed on
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Sutton, MG., Sharpe N. 2000. “Left Ventricular Remodeling After Myocardial Infarction.
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Sadoshima J, Jahn L, Takahashi T, et al. 1992. Molecular characterization of the stretch-
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Ades, P. 2011. Cardiac makeovers: Rehab and Prehab for a healthy heart. Video
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Velagaleti RS, Gona P, Levy D, Aragam J, Larson MG, Tofler GH, Lieb W, Wang TJ,
Benjamin EJ, Vasan RS. 2008. Relations of biomarkers representing distinct biological
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Verma, S., Dumont A.S., McNeill, J.H. 1999. Myocardial insulin resistance in cardiac
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Winston, D. 2011. Selenicereus grandiflorus. Native American Materia Medica.
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Winston, D. 2011. Centella asiatica. Ayurvedic Materia Medica.
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Winston, D. 2011. Scrophularia ningpoensis. Chinese Materia Medica.
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Winston, D. 2011. Ganoderma Lucidum. Chinese Materia Medica.
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Winston, D. 2011. Curcuma longa. Ayurvedic Materia Medica.
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Transforming Trauma Stored in the Body:
A Holistic Approach to Post Traumatic
Stress Disorder
Danielle Rissin- Rosenfeld
Post Traumatic Stress Disorder (PTSD) affects people’s lives profoundly but because it is
not something that is visibly debilitating it is often over looked. The purpose of this paper is
to provide a more comprehensive look at the reasons for PTSD and the ways that it
manifests itself in the body. It is also a platform to briefly overview supportive strategies,
healing practices and herbal therapeutics.
Post Traumatic Stress Disorder (PTSD) is a reaction to one or more traumatic events which
presents anywhere between one month and a year after the occurrence. People experience
trauma in situations that are emotionally/physically painful and distressing and overwhelm
their ability to cope. Trauma may begin as acute stress from a perceived life-threat or as
the end product of cumulative stress. (33) Trauma can stem from childhood abuse and
neglect, medical/ surgical interventions, war and violence, physical emotional and sexual
abuse, accidents and natural disasters, grief or witnessing acts of violence. (30) To be
diagnosed with PTSD one must exhibit the symptoms of mood functional disturbance,
substance abuse and suicidal thoughts. (35)
Symptoms of PTSD may include catatonia (speechless), black-outs (memory loss), robotic
actions (mind control), flashbacks (remembering when you don't expect to), sleeplessness,
irritability,
quickness
to
anger,
listlessness,
anger,
hopelessness,
purposelessness,
defeatism, depression, anxiety, panic attacks, nightmares, bad dreams, and disassociation.
(20) Risk factors for PTSD may include experiencing dangerous events or traumas, having a
history of mental illness, getting hurt, seeing people hurt or killed, feeling horror,
experiencing helplessness or extreme fear, having little or no social support after the event
or dealing with extra stress after an event such as loss of a loved one, pain and injury, or
loss of a job/ home. (20)
Hypthalamic-Pituitary-Adrenal Axis
During a traumatic event the individual usually mounts a “fight, flight, or freeze” response.
If the person’s body is unable to fully process the stressor and release the shock of the
event it gets stored in the cerebral cortex and muscle memory. (29) The stress during the
traumatic event, as well as ensuing stress, activates the Hypthalamic-Pituitary-Adrenal axis,
which leads to the suppression of DHEA, Testosterone and Estrogen synthesis, all of which
affect mood. Low estrogen is associated with lower serotonin production, which can impact
anxiety. While the Acute Stress Response is necessary for survival, prolonged stress is
ultimately damaging.
Allostatic load is a term for wear and tear on the body that
accumulates when an individual is exposed to repeated or chronic stress. A high allostatic
load can result in long-term physiological changes such as atherosclerosis and stroke. A
high allostatic load can cause insomnia, depression, and diabetes due to disruption of
endocrine function. (4, 29)
Chronic
stress
can
cause
prolonged
elevated
levels
of
Corticoliberin
CRF,
a peptide hormone and neurotransmitter. This may down-regulate CRF receptors in the
pituitary
and
brain.
Decreased
Adrenocorticotropic hormone (ACTH)
response and
decreased CRF receptor concentrations are found in the frontal cortex of depressed
individuals who commit suicide, as well as in people suffering from PTSD. (7)
Traumatic events can be replayed and re-experienced months to years after the event.
Fear related memories are stored in the cerebral cortex, and when triggered, may also
activate neural circuits in the temporal lobe and brain stem, potentiating feelings of panic.
(4) Panic, stress and emotional distress are perceived by the hypothalamus which signals
your body regulating hunger, thirst, sleep and wakefulness, as well as most involuntary
mechanisms, including body temperature.
When these signals are disturbed, the body is
confused about how to regulate itself (36). This can contribute to the symptoms of PTSD
and exacerbate self-destructive patterns.
Historical Trauma
Beyond the acute presentations of trauma, there are social, political and spiritual contexts
which engender ongoing trauma. Dr. Maria Yellow Horse Braveheart defines historical
trauma as:
“Cumulative emotional and psychological wounding over the lifespan and across
generations, emanating from massive group trauma. Native Americans have, for
over 500 years, endured physical, emotional, social, and spiritual genocide from
European and American colonialist policy. The effects of historical trauma include:
unsettled emotional trauma, depression, high mortality rates, high rates of alcohol
abuse, significant problems of child abuse and domestic violence.” (21)
It’s hard to heal from trauma when the conditions which created it haven’t changed.
Repeated on-going traumatic events such as
genocide, residential schools, slavery, war,
displacement, repeated sexual, emotional and physical abuse, environmental destruction
are not only held in an individual’s body but can be carried over to one’s descendants (14).
Although healing from trauma is important for the individual, it is also often a community
healing process which is required. When a person lives in isolation and is displaced from
their community or landbase and home it is a harder and longer journey towards healing.
(21)
In Judith Lewis’s book “Trauma and Recovery”, she says that, “recovery can take place only
within the context of relationships; it cannot occur in isolation.
recovery is the empowerment of the survivor.”(18)
The first principle of
There is a lot to be said about the
incredible strength and resilience of people who have endured so much. One of the most
major factors that encourages is community as well as positive feelings towards oneself and
healthy coping mechanisms like exercise and ritual. (25)
Therapeutic Practices for PTSD
Therapeutic protocols depend on a person’s symptoms, experiences and constitution. People
have found success with alternative therapies such as cranial sacral therapy, acupuncture
and somatic experiencing.
Somatic experiencing is a psychobiological method for resolving trauma symptoms and
relieving chronic stress. Other therapies include Eye Movement Desensitization and
Reprocessing (EMDR), Hypnosis and Emotional Freedom Technique (EFT). (35)
Somatic experiencing offers a framework to assess where a person is "stuck" in the fight,
flight, freeze, or collapse responses and provides clinical tools to resolve these fixated
physiological states.
Acupuncture is also a huge support in enabling victims to cope with trauma and to heal from
PTSD. When giving acupuncture treatments for PTSD acupuncturist Janette Cormier tends
to do the, “NADA (north American Detox Acupuncture) as a basic protocol combined with
more specific points for them as an individual” She also does, “'grounding' treatments and
treats many kidney issues (fear). It's often Kidney Yang deficiency.” (22)
Psychotherapy is also used as a healing modality for PTSD. However the pure mental health
focus, “often individualizes the experience, leaving people isolated with the impact and the
concrete circumstances of their specific situation.” (14)
Eye Movement Desensitization and Reprocessing (EMDR) is a therapy in which a person
moves their eyes rapidly from side to side while recalling a traumatic event.
Biofeedback is a therapy to help understand how the body reacts to stress.
It involves
using a machine, at first, to see bodily functions that are normally unconscious and occur
involuntarily like heart rate and temperature. The purpose is so that one will learn to control
the reactions, and eventually be able control their reactions to stress without using a
machine.
Hypnosis induces a deep state of relaxation, which may help people with PTSD feel safer
and less anxious, decrease intrusive thoughts, and become involved in daily activities again.
Emotional Freedom Technique (EFT) helps a person revisit traumatic events while tapping
on acupuncture points in order to release the experience. (36)
Ceremony encourages spiritual nourishment and release of a traumatic event especially
ceremony that incorporates shaking and crying. In Peter Levine’s Book Waking the Tiger he
talks about how when responding to an inescapable or overwhelming threat humans and
animals both use an immobility response. Levine believes that for humans to heal from
trauma they should mirror the fluid adaptation of wild animals, by shaking and passing
through the immobility response. This will enable them to move through the trauma and
becoming fully functional again. (26)
To begin the journey to healing a person must be able to look at their trauma and be ready
to transform it. When talking with clinical herbalist and acupuncturist Janette Cormier she
said,
“One of the most difficult things about healing from PTSD is that you need to gently,
but
firmly push people forward out of victimization. This can be really challenging for
the practitioner and the patient and must be done with care and integrity. There is also
a timing issue regarding a sort of 'grieving period'. Obviously it is not enough to
say/totally inappropriate to tell people they must "get over it", but within the context of
treatment and support this is still the ultimate goal - that they leave victimhood beyond
for a life of freedom from their past 'demons'” - whether they be people or experiences.
In order for people to move forward in this way they need to be strong, and I often find
myself working on strengthening their vitality and spirit, working on their constitution,
nourishing them and encouraging them always to move forward and not to stagnant.
Ceremony can be huge for this. I feel like acupuncture treatments are like a personal
ceremony when done appropriately... and can be massively profound at times.” (22)
Herbal Therapeutics for PTSD
Herbal medicine is only one of the many supportive strategies needed when approaching
PTSD.
When addressing PTSD it is important support the person’s endocrine function,
nervous system and help them adapt to the stress. When approaching it from Chinese
Medicine perspective, PTSD can be manifested as Shen disturbance or insufficient/ blocked
qi. In that case it may be useful to move or build the blood. (18) Addressing acute anxiety
and depression can also be useful in improving the quality of one’s daily life. The lasting
effects of PTSD can result in permanent physiological changes such as chronic pain and
illness (4,13,36). In this case one will want to support a person’s body by modulating their
immune system and supporting their neuroendocrine function. With acute symptoms of
PTSD such as insomnia, anxiety and panic it may be prudent to address physical pain and
emotional turmoil. However, suppressing these symptoms in the long term may prolong the
problem. Sedating someone is not addressing the underlying issue of why the trauma is
reoccurring. (27) Herbal actions may include nervines, adaptogens, blood builders and
movers, anxiolytics, immunomodulants and yin tonics etc. The herbs need to be different
for each person depending on their constitution, symptoms, barriers to healing and lifestyle.
In my research the herbs that were prominent:
Milky Oats (Avena Sativa) is a restorative nervine for self-induced adrenal exhaustion. The
milky tops are used internally as tea or fresh tincture. The fresh tincture is used for acute
nerve injury. The sooner taken the better. Milky oats are specifically indicated for
concussion, compressed nerve, cut nerves and traumatic brain injury.
It is helpful in
recovery from neurasthenia/chronic fatigue syndrome, insomnia, depression, anxiety, and
opiate withdrawal. They help restore, rebuild and regenerate nerves.
Dose: 3-5 ml 3xday (traumatic acute nerve (esp. brain) injury recovery) less for other
maladies. Tea: 6tbs/quart infusion preferably overnight. (9)
Hawthorn (Crataegus monogyna) Hawthorn nourishes and calms the heart, helping to settle
the Shen. At the same time, her thorns offer protection from those who would harm you.
Hawthorn can potentiate digitalis drugs, caution w/ bata blockers.
Dose: solid extract jam- Itsp TID (10)
Wood Betony (Stachys officinalis) is used for harmonizing the gut brain action,
parasympathetic tone, headaches and for aiding digestion in cases of all the consequences
of eating while experiencing stress. It is specifically indicated for grounding the solar plexis
for people who are fixated in mental patterns, providing protection from the belief in evil
spirits, nightmares and visions.
Dose: 1 teaspoon TID (17)
Anemone pulsatilla is for underlying anxiety, people who are sad, pale withdrawn and need
sleep. It is for people who are fearful and weep easily when everything that can go wrong
has. It is specifically used for panic attacks, insomnia, nervousness, and a generally
agitated emotional state with gloom and distress.
Dose: 3-10 drops, to 4X a day. USE WITH CARE. (30,31)
Dan Shen (Angelica sinensis) infuses courage where there is disturbance and fright. It is
specific in cases of insomnia, dementia, nourishes the blood while moving and has calming
effects. It is a blood tonic, mild analgesic for pain from stagnation and moves energy in the
body.
Dose: 3-15 g or 4-3 ml- 1-4 times daily. (9)
Ashwagandha (Withania somnifera) is indicated for the wired and tired person. It helps in
re-regulating the HPA axis and helps shift a person’s perception of stress and cognitive
decline. It is a yin tonic and is building, helping to store energy rather than use it.
Dose: 2-4 ml TID (2)
Skullcap (Scutellaria lateriflora) is a calming nervine for depression or anxiety, restless leg
syndrome, muscle spasms and obsessive compulsive behaviour. It is for those people who
are tired and wired. The eclectics used it for irritability of the nervous system and
restlessness.
Dose: 10g per day, tincture 1:2 30-150 drops TID. (9)
Frankincense (Boswellia sacra) is warm and pungent, and enters the heart and lung
meridians. It promotes blood circulation and movement of qi, and is used following acute
physical trauma. It can also relax tendons. Frankincense is especially suitable for conditions
where the joints and muscles are very stiff, swollen, and painful. (10)
Mimosa (Albizia julibrissin) is also used for disturbed shen, the bark and blossoms (more
calming). In Chinese tradition it is used for disturbed shen symptoms, including bad
dreams, irritability, anger, depression, and poor memory. Combined with Hawthorn berries
and Rose petals it is used for “broken hearts”, grief and deep sadness.
Mimosa blossoms (He Huan Hua) also can be used to calm the shen and elevate the mood,
but they are weaker and less effective than the bark. (32,17)
Dose: Tincture (1:5): 40-80 drops TID. (32)
Passionflower (Passiflora incarnata) is a mild anodyne, anxiolytic, hypnotic and nervine,
antispasmodic and hypotensive. It’s specifically used for circular thinking and people who
can’t relax or sleep because the mind is going around and around. Passionflower is an
antispasmodic relaxant and is a warmer alternative to blue vervain. It’s good for anxiety,
irritability, restlessness, stress induced spasm, backache, tension headache, bruxism
(grinding teeth) disturbed shen, convulsion, stress induced heart symptoms, nerve pain,
exhaustion with spasm and twitch, insomnia when you can’t turn off your mind, restless
sleep, sleeplessness from anxious irritability and worry. It is great combined with Jamaican
dogwood for someone who is sleepless with pain.
Dose: Fresh tincture (1:2 40%) 3-6 mls TID. For sleep 5ml at bedtime and for tea: 1-2
tsp/8 oz steep (30 min ideal) (6)
Rosa rugosa pedals are used for grief. They are used to astringe and protect the boundaries
of the heart. It can help people who feel disempowered feel more empowered. The
combination of mimosa, hawthorn and rose can help people who feel more deeply and help
deal with unresolved issue. (27,9)
Dose: petals 1:1 50%ETOH, 40%h2o,10%glycerin.
For astringency and anti-inflammatory effects- 3-5 ml
For emotional effects- 1-2 ml/day
Hips in syrup/jam- 1-2 TBS/day
Hip tea- 2-5 grams (9)
Ghost pipe (Monotropa uniflora) is used as a nervine to relieve symptoms of neurological
chemistry disruption and pain, to stop seizures, convulsions, insomnia, mental disorders,
and chronic muscle spasms. Ghost pipe is specific for: overwhelming physical pain when
combined with anodyne herbs, migraines associated with traumatic brain injury, anxiety and
panic associated with emotional or sensory overload, the triggering of emotional memories
that make the subject feel beside herself with unpleasantly intense mind altering
experiences.
Caution: consumption of 15 ml or more of Monotropa tincture can bring deep sleep and
ultra -vivid dreams, often bizarre, frequently erotic. (1,12)
Dose: start with three drops of the tincture, but go up to 1ml if the person doesn't respond
to a 3 drop dose. In cases of severe panic/agitation give 1ml drop doses at 5 minute
intervals. (1)
American Ginseng (Panax quinquefolius) is an endocrine amphoteric and adaptogen that is
useful for mild to moderate depletion of the HPA axis and adrenal glands. Because of its
effects on the HPA axis, it can help correct dysfunction of the immune system, including
depletion that leads to a susceptibility to catching colds. It is also a mood regulator, good
for regulating blood sugar in recovering junkies, chronic fatigue syndrome helping
regenerate the body in people with long term amphetamine use.
Dose: Do not use longer than 3 months, 50-80 drops TID (9)
Holy Basil (Ocimum tenuiflorum) is an adaptogen and helps re regulate a person’s
perception of stress in HPA dysregulation. It is also used specifically in eating disorders,
which are a common occurrence in PTSD because of the disassociation and body
dysmorphia that may occur.
Dose: Whole plant juice 1-3 ml, Tincture 3-5 ml in a formula, Tea 2-5 g (5)
Reishi (Ganoderma lucidum)
For women who have hyperimmunity (immune system hyper vigilant see everything outside
of itself as a threat) the caregiving type who are more prone to fibromyalgia. It is used for
disturbed Shen, anxiety, insomnia, bad dreams, and listlessness.
Dose: 1:2 ml 2 stage extract, 5ml BID, 2 tsp QD- BID powders, 7:10g in decoction (28).
Flower essences help deal with emotional and spiritual trauma. Some flower essences that
clinical herbalist Jasmyn Clift recommended for PTSD are:
Star of Bethlehem for shock and trauma. It comes with work. People will need a coping
mechanism because they will revisit the trauma to move through it. They need to be up for
the work. If they’re going through “crazy” times they shouldn’t take it. It is ideal to help
work with and transform triggers. (8, 16)
Mimulus helps a person get over fear. It is for the person who is shy and retiring and prone
to hide their anxiety. For the person who is deterred by chronic fears such as fear of the
dark, injury, poverty etc. (8, 16)
Aspen is an inability to explain the fear, sympathetic state and worry. For the person with
unexplainable fear, who has fears by day or night for no known reason, and fear
accompanied by trembling and sweating. (8, 16)
Rock Rose is for complete and utter terror and extreme fear caused by facing an
unexpected or unfamiliar experience. It is for the person who experiences fear from
terrifying sights or nightmares. When their fear and panic is so severe it is projected in the
atmosphere. Rock Rose enables a person to be calm, courageous and be able to look out for
the well-being of others. (8, 16)
Gentian is for people who are starting to lose faith in themselves. It is for people who
attract negativity because of their own negative state of mind and are experiencing a deep
depression from a known cause.
Gentian aids a person in finding faith in their own
resources. (8, 16)
Gorse is for people with no self- sufficiency who are living with chronic illness and/or in
poverty.
For people with diminished vision, lack of ambition and interest due to
hopelessness. Gorse helps confidence and enables one to overcome obstacles and not be
overly influenced by others. (8, 16)
Clematis is for people who cope by disassociating.
They are day dreamers that indulge
themselves in drugs and alcohol, TV and other distractions. Clematis helps a person live in
the present and complete tasks it is especially for people with A.D.D and PTSD. (8)
Honeysuckle is for people living in the past who can’t be present it is specifically for cases of
PTSD. Honeysuckle is for the people who dwell on thoughts of the past and hold a
pessimistic outlook both for the present and future. For the people who are chronically
nostalgic and regretful. Honeysuckle helps people overcome past experiences and be able to
creatively transform trauma and grow from it. (8, 16)
Olive is for people who are totally exhausted to the point of tears, drained of energy and
unable to cope with daily thing. It helps people find motivation, depend on their inner-self
and attract happiness and pleasure despite their exhaustion. (8, 16)
Pine is for people who have immense guilt and self-reproach. This is a common occurrence
in PTSD because people internalize their trauma and blame themselves for it. Pine is for
people who over work themselves and stress out because they are never good enough.
Pine helps resolve remorse and enables people to live without useless guilt. (8, 16)
Bach Rescue Remedy is for acute trauma situations and helps calm and ground a person in
times of panic and anxiety. (8)
Other flower essences that may be useful in PTSD are: Indian pink for remaining centered
and focused even under stress. Bleeding heart in a spirit dose of the whole is for mass
hysteria.
Eating the flower of borage will enhance courage. (25)
Red clover is used to create a calm and steady presence. (25)
Yarrow is useful for boundaries of psychic protection. (25)
Sunflower is for people who have relationship issues with their fathers. It also helps a
person express themselves fully, truly and vibrantly. (25)
Additional nutritional and supplementation support may include: Omega 3 fatty acids for
supporting mood. Eating kale and other leafy greens high in magnesium reduces spasms.
Co-Q10 and magnesium support immune and muscular support. It is good to avoid coffee
and other stimulants and it is recommended to look into other food sensitivities. (34)
Herbs are just one of the supportive strategies needed in the journey towards healing from
PTSD. The process of healing is different in each person. Healing is most effective when
done within community; the more support a person experiences the quicker and more likely
it is for transformation to occur.
Displacement and isolation hinder the healing process.
Ideally, a person receives multiple forms of care. Trauma is usually not a singular
occurrence and traumatic events may be unavoidable. When addressing PTSD, it is
important not just to look at it as an individual issue, but to look at the larger issues and
context of why the trauma has occurred.
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Case
Study
–
Anxiety,
Stress
management
Marguerite Gregory
RM is a 48 year old female, H 5’ 3 ½ “, W 133 lb., who came to the City Market clinic,
accompanied by her daughter, MM, in June, 2013. Her primary goals were to boost her
immune system, prevent Lyme Disease, and get help with insomnia related to extreme
stress and PMS. During this period of time her stress was tremendous – her daughter had
Lyme disease, she was going through a major break in an important family relationship, and
the proposed gas pipeline through Monkton was planned to pass close to her home well. The
initial visit and subsequent follow-up visits were conducted back-to-back with both mother,
daughter and two student clinicians present each time.
RM presented with frequent twitchy movements and seemed nervous, on the verge of tears.
She had cold hands and her face was pale, but with heat signs. At the initial visit her pulses
were thin, tense, and hard to occlude. They were somewhat weak in the Metal (LI/Lu), Fire
(TB/P) and Fire (SI/H) positions, and moderate in all other positions. Heart rate variability
was present, but slight. Her tongue was pink with a red tip and a slight white coat. It
appeared moist with slight quivering, lots of scallops and a crack near the tip. She had slight
blue sublingual veins.
Two years previously, in 2011, she was diagnosed with environmental illness from mold in
the house that was subsequently removed. She had also been diagnosed with candida on
the phone by a medical intuitive. She was leary of physicians and did not see a doctor
regularly.
During the client interview, most complaints centered around stress, although she reported
that during the last 3 months, her stress and related symptoms had begun to improve. She
was taking proactive steps to resolve the external factors causing her stress and was also
receiving Reiki that was helping. Symptoms of stress included insomnia, low energy, PMS,
global and specific anxiety, reduced libido and tinnitus. She also reported a loose, mushy
stool, PMS with breast tenderness (she has fibroids), increased appetite and craving for
sweet, insomnia and mild, dull cramps. Both mother and daughter were continuing to
experience cyclical symptoms that may have been related to the environmental illness. For
3 days every other week they experienced fatigue with brain fog, nausea and depression.
The constitutional summary was yin deficiency (false heat) with both Vata derangement
(tendency to cold, variable energy, nervous system disorders (insomnia and anxiety) and
shallow breathing and Pitta derangement (red tip of the tongue, hypersensitivity to mold).
The summary of relevant physiology included nervous tension affecting mood, sleep, GI
tract and libido, and immune system hypersensitivity.
Initial Goals:
1. Support adrenals and HPA-axis and increase energy.
2. Reduce perception of stress.
3. Support digestion.
4. Support sleep.
5. Support the immune system and reduce hypersensitivity.
Herbal actions centered around adaptogens, nerviness (trophorestorative and relaxing),
digestive tonic, immune modulators and immune tonics. She was given powders to make
into bliss balls: ashwagandha, shatavari, astragalus, and codonopsis (15 g/day), and a
tincture of blue vervain, skullcap, reishi, and yarrow (5 ml TID). It was recommended that
she and her daughter use air purifiers in their bedrooms, and that she continue with Reiki
and the community support group that she was involved in.
First follow-up, 6 weeks later, July 2013
All of RM’s pulses had strengthened, the weakest now being Fire (SI/H). It was further
noted that her tongue was swollen and had a jing saddle. She was fidgety and her eyes
blinked rapidly and frequently.
She reported that both her and her daughter’s health and emotional well-being were
improving. RM reported much less anxiety (2/10), though she felt that a baseline of anxiety
was part of her make-up. Sleep related to stress and PMS had improved (insomnia now only
1-2 days instead of 4), her energy was as good as it had been 5 years ago and she had not
noticed the tinnitus lately. PMS had generally improved except that she still had bothersome
fibroids and mild, dull cramps. There was no change in her loose stool, but the mystery
cycle of fatigue and depression had disappeared and she attributed this improvement to her
work with Barbara Clearbridge, a medical intuitive who practices Reiki and other healing
modalities.
Dampness (swollen tongue and mushy stool) was added to her constitutional summary, a
goal of reducing dampness also added, and astringent action introduced. The bitter taste,
which had been considered part of the “digestive tonic” action was revisited, because RM
could not stand the taste of the tincture, although she liked the bliss balls.
Herbal support formulas:
1. Bitters tincture: dandelion, blue vervain, yarrow (1 tsp TID).
2. Bliss balls: add reishi to ashwagandha, shatavari, astragalus, and codonopsis.
3. Nervine, astringing, and adaptogenic tea: tulsi, skullcap, gotukola, nettles, licorice.
It was also suggested that she could try eliminating some foods that tend to be allergenic
such as dairy, wheat, nuts and seeds.
Second follow-up, 8 weeks later, Sept. 2013
Her pulses continued to strengthen and to resemble one another in both strength and
quality, that is slightly deep, tense and thin. On her tongue, a coat that was white with
some yellow was noted only at the back now, and red papillae were noticed at the rear and
sides. Quivering was not seen this time.
RM reported much less anxiety. She had begun to enjoy social events with large groups of
people and felt she was managing better with events that formerly had caused her more
distress. Sleep and energy continued to improve, but she still felt unable to return to the
vigorous yoga she used to enjoy because she felt too depleted. She asked for a remedy that
she could take at times of acute stress. Her digestion had improved; she was more
comfortable, experiencing less gas and bloating and her stool was firmer. She had
eliminated wheat and was doing only very little dairy. Lately, stress was causing more PMS
breast tenderness. She had been diagnosed with fibroids in her 20’s (2 in one and 1 in the
other breast) and they were always tender during her periods, 6/10 on a pain scale.
She reported that she was not taking enough of her powders and wanted the daily amount
to be measure into separate baggies. She decided that she did not want to add any new
herbs yet, either for endurance or for PMS and fibroids, but wished to continue with the
herbs that were helping a lot.
Third follow-up, 8 weeks later, November, 2013
It was observed that RM looked very much better. Her face was shining and she seemed
very relaxed, even though her hands still twitched and her eyes still blinked fairly
frequently. Pulses and tongue observation were not done.
RM reported that she was managing stress much better, sleeping better and had less
anxiety and anger. PMS symptoms except for tender fibroids were fewer and less intense.
Endurance and stamina were improved but she wanted a boost. Her only digestive upset
was now with kale, so ways to cook it to lessen the indigestion were suggested to her. She’d
had the stomach flu and wanted an herbal remedy to help for another time. She’d had a
cold and was told how to make an elderberry, lemon and ginger remedy and a boneset
oxymel. She felt that this would now be a good time to begin working on the breast fibroids.
To the summary of relevant physiology was added:
Hormone imbalance (PMS, fibroids)
Stagnation (PMS, fibroids, blue sub-lingual veins)
Herbal actions: lymphatics and hormone modulators were added.
Herbal support formulas:
1-3 remain the same, with the option to substitute passionflower and oats when skullcap
was unavailable
4. Add eleuthero as a simple, ½ tsp TID.
5. Lavender bee balm as needed for the stomach flu
6. Vitex, 2 ml once a day in the AM
7. Tincture formula of viola, calendula and red root to add to castor oil as a liniment for a
breast massage every other day.
Other recommendations: It was suggested that she add omega-3’s, and legumes and avoid
methylxanthines (things with caffeine). It was also recommended she take vitamin E,
flaxseed oil and evening primrose oil, include seaweed in her diet 3 times a week, and
increase her exercise.
Email follow-up, February 2014
RM had stopped the vitex because she said it was giving her bad gas. She had been doing
the breast massage for about a month, but there was as yet no noticeable change to report.
Case
Study
–
Mood
support,
sleep
latency, menstrual difficulties
Emer McKenna
MC is age 30, 5’8.5”, and weighs about 140lbs.
I first saw her in clinic on January 22,
2013, she was 29 then. Her primary concerns were anxiety and depression, skin dryness
and eruptions, and poor sleep.
She described alternating between mild anxiety and
depression with one or the other being worse at different times in her life but in the past
three years there had been a shift that felt worse, less manageable, and more hopeless.
Her skin was sensitive to heat, cold, sun, and different foods particularly wheat and sugar.
She viewed her skin as the canary in the coalmine of her body. She expressed having poor
circulation, perennially cold feet, purple-looking legs in the winter, and blotchy skin on her
face and neck when she was stressed. The blotchy skin thing was new to the past two or
three years. Her sensitivity extended to her sleep concerns. When she ate wheat or sugar,
or even drank juice or ate a piece of fruit, too close to her bedtime, she would not be able
to get to sleep. If she drank alcohol she would not be able to get to sleep. If she stayed up
too late, past approximately 12:30 or 1 am, she would not be able to get to sleep. When
she was able to get to sleep she would sleep well, but lightly, and if she were awoken in the
night she would not be able to fall back asleep.
compounded one another.
Not being able to sleep and anxiety
She also described waking up in the morning with her heart
racing and feelings of panic.
M’s digestive system was sensitive, obviously. She described needing to eat simple foods to
avoid digestive upset and bloating.
She noted sensitivities to wheat, gluten, sugar, and
dairy. She moved her bowels about once a day. Her stool was generally a light to medium
brown and formed.
When her digestive system was not doing well she tended to loose
stools.
M said she drank at least a gallon of water a day and described herself as a very thirsty
person. Her urine tended to be clear and she felt as though she drank and drank but did
not feel hydrated.
During our intake, when the topic of menstruation came up, M informed me that recently
her periods had become very light and much further apart. Her cycle was 28-34 days long
and she bled for only 3 days. She used to have more “normal” periods and this change had
come on gradually in the past couple of years.
M has a history of migraines that began when she was a child, possibly related to a head
injury she sustained at age 5. They peaked in intensity about 3 or 4 years ago and that
lasted for 2 years. Eventually she eliminated several different foods from her diet and she
found that gluten and sugar were major triggers for her migraines. She also went through
a huge breakup and Hurricane Irene, moved houses, and became more physically active.
Her migraines were no longer a primary concern although she did describe getting more
minor headaches behind her eyes recently, perhaps related to her job working in front of a
computer.
Her pulse was thin, slack with some flooding in the first two positions, on the right hand
side, at the deep level. Her tongue was pale, very quivery, with a white coat only on the
back third of her tongue. It was moist on the edges and dry in the center.
My energetic assessment of M was Blood Deficiency and Liver Stagnation leading to Qi
Depression. Signs of Blood Deficiency included her thin and slack pulse, pale tongue, and
light menstruation.
Signs of Liver Stagnation were her light stool, very sensitive skin,
headaches behind her eyes, and her frustrated depression. Physiologically she seemed to
be suffering from adrenal insufficiency and HPA dysregulation. Clues of this were the recent
traumas of breaking up, Hurricane Irene, and having to move. Her issues with sleep and
waking up in the morning in a panic with her heart racing were also indicators.
My therapeutic goals were to support her adrenals and HPA function, build the Blood, and
move and support the Liver.
The actions required to achieve these goals were: nervine,
adaptogen, Blood builder/mover, hepatic.
M had told me that she was extremely sensitive to the bitter taste so we had a conversation
about all the benefits bitters could offer her and she agreed to be brave and try them for a
while. Since she was so sensitive, I wanted to give her a bitter formula that was mild, but
would still do the job.
I gave her a tincture formula as follows:
3mL dong quai
2mL ashwagandha
1mL burdock
1mL blue vervain
.5mL cardamom
The dosing instructions were to take 1/2 tsp, three times per day, before meals. I chose
dong quai for it’s blood building and moving qualities and mildly bitter and sweet taste;
ashwagandha as the primary adaptogen, to build the blood, and to promote sleep; burdock
as a mild bitter and hepatic and for her skin concerns; blue vervain for the liver and as a
nervine; and cardamom for flavor and as a catalyst.
I also gave her the following tea formula:
2g skullcap
2g wood betony
1g tulsi
1g anise hyssop
M did not flowery tasting teas at all so I was restricted considerably in the plants i could
choose for her. I wanted to give her a tea to encourage her to drink something other than
plain water in the hopes that that would prove more hydrating. I chose skullcap as a leafy
tasting anxiolytic; wood betony as a nervine and digestive; tulsi as an adaptogen and for
her skin, and anise hyssop as a nervine for her Heart and Liver and to make the tea
somewhat less drying. I also recommended that she drink switchel as an electrolyte better
to improve hydration.
I heard from M about one week later. She did not like the tea, it gave her an itchy feeling
in the back of her throat and she wondered if I could change it. She still was not open to
anything flowery-tasting. I wasn’t sure exactly what was going on with the throat itchiness
so I consulted with Betzy who advised me that it was likely the essential oils in tulsi and
advised me to add oats to make it more moist. I did this and dispensed the formula again
with an additional 2g of oats. Unfortunately, that did not help, M reported only drinking her
tea sporadically, and as far as I know she never refilled it. Looking back now, I think that M
was sensitive to dryness, likely related to her lack of Blood, and that the tea was too drying
for her. I think linden could have helped make the tea more palatable, but unfortunately
has a distinctly flowery taste and she likely would not have tolerated it anyway.
M is a friend of mine so we had a lot of informal communication regarding her progress. At
first she found the bitter taste very difficult to swallow and had to force herself to do it. A
few weeks later I received an excited report that her period was heavier and more red. This
trend of improvement continued and she got to the point where she loved the taste of her
bitters and would carry her bottle around and take swigs off it. She had reported that she
seemed to be increasing her dose slightly with the swigging and I gave her my blessing.
She also told me that bitters was making her stool darker and her bowel movements more
regular.
I next saw her in clinic on September 16. She was a little late to her appointment and had
some emotional stuff going on that she needed to talk about and that comprised most of
our follow up. She told me that improvements in her periods had continued, that she was
having much less difficulty falling asleep at night, and that her mood was feeling somewhat
better, even in the face of stress. I found her pulse to be thin, tight, and still slack. Her
tongue was still pale and quivery though more moist. She reported feeling muscle pain
while sitting. I felt that M needed even a little bit more blood building than she was getting
and i decided to add 3mL of white peony to her tincture, to synergize with the dong quai to
build blood and as an antispasmodic.
She took the new formula to California this fall to
work but her backpack was stolen and she lost it. Being off her formula for a couple months
made her even more aware of it’s benefits in her life. In correspondence with me she told
me that her sleep is much more solid now, her skin has mostly cleared up, her “poops are
AMAZING,” and that her periods have become more regular. She even found that taking
bitters before having alcohol prevents sleep problems and hangovers. Since she has been
off the bitters, for the past two months or so, her periods have gotten lighter again.
It
seems as though her Liver and Blood need some more tonifying but that she is on the right
path and that these plants have made a huge difference in her health and will likely
continue to do so.
Case
Study
–
Dermatographism,
recurring vaginosis
Elise Walsh
Female 36 y/o
Background / History:
The client’s primary concern was dermatographism (also called dermatographic urticaria or
skin writing). When any part of her body is scratched or rubbed, her skin becomes raised
and inflamed, forming wheals or welts. She experiences it on her back, and on seams of
clothing in particular. The condition is windy in nature, arising at different places on her
body. It becomes worst when she is lying in bed trying to sleep. She first experienced this
condition when she stopped lactating two years ago. She finds relief from anti-histamine
creams about once a week, but does not want to rely on them long-term. She has a sense
that it may be stress-related.
The client presented with high stress levels due to her work in the field of data assessment
and analysis. She did not report a sense of meaning in her work and her working
environment was one where she did not feel valued, which caused a sense of anxiety.
Working over 50 hours each week, she had a desire to spend more time with her daughter.
Her health was also a source of stress. She found alone time rare, mood “ok”, and was
waking unrested regularly. Upon rising she also felt stiff and sore in her back, which
resolved soon after rising.
Her second concern was reoccurring vaginal infection, which involved a greenish discharge
and occasional itching. A test done by her doctor after our first meeting confirmed it was
bacterial vaginosis. Her cycle lasts 30 days, with 4-5 days of bleeding. Over the past three
month period she had one month of “normal” flow and two months of nearly absent flow.
PMS involves some lower back pain, and mild emotional sensitivity. She has been anemic in
the past, although current hemoglobin levels are at the low end of normal at 12.7. The
client also reported pain with intercourse.
Her vegetarian diet is rich in vegetables, fruits, beans, soy, nuts, and seeds. The onset of
the dermatographism encouraged her to get tested for food sensitivities – she found she is
sensitive to eggs and brewer’s yeast. While she is not outright allergic to dairy, she eats it
sparingly. Having been vegan in the past, her oils sources include canola and olive oils,
avocado and Earth Balance for cooking.
Digestive symptoms involved some bloating, a mild alternating diarrhea and constipation
pattern which tends towards loose stool, passed 1-2x/day. She experiences hemorrhoids
every six weeks, which are somewhat painful and began with pregnancy. She applies a
topical salve to support wound healing.
She has a tendency to work through her illnesses, which generally reach the lower
respiratory system and persist up to two weeks. She had one sinus infection in the past
year, in previous years she did not become sick as readily.
Her blood pressure is low to normal 90/60, she experiences cold hands and feet, and
bruises easily. Skin and hair are dry.
Assessment:
The precipitation of her skin condition at the same time as she finished lactating was
suggestive of possible endocrine imbalance. The dermatographism, recurrent vaginal
infection, painful intercourse and dry skin were suggestive of poor tissue integrity.
The client presented as a vata-pitta constitution. She is highly driven, action oriented,
experiences poor circulation to the periphery and work-related anxiety, suggestive of a pitta
imbalance. Her pulses were thin suggesting deficiency of fluids (possibly blood and yin).
They had generally good force though the fire pulses were the weakest. Tongue was
scalloped, with a sulcus, which along with her digestive symptoms and hemorrhoids pointed
towards a need for digestive support. The variability in her digestion, windy skin rash,
absent sense of social safety, and tendency to forget to breathe were suggestive of a vata
constitution and/or imbalance.
Plan:
Our strategy has been to support tissue integrity, promote endocrine system balance, tone
down her inflammatory response through tonification of the liver, support digestive function,
build blood, reduce perception of stress and shift stressors. The following tinctures and tea
along with dietary suggestions were utilized:
Tincture:
5ml Fresh Nettle leaf
3ml White Peony root
3ml Shatavari root
2ml Mugwort leaf and flower
1ml Burdock seed
1ml Stoneroot
= 15ml daily dose: 1tsp TID
Tea infusion:
5g Goldenrod flower
4g Tulsi leaf and flower
3g Gotu Kola leaf
3g Lemon Balm leaf
=15g/day
Other recommendations:
Algae-based source of Omega-3 EFAs
Blueberries as vascular tonic
Focus on colorful fruits and veggies
Follow-up:
Client returned two months later (Follow-up #1, June) having utilized the tincture, tea and
omega-3 supplement consistently. As well as starting a new, more meaningful job, she
found improvement in her skin condition. In the past years, May has been the worst month
for her skin condition, but this year she has seen improvement.
She found an asthmatic pattern arising, however, involving a sense of tightness in her lungs
and an inability to get enough air into her lungs. The triggers seem to be anxiety-provoking
experiences (speaking in front of large groups) and when out of breath (pulling her
daughter up a hill). We added 1ml of Reishi to her tincture (replacing the Stoneroot), to give
her formula more of a focus on reducing the inflammatory response in her skin and lungs.
Bacterial vaginosis has continued to persist for her, we discussed using a garlic suppository
and boric acid protocol, along with tissue tonification and endocrine balancing strategies
through herbs and diet.
After using her formula for four months (Follow-up #2, September) and shifting job
stressors she found complete relief from pre-sleep onset dermatographism. When she
ceased using her herbal formulas, the itching returned, along with asthma and hemorrhoids
(stoneroot was added to her formula again).
Her emotional health has been good, though her menses are still scant. Energy is all right,
she still feels tired upon waking after seven hours of sleep. We discussed using a whole food
fat source such as butter, coconut oil, and olive oil to replace Earth Balance.
Discussion:
The herbal formulation has been effective for management of the inflammatory skin
condition through minimizing the hyper-reactive mast cell response in her skin and
supporting tissue integrity. The herbs also support her endocrine system balance by
estrogen enhancement, yin and blood building, and liver tonification. The client plans to
continue to work with these formulas in the coming months. While this client-practitioner
relationship will conclude at the end of the clinical internship, future goals should be to build
blood in order to support a menstrual flow. The client plans to continue her own tea blends
and to work with a Burlington herbalist as the need arises.
Case Study – Lower leg edema, sugar
cravings
Susan Nova Staley
I first met this client on July 16, 2013 at the VCIH Student Clinic in Montpelier, VT.
Client is a 37yr old female, roughly 5’4’’ and 140lbs. Tongue appeared pink in color
with a slight white coat that yellowed and darkened towards the back. The tongue
was dry in quality with a slight quiver. It was slightly swollen with a red tip that was
a bit pointy. Pulses were tight in quality and more deep than superficial; some
weakness in the Kidney and Pericardium positions, otherwise present.
Primary concerns were to reduce swelling and pain in her lower legs, improve the
skin condition on her face and reduce her sweet tooth. Client works as a full time
pastry chef where she is constantly on her feet (which contributes greatly to the
lower leg edema).
I observed varicosities and spider veins on her legs. Her
complaint of edema was visually represented and presented as non-pitting on both
sides. She had experienced this swelling for about three weeks. Current pain was
around 1 on a scale from 1-10 though rated at a 5 during running (which she had
stopped due to discomfort). Also found relief from compression stockings. 3-second
capillary refill time on exam. Also acutely presenting was a swelling that her
acupuncturist identified as a Baker’s Cyst behind her right knee; this was causing her
pain and difficulty reaching full range of motion. There was also an acute pain in her
right ankle.
Client has a history of asthma that was significant as a child but now presents only in
the very cold weather, as well as allergies (mold and pollen). Diagnosis of Plantar
Fasciitis 15 years ago and has since changed to barefoot running shoes that have
offered great relief. She wears these shoes at work now. Family history of
Cardiovascular system weakness (stroke, heart disease, high blood pressure and
diabetes) as well as some thyroid disorder.
Client’s experience of edema started 15 years ago. In the past she experienced some
“arm bloating” that was relieved by lymph massage. Client exercises daily preferring
running, yoga, and weight training. Edema had stopped her present running practice.
Client reports experience of heat and sweating after exercise well after stopping
exercise. She rated her daily energy levels around 7.5, though she says that her
husband would rate her at a 12.  Without daily exercise she feels “cranky” and as
though “something is missing”. Client also reports having experienced low libido and
poor concentration over the past year.
Sleep is variable; it takes her a while to fall asleep and she wakes 2x/night on
average to pee. (Stops fluid intake around 8pm each night). She can be distracted
by making lists in her head regarding past, present and future as well as minor
obsession with “doing the right thing” for self and others. Part of her difficulty
sleeping is that her schedule doesn’t permit her to sleep the hours she prefers (2am9pm) so she uses an alarm clock and feels unrested upon waking (6am).
Client sips water throughout the day, drinking an average of 64oz . She reports that
she urinates all the time and that the urine is clear or close to clear in color. And
although she reports that she “feels pretty quenched” she will frequently pee before
leaving her house in the morning and arrive to work feeling the need to urinate
again, which may only be 10 minutes later. She also says that she doesn’t feel fully
voided. No history of UTIs or painful/burning upon urination.
Client reports sensitivity to changes in temperature; that her hands and feet will be
freezing cold in the winter-time and that her veins will tend to pop out and swell
during warm weather. Hands swell in heat. Skin becomes “worse” in heat and
humidity with increase in “bumps” and be oiler. Client generally prefers cold over
hot. Muscles store tension easily (esp bisepts and neck) Tends to pull muscles in her
back.
28 day menses cycle. Scant, 2 days of bleeding for the past 10 years, down from 3
days. Starts red with no clotting. She experiences some swelling in her breasts and a
little moodiness premenstrual with little to no experience of cramping (1x/year mild).
Menses is not a disturbing experience.
Diet is well rounded and has variety. It includes ample fruits (berries) and
vegetables. Sweet tooth causes client to indulge in daily desserts (usually in the form
of a baked good). She also may avoid “rich” foods because they “make her feel
terrible”. My impression was that she feels heavy and uncomfortable after eating
greasy foods and that she avoids them. My impression was that she thinks greasy
foods make everyone feel bad and everyone should avoid them, although this may
point to some insufficiency of liver function. She practices intermittent fasting
1x/week. Whole grains in diet in addition to refined carbs. Some use of cooking with
olive oil (her favorite fat).
Initial constitutional assessment was imbalance between water and fire, and some
interaction between the two. Excess heat (potentially coming from dryness) seen in
her preference for cold over heat, tendency to become irritated in hot weather and
the redness at the tip of her tongue. Some suggestion of Pita from relief felt through
exercise. Water element is suggested from the fluid imbalance seen in edema,
history of lymphatic insufficiency, frequent urination and dry tongue. Other notable
phases are wood related to liver function, issues with tendons and ligaments and
muscular tension. Potential tension/stagnation in Liver. She also gave the impression
of “brewing beneath the surface” so to speak, or perhaps the feeling that she works
to present everything as “ok”. Also worth noting is the Earth element seen in sweet
tooth and tendency to worry/want the best for others.
Initial
physiological
circulation/Lymphatic
assessment
weakness
would
show
(decreased
some
liver
venous
function,
insufficiency/poor
family
history
of
cardiovascular challenge, sugar consumption, being on feet all the time and tension
in the musculature). This insufficiency looks like edema, varicosities, swollen hands
and feel in the heat and frozen hands and feet in the cold. Lymphatics may be a lifelong area of weakness. Liver function is diminished/burdened and seen in skin
rashes, tension, poor circulation of blood and trouble digesting fats.
Initial goals included: support liver function, decrease sweet tooth, increase
circulation, support lymphatic function, support cardiovascular system, decrease
tension (improve sleep), decrease edema and decrease stress.
Herbal
Actions:
Hepatic/bitter,
circulatory
stimulant,
lymphatic,
astringent,
cardiovascular tonic, adaptogen, nervine (mild/relaxant), anti-inflammatory.
There were 3 initial formulas. The first was a tonic 15ml (1.5tsp BID) and included 5
parts Hawthorne, 4 Dan Shen, 3 Schisandra and 2 Prickly Ash. Second was to be
taken during acute edema and was comprised of 2 parts cleavers, 2 parts Red Root
and 1 part Horse Chestnut, 5ml BID. Also included was a tea totally 5g/day this
included 2 parts Dandelion Leaf, 2 parts Linden, 1 part Peppermint and 1 part Tulsi.
Last piece of the protocol was a bitter formula to be taken in the evening before
dinner or afterwards in an effort to begin the wind down process as well as reduce
the sweet craving some through the bitter taste. This formulas was 2 parts
Dandelion root, 1 part Mugwort, 1 part Chamomile and 1 part Lavender to be taken
5ml prn.
Hydrotherapy was suggested for supportive therapy and dietary suggested included
1/2c of blueberries daily, increasing garlic in her diet and eating more greens to
decrease sugar cravings. Also to switch to saturated fats for cooking and to reserve
olive oil for dressings.
Follow-up concerns were to ask into blood pressure, cholesterol levels and if she is
experiencing any heart palpitations. Also questions regarding blood sugar levels
(tingly feet? Vision?) And if she has had her thyroid levels tested in recent history or
to suggest such tests in the future because of family history.
Client returned for a follow-up visit on September 3rd of the same year. She disclosed
that she had been very compliant and followed the protocol completely since
receiving the formulas and had refilled them twice. (yay!) She reported that during a
gym class she found herself in a kneeling position she had otherwise been unable to
achieve and she accounted her success to the herbs. She also said that her eyes are
a little blurry in the morning and increasingly so. She spoke of worry about a mole
on her husband and I encouraged her to make an appointment at the dermatologist
for him. Her tongue was slightly less swollen looking though otherwise the same and
pulses the same.
I want to keep an eye on the client with Dan Shen because of her scanty periods. 2
ml of Dan Shen was added to the tonic formula to help build blood, Yin and provide a
bit more antispasmodic action. New formula as of September 13th 2013 is: 5 parts
Hawthorne, 4 parts Dan Shen, 2 parts Schisandra, 2 parts Prickly Ash, 2 parts White
Peony. Other formulas remained the same. No further contact with client at this time
as she lost access to her car and was having trouble getting to the clinic. Will be in
touch through email shortly.
Health Access Issues
Emer McKenna
Migrant workers in Vermont face a variety of challenges when it comes to accessing
health care. Firstly, many agricultural migrant workers in Vermont have not arrived through
official channels and therefore lack the proper documentation to work in the United States. 1
There are programs that allow for migrant workers to enter the United States legally, but
few permits are given out (400 for the entire state of Vermont) 2, and they have stipulations
which allow them to be given only to laborers who are both migrant AND seasonal. 3
In
4
Vermont, the largest industry employing migrant workers is dairy . These jobs are yearround, so these H2-A visas are not available to workers in this field. 5
Lack of
documentation prevents workers from accessing state programs such as VHAP or
Catamount, which are available to residents and foreign workers with visas. 6
A lack of documentation also puts workers at risk of deportation by US Immigrations
and Customs Enforcement (ICE), a department of Homeland Security. 7 To avoid potential
exposure to law enforcement, some workers avoid leaving their farm at all for any reason. 8
Of course, some workers do leave their farms to buy groceries, visit nearby friends or family
members, and to visit doctors. 9
Quite recently, outside of a dental clinic in Richmond, a
migrant worker was stopped by local authorities for “suspicious activities” and subsequently
turned over to ICE. 10
It can be extrapolated, then, that state and local police or
immigration officials may target health clinics and other organizations that serve migrant
workers and engage in racial profiling to apprehend undocumented foreign nationals.
Though some districts in Vermont have passed Bias-free Policing Policies 11 racial profiling is
still considered a problem in much of Vermont. 12 Vermont has been named by the Mexican
Consulate in Boston as the state with the most severe immigration enforcement in the
Northeast 13 and fear of deportation was ranked highest among barriers to receiving health
care in one study which surveyed 70 workers in northern and central Vermont. 14
The other most frequently reported barriers to health care were lack of insurance
(discussed above) and high cost of care 15
16
.
Most migrant workers who leave their
countries of birth to work in the US plan on coming for a short time, working as much as
possible, saving money, supporting family members abroad, and then returning to their
countries. 17 Therefore, many workers are reticent to spend money on health care unless
facing a serious medical condition, in which case workers often return to their home country
to receive care. 18 When workers were asked if they would be more likely to seek health
care if they had access to a free or sliding-scale community clinic, one hundred percent of
those surveyed said yes. 19
Other frequently reported issues for migrant workers in Vermont are transportation
and language barriers. 20
21
Population Demographics
An accurate estimate of the number of migrant farm workers in Vermont is difficult
to attain because of issues such as obtaining access to marginalized and vulnerable
populations, the desire of these populations to avoid interaction with government officials
(or those perceived as such), and the inherent fluctuation of migrant populations due to
political or economic factors. 22 That said, the most frequently cited figures come from the
Vermont Agency of Agriculture, who commonly cite between 2000 and 3000 workers 23 and
from the Vermont Migrant Education Project who estimated 1500 workers in Vermont in
2009. 24
A study conducted by the Vermont Department of Health in 2007 cited a total
migrant worker population of 2500, 1200 of whom resided in Franklin, Grand Isle, and
Addison Counties. 25
Compatibility with the Clinic
A number of historic influences have combined to create the modern cultural makeup of Mexico and Central America.
The ancient Maya 26, Aztecs 27, conquistadores from
Europe 28, and Africans brought to the region as slaves, 29 have all contributed to the pool of
knowledge which informs modern day traditional medicine of Mexico and Central America.
This is significant since most migrant farm workers in Vermont come from Mexico or
Guatemala, with an increasing number migrating from indigenous communities in southern
Mexico. 30
The use of traditional herbalists ([email protected] 31), healers ([email protected]), midwives
([email protected]), bone setters ([email protected]), and massage practitioners (sobadores) is
common, in both indigenous and non-indigenous communities in Mexico and immigrant and
native-born populations in the United States. 32
33
34
.
Even without the services of an
herbalist, people of Latina/o or Chicano/a heritage in the United States and Mexico
frequently use herbs such as peppermint, cinnamon, chamomile, eucalyptus, aloe vera,
yarrow, et al for various complaints. 35
The most commonly reported health issues of
migrant workers in Vermont have been skin problems such as dermatitis and fungal
infections of the feet, soreness and/or injuries caused by repetitive stress and hard physical
labor, respiratory conditions, gastrointestinal issues, dental concerns, and vision problems. 36
Also mentioned were high blood pressure, parasites, anxiety, and depression. 37
38
Migrant
farm workers are an underserved population, in terms of health care, in the United States in
general, and Vermont, in particular. 39
They are also a population under a significant
amount of stress, due to long hours, hard labor, social/cultural isolation, fear of lawenforcement authorities, and exposure to chemicals and other occupational hazards. 40 Our
clinic could be an incredible resource to these populations, and be an excellent health care
adjunct, capable of addressing many commonly reported health complaints.
Issues for the Clinic at VCIH
In order for the clinic to become more of an open resource to migrant farm workers
in the area, there are certain issues that will need to be addressed.
Matters involving
interpretation will require significant attention. Intake documents will need to be translated
into Spanish and once these documents are filled out by the client, a practitioner may need
assistance in comprehending them.
Setting appointments may also be an issue for our
clinic if there are not bilingual staff members answering the phones. Since interpretation
will take away from the actual time spent in conversation with a client, the length of
appointments may also warrant consideration.
For the purpose of this research paper, extensive enumeration of potential clients
within our service area was not conducted. Due to the transience and immigration status of
migrant farm workers, these populations are not particularly visible or easily accessible to
outsiders.
If the clinic decides to go forward this project, outreach will be conducted to
both workers and their employers. I believe this process will give a much more concrete
estimate of the number of people our clinic could look forward to serving.
There are still many questions in my mind, regarding transportation, length of travel,
timing of appointments, safety from immigration, and the efficacy of serving clients in
Montpelier, Burlington, or elsewhere.
I believe the connections made with nearby
communities through outreach would greatly help illuminate the best ways to provide herbal
resources to migrant workers in Vermont.
1
Buskey, T., Ed. (2005). VT Farm Bureau Dairy Industry Labor Survey - Final Results. Richmond, VT, Vermont
Farm Bureau.
2
Chappelle, D. and Baker, D. (2010). Migrant Worker Health Needs Assessment: Central and Northeastern
Vermont. Prepared for Bi-State Primary Care Association. University of Vermont, Burlington, VT
3
Department of Labor (2010) Employment Law Guide. Website: http://www.dol.gov/compliance/guide/taw.htm Accessed February, 2012.
4
Wilson Ring, Vermont Dairy Farms Count on Illegal Immigrants, Associated Press, May 13,
2009, available at http://www.immigrationworksusa.org/uploaded/file/051309Vermontdairyfarmscounton
illegalimmigrants.pdf.
5
Id., at 3.
6
Ona, F. (2007). Assessing the Health Status, Health Care Needs, and Barriers to Care for Migrant Farm Labor in
Franklin, Addison and Grand Isle Counties 2006. Burlington, VT, VT Department of Health.
7
Wilson Ring, Vermont Dairy Farms Count on Illegal Immigrants, Associated Press, May 13,
2009, at 2, available at http://www.immigrationworksusa.org/uploaded/file/051309Vermontdairyfarmscounton
illegalimmigrants.pdf.
8
Id, at 2.
9
Ibid
10
Cohen, M., The Ethnomedicine of the Garifuna of Rio Tinto, Honduras, Ethnomedicine Quarterly.
11
Notably Burlington and Middlebury. For an example see: Burlington Police Department, Department Directive
01-­DD08.03, Bias Free Policing, Updated May 19, 2010
12
Reed, Curtis Jr. (2009). Racial Profiling In Vermont: Briefings before the Vermont Advisory Committee to the
United States Commission on Civil Rights. Vermont State Advisory Committee, Montpelier, VT.
13
Flowers, J. (2007) Views on Migrant Workers Discussed. Addison Independent: February 15, 2007.
14
Id, at 2.
15
Ibid
16
Id, at 6.
17
Id., at 2.
18
Id., at 2.
19
Ibid.
20
Id., at 2.
21
Id., at 6.
22
Id., at 2.
23
National Agricultural Statistics Service (2010) Vermont Agricultural Overview Factsheet. Website:
www.nass.usda.gov/statistics_by_state/Vermont. Accessed February, 2009.
24
Shea, Erin, S. (2009). Are Apples More Important than Milk? Migrant Labor Turnover among Dairy Farm
Workers: Insights from the Vermont Migrant Education Program. M.Ed Action Research, Leadership and Policy.
University of Vermont.
25
Id., at 6. They, however, did not cite their source for this figure.
26
Peren, Hugo (2007). Revival of Maya medicine and impact for its social and
political recognition (in Guatemala). The Health Systems Knowledge Network, World Health Organization
Commission on the Social Determinants of Health.
27
Sahagun, Bernardino de (1961-1981). Florentine Codex: General History of the Things of New Spain, Vol 10.
Translated by Arthur J.O. Anderson and Charles E. Dibble. University of Utah Press, Salt Lake City, Utah.
28
Ibid.
29
“You Can’t Jail Hope” video available at migrantjustice.net, accessed February, 2012.
30
2011 Assessment of the Eastern Stream of Migrant and Seasonal Farmworkers. Migrant Health Services,
Peekskill, NY.
31
The use of the “@” symbol is used here to signify that the word ending may be ‘a’ or ‘o’ depending on the gender
of the practitioner.
32
Mines, Richard (2010). California’s Indigenous Farmworkers: Final Report of the Indigenous Farmworker
Society to the California Endowment.
33
Carrillo, Frank R. (2008). The Practice of Pluralistic Medicine by Long-term Immigrant and Native-born
Mexican-Americans in Santa Ana, California: The Persistence of Traditional Medicine. University of Southern
California, Los Angeles, CA.
34
Grieshop, James I. Transnational and Transformational: Mixtec Immigration and Health Belief, 1997.
35
Id., at 32. This statement also reinforced by the personal experience of the author, from time spent travelling and
living in Mexico and Central America and from experiences working with indigenous and/or migrant communities
in the US.
36
Id., at 6.
37
Ibid.
38
Baker and Chapelle, in the qualitative results section of their report, emphasize that anxiety and depression must
not be overlooked, though they may be under-reported (due to cultural factors), as health issues of migrant
farmworkers. Id., at 2.
39
Hansen, Eric and Martin Donahoe. Health Issues of Migrant and Seasonal Farmworkers, Journal of Healthcare
for the Poor and Underserved, Vol. 14, Issue No. 2, July, 2001.
40
Id., at 2 and 6.
Why You Should Chill Out:
Stress Hormones Affecting Endogenous
and Exogenous Sex Hormones
Kelly McCarthy
I want to explore the interconnection between stress hormones and our endogenous sex
hormones. Humans have evolved to cope with life-threatening stress quickly and efficiently,
but these mechanisms can get out of balance when the stress is chronic or prolonged,
without a chance to recover and come back to a state of relaxation. I want to focus on what
the effects are when our bodies prioritizes making cortisol, a stress hormone, instead of
making our endogenous sex steroid hormones. I hope to work with trans* clients (including
those who choose to take exogenous sex steroid hormones) so first understanding the
body’s process regulating its endogenous sex steroids under stress is a key part of my
understanding.
The Hormone Cascade
The hypothalamic-pituitary-adrenal (HPA) axis controls our stress response via hormones.
The hypothalamus is considered the master gland, directing many life sustaining functions.
It secretes Corticotropin Releasing hormone (CRH) in response to stress, which stimulates
the anterior pituitary to release Adrenocorticotropic hormone (ACTH), which increases the
production and secretion of corticosteroids, most notably cortisol and aldosterone. When
cortisol is released from the adrenal cortex, it provides a negative feedback to CRH and
ACTH, telling both of them to decrease activity so less cortisol is produced. The smooth
function of these feedback loops are essential to regulated HPA activity.
As seen in the hormone cascade chart, all steroid hormones are derived from
cholesterol. Cholesterol converts to pregnenolone which can take one of two paths, to either
be converted to progesterone or DHEA. From progesterone, we primarily get cortisol,
although progesterone can convert to androstenedione (instead of cortisol) which can
convert to testosterone or estrogens . From DHEA, we first get androstenedione, which then
converts to testosterone and then estrogens.
Pregnenolone and progesterone are the places along the hormone cascade at which
the production of cortisol can be favored over that of the sex hormones. Evolutionarily,
surviving the stress of a given moment gets prioritized over the potential to make a baby in
the future. When people experience high levels of stress, be it physical or mental, the body
will use the pregnenolone or progesterone to make cortisol rather than making DHEA or
androstenedione. This prioritization of cortisol is one of the ways hypothalamic-pituitaryadrenal (HPA) axis dysregulation can manifest.
Cortisol and DHEA are measurable ways to assess level of stress in the body and
many studies are conducted assessing the ratio of cortisol and DHEA. Because cortisol and
DHEA act in the body to balance each other, when blood levels of one are high, the other is
low. DHEA and cortisol have an inverse relationship. I will look at their physiological effects
and some of their pathophysiological effects when they are out of balance.
Cortisol is a glucocorticoid steroid hormone, released from the adrenal cortex in
response to stress and low blood glucose levels. Its primary functions in the body are to
suppress the immune system, metabolise macronutrients, and increase blood glucose levels
through gluconeogenesis. Cortisol uses two types of receptors, glucocorticoid and
mineralocorticoid. The
glucocorticoid
receptors have less binding
affinity, and
the
mineralocorticoid have more. Because plasma levels of cortisol have not only circadian
fluctuations throughout the day, but can also spike in response to stress, both receptor
systems ensure that cortisol can be fast acting (glucocorticoid receptors) or slow acting
(mineralocorticoid receptors), depending on need. “Under pathological conditions, for
example, severe major depression or Cushing's syndrome, continuing corticosteroid
hypersecretion
leads
to
overexposure
of
GRs
(glucocorticoid
receptors)
and
MRs
(mineralocorticoid receptors) which, in turn, are down-regulated.” (Holsboer). This offers
one explanation of how having chronically high plasma levels of cortisol can disrupt the
negative feedback loops that regulate our stress response.
Cortisol is kept in balance by DHEA-S’s antiglucocorticoid activity. DHEA-S is the
most abundant circulating steroid in the body, produced by the adrenals. Testing serum
levels of DHEA-S is one way to test for adrenal dysfunction, as a progression towards
adrenal fatigue is characterised by the inability of the adrenals to produce adequate DHEAS. The sulfate group (-S) can get removed to create DHEA, and DHEA can have the sulfate
group added back on the create DHEA-S.
DHEA functions primarily as a metabolic
precursor to testosterone and estrogens; there is limited information about its function in its
own right but it seems to act as a neurosteroid and to have mild androgenic properties
(Friess). Healthy levels of DHEA means healthy LDL levels, strong bone density, normal
sleep patterns, as well as positively affecting emotional mental health, memory, and
cognition. DHEA helps us recover from emotional and physical stress. It is sold as a
supplement with claims that it is the source of the fountain of youth. If only.
As the primary precursor to our endogenous sex hormones, DHEA is responsible for
converting into testosterone and estrogen. Testosterone acts as an anabolic and androgenic
hormone in people of all genders, although it is circulating unbound to sex hormone binding
globulin (and therefore more readily available) at about a 7 times greater concentration in
people with testes. Testosterone increases muscle mass and strength, increases bone
density, acts as the precursor to DHT, which is responsible for secondary sex characteristics
like deepening voice, pubic, facial, and armpit hair, and adult body odor. It is also
responsible for the maturation of genitalia and plays a role in sexual arousal. Testosterone
inhibits alpha-2 receptor formation, which are adrenergic cell receptors that sense the
circulating epinephrine and tell the hypothalamus there is enough epinephrine circulating,
which stimulates lipolysis. So testosterone acts as a direct feedback inhibition of the
hypothalamic sympathetic discharge and inhibits fat storage. (Mitrovic)
Testosterone can be aromatized to three forms of estrogen - estrone, estradiol, and
estriol. Estrogens are responsible for female secondary sex characteristic, such as breast
development and are involved in the build up of the endometrial lining. They also have an
important role in healthy bone density, encourage fat stores, influence a healthy lipid
profile, protect vascular endothelium, affect blood coagulation. This is all to say these sex
steroids do have profound effects on our bodies other than activities related to reproductive
sex.
In order for there to be adequate plasma levels of DHEA from which to make these
sex hormones, there needs to be a healthy ratio of DHEA and cortisol. I will look at two
possible ways for cortisol and DHEA to get out of balance, first high cortisol/low DHEA, then
high DHEA/low cortisol.
Having high levels of cortisol circulating in the blood raises blood sugar, and high
levels of blood sugar over prolonged periods of time will lead to insulin resistance by
downregulating the GLUT-4 insulin receptor. The detrimental effects of insulin resistance are
beyond the scope of this paper, but it is directly implicated in some of the most prevalent
health
concerns
of
modern
American’s:
Type
II
Diabetes,
Metabolic
Syndrome,
atherosclerosis, heart disease, and obesity. Cortisol in the bloodstream also downregulates
the inflammatory process by inhibiting IL-2 receptors on helper T-cells, which means the
interleukin 2 cannot produce as much Th2 response, leading to a Th1 dominant immune
response.. Th1 dominance is often expressed in auto-immune and high inflammatory
conditions. So prolonged high cortisol will have a negative effect on immune function.
The correlating low levels of DHEA have been implicated in a variety of medical
conditions, including rheumatic disease, cardiovascular disease, and immune system
disorders. (Imrich, 2002; Thijs, 2003; Chen, 2004; Dharia, 2004). Low DHEA is often seen
in people with clinical depression. (Zaluska). A 2013 study showed women with major
depression have lower levels of androgens (which are metabolites of DHEA), as compared to
the control group, and within the women with major depression , there were even lower
androgens if they had severe anxiety. (Oulis) Paradoxically, another 2013 study looked at
DHEA-S levels in women with PCOS as compared to women with PCOS and diagnosed with
either Major Depressive Disorder or Generalized Anxiety Disorder; the women with either
MDD or GAD had significantly higher levels of DHEA-S than those without these
psychological conditions. (Zaluska).
PCOS is a condition characterised by sex hormone
dysregulation in people with ovaries, and comparing these two recent studies illustrates the
interconnectedness (and complicatedness) of stress, DHEA, and sex hormones.
If cortisol levels stay high over a prolonged period of time, eventually the cortisol
producers - adrenals, ovaries, and testes, will not be able to keep producing adequate
amounts. Low levels of cortisol are often described as a flatline, where there is no cortisol
spike upon waking in the morning, people experience high levels of inflammation, low
immune function, and generally feel exhausted. Low cortisol levels will be seen with
corollary high DHEA. Elevated levels of DHEA have been observed in connection with obesity
and Type II diabetes, female hirsutism, and in people subjected to prolonged physical stress
(Krobath. Bergfield 2000.) There is a strong connection between PCOS and elevated DHEA
(Yildiz). These are also conditions associated with elevated levels of androgens, which
makes sense considering DHEA has mild androgenic properties and is the precursor to
testosterone and DHT. Elevated levels of DHEA will inhibit cortisol binding, meaning cortisol
cannot aid in mounting an appropriate stress response.
All people should have testosterone and estrogens acting in their body. In people
with ovaries, about 60% of testosterone comes from the conversion of adrenal DHEA, the
remaining 40% is produced by the ovaries. DHEA is also estimated to contribute 70% of
estrogens before menopause and nearly all after menopause. Compare that to people with
testes, where about 95% of the testosterone is produced in the testes; the remaining five
percent is supplied by conversion of adrenal DHEA to testosterone. (McCormick) People
without testes, therefore, are more at risk for overworked adrenals, because the body needs
to use the adrenals for producing cortisol and sex steroids, and cannot rely on the testes to
produce testosterone. The adrenals will prioritize making cortisol over making sex
hormones, and an imbalance of these hormones has numerous, noted negative effects.
Considerations With Trans* Clients
This paper will look briefly at potential effects on the HPA axis in transpeople who are taking
exogenous
hormones.
Identifying
as
trans*
does
necessitate
cross-sex
hormone
replacement therapy, nor does it imply a gender binary, and many trans* people choose not
to take exogenous hormones. Because of the immense variables, this paper can only hope
to generalize some possible interactions between exogenous hormones and our bodies
stress hormones.
Mental Health and Stress
Much of the literature looking at trans* people focuses on people who choose to take
exogenous sex steroid hormones, although there is a significant amount of research looking
at LGB and queer people, which can include trans* people who are and are not taking
hormones.
There
is
much
research
documenting
that
trans*
people
experience
disproportionately high levels of stress, depression, anxiety, and suicide attempts.
(Mustanski 2008. Nuttbrock 2002.)
A 2011 study of nearly 200 trans patients reported
61% of them to experience depression and anxiety before beginning cross-sex hormone
treatment. (Gomez-Gil)
In 2013, 70 transsexual patients had their cortisol awakening
response measured before beginning cross-sex hormone replacement -- overall, their
cortisol levels were higher than non-trans patients. (Colizzi). According to a 2001 British
study,
“socio-economic and psychosocial handicaps are probably central inducers of
hyperactivity of the hypothalamic-pituitary adrenal (HPA) axis” (Björntorp). Knowing this,
and not because trans* identity is one to be pathologized, a practitioner would be wise to
inquire if a trans* patient experienced or perceived a high level of stress (whether currently
or in the past), by virtue of being trans* in a gender-binary world.
Exogenous Hormones
Female-to-Male Transmen
Transmen who choose to take testosterone can opt for a range of doses, and
commonly patients are aiming for similar circulating blood levels as cismen. I have looked
at studies looking at the effects of testosterone in cismen to know how testosterone and
cortisol possibly interact under “normal” circumstances.
In trials involving cismen, high cortisol inhibits the effects of T on target tissues and
also downregulates androgen receptors. Chen et al. found “evidence that the opposing
physiological effects of the androgen and glucocorticoid hormones are due to the direct
physical interaction between their receptors at the transcriptional level,” From this, one
could extrapolate that even if someone is taking exogenous testosterone, if the cortisol
levels are high, the testosterone may not be able to bind to receptors and act on target
tissues.
There is also a concern with exogenous testosterone being aromatized to estrogen.
In general, “the conversion of androgens into estrogens is favored by a pro-inflammatory
environment.” (Edwards). So if someone is in a state of adrenal exhaustion with lots of
inflammation and they are trying to transition or maintain masculinity with exogenous
testosterone, it could be possible that the exogenous testosterone is getting aromatized and
not having the desired effect.
OB-GYN Nurse Practitioner Marcelle Pick focuses her practice on ciswomen with
adrenal fatigue. According to her literature, she sees a strong connection where postmenopausal (or post-hysterectomy) ciswomen have pathologically high DHEA and this high
DHEA makes imbalanced conversions either strongly towards testosterone overproduction or
creating a situation of estrogen dominance (Pick) Both overproduction of testosterone or
estrogen would have negative implication when someone is taken exogenous testosterone.
Male-to-Female Transwomen
Transwomen often will use an anti-androgen (such as spironolactone or finasteride)
to suppress testosterone and a form of estrogen (oral, injectable, or transdermal) to
encourage feminization. Spironolactone competitively binds with aldosterone, increasing
testosterone clearance and estradiol production. It also blocks the conversion of potent
androgens to weaker ones at target tissues. It has been shown in multiple studies that the
administration of estrodiol in ciswomen leads to elevated cortisol. Studies have examined
the effect of exogenous estradiol in post-menopausal ciswomen on cortisol levels. In 2008,
2mg estradiol administered daily (which is a common dose for transwomen) to postmenopausal women was found to increase plasma levels of cortisol. (Edwards) A Mexican
study showed administering estrogen to post-menopausal women increased DHEA and
ACTH, both of which were low because of hypoestrogenism. The authors hypothesized this
was because the estradiol was having a stimulating effect on the pituitary gland. (Fonseca).
Our body’s propensity to prioritize cortisol combined with a high stress culture means
HPA dysregulation is all too common. It is clear that endogenous sex hormones interact with
the HPA axis, although we still have a limited understanding here. People taking exogenous
hormones, whether to present in the world with a certain gender identity or to regulate their
menopause, especially want to modulate their stress so at the very least, their bodies
endogenous sex hormones and stress hormones are functioning as smooth as possible. It is
in optimal health that our body can best take in foreign substances (be it food, drugs, or
hormones) and process those substances to use or pass through.
Works Cited
Annagür, Bilge Burçak, et al. "Biological correlates of major depression and generalized
anxiety disorder in women with polycystic ovary syndrome." Journal of psychosomatic
research (2013).
Bergfeld, W.F. (2000). Hirsutism in women: Effective therapy that is safe for long-term use.
Postgrad Med 107(7),93-4
Brownlee, Kaye K., Alex W. Moore, and Anthony C. Hackney. "Relationship between
circulating cortisol and testosterone: influence of physical exercise." J Sports Sci Med 4
(2005): 76-83.
Colizzi, M., Costa, R., Pace, V., & Todarello, O. (2013). Hormonal Treatment Reduces
Psychobiological Distress in Gender Identity Disorder, Independently of the Attachment
Style. The journal of sexual medicine.
Chen, Sei-yu, et al. "Androgen and Glucocorticoid Receptor Heterodimer Formation A
POSSIBLE MECHANISM FOR MUTUAL INHIBITION OF TRANSCRIPTIONAL ACTIVITY." Journal
of Biological Chemistry 272.22 (1997): 14087-14092.
Cumming, D. C., M. E. Quigley, and S. S. C. Yen. "Acute suppression of circulating
testosterone levels by cortisol in men." Journal of Clinical Endocrinology & Metabolism 57.3
(1983): 671-673.
Björntorp, Per, and
Roland Rosmond. "The metabolic syndrome—a neuroendocrine
disorder?." British Journal of Nutrition 83.S1 (2000): S49-S57.
Colizzi, Marco, et al. "Hormonal Treatment Reduces Psychobiological Distress in Gender
Identity Disorder, Independently of the Attachment Style." The journal of sexual medicine
(2013).
Edwards, Kate, and Paul Mills. “Effects of estrogen versus estrogen and progesterone on
cortisol and interleuken-6.” Maturitas. 2008 December 20; 61(4): 330–333.
Fonseca,
Eugenia,
et
al.
"Hormone
replacement
therapy
increases
ACTH/dehydroepiandrosterone sulfate in menopause." Maturitas 39.1 (2001): 57-62.
Friess E, Schiffelholz T, Steckler T, Steiger A (December 2000)."Dehydroepiandrosterone--a
neurosteroid".
European
Journal
of
Clinical
Investigation.
30
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3:
46–50.
doi:10.1046/j.1365-2362.2000.0300s3046.x.PMID 11281367
Gómez-Gil, Esther, et al. "Hormone-treated transsexuals report less social distress, anxiety
and depression." Psychoneuroendocrinology 37.5 (2012): 662-670.
Holsboer, Florian. “Neuroendocrinology of Mood Disorders.” Neuropsychopharmacology: The
Fifth Generation of Progress (2002)
Krobath, P.D., Salek, F.S., Pittenger, A.L. et al. (1999). DHEA and DHEA-S: A review.
J Clin Pharmacol 39, 327-48
McCormick, Kathleen. “DHEA: Surviving and Thriving” Connections: An Educational
Resources of Women’s International Pharmacy. March 2012 (1).
Mehta, Pranjal H., and Robert A. Josephs. "Testosterone and cortisol jointly regulate
dominance: Evidence for a dual-hormone hypothesis." Hormones and Behavior 58.5 (2010):
898-906.
Mitrovic MD, Igor . “Introduction to the Hypothalamo-Pituitary-Adrenal (HPA) Axis.” UCSF
Biochemistry.
http://biochemistry.ucsf.edu/programs/ptf/mn%20links/HPA%20Axis%20Physio.pdf
Mustanski, Brian S., Robert Garofalo, and Erin M. Emerson. "Mental health disorders,
psychological distress, and suicidality in a diverse sample of lesbian, gay, bisexual, and
transgender youths." American Journal of Public Health100.12 (2010): 2426-2432.
Nuttbrock, Larry, Andrew Rosenblum, and Rosalyne Blumenstein. "Transgender identity
affirmation and mental health." The International Journal of Transgenderism 6.4 (2002):
97-03.
Oulis, Panagiotis, Vasilios G. Masdrakis, and Manolis Markianos. "Testosterone and
dehydroepiandrosterone sulfate in female anxious and non-anxious major depression."
International journal of psychiatry in clinical practice (2013): 1-4.
Pasquali, Renato, et al. "The Hypothalamic‐Pituitary‐Adrenal Axis Activity in Obesity and the
Metabolic Syndrome." Annals of the New York Academy of Sciences 1083.1 (2006): 111128.
Pasquali, R., et al. "Sex-dependent role of glucocorticoids and androgens in the
pathophysiology of human obesity." International Journal of Obesity 32.12 (2008): 17641779.
Pick,
Marcelle.
“DHEA
and
Adrenal
Imbalance.”
Women
to
Women
Clinic.
http://www.womentowomen.com/adrenal-health-2/dhea-and-adrenal-imbalance/
Sharma, Animesh, et al. "Gender determines ACTH recovery from hypercortisolemia in
healthy older humans." Metabolism 62.12 (2013): 1819-1829.
Tilbrook, A. J., A. I. Turner, and I. J. Clarke. "Effects of stress on reproduction in non-rodent
mammals: the role of glucocorticoids and sex differences." Reviews of reproduction 5.2
(2000): 105-113.
Yildiz, Bulent O., and Ricardo Azziz. "The adrenal and polycystic ovary syndrome." Reviews
in Endocrine and Metabolic Disorders 8.4 (2007): 331-342.
Zaluska, M. Janota, B. “Dehydroepiandrosterone in the mechanisms of stress and
depression.” Pyschiatra Polska (2013).
Some
reflections
on
action-based
classification of medicinal plants
Linden de Voil
For many contemporary herbal practitioners, the categorization of medicinal plants
according to action on the body can seem as common as the air we breathe; the
classification of a plant as astringent, expectorant, or vulnerary may be one of the first ways
we understand that plant and its role as medicine. This system is so familiar that we may
forget that classifying and applying herbs according to these action categories is just one
approach to their use - certainly one with many useful applications, but not without its
limitations.
We can gain some insight into the historical application of such classification by
looking at a partial history of terms applied to the common medicinal plant mullein
(Verbascum thapsus) within the Western European herbal tradition.
Although Dioscorides uses the classification astringent for other plants, he does not
apply it to mullein, which is listed as a specific remedy "for old coughs" and said to help with
the spitting of pus. i Hildegard of Bingen also suggests specific indications, recommending
Mullein for "one who is hoarse or has pain in his chest." ii
By the time of the electic
physicians we see a clear transition into use of categories of actions; mullein is classified as
a demulcent and anti-spasmodic, and a specific for cough with catarrh, iii as well as an
alterative. iv Maude Grieve's 1931 herbal highlights its "markedly demulcent, emollient and
astringent properties, which render it useful in pectoral complaints." v
Modern research on the uses of verbascum is limited. Contemporary herbalists
commonly continue to apply the same primary categorizations seen since the eclectic era
with varying emphasis on its demulcent, astringent and expectorant qualities. vi We often
see it listed as having a virtual parade of actions;
a quick glance into just one desktop
reference text lists twenty-one actions for mullein, ranging from alterative to yin tonic. vii
Some of these (antihistamine) may be specific enough to assist in applied use, though many
(anti-inflammatory) are extremely broad. This points to one of the potential shortcomings
of the action-based classification system: the application of an extremely long list of actions
for a single herb, which can quickly defeat its own usefulness, overwhelming any sense of
how the herb is most appropriately applied.
Jim McDonald offers one potential
clarification by dividing classes of action into foundational actions and secondary properties.
McDonald is not the only herbalist to offer an explanation of a subcategorical system.
Culpeper famously interpreted Galen's system of degrees in his 17th century herbal; viii
Hoffman offers another approach to primary and secondary uses, ix while Wood delineates a
system very similar to McDonald's, based on pathological tissue conditions and affinities to
specific organ systems. x
McDonald's foundational classes include astringent, demulcent, bitter, and nervine,
among others, while secondary actions are "those properties attributed to it that owe their
effect to one or more of the plant's primary actions," including categories such as antiinflammatory, expectorant, or lymphatic. By this system, we understand mullein to have
foundational astringent, demulcent, and relaxant action, with secondary actions including
expectorant, anti-inflammatory, and lymphatic qualities. xi
In addition to the sheer number of actions applied to any given plant, there may be
confusion about or overlap in meaning of some terms; the breadth of definition applied to
some terms of classification may be another limitation within an action-based organizational
system.
Expectorant herbs provide a relevant example here. Hoffman points out that the
term 'expectorant' itself is often "used somewhat loosely to refer in a general way to
remedies that 'do something' for the respiratory system," xii as do the terms 'pulmonary' and
'respiratory tonic,' although pharmacologically expectorants are "agents that promote
removal of mucus secretions from the lungs, bronchi and trachea." xiii Translations of
historical texts present their own challenges in this arena. To return to a previous example:
we read Dioscorides in translation to state that mullein helps with the spitting of pus. Does
this simply mean that it has expectorant qualities, and if so by what action? Might there be
alternative translations that suggest additional qualities, or more specific action?
As terminology continues to evolve with our understanding and interpretation of
herbal actions, there is at least one instance where we we encounter the problem of
significantly differing definitions for a single term, arising through shifting historical use.
Medical phytotherapist Kerry Bone argues against the use of the categories of 'relaxing' and
'stimulating' expectorants, equating them with antiquated divisions in which expectorants
"were formerly classified into stimulating and depressing groups, the former being supposed
to increase blood pressure and diminish secretion, the latter to lower blood pressure,
increase secretion and promote expulsion. These terms are now generally discarded." xiv
However, other contemporary herbalists continue to use these categorizations to
differentiate between those expectorants that facilitate increased mucosal secretion via
irritation of bronchioles or thinning of sputum, and those that act, via reflex, as demulcents
within the lower respiratory tract, simultaneously encouraging expectoration and loosening
mucous by production of less sticky sputum that effectively 'pushes' out stickier mucous. xv
Not
surprisingly,
increased
understanding
of
physiology
and
emphasis
on
pharmacology at the molecular level has shifted and complicated our understanding and
usage of the action-based classification system; again expectorants provide an interesting
lens to watch this development.
In 1927 Dr JA Gunn offered a system of categories of expectorants based on their
site of action: local, via central nervous stimulation, directly on vagal nerves, or directly on
secretory glands, and specified the drugs which have most action for each category, and for
certain clinical presentations. He explained, "This classification is not to be regarded as a
mere academic curiosity. It is upon differences in site of action that the superior suitability
of certain expectorants for certain actions largely depends." xvi
Subsequent research clarified the expectorant action of substances which trigger the
gastropulmonary reflex, inducing the preliminary stage of emesis, salivation, and thin
watery secretion from goblet cells in bronchial glands, and linked the action with saponincontaining plant extracts. xvii
Research also shows that expectorant herbs containing
saponins function to reduce the surface tension of the secretions, facilitating their
separation from the mucous membranes. xviii The demonstrated demulcent action of
mucilaginous polysaccharides, which form a protective coating lining the respiratory
mucosa, has been hypothesized to work through a similar reflexive action. xix
After tracing its historical legacy in traditional medicine, it comes as no surprise that
mullein contain both saponins xx and polysaccharides. xxi By comparing the biomedical,
evidence-based arc of classification with the action-based system of traditional herbalist
McDonald, we arrive at some similar conclusions.
This leads us finally to a major strength
of the action-based classification system, which makes it so useful at this particular moment
in time: the ability to help bridge traditional uses of herbs with the language and paradigm
of orthodox western medicine.
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Medicines. Austin TX: American Botanical Council, 1998. Web. American Botanical Council.
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"Phytotherapy for the Lower Respiratory System," Townsend Letter for
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Bylka, W., I. Matławska, and E. Witkowska-Banaszczak. "Expectorant herbal medicines in
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Culpeper, Nicholas.
Culpeper's Complete Herbal.
Glenwood, IL: Meyerbooks 1990. 376-
380.
Dioscorides. The Herbal of Dioscorides the Greek (De Materia Medica.) N.p, n.d.
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Henriette's Herbal Homepage. Feb 11 2013.
Felter, H.W. and John Uri Lloyd. "Verbascum." King's American Dispensatory. N.p:1898.
Web. Henriette's Herbal Homepage. Feb 11 2013.
Gunn, JA. British Medical Journal, Nov 26, 1927. Web.
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71 (1958): 417-424.
Hoffman, David. "Expectorants." Web. Healthy Net. Feb 14 2013.
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ii
Permeability Matters:
A Primer on Leaky Gut and Related Autoimmune Conditions
Kelly McCarthy
Clinical herbal practitioner, Betzy Bancroft, relates that often people who come to the
VCIH clinic are people with auto-immune conditions for which western medicine does not
offer promising treatments. (Bancroft 2013) According to herbalist Paul Bergner, primitive
people did not suffer from auto-immune conditions with the same frequency that modern
people do. (Bergner 2001) Current research is showing the connection between lack of gut
health and many auto-immune conditions. If looking at the human body as a microcosm of
the macrocosm, one can see that as our external ecosystem is seriously struggling because
of resource extraction, overuse, and factors too various to list for the scope of this paper,
the internal ecosystem of our gut is in a state of disharmony for many people and autoimmune conditions are often seen in clinic. Herbal medicine has an important place in the
intervention and prevention of leaky gut and the related auto-immune conditions.
The epithelial cells in the gut serve multiple functions: they create a protective
barrier and they regulate the exchange of contents of the lumen (the external environment)
with the inside of the body. (Silverthorn 2001). As a protective barrier, the cells are
responsible for keeping out bacteria, pathogens, parasites, and other antigenic substances.
But simultaneously the cells must allow nutrients from food and drink to pass from the
lumen to the bloodstream. The inherently “leaky” junctions between these cells allow
solutes across the barrier according to their size and charge. (Shen 2006) The lumen of the
gut is also home to the largest concentration of mucosal cells in the body, known as the
Mucosa Associated Lymphoid Tissue (MALT), which plays a major role in immune function.
It is estimated about 80% of lymphocytes are located here. (Silverthorn 2001) MALT
constitutes sites of great importance for both innate and acquired immune functions.
(Turner 2009) If the mucosa is damaged, so is the body's ability to differentiate self from
non-self and when the body can’t differentiate self from non-self, immune cells can attack
healthy self. (Fassano 2005)
Ideally, the intercellular junctions are tight enough to keep antigenic material from
passing through into the bloodstream. Many things in the modern world have been shown to
irritate the lining of the gut, causing small perforations and therefore creating a larger
junction for antigenic material to pass through. Some known irritants are, according to
medical herbalist and Ayurvedic practioner Todd Caldecott, “antibiotics, alcohol, caffeine,
parasites, pathogenic bacteria, peroxidized fats, some food preservatives and food
additives,
enzyme
deficiencies
(e.g.
celiac
disease,
lactose
intolerance),
NSAIDs,
corticosteriods, refined carbohydrates, oral contraceptives and mycotoxins (fungal toxins
found in stored grains and dried fruit)” (Caldecott 2000) Damage to the lining of the gut
creates wider junctions and damages mucosal immune tissue.(Lichtenberger 2012) When
antigens are allowed by an overly leaky gut to pass from the lumen into the bloodstream,
an immune response is initiated. The immune system creates antibodies to these antigens.
(Caldecott 2000) Unfortunately, many tissues possess antigens that are similar enough to
these exogenous antigens that the antibodies that have been created attack the self.
Hence, the pathogenesis of an autoimmune condition. (Bergner 2001)
It is more obvious to see how a damaged gut epithelium could lead to digestive
system related auto-immune conditions such as Crohn’s disease and Ulcerative Colitis. (Ma
1997; Zanjanian 1976)
Research has shown a link between leaky gut and many non-
gastrointestinal related auto-immune conditions including multiple sclerosis, ankylosing
spondylitis, Behcet's syndrome, diabetes, and rheumatoid arthritis (Orlando 2002; De
Keyser 2002; Fresco 2001; Vaarala 2002; Malosse 1992). To see the mechanism of action,
take for example Diabetes mellitus. According to researchers de Kort, Keszthelyi, and
Masclee, the increased immune reaction caused by the leaky gut leads to the destruction of
beta cells in the pancreas which can lead to increased cytokine production which can lead to
insulin resistance. (de Kort et al 2011).
It could be said that auto-immune conditions are a product of the modern world and
its associated ills. It would behoove people suffering from auto-immune conditions to look to
more primitive times for potential solutions: diets high in fiber and exercise, eating bitter
foods, avoiding toxic substances like pharmaceutical drugs. Herbal medicine can be useful
because so many plants can lower inflammation, soothe the gut lining, balance the immune
system, and tone epithelial tissue. Because there is limited historical herbal treatment
protocols for these specifically modern conditions, auto-immune conditions exemplify the
need to combine an energetic approach with current medical research.
Works Cited
Bergner, Paul. “Gastrointestinal: Leaky Gut, Molecular Mimickry, Microchimerism, and
Autoimmunity.” Medical Herbalism 9(4):14-17
Caldecott, Todd. "Leaky gut syndrome." http://www.toddcaldecott.com/leaky_gut.html
(2006).
Cuvelier C, Barbatis C, Mielants H, De Vos M, Roels H, Veys E. 1987. Histopathology of
intestinal inflammation related to reactive arthritis. Gut. Apr;28(4):394-401
de Kort, S., D. Keszthelyi, and A. A. M. Masclee. "Leaky gut and diabetes mellitus: what is
the link?." Obesity Reviews 12.6 (2011): 449-458.
6.
Fasano, Alessio, and Terez Shea-Donohue. "Mechanisms of disease: the role of intestinal
barrier function in the pathogenesis of gastrointestinal autoimmune diseases." Nature
clinical practice Gastroenterology & hepatology 2.9 (2005): 416-422.
Fresko, I., et al. "Intestinal permeability in Behçet's syndrome." Annals of the rheumatic
diseases 60.1 (2001): 65-66.
Lichtenberger, Lenard M., et al. "Insight into NSAID-induced membrane alterations,
pathogenesis
and
therapeutics:
Characterization
of
interaction
of
NSAIDs
with
phosphatidylcholine." Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of
Lipids (2012).
Ma, Thomas Y. "Intestinal epithelial barrier dysfunction in Crohn's disease." Proceedings of
the Society for Experimental Biology and Medicine. Society for Experimental Biology and
Medicine (New York, NY). Vol. 214. No. 4. Royal Society of Medicine, 1997.
Malosse, D., et al. "Correlation between milk and dairy product consumption and multiple
sclerosis prevalence: a worldwide study." Neuroepidemiology 11.4-6 (1992): 304-312.
Orlando, Ambrogio, et al. "Gastrointestinal lesions associated with spondyloarthropathies."
World journal of gastroenterology: WJG 15.20 (2009): 2443.
Shen, Le, and Jerrold R. Turner. "Role of epithelial cells in initiation and propagation of
intestinal inflammation. Eliminating the static: tight junction dynamics exposed." American
Journal of Physiology-Gastrointestinal and Liver Physiology 290.4 (2006): G577-G582.
Silverthorn, Dee Unglaub, and Bruce R. Johnson. Human physiology. Pearson/Benjamin
Cummings, 2001.
Turner, Jerrold R. "Intestinal mucosal barrier function in health and disease."Nature Reviews
Immunology 9.11 (2009): 799-809.
Vaarala, Outi. "The gut immune system and type 1 diabetes." Annals of the New York
Academy of Sciences 958.1 (2002): 39-46.
Vaarala, Outi, Mark A. Atkinson, and Josef Neu. "The “Perfect Storm” for type 1 diabetes the
complex interplay between intestinal microbiota, gut permeability, and mucosal immunity."
Diabetes 57.10 (2008): 2555-2562
Yacyshyn, Bruce, et al. "Multiple sclerosis patients have peripheral blood CD45RO+ B cells
and increased intestinal permeability." Digestive diseases and sciences 41.12 (1996): 24932498.
Zanjanian, M. H. "The intestine in allergic diseases." Annals of allergy 37.3 (1976): 208.
Selecting native plants for a beneficial
insects garden
Denise Quick
The Community Teaching Garden (CTG) is a project of the Friends of Burlington Gardens
(FBG) whose goal is teaching organic gardening to adults. It is located at the Ethan Allen
Homestead in Burlington, Vermont, a site where there have been community gardens since
the1976 (Flint, 2007). In addition to the CTG, the Ethan Allen Homestead is currently the
location of 50 community garden plots and the Visiting Nurses Association’s Family Room
Garden (FBG, n.d.).
As gardens have been established at this site for over 35 years, there are also established
populations of garden pests. For example, during the summers of 2009 and 2010, there
was a noticeable population of Colorado potato beetles (Leptinotarsa decemlineata) on
solanaceous crops, especially potatoes, and relatively high populations of Mexican bean
beetles (Epilachna varivestis) on pole beans.
Damage from striped cucumber beetles
(Acalymma vittatumwas) was evident on cucurbits during the summers of 2009, 2010 and
2011, while significant impact from flea beetles (family Chrysomelidae) was seen on leafy
brassicas during the early summer in 2011.
As the CTG is an organic garden, cultural
methods are emphasized, and students picked pest insects from crops regularly during the
growing season. Use of ORMI-listed (Organic Materials Review Institute) pesticides has also
occurred at the CTG (personal observation). Additional pest control methods that support
the local ecosystem are desired at the garden.
In late summer 2011, the board of the
Winooski Valley Park District (WVPD), who manages the land where the CTG in located,
approved development of a beneficial insect garden. This garden is to be located on land
contiguous to the CTG garden (Yumi Jakobcic, personal communication, 28 Oct 2011).
Healthy populations of predatory and parasitoid insects are desirable in agricultural settings
because they feed on herbivorous pest insects during at least one life-stage. A review of the
literature by Fielder and Landis (2007a) reveals that plant foods are also important to these
insects. Adult parasitoid insects with access to nectar have shown increased fecundity or
length of life, and pollen resources are needed by some predatory insects to produce
mature eggs. Therefore, the availability of appropriate plant resources for beneficial insects
may reduce populations of pest insects in fields and gardens.
A number of non-native, annual plants are commonly recommended to support populations
of beneficial insects, but Fielder and Landis (2007a, 2007b) suggest there are advantages to
using perennial, native plants rather than non-native annuals. Native plants are adapted to
local environments, so may have a reduced likelihood of invasiveness.
It is likely that
perennial plants provide better overwintering habitats for beneficial insects, thus assisting in
establishing a more permanent community of beneficial insects.
Additionally, the use of
native plants can increase native biodiversity in a given area (2007a, 2007b).
Some plants that appear attractive to beneficial insects also attract pests. For example, in
Michigan Fielder and Landis (2007a) observed a high number of herbivorous Japanese
beetles (Popillia japonica) on common evening primrose (Oenothera biennis), a native
Michigan perennial. They also found a number of Phyllotreta spp. flea beetles, common
pests of brassica, on sweet allysum (Lobularia maritima).
So, although sweet allysum is
often recommended as a beneficial insect attractor, planting it near brassicas may increase
the pest load on those crops (2007a).
Research on an organic farm in California’s Central Valley compared insect occurrences in
hedgerows of native shrubs, native perennial grasses and weedy patches (dominated by
mustard and knotweed species) located between farm fields.
Over two growing seasons,
the levels of beneficial insects (both predators and parasitoids of pest insects) and pest
insects (herbivores on crop plants) were tracked. Researchers found a ratio of beneficials to
pest was approximately 4:1 on the native shrubs, approximately 1.5:1 in the perennial
grasses, and approximately 1:1.5 in the weedy patches.
The shrubs held the highest
numbers of beneficial insects while they were in bloom, suggesting that floral resources
were being used. (Morandin et al, 2011).
Another research study, performed at a research farm in Ingham County, Michigan,
compared the presence of beneficial and herbivorous insects on native perennial plant with
insects found on commonly recommended non-native annuals.
Forty-three native plant
species were tested, and 24 of those species were found to contain beneficial insect
populations at least as large as the populations found on the five non-native annuals. Some
of those 24 species also held a high population of pest insects, so were considered unlikely
to be useful as host plants for beneficial insects (Fielder and Landis, 2007a).
In the work of both Morandin etal (2011) and Fielder and Landis (2007a), the number of
beneficial insects observed on the native plants increased over the two years of the study,
suggesting that an established population of perennial plants can help to support a healthy
population of beneficial insects. As the research of Fielder and Landis (2007a) was
performed in Michigan, it has more applicability to Vermont (the current USDA Plant
Hardiness Zone Map shows Ingham County, Michigan as zone 5b, while Burlington, Vermont
is categorized as zone 5a (USDA ARS, 2012)). Table 1 lists plant evaluated by Fielder and
Landis (2007a) whose home range includes Vermont.
These plants should grow well in
Burlington, Vermont, and should provide floral resources thought out the growing season.
Table 1: Native plants found to be used by beneficial insects in Michigan (Fielder and Landis,
2007a), whose range includes Vermont (USDA NRCS, 2012).
Scientific Name
Common name (s)
Zizia aurea
Golden zizia or golden Alexanders
Angelica atropurpurea
Purplestem angelica
Coreopsis lanceolata
Lanceleaf tickseed
Ratibida pinnata *
Barnhart pinnate prairie coneflower
Spiraea alba
White meadowsweet
Monarda punctata *
Spotted beebalm
Silphium perfoliatum
Cup plant
Eupatorium perfoliatum
Common boneset
Lobelia siphilitica
Great blue lobelia
Symphyotrichum novae-angliae
New England aster
* The USDA Plants Database shows Vermont to be the far eastern edge of the ranges for
Ratibida pinnata and Monarda punctate.
Works cited
Fiedler, A. K., and D. A. Landis (2007a). Attractiveness of Michigan native plants to
arthropod natural enemies and herbivores. Environmental Entomology 36 (4): 751-765.
Fiedler, A. K., and D. A. Landis (2007b). Plant characteristics associated with natural enemy
abundance at Michigan native plants. Environmental Entomology 36 (4): 878-886.
Flint, Jim (2007). 35 Years and Still Growing: The history of Burlington Area Community
Gardens,
1972-2007.
Friends
of
Burlington
Gardens,
Burlington,
VT. http://www.burlingtongardens.org/BACG_History_1972-2007.pdf
Friends of Burlington Gardens (n.d.) Burlington Area Community Gardens (BACG)
sites. http://www.burlingtongardens.org/virtual.htm
Morandin, Lora, Rachael F. Long, Corin Pease, and Claire Kremen (2011). Hedgerows
enhance beneficial insects on farms in California’s Central Valley. California Agriculture 65
(4):197-201. http://www.escholarship.org/uc/item/1rh197qj
USDA
ARS
(2012)
USDA
Plant
Map. http://planthardiness.ars.usda.gov/PHZMWeb/#
USDA NRCS (2012) Plants Database. http://plants.usda.gov/java/
Hardiness
Zone
Heating or Cooling?
Amphotericity
of
Zingiber
officinale
and Capsicum annuum in Pyrogenesis
Robin Shapero
The famous nineteenth century herbalist Samuel Thomson refers to cayenne(Capsicum
annuum) as “being powerful only to raise and maintain that heat on which life depends,”
and ginger(Zingiber officinale) as “being the next best thing to raise the inward heat and
promote perspiration.”i These two plants do indeed have an undeniably “hot” taste to them.
That being said, many an herbal refers to them each as diaphoretic,ii and diaphoresis, or
sweating, while being a well-­‐known part of the fever process, is actually cooling to our
body.iii There are several ways in which plant constituents can insert themselves into the
complex process of the pyrogenic cascade to show marked effect, and I will explore just a
few of the ways these two plants can do so.
Fever, or pyrexia, is not simply a symptom of the disease process but a deliberate and
necessary action of our body’s internal defense system.1 Indeed, “fever is not failure of the
body to regulate temperature, rather, body temperature is being regulated at higher level
than normal.”iv The main regulator of temperature in the body is our hypothalamus. A
simplified view of the pyrogenic cascade is that “a trigger of the fever, called a pyrogen,
causes a release of prostaglandin E2 (PGE2). PGE2 then acts on the hypothalamus, which
generates a systemic response back to the rest of the body, causing heat-­‐creating effects to
match a new temperature level.”v
Arachidonic acid is the first rate-­‐limiting factor of the pyrogenic cascade. It is necessary for
the synthesis of prostaglandin E2(PGE2)vi, and constituents of ginger inhibit the metabolism
of arachidonic acid.vii This could cause more AA to be available for conversion to PGE2, and
therefore be helpful in raising a higher fever response. However, in pharmacological trials on
rats, ginger was actually shown to lower PGE2 levels.viii Cyclooxygenase(COX), an enzyme
that is responsible for the conversion of arachidonic acid into prostaglandin precursors, has
been shown to be inhibited by a breakdown-­‐constituent of ginger, shogaol, in certain isolated
tissues. COX inhibition is also the mechanism of
action by which common NSAIDs such as aspirinix and ibuprofenx effect their anti-­‐pyrexial
action.
These seemingly contradictory effects of ginger constituents on the body’s
biochemical activities are characteristic of the often amphoteric effects engendered by whole­‐plant use of medicinal herbs.
Capsaicin is the principle active constituent of cayenne and is what gives its characteristic
hot taste.xi Capsaicin, like certain ginger constituents, has also been shown to have an
amphoteric effect on fever and inflammation, although unlike ginger, this has been shown
to be dose-­‐dependent(this effect may well be dose-­‐dependent for ginger as well, but this
has not been studied).xii
A 1996 study stated that “…acute treatment at low concentrations
will produce an increase of IL-­‐l-­‐a.”xii An increase of interleukin-­‐1-­‐alpha(IL-­‐1a) causes
increased PGE2 production, which, as stated earlier, causes the hypothalamus to raise its
set point, inducing increased thermogenesis. vi Capsaicin has also, in low doses, “been
reported to increase thermogenesis by enhancing catecholamine secretion from the adrenal
medulla in rats, mainly through activation of the central nervous system.”xiii
This same
study, however, also shows that high doses of capsaicin over a longer time period
would increase nitric oxide production. NO is a potent vasodilator, causing increased blood
circulation to peripheral tissue, which effects lowered core body temperature and possible
increased diaphoresis. xiv Once again, a herb's amphoteric qualities are proved and ratified
by scientific data.
The contradictory indications of ginger and cayenne that are evidenced by the scientific
literature can be quite confusing. We as herbalists, though, have other resources than just
pure scientific data for our clinical applications of these two plants. Historic texts of herbal
practice give us many recommendations on how to use a phytomedicine appropriately.
Samuel Hahnemann, the originator of homeopathy, states that “if experience should show
that by medicines that possess similar symptoms to the disease the latter would be most
certainly and permanently cured, we must select for the cure medicines with similar
symptoms.”xv
Anyone who has ever eaten a hot pepper can attest to the fever-­‐like
symptoms that occur immediately thereafter. The Materia Medica of the Hindus, a collation of
thousands of years of traditional knowledge compiled from original Sanskrit works, declares
ginger to be “heating.”xvi In the Galenic system both ginger and cayenne are considered to
be “heating in the third degree.” That is, capable of causing and maintaining fever.xvii
The only conclusion that can be drawn from such a wealth of contrary information is that
ginger and cayenne can each, given the right dose, the right client, the right timing and the
right state of disease can assist in either abatement or enhancement of fever response. The
many factors involved and the importance of outcome necessitates further research and
experiential learning in this matter.
Resources Cited:
i Thomson, Samuel. New Guide to Health: Or, Botanic Family Physician. Columbus, OH:
Jarvis
Pike, 1833. Print.
ii
Ody, Penelope. The Complete Medicinal Herbal. London: Dorling Kindersley, 1993. Print.
iii "Sweating: MedlinePlus Medical Encyclopedia." U.S National Library of Medicine.
U.S. National Library of Medicine, n.d. Web. 19 Feb. 2013.
<http://www.nlm.nih.gov/medlineplus/ency/article/003218.htm>.
iv Conti, Bruno, et al. "Cytokines and fever." Front Biosci 9 (2004): 1433-­‐1449.
v Boulan, J. "Thermoregulation." Fever: Basic Mechanisms and Management. By Philip
A. Mackowiak. Philadelphia: Lippincott-­‐Raven, 1997. N. pag. Print.
vi Dinarello, Charles A., Silvia Gatti, and Tamàs Bartfai. "Fever: links with an
ancient receptor." Current biology 9.4 (1999): R143-­‐R146.
vii Mills, Simon, and Kerry Bone. Principles and Practices of Phytotherapy. N.p.: Churchhill
Livingstone, 2000. Print.1st edition
viii Chrubasik, S., M. H. Pittler, and B. D. Roufogalis. "Zingiberis rhizoma: a
comprehensive review on the ginger effect and efficacy profiles." Phytomedicine 12.9
(2005): 684-­‐701.
ix "Aspirin: Drug Information Provided by Lexi-­‐Comp: Merck Manual Professional."
Merckmanuals.com. Merck, Jan. 13. Web. 19 Feb. 2013.
<http://www.merckmanuals.com/professional/lexicomp/aspirin.html>.
x "Ibuprofen: Drug Information Provided by Lexi-­‐Comp: Merck Manual Professional."
Merckmanuals.com. Merck, Jan. 13. Web. 19 Feb. 2013.
<http://www.merckmanuals.com/professional/lexicomp/ibuprofen.html>
xi Hoffmann, David. Medical Herbalism: The Science and Practice of Herbal
Medicine. Rochester, VT: Healing Arts, 2003. Print.
xii Panossian, A., E. Gabrielian, and H. Wagner. "Dose-­‐dependent reversal effects of
Capsaicin on Interleukin-­‐1α production is associated with the metabolism of arachidonic acid
(leukotriene B< sub> 4</sub> and prostaglandin E< sub> 2</sub>) as well as nitric oxide
production in human leukocytes." Phytomedicine 3.2 (1996): 169-­‐174.
xiii Westerterp-­‐Plantenga, Margriet, et al. "Metabolic effects of spices, teas, and caffeine."
Physiology & behavior 89.1 (2006): 85-­‐91.
xiv Moncada, S. R. M. J., R. M. Palmer, and E. A. Higgs. "Nitric oxide: physiology,
pathophysiology, and pharmacology." Pharmacological reviews 43.2 (1991): 109-­‐142.
xv Hahnemann, Samuel. Organon of Medicine. Los Angeles: J.P. Tarcher, 1982. Print.
xvi Dutt, Udoy Chand., and George King. The Materia Medica of the Hindus, Compiled from
Sanskrit Medical Works. Calcutta: Thacker, Spink, 1877. Print.
xvii Wood, Matthew. "Greek Herbal Medicine: The Four Qualities and the Four Degrees."
Plant Healer Magazine (Spring 2012): n. pag. Web. 19 Jan. 2013.
<http://planthealermagazine.com>.
The
Use
of
Animal
Fats
in
Topical
Applications
Anna Powell
By the ninth edition of the US pharmacopeia (1916) lard had been replaced by
petrolatum in many of the official ointments and pastes. By the 1940’s it was common
thought that hydrogenated oils were better than lard as an ointment base due to the fact
that they are less susceptible to rancidity and more stable (Fiero, 1940). Before the
introduction of petroleum, most ointments were prepared from animal fats. The animal oils
used were numerous including, bear’s grease, dog fat, beaver fat, bat oil, eel oil, porpoise
oil, raccoon oil, rattlesnake oil and skunk oil. Lard, tallow, wool fat and goose grease were
more commonly used up until the early 1900’s (American Druggist and Pharmaceutical
Record, 1912).
The use of animal fats in medicine dates back to early human history.
Ancient Egyptian papyrus scrolls, from 1700 BC contain information on their medical
remedies of the time. Animal products appear in 42% of the prescriptions found on the
Ebers papyrus, and approximately 1/3 of these contain fat or grease, both of which were
likely used as vehicles. Animals that were mentioned included cows, geese, donkeys,
humans, cats, pigs, mice, goat, sheep, bats, hippopotami, antelope, dogs, fish , ostrich,
pigeons, pelicans, ravens, frogs, lizards, snakes, tortoises and crocodiles (Parkins, 2001). In
a review of medieval cosmetics, butter, bear, deer, goat, hen, and pig fat are referred to as
being used topically and in ointments (Cavallo, 2008). Wilhelm Fabry, a "surgeon-inordinary", published a book in 1614 on burns, De Combusionibus, which utilizes bear and
hen grease as a part of a formula to smooth and soften the scars (Naylor, 1996). In studies
done of the compositions of residues of apothecary jars from eighteenth century Italy and
Spain, traces of fatty material possibly belonging to a pig and also to a ruminant animal
were identified in samples (Saliu, 2011). In another study on the organic materials found in
a series of glass jars recovered from a Roman villa in the ancient town of Oplontis traces of
lipid based materials were detected, including beeswax, animal fat and vegetable oils.
These are thought to have been used for the macerations and/or enfleurage of plant based
materials (Ribechini, 2008). Records of Native American medicine cite the use of eagle fat,
raccoon grease, fish oil, hog grease, seal oil, pond frog fat, bear grease, fox oil, rattlesnake
fat and oil, skunk oil, goose fat, beaver fat, mountain goat fat, tallow and buffalo fat being
used as liniments and for the bases of ointments (Duke, 1986) (Josselyn, 1886) (Lloyd,
1951) (Moerman, 1998) (Youngken, 1925). The Noatak Eskimos used seal oil and whale
blubber in their topical ointments (Lucier, 1971). Sauer’s eighteenth-century colonial
American herbal mentions goose fat, butter, and lard as emollients. Goose fat is said to be
used in place of olive oil when it was too expensive or unavailable (Weaver, 2000).The
Eclectics used lard in ointments, cerates, liniments, laxative enemas, and as simple dressing
for ulcer and blisters (Cook, 1869) (Sayer, 1917) (Scudder, 1898) (Thomson, 1905) In the
Foxfire collections of traditions of the Appalachian peoples mutton tallow, ground hog oil,
goose fat, wild cat oil, and beef tallow are included in a list of home remedies for various
ailments (Fund, 1972).
Today in Poland, badger fat is sought after via the Internet and
press ads and is widely used as a salve for rheumatism by folk medicine practitioners
(Zalewski, 2007).
The penetration of materials from the outer world into and through the skin has long
been an object of discussion and investigation (MacKee, 1945). Wild (1926) experimented
with the absorption of various mercurials with different ointment bases, including lard,
hydrous wool fat and paraffin. Lard showed the greatest absorption, increasing with
prolonged rubbing. Hydrous wool-fat was absorbed to a greater extent than lard, but the
absorption of mercury was actually less than from lard ointment. The paraffin base
absorptions were always less than the lard bases (Wild, R.B., 1926). Soft- paraffin remains
on the skin as a protective layer for a considerable period and appears to be hardly
absorbed at all. From some hundreds of cases of impetigo, it was found that patients
treated with the paraffin base required on an average three weeks of treatment compared
with two weeks for those who had the same ointment, but with a lard base (Wild, 1911).
Petrolatum poorly penetrants the skin unless applied with friction (Sutton, 1908) (Sayer,
1917). The poorest vehicles are the ones which have been most frequently incorporated in
ointments, namely, petrolatum, mineral oil and lanolin (Laug, 1947).
When choosing a base for an ointment it is important to consider if the ointment is to be
absorbed by the skin, as seen with lard and hydrous wool fat, or if a protective coating is
desired where only the epidermal layer is affected, as seen with paraffin and petroleum
bases (Wild, 1911).
Sources:
American Druggist and Pharmaceutical Record, Volume 60(1912): 376-78.
Bamber, G. "Notes on some ointment bases." British Journal of Dermatology 52.1 (1940):
21-25.
Cavallo, P., et al. "The first cosmetic treatise of history. A female point of view."
International journal of cosmetic science 30.2 (2008): 79-86.Cobb, C. M. “Some medical
practices among the New England Indians and early settlers.” The Boston Medical and
Surgical Journal. CLXXVII.4 (1917): 97-105.
Cook,
W.
"The
physiomedical
dispensatory."
Online
version
http://www.
ibiblio.org/herbmed/eclectic/cook/BAROSMA_CREN ATA.htm (1869).
Duke, J. A. Handbook of northeastern Indian medicinal plants. Lincoln, MA: Quarterman
Publications, 1986.
Ellingwood,
F.,
and
J.
U.
Lloyd.
"American
Materia
Medica,
Therapeutics
and
Pharmacognosy. Volume II; 1919 Portland." 457-9.
Fiero, G. W. "Hydrogenated oil as an ointment base. II."
Journal of the American
Pharmaceutical Association 29.1 (1940): 18-23.
Fiero, G. W. "Hydrogenated castor oil as an ointment base. V. jellified ointments." Journal of
the American Pharmaceutical Association 29.11 (1940): 502-505.
Fund, Foxfire. The Foxfire Book: Hog Dressing, Log Cabin Building, Mountain Crafts and
Foods, Planting by the Signs, Snake Lore, Hunting Tales, Faith Healing, Moonshining. Vol. 2.
Anchor, 1972.
Goodman, Herman, and C. P. Wimmer. "Lard versus petrolatum in ointments and pastes for
dermatologic use." Archives of Dermatology 44.5 (1941): 914.
Josselyn, John. New England's rarities discovered. Applewood Books, 1986.
Laug, E. P., et al. "A study of certain factors governing the penetration of mercury through
the skin of the rat and the rabbit." Journal of Pharmacology and Experimental Therapeutics
89.1 (1947): 52-63.
Lloyd, G. K. “Interesting animal foods, medicines and omens of the Eastern Indians.”
Journal of the Washington Academy of Sciences 41.7 (1951): 229-235.
Lucier, C. V., J. W. VanStone, and Della Keats. "Medical practices and human anatomical
knowledge among the Noatak Eskimos." Ethnology (1971): 251-264.
Mackee, G. M., et al. "Histologic studies on percutaneous penetration with special reference
to the effect of vehicles." J Invest Dermatol 6 (1945): 43-61.
Moerman, D. E. Native American Ethnobotany. Vol. 879. Portland, OR: Timber Press, 1998.
Naylor, I. L., B. Curtis, and J. J. Kirkpatrick. "Treatment of burn scars and contractures in
the early seventeenth century: Wilhelm Fabry's approach." Medical History 40.4 (1996):
472.
Parkins, M. D. "Pharmacological practices of ancient Egypt." History of Medicine Days 5
(2001).
Petersen, F. J. Materia Medica and Clinical Therapeutics. The author, 1905.
Pieroni, A., et al. "Ethnopharmacognostic survey on the natural ingredients used in folk
cosmetics, cosmeceuticals and remedies for healing skin diseases in the inland Marches,
Central-Eastern Italy." Journal of Ethnopharmacology 91.2-3 (2004): 331-344.
Ribechini, E., et al. "Gas chromatographic and mass spectrometric investigations of organic
residues from Roman glass unguentaria." Journal of Chromatography A 1183.1 (2008):
158-169.
Rishel, J. The Indian Physician: Containing a New System of Practice Founded on Medical
Plants, Together with a Description of Their Properties, Localities, and Method of Using and
Preparing Them: a Treatise on the Causes and Symptoms of Diseases, which are Incident to
Human Nature, with a Safe and Sovereign Cure for Them, and the Mode of Treatment, in
Any Stage of Disease for the Use of Families and Practitioners of Medicine. Ohio State
University Libraries Publications Committee, 1980.
Saliu,
F.,
et
al.
"HPLC–APCI-MS
analysis
of
triacylglycerols
(TAGs)
in
historical
pharmaceutical ointments from the eighteenth century." Analytical and bioanalytical
chemistry 401.6 (2011): 1785-1800.
Sayre, L. E., and Stevens, W. C. A Manual of Organic Materia Medica and Phamacognosy. P.
Blakiston's son & Company, 1900.
Scudder, J. M. The American Eclectic Materia Medica and Therapeutics. author, 1898.
Sutton, R. L. "The Absorption of Ointments." British Medical Journal 1.2473 (1908): 1225.
Thomson, S. The Medicines of Nature: The Thomsonian System. Quakertown, PA: The
Humanitarian Society, 1905.
Weaver, W. Sauer's Herbal Cures. Routledge, 2000.
Wild, R. B. "Part I: On the official ointments, with special reference to the substances used
as bases." British Medical Journal 2.2638 (1911): 161-162.
Wild, R.B. “Part II: On Certain Non-Official Fats as Ointment Bases.” British Medical Journal.
October 18, I9I3.
Wild, R. B., and Ivy Roberts. "The Absorption of Mercurials from Ointments Applied to the
Skin." British medical journal 1.3416 (1926): 1076-1079.
United States Patent Office (1872). “Ephpraim Wilson, of Buchanan, Michigan. Improvement
in Medical Compounds or Salves. Patent No. ISO,263.” August, 1872.
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Patent No. 320,836.” June 23, 1885.
Youngken, H. W. “Drugs of North American Indians.” American Journal of Pharmacology.
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185.
Zalewski, K., Martysiak- Żurowska, D., Iwaniuk, M., Nitkiewicz, B.,
Stołyhwo, A.
“Characterization of Fatty Acid Composition in Eurasian Badger (Meles meles).” Polish
Journal of Environmental Studies, 16. 4(2007:) 645-650.
Late Autumn & Early Winter Grain Bowl
For Optimal Immunity
Al Scotton
Bowl:
Wild Rice
Quinoa
Shiitake mushrooms
Carrots
Kale
Broccoli
Nori
Almonds
Walnuts
Pepitas
Sunflower Seeds
Sauerkraut
Sprouts (any sort!)
Sauce:
Raw Garlic
Olive Oil
Tamari
Ginger
To make sauce, chop 1 head of garlic and 1 thumb of ginger and blend with 1 part tamari or
soy sauce. With blender running, slowly pour in 2 to 3 parts olive oil, until sauce thickens.
To assemble bowl, soak, rinse, and cook grains. Sautee shiitake mushrooms and mix with
shredded nori in a bowl; add the warm grains. Steam chopped carrots, kale, and broccoli,
and add to bowl. Top with a handful of nuts and seeds, sauerkraut, and sauce. Also great
with avocado and sprouts!
Carrots, broccoli, and kale are rich in many vitamins and minerals including carotenoids,
which protect the mucous membranes of the lung and intestine during the onslaught of
viruses in cold and flu season. Kale helps to dispel mucous, and shiitake helps to balance
the immune response.
Garlic is aromatic, pungent, and dispersive, warming, and highly
antimicrobial, with an affinity for the upper respiratory system. Nori helps to moisten
dryness during late autumn and winter, nourish the kidney yin (governed by the water
element in TCM), support the nervous system and endocrine systems with key minerals,
and also helps to bring body warmth inward.
Almonds and seeds nourish the jing and
moisten the body with healthy fats, while walnuts, quinoa, and wild rice nurture the kidney
yang. Ginger is pungent and warming, and benefits the metal element in late fall.
Most of these foods are fibrous, helping to maintain a healthy colon, healthy gut flora, and
stable blood sugar levels, all of which contribute to healthy immune function. Most are also
sweet, nourishing, and moistening, which is important during the dry and cold Vata season.
The grain bowl is filled with sources of omega-3s, protein, complex carbohydrates, vitamins,
minerals, and phytonutrients. The meal is a good source of magnesium, phosphorus,
copper, iron, vitamin A, vitamin C, vitamin K, and manganese. All five tastes are present:
pungent (garlic), bitter (kale), sour (sauerkraut), salty (nori, tamari), sweet (grains,
nuts/seeds, carrots).
Each of these tastes works on different body systems, bringing
nourishment and balance to the entire organism for optimal health and optimal immunity.