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Aloe's Benefits More Than Skin Deep
NEW YORK (Reuters) -- Studies in rats suggest that a gel extracted from
the aloe
plant may help prevent disease and extend life-spans.
Although many Americans use aloe-based skin creams, Dr. Jeremiah Herlihy,
associate
professor of physiology at the University of Texas Health Science Center
in San Antonio,
points out that "people worldwide use it for medicinal purposes... (and)
we wanted to
begin to document what the effects actually are."
To do that, Herlihy and other researchers tracked the diets of 360 rats
over the course of
their respective life-spans. Some of the rats were fed a diet of rat food
mixed with 1%
dried aloe gel, extracted from the Aloe barbadensis plant. Some were fed
unadulterated
rat food, but received aloe gel in their water supply. Others ate a normal,
aloe gel-free
diet.
Pathologist Dr. Yuji Ikeno performed autopsies on all the rats after their
deaths, and
discovered that the advancement of kidney disease, common to rats at the
end of their
life-span, was "reduced" in the aloe gel-eaters when compared with rats
who were not
fed the aloe gel.
He also found that aloe gel-eating rats displayed reduced rates of heart
muscle disease,
clot formation in the chambers of the heart, and cancer.
"Multiple causes of death were reduced, suggesting that the disease burden
was lighter in
the aloe-fed rats," Ikeno said.
This news may come as little surprise to believers in 'traditional' or
'folk' medicine. Herlihy
acknowledges that "people worldwide use (aloe gel) for medicinal purposes
including
burns, digestion, and as a cathartic (laxative)." While people in the affluent
West may
think of aloe gel as a dermatological aid, Herlihy says, "more people in
the world take the
(extracted) gel internally than use it as a skin treatment."
But a note of caution: Dr. Ernest DeMarie, curator of desert plants at
the New York
Botanical Garden doesn't encourage people to start eating aloe, or drinking
tea made
from the plant. "At least one African species of aloe is toxic when an
infusion is made
from it," he explained. "If the study has merit,... then they will probably
identify the active
principle ingredient and make a pill form of it. That would be a lot safer."
The secrets to aloe's benefits to health are complex and still unfolding.
"Aloe gel has many
active ingredients," says study director Dr. Byung Pal Yu, "only two of
which -- an
antioxidant and an anti-inflammatory agent -- have been identified."
His team plan more studies into the plant's medicinal powers. "We still
need to determine
the optimum dose of (extracted aloe gel) and identify the active ingredients
responsible
for the observed benefits," Yu explained.
Copyright 1997 Reuters Limited.
The DHEA Craze – What Pharmacists Should Know
By: James B. LaValle, R.Ph, DHM, DHPh
TV, newspapers and the popular press have proclaimed DHEA as the revolutionary
"fountain of youth." And just as consumers rushed to buy Melatonin in droves,
the lines to
purchase of DHEA are lengthening as well. As pharmacists, a working knowledge
of
DHEA is important in order to help the consumer and patient to make a well-informed
choice. Health professionals’ opinions on DHEA run from dangerous to anecdotal
to the
indiscriminate recommending of it. In reality, upon examining the facts
and some of the
more recent studies on DHEA, you will see the truth lies somewhere in between.
Experts
feel DHEA is probably not going to extend life or retard the aging process.
However, an
increasing number do feel it can improve the quality of life if used correctly
and may be of
significant help in the treatment of various disease processes. In addition
to the recent
controlled studies supporting DHEA use, a deluge of positive anecdotal
reports have
surfaced from the public.
Dehydroepiandosterone and its sulfate conjugate are primarily produced
in the adrenal
cortex. DHEA is a metabolic intermediate for hormones converting on demand
to
estrogen, estradiol, testosterone and corticosteroids. Scientific evidence
points to the fact
that DHEA concentrations drop with age as well as in numerous chronic conditions
such
as obesity, elevated cholesterol, arthritis, fatigue, age-related endocrine
decline and
autoimmune diseases such as SLE. Only time will tell if DHEA administration
will have
long term benefits without significant risks.
DHEA production surges at birth, peaks again around age seven and then
crests to peak
again between the ages of 25 and 30. DHEA shows a definite circadian rhythm
in the
body while DHEA-S does not. With aging comes a linear decline in DHEA until
age
eighty, where we are producing only 10-20% of levels from our twenties.
Under stress,
the hypothalamic/pituitary axis shifts to increase the production of glucocordicoids,
cortisol and a resultant decrease in productions or mineral corticoids.
This can result in
fatigue and open the door for a whole host of chronic illnesses. DHEA blocks
the enzyme
G6PD which promotes cancer cell division and fat production.
Through monitoring of blood levels or a new saliva test which is available,
supplemental
DHEA dosages can be recommended more accurately. However, no one really
knows
the proper replacement dose for DHEA or the differences in how men and
women
metabolize it. The dosage range for DHEA is anywhere from 5-50mg daily.
Anything
over 25mg a day would be best served by having periodic testing. Recommending
5mg
increments and then observing the results is a good conservative approach
because some
people may not tolerate as little as 5mg while others can easily tolerate
50mg. It is true
that no one knows the potential long term risks of DHEA use, but research
has been
going on for some 40 years with a relatively good report for a margin of
safety. The
concern for use is around the conversion of DHEA into both estrogen and
testosterone in
the body. Masculinization in women most notably shows up in dosages over
25mg a day.
DHEA may restore T cell and natural killer cell function. It has also shown
the ability to
activate insulin growth factor levels to that of a 30 year old. The average
dose for a 60
year old male under supervision is 50mg daily.
Some cautions, Contra-indications and Toxicities:
• Side effects tend to be uncommon in low or appropriate dosing, and most
disappear
with decrease or discontinuance of use.
• DHEA levels are generally lower in vegetarian diets. This is mostly because
vegans eat
a large amount of dairy and starches, and do not balance their diet with
legumes. Very
low fat diets may also affect DHEA levels. When we remove quality sources
of fatty
acids (such as olive oil) from our diet, our body does not receive the
needed nutrients to
make precursors to steroid structures.
• Overstimulation or insomnia/fatigue or low energy.
• DHEA should not be recommended to men with a history of prostate cancer
or women
with a history or breast, ovarian or uterine cancer.
• Excessive hair growth and masculinization in women
• The development of oily skin.
• Reports of infrequent headaches, aggressiveness and menstrual irregularities.
• Question the source of DHEA. Is it from a reputable source that guarantees
quality and
can provide you information on it? Fears are well supported from the poor
quality control
that created the tryptophan issue.
Though there is enough supportive evidence to suggest that DHEA may offer
a key to
previously unknown metabolic pathways, there are risks. People will be
asking you for
your opinion as it applies to aging, cancer, diabetes, heart disease, weight
loss, etc. Keep
in mind that many of these people will not want to seek a medical test
in order to find out
if they are good candidates for DHEA therapy. So you need to stay current
with DHEA
studies. Read…New studies will be coming out.
FTP’s Natural Medicines author Jim LaValle is a registered pharmacist with
more than
10 years of clinical experience in the Natural Medicine Industry. Jim is
an adjunct
instructor of Natural Medicine at the University of Cincinnati College
of Pharmacy.
TOPIC: Feverfew
SCIENTIFIC NAMES: Tanacetum parthenium Schulz-Bip. synonymous with
Chrysanthemum parthenium L. Bernh., Leucanthemum parthenium (L.) Gren and
Godron, and Pyrethrum parthenium (L.) Sm.1 Alternately described as a member
of the
genus Matricaria. Family: Asteraceae Compositae.
COMMON NAMES: Feverfew, featherfew, altamisa, bachelor's button, featherfoil,
febrifuge plant, midsummer daisy, nosebleed, Santa Maria, wild chamomile,
wild quinine2
3 4 5
BOTANY: A short bushy perennial that grows from 15 to 60 cm tall along
field and
roadsides. Its yellow-green leaves and yellow flowers resemble those of
chamomile
(Matricaria chamomilla), for which it is sometimes confused. The flowers
bloom from July
to October.
HISTORY: The herb feverfew has had a long history of use in traditional
and folk
medicine, especially among Greek and early European herbalists. However,
during the
last few hundred years feverfew had fallen into general disuse, until recently.6
It has now
become popular as a prophylactic treatment for migraine headaches and its
extracts have
been claimed to relieve menstrual pain, asthma, dermatitis and arthritis.
Traditionally, the
herb has been used as an antipyretic, from which it's common name is derived.
The
leaves are ingested fresh or dried, with a typical daily dose of 2 to 3
leaves. These are
bitter and are often sweetened before ingestion. It has also been planted
around houses
to purify the air due to its strong, lasting odor, and a tincture of its
blossoms doubles as
an insect repellant and balm for their bites.3 It was once used as an antidote
for
overindulgence in opium.2
CHEMISTRY: The chemistry of feverfew is now well-defined. The plant is
rich in
sesquiterpene lactones, the principal one being parthenolide.7 Parthenolide
comprises up
to 85% of the total sesquiterpene content.1 Other active sesquiterpene
lactones are
canin, secontanapartholide A, artecanin, and 3-beta-hydroxyparthenolide.8
Other
members of this class have been isolated and have been shown to possess
spasmolytic
activity perhaps through an inhibition of the influx of extracellular calcium
into vascular
smooth muscle cells. The plant contains several flavonoid glycosides, the
main ones being
luteolin and apigenin.9
PHARMACOLOGY: Feverfew action does not appear to be limited to a single
major
mechanism; rather, plant extracts affect a wide variety of physiologic
pathways.
In vitro: Feverfew appears to be an inhibitor of prostaglandin synthesis.
Extracts of the
above-ground portions of the plant suppress prostaglandin production by
up to 88%; leaf
extracts inhibit prostaglandin production to a lesser extent (58%). Neither
the whole plant
nor leaf extracts inhibit cyclooxygenation of arachidonic acid, the first
step in
prostaglandin synthesis.10
Aqueous extracts prevent the release of arachidonic acid and inhibit in
vitro aggregation
of platelets stimulated by ADP or thrombin.11 Whether these extracts block
the synthesis
of thromboxane, a prostaglandin involved in platelet aggregation, is controversial.12
13
Data suggest that feverfew's inhibition of prostaglandin synthesis differs
in mechanism
from that of the salicylates. Extracts may inhibit platelet behavior via
effects on platelet
sulfhydryl groups. 14 15
Feverfew extracts are potent inhibitors of serotonin release from platelets
and
polymorphonuclear leucocyte granules, providing a possible connection between
the
claimed benefit of feverfew in migraines and arthritis. Feverfew may produce
an
antimigraine effect in a manner similar to methysergide maleate (Sansert),
a known
serotonin antagonist.16 17 Extracts of the plant also inhibit the release
of enzymes from
white cells found in inflamed joints, a similar anti-inflammatory effect
may occur in the
skin, providing a rationale for the traditional use of feverfew in psoriasis.
In addition, feverfew extracts inhibit phagocytosis, inhibit the deposition
of platelets on
collagen surfaces, exhibit antithrombotic potential, have in vitro antibacterial
activity,
inhibit mast cell release of histamine18 and exhibit cytotoxic activity.9
Monoterpenes in
the plant may exert insecticidal activity, and alpha-pinene derivatives,
may possess
sedative and mild tranquilizing effects.
Clinical Uses: Much interest has been focused on the activity of feverfew
in the treatment
and prevention of migraine headaches.19 The first significant, modern,
public account of
its use as a preventative for migraines appeared in 1978. This story, reported
in the
British health magazine, Prevention, concerned a Mrs. Jenkins who had suffered
from
severe migraines since the age of 16. At the age of 68, she began using
three leaves of
feverfew daily, and after ten months her headaches ceased altogether. This
case
prompted studies by Dr. E. Stewart Johnson.6
A study in eight feverfew-treated patients and nine placebo-controlled
patients found that
fewer headaches were reported by patients taking feverfew for up to six
months of
treatment. Patients in both groups had self-medicated with feverfew for
several years
before enrolling in the study. The incidence of headaches remained constant
in those
patients taking feverfew but increased almost three-fold in those switched
to placebo
during the trial (p<0.02).20 The abrupt discontinuation of feverfew
in patients switched to
placebo caused incapacitating headaches in some patients. Nausea and vomiting
were
reduced in patients taking feverfew. The statistical analysis has been
questioned but the
results provide a unique insight into the activity of feverfew.21 These
results were
confirmed in a more recent placebo-controlled study in 72 patients suffering
from
migraine.22 On the basis of their research, Johnson, et al, predict that
feverfew will be
useful not only for the classical migraine and cluster headache, but for
premenstrual,
menstrual and other headaches, as well.23
However, studies at the London Migraine Clinic24 found that the experimental
observations may not be clinically relevant to migraine patients taking
feverfew. Ten
patients who had taken extracts of the plant for up to 8 years to control
migraine
headaches were evaluated for physiologic changes that may have been related
to the
plant. The platelets of all treated patients aggregated characteristically
to ADP and
thrombin and similarly to those of control patients. However, aggregation,
in response to
serotonin, was greatly attenuated in the feverfew users.
Feverfew has been investigated in the treatment of rheumatoid arthritis.
In one major
study, 41 female patients received feverfew (70 to 86 mg) or placebo once
daily for 6
weeks under double-blind conditions. No significant differences were observed
in more
than 15 parameters between the test groups suggesting no apparent benefit
from oral
feverfew therapy.25
Canada's Health Protection Branch has granted a Drug Identification Number
(DIN) for
a British feverfew (Tanacetum parthenium) product. This allows the product's
manufacturer, Herbal Laboratories, Ltd., to make the claim as a nonprescription
drug, for
effectiveness in the prevention of migraine headache. Canada's Health Protection
Branch
recommends a daily dosage of 125 mg of a dried feverfew leaf preparation
from
authenticated Tanacetum parthenium containing at least 0.2% parthenolide
for the
prevention of migraine.26
TOXICOLOGY: Much has been learned about the safety of feverfew over the
last
decade. In the study conducted by Johnson, et al, patients received 50mg/day,
roughly
equivalent to two leaves. Adverse effects noted during 6 months of continued
feverfew
treatment were mild and did not result in discontinuation. Four of the
eight patients taking
the plant had no adverse effects. Heart rate increased dramatically (by
up to 26
beats/min) in two treated patients. There were no differences between treatment
groups
in laboratory test results.
Patients who had been switched to placebo after taking feverfew for several
years
experienced a cluster of nervous system reactions (rebound of migraine
symptoms,
anxiety, poor sleep patterns), along with muscle and joint stiffness; Johnson
refers to this
as the "postfeverfew syndrome."
In a larger series of feverfew users, 18% reported adverse effects, the
most troublesome
being mouth ulceration (11%). Feverfew can induce more widespread inflammation
of
the oral mucosa and tongue, often with lip swelling and loss of taste.20
Dermatitis has
been associated with this plant.27 28
No studies of chronic toxicity have yet been performed on the plant and
the safety of
long-term use has not been established scientifically. The plant should
not be used by
pregnant women, as the leaves have been shown to possess potential emmenagogue
activity, and is not recommended for lactating mothers or children under
the age of 2. 26
Although an interaction with anticoagulants is undocumented, this may be
clinically
important in sensitive patients.
One study has evaluated the potential genotoxic effects of chronic feverfew
ingestion.
Analysis of the frequency of chromosomal aberrations and sister chromatid
exchanges in
circulating lymphocytes from patients who ingested feverfew for 11 months
found no
unexpected aberrations suggesting that the plant does not induce chromosomal
abnormalities.29
SUMMARY: Feverfew has been used for the treatment of disorders often controlled
by
aspirin, such as fever, rheumatic inflammations and headache. The chemistry
and
pharmacology of feverfew have been reasonably well defined. The ability
of the plant to
aid in the control of migraine has been under close study. To date, the
studies comparing
the plant to placebo have generally found a significant clinical benefit
from the
administration of feverfew. Preliminary safety data from clinical trials
suggest that the plant
is relatively safe, although the incidence of mouth ulcers has been disturbingly
high in
some trials. The plant does not appear to be mutagenic and should not be
used by
pregnant women.
REFERENCES:
1.Awang DVC. Herbal medicine, feverfew. Can Pharm J 1989;122:266.
2.Duke JA. Handbook of Medicinal Herbs. Boca Raton, FL:CRC Press, 1985.
3.Dobelis IN, ed. Magic and Medicine of Plants. Pleasantville, NY: Readers
Digest
Assoc., 1986.
4.M;eyer JE. The Herbalist. Hammond, IN: Hammond Book Co., 1934.
5.Castleman M. The Healing Herbs, Emmaus, PA: Rodale Press, 1991.
6.Hobbs, C. The Modern Rediscovery of Feverfew. National Headache Foundation
Newsletter Winter 1990:11. 3 Ibid. 2 Ibid.
7.Bohlmann F, Zdero C. Sesquiterpene lactones and other constituents from
Tanacetum parthenium. Phytochemistry 1982;21:2543. 1 Ibid.
8.Groenewegen WA, et al. Compounds extracted from feverfew that have
anti-secretory activity contain an alpha-methylene butyrolactone unit.
J Pharm
Pharmacol 1986;38:709.
9.Hobbs C. Feverfew, Tanacetum parthenium. Hergal Gram 1989;20:26.
10.Collier HOJ, et al. Extract of feverfew inhibits prostaglandin biosynthesis.
Lancet
1980;2:922. Letter.
11.Loecshe EW, et al. Folia Haematol 1988;115:181
12.Makheja AN, Bailey JM. The active principle in feverfew. Lancet
1981;2:1054.Letter
13.Heptinstall S, et al. Extracts of feverfew inhibit granule secretion
in blood platelets
and polymorphonuclear leucocytes. Lancet 1985;1:1071.
14.Heptinstall S, et al. Extracts of feverfew may inhibit platelet behavior
via
neutralization of sulphydryl groups. J Pharm Pharmacol 1987;39:459.
15.Voyno-Yasenetskaya TA, et al. Effects of an extract of feverfew on endothelial
cell integrity and on cAMP in rabbit perfused aorta. J Pharm Pharmacol
1988;40:501.
16.Tyler VE. The New Honest Herbal. Philadelphia, PA: GF Stickley Co.,
1987.
17.Olin BR, Hebel SK, eds. Drug Facts and Comparisons. St. Louis: Facts
and
Acomparisons, Oct 1991:257.
18.Hayes NA, Foreman JC. The activity of compounds extracted from feverfew
on
histamine release from rat mast cells. J Pharm Pharmacol 1987;39:466. 9
Ibid.
19.Feverfew-a new drug or an old wives' remedy. Lancet 1985;1:1084. Editorial
6
Ibid.
20.Johnson ES, et al. Efficacy of feverfew as prophylactic treatment of
migraine. BR
Med J 1985;291:569.
21.Waller PC, Ramsay LE. Efficacy of feverfew as prophylactic treatment
of
migraine. Br Med J 1985;291:1128. Letter.
22.Murphy JJ, et al. Randomised double-blind placebo-controlled trial of
feverfew in
migraine prevention. Lancet 1988;2:189.
23.Hobbs C. Feverfew. National Headache Foundation Newsletter Winter 1990:10.
24.Biggs, et al. Platelet aggregation in patients using feverfew for migraine.
Lancet
1982;2:776. Letter
25.Pattrick M, et al. Feverfew in rheumatoid arthritis: a double blind,
placebo
controlled study. Ann Rheum Dis 1989;48:547.
26.Awang DVC. Feverfew Fever. HerbalGram 1993;29:34. 20 Ibid.
27.Vickers HR. Feverfew and migraine. BR Med J 1985;291:827. Letter
28.Schmidt RJ, Kingston T. Chyrsanthemum dermatitis in South Wales; diagnosis
by
patch testing with feverfew (Tanacetum parthenium) extract. Contact Derm
1985;13:120. 26 Ibid.
29.Anderson D, et al. Chromosomal aberrations and sister chromatid exchanges
in
lymphocytes and urine mutagenicity of migraine patients: a comparison of
chronic
feverfew users and matched non-users. Human Toxicol 1988;7:145.
Reprinted with permission from The Lawrence Review of Natural Products®
Copyright© 1994 by Facts and Comparisons (ISSN 0734-4961) All rights
reserved.
TOPIC: Ginger
SCIENTIFIC NAMES: Zingiber officinale Roscoe; occasionally Z. capitatum
and
Z. zerumbet Smith are used. Family: Zingiberaceae.
COMMON NAME: Ginger
BOTANY: This perennial grows in warm climates such as India, Jamaica and
China. The
plant carries a green-purple flower in terminal spikes; the flowers are
similar to orchids.
The rhizome is aromatic and is the source of the dried powdered spice.1
HISTORY: The roots and rhizomes of ginger have been used as a seasoning
and have
played an important role in Chinese, Indian and Japanese medicine. Ginger
is though to
possess carminative, stimulant, diuretic and antiemetic properties.2 Fluid
extracts of
ginger have been used since the 1500s for the treatment of gastrointestinal
distress. In
China, ginger root and stem are used as pesticides against aphids and fungal
spores.3
CHEMISTRY: A number of investigations led to the isolation of a variety
of chemical
components from ginger root. It had long been believed that the "pungent
principles" of
ginger were also responsible for it pharmacologic activity, and this has
been found to be
accurate. The characteristic aroma of ginger is due to a volatile oil present
in a
concentration of 1% to 3%.4
Analyses of the "pungent principles" have resulted in the identification
of a class of
structurally related cardiotonic compounds called gingerols. These occur
at levels of less
than 1% of the root by weight. In addition, the pharmacologically active
compounds(6)-shogaol5 [a dehydroxylated analog of (6)-gingerol], (6)-and
(10)-dehydrogingerdione, (6)-and (10)-gingerdione and zingerone have been
identified.6
PHARMACOLOGY: The gingerols and the related compounds shogaol have been
found to possess cardiotonic activity. Crude methanol extracts of ginger
were known to
have a powerful positive inotropic effect on animal hearts. The gingerols
have been found
to exert a dose-dependent positive inotropic action at doses as low as
10-4 g/ml when
applied to isolated atrial tissue.2
Administration of (6)-gingerol and (6) shogaol (1.75 to 3.5 mg/kg IV and
70 to 140
mg/kg orally) inhibited spontaneous motor activity, produced antipyretic
and analgesic
effects and prolonged hexobarbital-induced sleeping time in laboratory
animals.
(6)-gingerol and showed an intense antitussive effect when compared to
dihydrocodeine
phosphate. Interestingly, (6)-shogaol inhibited intestinal motility when
given IV, but
facilitated GI motility after oral administration. Both compounds were
cardiodepressant at
low doses and cardiotonic at higher doses.5 (6)-gingerol, the dehydrogingerdiones
and
the gingerdiones are potent inhibitors of prostaglandin biosynthesis through
the inhibition
of prostaglandin synthetase.6
The volatile oil of ginger root was capable of inhibiting the growth of
bacteria in a closed
chamber,7 and a commercial applications of this activity are being investigated.
The cytotoxic compound zerumbone and its epoxide have been isolated from
the
rhizomes of Z. zerumbet. This plant, also a member of the family Zingiberaceae,
has
been used traditionally in China as an antineoplastic. The isolates inhibited
the growth of a
hepatoma tissue culture.8 In addition, juice prepared from ginger root
has been found to
inactivate the mutagenicity of tryptophan pyrolysis products in vitro.9
The root stock of the related Z. capitatum contains a heat-stable interferon
that
possesses some immune-stimulating activity. It has no direct virucidal
or antitumor
activity.10
Little is known about the human pharmacology of ginger. One widely publicized
double-blind study was conducted to compare the effect of 940 mg of powered
ginger
root, 100 mg dimenhydrinate(eg, Dramamine, an antihistamine) and placebo(chickweed
herb) in the prevention of motion sickness. Thirty-six subjects were given
the
preparations and were placed blindfolded in a rotating chair. Subjects
who received
ginger root remained in the chair an average of 5.5 minutes, compared to
3.5 minutes for
the dimehydrinate group and 1.5 minutes for the placebo group. Half of
the
ginger-treated subjects remained in the chair for the full 6 minutes of
the test; none of the
subjects in the other groups completed the test. In general, it took longer
for the ginger
group to begin feeling sick, but once the vomiting center was activated,
sensations of
nausea and vomiting progressed at the same rate in all groups. The authors
postulated
that, unlike antihistamines, which act on the CNS, the aromatic, carminative
and possibly
absorbent properties of ginger ameliorate the effects of motion sickness
in the GI tract
itself. It may increase gastric motility, blocking GI reactions and subsequent
nausea
feedback.11
More recently, pregnant women suffering from hyperemesis gravidarum received
ginger(250 mg four times daily) or placebo for 4 days. A significant(p=
0.003)
percentage of women(70.4%) subjectively preferred ginger treatment, with
greater
symptomatic relief being observed compared to placebo.12 There is no good
evidence
regarding the safety of ingesting large amounts of this material by pregnant
women.
SUMMARY: Ginger root is an ancient spice that has had a role in herbal
medicine for
hundreds of years. Recent research indicates that the root contains pharmacologically
active compounds that maybe of benefit in the treatment of dizziness and
vestibular
disorders. Further investigation into the pharmacology and therapeutic
potential of the
root is warranted.
TOPIC: Ginkgo
SCIENTIFIC NAME: Ginkgo biloba L. Family: Ginkgoaceae
COMMON NAMES: Ginkgo, maidenhair tree, Kew tree
BOTANY: The ginkgo is the world’s oldest living tree species, and it can
be traced
back more than 200 million years to the fossils of the Permian period.
It is the sole
survivor of the family Ginkgoaceae. Individual trees may live as long as
1,000 years.
They grow to a height of about 125 feet and bear fan-shaped leaves. The
species is
dioecious; male trees more than 20 years old blossom in the spring. Adult
female trees
produce a plum-like gray-tan fruit that falls in late autumn. Its fleshy
pulp has a foul,
offensive odor and causes contact dermatitis. The edible inner seed resembles
an almond
and is sold in oriental markets.1
HISTORY: The gingko species was almost destroyed during the ice age but
survived in
China, where it was cultivated as a sacred tree and is still found decorating
Buddhist
temples throughout Asia. Preparations have been used as health remedies
for more than a
thousand years. Traditional Chinese physicians used ginkgo leaves to treat
asthma and
chillblains, which is the swelling of the hands and feet from exposure
to damp cold. The
ancient Chinese and Japanese ate roasted ginkgo seeds, and considered them
a digestive
aid and preventive for drunkenness.2
Currently, oral and intravenous forms are available in Europe, where it
is one of Europe’s
most widely prescribed medications. Neither form has been approved for
general use in
the United States.
CHEMISTRY: Chemical analysis of the ginkgo has identified a number of terpenes,
pro-anthocyanidines, heterosides and bioflavones, the most common of which
are
sciaopitysin, ginkgetin, isoginkgetin, bilobetin and ginkgolic acid. There
is a seasonal
variation in the content of these compounds in leaves, with the highest
amounts being
present in the autumn.3 Although a number of individual components have
been
identified, almost all clinical studies have been conducted with whole-plant
extracts that
are generally not well characterized.
PHARMACOLOGY: The physiologic mechanisms of action of ginkgo extract are
poorly understood. Some data indicate that it is an inhibitor of COMT,
but its lack of
central nervous system effects suggests that this may not be an important
mechanism of
action.4 The extract has a "scavenging" effect on free radicals, which
may contribute to its
protective effect on vascular walls.5
In man, dietary supplementation with ginkgo extracts for 14 days indicated
that the
extract was slightly less effective than selenium but more effective than
beta-carotene and
vitamin E as an oxidative scavenger.6 Oral administration of leaf extract
to rats resulted in
the partial suppression of experimental microembolus formation in cerebral
vessels. The
extract also caused an increase in flow rates through experimentally occluded
rat cerebral
blood vessels, with a concomitant increase in tissue oxygen consumption.7
In man, intravenous injection of 50 to 200 mg of ginkgo extract caused
a
dose-dependent increase in microcirculation and blood viscoelasticity in
patients with
pathologic blood flow disorders.8
Vasoconstriction can occur after administration of ginkgo extract, especially
when
cerebral vessels are already maximally dilated.9
When the extract was given to diabetic patients, peripheral blood flow
increased by 40
percent to 45 percent, compared with an increase of 35 percent after administration
of
nicotinic acid.10 In patients with hearing disorders secondary to vascular
insufficiency of
the ear, about 40 percent of those treated orally with a leaf extract for
two to six months
showed improvement in auditory measurements. The extract also was extremely
effective
in relieving vertigo associated with vestibular dysfunction. It appears
useful in
management of peripheral vascular disorders such as Raynaud’s disease,
acrocyanosis
and post-phlebitis syndrome.11 A six month, double blind trial suggested
some efficacy
in treating obliterative arterial disease of the lower limbs.5 Patients
who received extract
showed a clinically and statistically significant improvement in pain-free
walking distance,
maximum walking distance and plethysmographic records of peripheral blood
flow.
Rabbit aortas treated with ginkgo leaf extract showed a dose-related increase
in tone, an
effect that may in part be due to a release of endogenous catecholamines.12
The extract
has a slightly anti-inflammatory effect. It is slightly spasmolytic, with
an activity similar to
that of papaverine although its effects on intestinal tissue are inconsistent.
The extract
appears to inhibit histamine and serotonin to a degree similar to that
of cyproheptadine. It
is devoid of CNS activity.13
In man, intravenous administration of the extract increased cerebral blood
flow in about
70 percent of the patients evaluated. This increase was age related: patients
between the
ages of 30 and 50 years had a 20 percent increase from baseline, compared
with 70
percent in those 50 to 70 years old. Further, the time to reach peak blood
flow was
shorter in the elderly.14
In elderly men with slight age-related memory loss, ginkgo supplementation
significantly
improved the speed required to process visual information.15 However, a
critical review
of 40 published trials of ginkgo in cerebral insufficiency identified only
eight studies that
did not have major methodological flaws; the results from these better
studies were,
nevertheless, difficult to interpret. They suggested that long-term treatment(greater
than
six weeks) is required and that any effect is similar to that observed
following treatment
with ergoloids.16
A number of other potentially beneficial pharmacologic effects have been
observed for
ginkgo, including its ability to prevent the deterioration of lipid profiles
when subjects
were challenged with high-cholesterol meals over an extended holiday season
17,
improvement in the symptoms of PMS, particularly breast-related symptoms18,
and in
vitro and in vivo activity against Pneumocystis carinii19, Ginkgo inhibits
platelet activating
factor (PAF), thereby preventing PAF-induced clot formation and promoting
clot
breakdown. Similarly, ginkgo inhibits PAF-induced bronchospasm. 20
TOXICOLOGY: Ingestion of the extract has not been associated with severe
side
effects. Mild adverse reactions have included gastrointestinal upset and
headache. By
contrast, contact with whole ginkgo plants has been associated with severe
allergic
reactions. A cross-allergenicity exists between ginkgo fruit pulp and poison
ivy. Ginkgolic
acid and bilobin are structurally similar to the allergens of poison ivy,
mango rind and
cashew nut shell oil. Contact with the fruit pulp causes erythema and edema,
with the
rapid formation of vesicles accompanied by severe itching. The symptoms
last seven to
ten days. Ingestion of as little as two pieces of pulp has been reported
to cause perioral
erythema, rectal burning and tenesmus (painful spasms of the anal sphincter).1
A toxic syndrome has been recognized in the Orient in children who have
ingested ginkgo
seeds. Approximately 50 seeds produce tonic/clonic seizures and loss of
consciousness.21 Ginkgo pollen can be strongly allergenic.22
SUMMARY: The ginkgo is the oldest known living tree species. An extract
of the
leaves has been shown to have pharmacologic activity generally associated
with
vasodilation. The chemistry of the extract and its mechanism of action
are poorly
understood. In human clinical trials an extract has been effective in treating
symptoms of
Raynaud’s disease and appears to increase cerebral and otic blood flow.
It is generally
devoid of adverse effects, but contact with the fruit pulp causes a severe
poison-ivy-like
dermatitis. The pulp and seed are toxic if ingested.
Back to the Top of Page
REFERENCES:
1. Becker LE, Skipworth GB. Ginkgo-tree dermatitis, stomatitis and proctitis.
JAMA
1975;231:1162.
2. Castleman, M. Healing Gifts from the Ancient Ginkgo. The Herb Quarterly
1990;
Spring:26.
3. Briancon-Scheid F, et al. HPLC separation and quantitative determination
of
biflavones in leaves from Ginkgo biloba. J Med Plant Res 1983;49:204.
4. Herz W. Panel Discussion. Minerva Med 1973;79:4202.
5. Bauer U. 6-Month double-blind randomized clinical trial of ginkgo biloba
extract
versus placebo in two parallel groups in patients suffering from peripheral
arterial
insufficiency. Arzneim Forsch 1984;34:716.
6. Pietschmann A, et al. Protection from uv-light-induced oxidative stress
by nutritional
radical scavengers. Z Gesamte Inn Med 1992;47:518.
7. le Poncin Lafitte M et al. Effects of Ginkgo biloba on changes induced
by quantitative
cerebral microembolization in rats. Arch Int Pharmacodyn 1980;243:236.
8. Koltringer P et al. Hemorheologic effects of Ginkgo biloba extract EGb
761.
Dose-dependent effect of EGb 761 on microcirculation and viscoelasticity
of blood.
Fortschr Med 1993;111:170.
9. Condorelli S. Panel Discussion. Minerva Med 1973;79:4172.
10. Bartolo M. Panel Discussion. Minerva Med 1973; 79:4192.
11. Nazzaro P, Dicarlo A. Risultati del trattamento con ginkgo biloba nelle
dermopatie
angiodistrofiche. Minerva Med 1973;79:4198.
12. Hellegouarch A et al. Comparison of the contractile effects of an extract
of Ginkgo
biloba and some neurotransmitters on rabbit isolated vena cava. Gen Pharmacol
1985;16:129.
13. Herz W. Farmacologia sperimentale della Ginkgo biloba. Minerva Med
1973;79:4160.
14. Pistolese GR. Risultati preliminari sulle modificazioni del flusso
cerebrale con lo
xenon-133 durante somminisrazione della Ginko biloba. Minerva Med 1973;79:4166.
15. Allain H et al. Effect of two doses of Ginkgo biloba extract (EGb 761)
on the dual
coding test in elderly subjects. Clin Ther 1993;15:549-58.
16. Kleijnen J, Knipschild P. Ginkgo biloba for cerebral insufficiency.
Br J Clin
Pharmacol 1992;34:352.
17. Kenzelman R, Kade F. Limitation of the deterioration of lipid parameters
by a
standardized garlic- ginkgo combination product. A multicenter placebo-controlled
double-blind study. ArzneimForsch 1993;43:978.
18. Tamborini A, Taurelle R. Value of standardized Ginkgo biloba extract
(EGb 761) in
the management of congestive symptoms of premenstrual syndrome. Ref Fr
Gynecol
Obstet 1993;37:1492.
19. Atzori C et al. Activity of bilobalide, a sesquiterpene from Ginkgo
biloba on
pneumocystis carinii. Antimicrob Agents Chemother 1993;37:1492.
20. Ginkgo biloba extract (Egb761) in perspective. Adis Press International, 1990.
21. Yagi M et al. Studies on the constituents of edible and medicinal plants.
IV.
Determination of 4-O methylpyridoxine in serum of the patient with ginnan
food poisoning
Yakugaku Zasshi 1993;113:596.
22. Long R et al. Partial purification and analysis of allergenicity, immunogenicity
of
Ginkgo biloba L.Pollen. Hua Hsi l Ko TA Hseuh Hsueh Hsueh Pao 1992; 23:429.
________________________________________________________________________
Reprinted with permission from The Lawrence Review of Natural Products®
Copyright
© 1994 by Facts and Comparisons (ISSN 0734-4961).
Glucosamine: a nutraceutical with great hope for arthritis
By: James B. LaValle R.Ph., D.H.M., D.H.Ph.
More and more articles are being written on glucosamine and its value in
osteoarthritis.
For several years now, glucosamine has been studied with very promising
results. As we
age, many of us stop producing glucosamine. This, coupled with the excessive
wear and
tear we place on our joints, results in cartilage destruction and hardening,
as well as bone
spur formation. Most of us will experience some discomfort from osteoarthritis
in our
lifetime. In fact, statistics show the 80% of us over the age of 50 have
some osteoarthritis
complaints.
Glucosamine is part of a group of agents called glucosaminoglycans (GAG’s).
Glycosaminoglycans are the principal components of our cartilage. Glucosamine
can be
taken orally and is the precursor to chondroitin sulfate, which is also
used orally and is the
precursor to chondroitin sulfate, which is also used orally. It provides
a nutrient source
for the body to utilize in rebuilding the collagen matrix of the affected
joint by stimulating
proteogycan production. Several have shown that glucosamine may actually
more
effective and better tolerated than some NSAID’s in relieving pain, decreasing
inflammation, and improving joint mobility. Long term use of NSAID’s and
aspirin may
contribute to the long term progression of arthritis by inhibiting cartilage
repair and
potentially accelerating its destruction. Also, it should be noted that
NSAID’s may
aggravate the GI mucosa and lead to increased membrane permeability. Cardiovascular
or hypertensive individuals may exhibit increased peripheral resistance
due to
atherosclerotic tendencies in the GI tract. Beginning with glucosamine
may be a more
desirable option, instead of potentially aggravating this situation. The
beneficial effects of
glucosamine use increase with the length of time taken. It should also
be noted that it will
take as long as 6-8 weeks to see any results with its use. There are also
some very
promising studies using indictable glucosamine to build up intra-articular
collagen. In the
future, you will probably see glucosamine combined with type I or II collagen
in an
indictable form that will be superior to glucosamine alone.
Please note that studies were performed using glucosamine hydrochloride
and sulfate. In
fact, many studies performed today are using hydrochloride because it can
be used in a
BID dosage thus enhancing compliance. The HCL form is 83 percent glucosamine,
which
the sulfate form is 62 percent glucosamine. The debate over superiority
is now heating
up, but remember the sulfate form is the one most commonly seen and has
established an
excellent track record. Other derivatives such as N-acetyl-glucosamine
do not have the
same supportive data from studies. Likewise, there are a variety of sources
of GAG’s
such as green-lipped mussels, shark cartilage, and chondroitin sulfate.
All supply the
needed nutrients, but not to the same extent nor with the same track record
as
glucosamine.
Some cautions, contra-indications and toxicities: None known at this time.
Dosage is
500mg t.i.d. sulfate or 750mg b.i.d. for HCl. Obese individuals may need
an increased
dose for effectiveness.
TOPIC: Goldenseal
SCIENTIFIC NAME: Hydrastis canadensis L. Family: Ranunculaceae
COMMON NAMES: Eye balm, eye root, goldenseal, ground raspberry, Indian
dye,
jaundice root, orange root, tumeric root, yellow Indian paint, yellow puccoon,
yellow
root.1
BOTANY: A stout perennial found deep in rich woods from Vermont to Arkansas
in the
USA. The 5 to 9-lobed plant palmate leaves can grow to ten inches. It produces
dark
red berries in April and May from green-white flowers. The rhizomes are
golden-yellow
and knotted in appearance.
HISTORY: The use of goldenseal dates to the settlers who learned of its
use from the
American Indians who used it as a dye and for its medicinal properties.
It had been used
as a bitter stomachic for the relief of catarrhal conditions and as an
eye wash. After the
Civil War, goldenseal enjoyed a golden age, as it was an ingredient in
many patent
medicines. It was collected to the point of near extinction.2 Today, it
is farmed, but still
costly,2 and in many it has been almost exterminated by commercial harvesting.1
Preparations containing goldenseal have been marketed for the treatment
of menstrual
disorders, pain of minor sciatica, rheumatic or muscular pain, and as an
antispasmodic. It
is said to enhance the potency of other herbs as well.1 Today goldenseal
finds some use
as an ingredient in commercial sterile eye washes.
CHEMISTRY: Goldenseal contains the alkaloids hydrastine(about 4%) and
berberine(up to 6%) with smaller amounts of hydrastinine, canadine and
related
alkaloids.3 It also contains a small amount of a volatile oil.
PHARMACOLOGY: The activity of goldenseal is largely due to the presence
of
hydrastine and to a lesser extent from berberine.4 Goldenseal has been
used as a uterine
hemostatic but was found to be unreliable in its action; its activity was
inferior to that of
the ergot alkaloids in the treatment of postpartum hemorrhage. Berberine
stimulates bile
secretion and is used as a sedative in mice. It has weak antibiotic activity
and some
antineoplastic activity.5 Several reports show berberine to be effective
against many
bacteria that cause diarrhea, including cholera bacteria. Several animal
studies also show
goldenseal helps shrink tumors.2
Hydrastine constricts peripheral blood vessels and has been investigated
for the treatment
of gastric inflammation. Hydrastine administered internally can result
in a rise in blood
pressure, where as berberine can induce hypotension.4 The plant has been
associated
with a hypoglycemic effect.6 Empirical evidence and clinical experience
suggest
goldenseal may be useful in helping to "cleanse" the liver or blood and
restore digestive
function in alcoholics.7
Goldenseal had gained the reputation of being able to prevent the detection
of morphine,
marijuana or cocaine in urine samples.8 This notion arose from a plot in
John Uri Lloyd’s
novel Stringtown on the Pike(Dodd Mead, 1900), and was given further credence
by
the fact Lloyd was an internationally known plant pharmacist.7 However,
studies have
found no basis for this belief.9
TOXICOLOGY: In higher doses, hydrastine can cause exaggerated reflexes,
hypertension, convulsions, and death from respiratory failure. Large doses
of the plant
irritate the mouth and throat and cause nausea, vomiting, diarrhea, and
paresthesias.
CNS stimulation and respiratory failure induced by the plant can be fatal.
Moderate
doses of the alkaloid hydrastinine cause peripheral vasoconstriction and
increased
cardiac output. A 10% solution of hydrastinine causes pupillary dilation.10
SUMMARY: The topical use of goldenseal extracts in sterile eye washes persists
although there is little clinical evidence for its effectiveness. The plant
possesses astringent
and weak antiseptic properties which may be modestly effective in treating
minor oral
problems.11 12 While small amounts of the plant can be ingested with no
side effects as a
component of bitter tonics, large doses can be toxic. The effects of the
plant and its
extracts in pregnant women are inconclusive. Some animal studies show berberine
calms
the uterus, while others have shown it stimulates uterine contractions.
Goldenseal should
be avoided during pregnancy.
Grape Seed Extract (Proanthocyanidins)
By James B. LaValle R.Ph., D.H.M., D.H.Ph.
Standardized to: 40-80% proanthocyanidins or 95% polyphenols
Active constituents: proanthocyanidins (also known as leucocyanidins or PCO's)
Dosage: 25-100 mg. 1-3 times a day
Traditional Uses:
Allergies and asthma
Prevention of atherosclerosis
Improves microcirculation of the brain, heart and periphery
Decreases platelet aggregation; improves blood flow
Variscosities
Retinopathy and macular degeneration
Improves elastic fibers of collagen and elastin of capillaries
Arterial or venous insufficiency, intermittent claudication
Preventative and anti-aging effects
Introduction
PCO's could be one of the most important natural products to be discovered
in the last
several years. Some call it a neutraceutical, and yet others consider it
an herb. It is a
flavonoid rich compound which is being heavily touted as one of the most
potent free
radical scavengers known, being about 20 times more powerful than Vitamin
E, and as
much as 50 times as strong as Vitamin C. It enhances absorption of and
works
synergistically with Vitamin C. Pine bark extract (Pycnogenol) is closely
related to Grape
Seed Extract..
Pharmacology
Proanthocyanidins have the incredible ability to support collagen structures
and inhibit the
destruction of collagen. They accomplish this via several mechanisms of
action. First, they
protect 1-antitripsen, a chemical which keeps enzymes from breaking down
collagen,
elastin, and hyaluronic acid. PCO's also directly inhibit the damaging
enzymes. Secondly,
proanthocyanidins also neutralize lipid peroxidation damage to cell membranes
through
their free radical activity. This collagen protection is very important
for health. It allows
for red blood cells to penetrate into the microcapillary system and won't
allow fluids to
leak out of the blood. They tend to strengthen the capillary walls and
skin. PCO's also
inhibit the release of mediators of inflammation, such as histamine and
prostaglandins.
Proanthocyanidins neutralize many free radicals, including: hydroxyl, lipid
peroxides and
iron induced lipid peroxidation. They also inhibit the enzyme xanthine
oxidase. PCO's use
in allergies has been quite successful because of its ability to inhibit
the degradation of
mast cells and the subsequent release of histamine and other mediators
of inflammation.
Toxicities, Cautions and Contraindications
Extremely safe with no known toxicity or adverse effects noted even under
extremely
high doses.
PANAX GINSENG and SIBERIAN GINSENG:
By: Jim LaValle
Overview:
Ginseng may be the most famous herbal medicine in the world. It is certainly
the most
widely used herbal in the U.S and has helped retail pharmacy to stimulate
interest in the
herbal market in this country. Historically Ginseng has been used for a
wide variety of
health benefits - especially for its adaptogenic and prophylactic effects
on individuals
under stress or fatigue. In the past, its benefit has been exaggerated,
but today Ginseng
has proven to be of true value. There are several species of Ginseng which
find their way
onto the pharmacy shelf. Most common are Chinese or Korean (the most prized),
American and Siberian species (considered distinct from the Panax species).
Each may
have a slightly different application.
As pharmacists, we should be aware of these differences and know when it
is
appropriate to recommend each. Care should be given in recommending Ginseng
because it could aggravate or exacerbate certain conditions. Standardized
extracts should
be chosen. Without standardization, the content of the active compounds
can vary widely
from bottle to bottle and brand to brand; and the lack of quality may give
erratic if not
potentially toxic effects.
Pharmacology:
As adaptogens, both the Panax Ginseng and Elucthcroccus Senticosus (Siberian)
exhibit
the ability to increase non-specific resistance of the body to a wide range
of chemical,
physical, psychological and biological stressors. Adaptogens have the ability
to switch
from stimulating or sedative effects depending on the biochemical terrain.
The chief
constituents responsible for the activity of Panax Ginseng are the ginsenosides.
American
Ginseng, exhibits sedative and relaxing properties, weak anti-inflammatory
activity,
improved stamina and increased learning capacity and may be better suited
for females in
addition to males, younger people and elderly populations. The triterpenoid
structure is
similar to steroid hormones. It is thought ginsenoside terpenes act at
hormonal receptor
sites, especially in the hypothalamus and pituitary glands stimulating
secretion of ACTH.
Ginsenosides stimulate RNA, protein synthesis and cholesterol production
in the liver,
increase hepatic rough endoplasmic reticulum, show carbohydrate-sparing
and stamina
increasing activity in muscle tissue, increase enzymatic activity and fatty
acid production
as well as increase adrenal cholesterol by 20%. Other components of ginseng
have
shown the ability to lower blood sugar in diabetic mice and yet have no
effect on normally
functioning lab animals. Studies show ginseng lowers cholesterol levels
in diabetics having
a positive benefit in regards to insulin regulation. Other activities of
ginseng include
anti-cancer and anti-aging effects on cells as well as immunostimulating
activity to the
reticulo-endothelial system. Studies show use of ginseng will reduce the
risk of viral
infection. Ginseng has shown both hypertensive and hyptotensive effects
which are dose
dependent. Lower doses have shown a hypertensive effect and higher doses
a
hypotensive effect. Ginseng may have the ability to decrease total cholesterol,
triglycerides, platelet adhesiveness and increase HDL cholesterol which
makes it valuable
in cardiovascular disease prevention. Ginseng may have protective effects
for those
people undergoing chemotherapy. Studies show a decrease in weight loss
and greater
white blood cell counts in lab animals administered Ginseng simultaneously
with
chemotherapies. Panax ginseng exhibits some estrogen like activity and
may improve
vaginal lubrication in menopausal women.
Siberian Ginseng owes its activity to glycosides known as eleutherosides.
It has been
studied extensively in Russia with promising results in performance enhancement
protection against environmental pollutants, strong immune stimulating
effects, for allergies
in addition to the other benefits listed. Some herbalists feel Siberian
Ginseng offers more
positive activity and less potential toxicity than the Panax species.
Key actions and indications for Ginseng:
Adaptogenic Activity
Anti-fatigue (both physical and mental)
Anti-stress
Anti-aging
Convalescence and weakness
Insulin regulating (diabetic and hypoglyce