Benefits of many herbs...

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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.

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 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.

Back to the Top of Page

 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 hypoglycemic)
           Anti-cancer effects
           Adjunct for chemotherapy
           Immunostimulating effects
           Liver effects

      Contra-indications, cautions, warnings:

           Because of the potential for high germanium content in ginseng, it should not be
           recommended to people with kidney failure, and one case has been sited where
           ginseng may have precipitated kidney event.
           Ginseng may cause breast tenderness in some women
           Ginseng should not be taken in stage 2 or higher hypertension
           Ginseng should not be recommended in acute inflammatory diseases or bronchitis
           Do not use if chronic disease of the GI tract such as diverticulitis, esophageal
           reflux, etc. is present
           If used as stress support a regimen of 3 weeks on 1-2 weeks off is best
           Do not recommend in high doses during acute phases of infection especially with
           high fever. It may actually suppress immunity.
           Do not take if pregnant or nursing unless prescribed by a doctor
           As with any herb do not use in children under 2 years of age unless instructed by a
           physician.
           Do not take if suffering from anxiety and extreme nervousness

      Dosage:

      Approximately 200-600mg daily of standardized extract (standardized at 5-15%
      ginsenoside content). If excitability occurs reduction in dosage may be needed. Siberian
      ginseng standardized to .8% eleutherosides 200-600mg daily. Adverse effects include
      diarrhea, insomnia, nervousness, nausea and vomiting. Side effects are infrequent in
      recommended doses.

      The Verdict:

      Ginseng may offer some positive benefits as a general tonic for overall health, especially
      for stress conditions, fatigue, concentration, recovery from some illness and for improved
      stamina.

      Jim LaValle is a registered pharmacist with over 10 years of clinical experience in
      the Natural Medicine Industry. Jim is an adjunct instructor for Natural Medicine at
      the University of Cincinnati College of Pharmacy.

 TOPIC: Peppermint

      SCIENTIFIC NAME: Mentha x piperita L. Peppermint is a hybrid of M. spicata L.
      (spearmint) and M. aquatica L. Family: labiatae

      COMMON NAME: Peppermint

      BOTANY: This well-known perennial is a classical member of the mint family. It has a
      squarish purple-green stem with leaves of dark green or purple and lilac-colored flowers.
      The plant is generally sterile and spreads by means of stolons(basal branches). A variety
      of types of peppermint exist and these are cultivated worldwide.

      HISTORY: Peppermint and its oil have been used in Eastern and Western traditional
      medicine as an aromatic, antispasmodic and antiseptic in treating indigestion, nausea, sore
      throat, colds, toothaches, cramps and cancers. Today, the oil is used widely as a
      flavoring and as an ingredient in cough and cold preparations. It is also found in numerous
      antiseptic and local anesthetic preparations.

      CHEMISTRY: The chemistry of peppermint oil is complex. More than a hundred
      components have been found in the oil and their relative concentrations vary between
      cultivars and geographic location.1 Peppermint yields 0.1% to 1% of a volatile oil that is
      composed primarily of menthol(29% to 48%), menthone(20% to 31%) and methyl
      acetate(3% to 10%).

      PHARMACOLOGY: As is observed with numerous other volatile oils peppermint oil
      possesses antibacterial activity in vitro. However, this has not been of significant clinical
      benefit. Peppermint extracts have been reported to have antiviral activity against
      Newcastle disease, herpes simplex, vaccinia and other viruses in culture(Leung).
      Peppermint oil has been shown to exhibit spasmolytic activity on smooth muscles.
      Commercial preparations are available for use in the treatment of irritable bowel,
      abdominal pain and related symptoms. When administered orally, these
      peppermint-containing drugs appear to be effective.2 Generally administered as
      enteric-coated capsules, these preparations release their contents in the large intestine
      and colon; peppermint, therefore, appears to act directly on this smooth muscle. The
      spasmolytic activity is related to menthol content and it has been demonstrated that this
      activity is due to the calcium antagonist effect of menthol.3
      The flavonoids in peppermint leaves reportedly have choleretic(bile stimulating) effects in
      dogs(Leung). A related effect was confirmed in one study in which guinea pigs were
      administered intravenous doses of the essential oil of peppermint in doses of 0.1 to 50
      mg/kg. Prior to dosing, the sphincter of Oddi had been concluded by the administration
      of morphine. Following a single dose of 1 mg/kg of peppermint oil, a rapid and complete
      opening of the sphincter was observed. However, in doses of 25 or 50 mg/kg,
      peppermint oil again constricted the sphincter.4
      Azulene, which is found in small quantities in peppermint oil, is known to have
      anti-inflammatory and antiulcerogenic effects in animals.

      TOXICOLOGY: Peppermint is generally recognized as safe for human consumption as
      a seasoning or flavoring, as are other mints from which menthol is derived as a plant
      extract.
      Menthol, the major component of peppermint oil, may cause allergic
      reactions(characterized by contact dermatitis, flushing and headache) in certain
      individuals(Leung). The application of menthol-containing ointment to the nostrils of an
      infant for the treatment of cold symptoms has been reported to have caused instant
      collapse(Leung).
      Rats fed peppermint oil in daily doses of up to 100 mg/kg for 28 days developed
      dose-related brain lesions. These were similar in nature to the neuropathy induced
      byhexachlorophene.5 However, one would only expect to observe doses of this
      magnitude ingested in a case of overdosage with the oil.
      Because of the oil's ability to relax gastrointestinal smooth muscle, persons with hiatal
      hernia may experience worsening of symptoms while ingesting peppermint-containing
      preparations.

      SUMMARY: Peppermint and its oil are used extensively in foods and drugs. The oil is a
      complex mixture of more than one hundred compounds. Menthol, which is found in the
      highest concentration, is pharmacologically active in relatively small doses. Extracts have
      been used with preliminary success in the treatment of certain gastro-intestinal disorders.

      REFERENCES:

      1 Hoffman BG and Lunder LT, Planta Medica 50:361, 1984; Maffei M and Sacco T,
      Planta Medica 53:214, 1987. 2 Rees WDW et al, Brit Med J:835, 1979. 3 Taylor BA
      et al, Proceedings of the British Pharmacol Soc, April, 1985. 4 Giachetti D et al, Planta
      Medica 54:389, 1988. 5 Olsen P and Thorup I, Arch Toxicol Suppl 7:408, 1984.
      ________________________________________________________________________

      Reprinted with Permission from The Lawrence Review of Natural Products© 1990
      Facts and Comparisons (ISSN 0734-4961). All rights reserved.
 
 

 Red Pepper Peps Runners

      NEW YORK (Reuters) -- Athletes seeking to gain a competitive edge might someday
      consider spicing up their meals with red hot pepper, a study suggests.

      Korean runners who ate a breakfast laced with 10 grams (0.3 oz.) of dried hot red
      pepper powder burned carbohydrates faster both at rest and during exercise. They also
      showed increased blood levels of stress-related hormones.

      Hot red chili peppers have become one of the most popular spices for flavoring foods.
      Capsaicin is the pepper's active ingredient, and studies have shown that it can increase fat
      and energy metabolism by increasing blood levels of the so-called "fight or flight"
      hormones epinephrine and norepinephrine, collectively known as adrenaline.

      For that reason, researchers from the University of Inchon in Korea, and Fukuoka
      University in Japan wanted to study capsaicin's effects on an athlete's ability to burn
      carbohydrates, both at rest and during exercise.

      The researchers fed eight male middle- and long-distance runners a standard Korean
      meal the night before the race, and a low-fat breakfast the following morning containing
      10 grams of dried hot red pepper powder.

      "The amount of hot red pepper powder used in this study was about 1.5 times the
      average daily consumption in Korean individuals," the researchers state.

      Following the meals, the researchers collected blood and breath-gas samples every 30
      minutes for 2 1/2 hours. The men then exercised on stationary bicycles for one hour at
      moderately hard levels. Again, blood and gas samples were collected, this time every 10
      minutes.

      On two other occasions, for comparison data, the runners were tested after eating a
      breakfast without the pepper powder.

      The analysis of gas and blood measures suggested that, both at rest and during exercise,
      eating red hot pepper increased the breakdown and use of carbohydrates for exercise
      energy fuel. At rest, the pepper-laden meal increased oxygen consumption by 13% and
      energy expenditure by 10%. But during exercise, oxygen consumption and energy
      expenditure "were not different between the hot red pepper and control trials," the
      researchers state.

      But what does this mean for high-powered athletes?

      "It's not clear from this report whether this is going to hurt performance or improve
      performance," says exercise physiologist Dr. Edward Coyle, director of the Human
      Performance Laboratory at the University of Texas in Austin.

      Coyle says the runners "are obviously showing a stress reaction, which is not surprising
      from eating hot red pepper."

      He notes that increased stress, which can also be induced by dehydration and increasing
      exercise intensity, is known to help boost blood levels of these stress-related
      "catecholamine" hormones, which cause faster carbohydrate burning.

      "These are interesting preliminary findings that I don't think are conclusive," he says.

      SOURCE: Medicine and Science in Sports and Exercise (1997;29:355-361)

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 TOPIC: Rose Hips

      SCIENTIFIC NAMES: Commonly derived from Rosa canina L., R. rugosa Thunb.,
      R. acicularis Lindl, or R. cinnamomea L. Numerous other species of rose have been
      used for the preparationof rose hips. Family: Rosaceae

      COMMON NAMES: Rose hips, "heps"

      BOTANY/SOURCE: Rose hips are the ripe ovaries or seeded fruit of roses forming on
      branches after the flower.1

      HISTORY: Rose hips are a natural source of vitamin C, which has lead to their
      widespread use in natural vitamin supplements, teas and various other preparations
      including soups and marmalades.2 Although these products have been used historically as
      nutritional supplements, they have also found use as mild laxatives and diuretics. One
      newspaper account indicated that a mixture of parsley, licorice, hot pepper and rose hips
      could lower the cholesterol content of eggs from chickens fed the herbal mixture.3

      CHEMISTRY: Fresh rose hips contain from 0.5% to 1.7% vitamin C2, usually
      determined as a combination of I-dehydroascorbic acid and I-ascorbic acid.4 However,
      the content of dried commercially available rose hips products varies considerably. Rose
      hips also contain pectin (11%), malic and citric acids, carotenoids, polyphenols and a
      variety of minor components.

      While some accounts suggest that rose hips arethe richest natural source of vitamin C, a
      number of more concentrated sources have been identified. Citrus fruits contain
      approximately 50 mg vitamin C per 100 g. Uncooked broccoli, kale and kiwi fruit,
      approximately 100 mg; black currants, guavas and some tropical vegetables, 200 to 300
      mg; rose hips (Rosa canina), 1250 mg; acerola or Barbados cherry (Malpighia
      punicifolia), 1000 to 2330 mg; and Terminalia ferdinandiana, up to 3150 mg.5

      PHARMACOLOGY: Vitamin C is used as a nutritional supplement for its antiscorbutic
      properties. Because a significant amount of the natural Vitamin C in rose hips may be
      destroyed during drying and processing, many "natural vitamin supplements" have some
      form of vitamin C added to them. One must read the label carefully to determine what
      proportion of the vitamin C is derived from rose hips versus other sources. Unfortunately,
      this information is not always available on the package label.

      The laxative activity of rose hips may be related to the presence of malic and citric acids
      or to purgative glycosides (multiflorion A and B).6

      TOXICOLOGY: Rose hip ingestion is not generally associated with toxicity. More than
      100 g of plant material would have to be ingested to obtain a 1200 mg dose of vitamin C,
      an impractical amount to ingest. Most people do not have any side effects from ingesting
      small gram quantities of the plant. Adverse effects associated with the long-term ingestion
      of multi-gram doses of vitamin C (i.e., oxalate stone formation)7 have not been reported
      with rose hips. Production workers exposed to rose hip dust have, however, developed
      severe respiratory allergies, with mild to moderate anaphylaxis.1

      SUMMARY: Rose hips are a pleasant-tasting source of natural vitamin C. Because the
      concentration of the vitamin is relativelylow, one must ingest large amounts of the product
      to serve as a viable nutritional supplement. Many natural rose hip products are fortified
      with ascorbic acid.

      _____________________________________________________________________

      Reprinted with permission from The Lawrence Review of Natural Productsâ 1991 by Facts and
      Comparisons (ISSN 0734-4961).
 
 

 TOPIC: Shark Cartilage and Squalamine

      SCIENTIFIC NAMES: Squalus acanthias(spiny dogfish shark), Sphyrna lewini
      (Hammerhead Shark) and other shark species.

      COMMON NAMES: Spiny dogfish shark, hammerhead shark and other species

      SOURCE: Shark cartilage is prepared from the cartilage of freshly caught sharks in the
      Pacific Ocean. The cartilage is cut from the shark, cleaned, shredded and dried. One of
      the main processing plants for dogfish shark is in Costa Rica. The finely ground cartilage
      is uniformly pulverized (in a 200 mesh screen), sterilized and encapsulated. Gelatin
      capsules contain 740 mg, usually without additives or filler, and are claimed to be "all
      natural." The 100% pure shark cartilage is also available in 200 g and 500 g capsules in
      safety-sealed bottles (eg, Cartilade®). 1 2

      Squalamine was originally isolated from shark stomachs, but has subsequently been
      synthesized.1 This compound is still in the experimental stage and is not yet commercially
      available.

      CHEMISTRY: Early claims were made that extracts of shark cartilage inhibited tumor
      anglogenesis when implanted in rabbit corneas. The active principle(s) has not been
      found, although some believe it might be a protein.1 2 Several studies have been done on
      various sharks. Pettit and Ode3 isolated and characterized sphyrnastatin 1 and 2 from the
      hammerhead shark. Neame et al4 recently reported on the isolation of a protein from reef
      shark(Carcharhinus springeri) cartilage which bears a striking resemblance to human
      tetranectin. Moore et al5 discovered a broad-spectrum steroidal antibiotic from the
      dogfish shark which they named squalamine; chemically it is 3-beta-N-(N-[3-(4-
      aminobutyl)]-1,3-diaminopropane)-7 alpha, 24 zetadihydroxy-5 alpha-cholestane
      24-sulfate.

      PHARMACOLOGY: Many claims have been made that shark cartilage can cure
      cancer. The rationale includes the fact that sharks rarely get cancer, that sharks are
      cartilaginous fish and that cartilage is avascular and contains agents that inhibit
      vascularization (anglogensis). The reasoning then follows that sharks do not get cancer
      because the inhibited vascularization prevents the formation of tumors; hence, giving it to
      humans may inhibit tumor angiogenesis and thus cure cancer.1

      In late 1992, incomplete and since non-replicated clinical studies(unpublished) in Havana,
      Cuba, purported to show some progress in terminally ill cancer patients. The National
      Cancer Institute reviewed these studies and decided against researching shark cartilage.1
      Recently, however, the FDA granted an IND application for a shark cartilage product,
      BeneFin, by Lane Labs-USA, Inc. to investigate benefits in prostate cancer and AIDS
      associated Kaposi’s sarcoma.6

      Certainly, future work should continue to focus on the isolation of the responsible
      proteins or small molecules. The tetranectin-like protein from the reef shark is important
      since, in man, tetranectin enhances plasminogen activation catalyzed by the tissue
      plasminogen activator. It may also play a role in cancer metastasis. Research along these
      lines by Moore et al5 has demonstrated the presence of a broad-spectrum aminosterol
      antibiotic in the dogfish shark which they named squalamine. It shows significant
      bactericidal activity against both Gram-negative and Gram-positive bacteria. It is also
      fungicidal and induces activity against protozoa.5 This discovery implicates a unique
      steroid acting as a potential host-defense agent in vertebrates and provides unique
      concepts of chemical design for a new family of much needed broad-spectrum
      antibiotics.

      TOXICOLOGY: No toxicity data has appeared in current literature on either shark
      cartilage or squalamine.

      SUMMARY: Initial interest on the purported anticancer effects of cartilage from dogfish
      shark has waned since the National Cancer Institute decided against supporting studies
      on it. A few studies on related species show interesting active protein substances that
      may be useful as cancer control agents. However, the only active small molecule with
      promise is the aminosterol called squalamine. Its major activity experimentally has been
      as a unique and potent antibiotic with fungicidal and antiprotozoal activity. Clinical data
      should be forthcoming.

      ____________________________________Back to the Top of Page____________________________________

      Reprinted with permission from The Lawrence Review of Natural Products®
      Copyright© 1995 by Facts and Comparisons(ISSN 0734-4961). All rights reserved.
 
 

 Vitamin E Boosts Elderly Immunity

      NEW YORK (Reuters) -- Vitamin E, already much in the news for its benefits in
      combating heart disease and Alzheimer's disease, may help boost the waning immune
      system of the elderly, a new study shows.

      A group of people over age 65 who took 200 milligrams (mg) of vitamin E a day for
      eight months showed large improvements in their bodies' ability to produce antibodies
      that fight off a variety of infectious diseases, including hepatitis B and tetanus.

      The new findings appear this week in The Journal of the American Medical Association.

      Dr. Simin Nikbin Meydani, nutritionist and immunologist at the U.S. Department of
      Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston,
      Massachusetts, says the discovery is important because it suggests that elderly people
      ought to be taking about 20 times more vitamin E daily than the current recommended
      amount of 8 to 10 mgs.

      "What we've been trying to do is see if there are dietary factors that can reverse the
      decline in the immune system with aging," she says.

      "Many studies have shown that with aging, there is a dysregulation in parts of the immune
      system which contributes to an increase in infectious diseases, an increase in tumors, and
      to immune diseases like arthritis. It is a big problem for the elderly," she adds, noting that
      infections such as pneumonia and influenza are among the leading causes of death in older
      people.

      The researcher points out that although they get flu vaccinations in the fall, "it is only 60%
      as effective in older people as it is in younger people. They don't develop as much
      antibody."

      Meydani and her colleagues from Harvard and Boston universities divided 88 study
      participants into four groups, who were then given daily doses of either 60, 200, or 800
      milligrams (mg) of vitamin E or given an inactive placebo. All participants were in good
      health and lived in the community rather than in institutions.

      The subjects were given a skin sensitivity (DTH) test to observe their immune reactions
      to a number of infectious agents, including tetanus, diphtheria, and streptococcus
      bacteria. They also received a series of vaccinations and booster shots against
      pneumonia, hepatitis B, and tetanus/diphtheria. Blood samples were later evaluated for
      antibodies against these diseases and compared with blood samples taken when the
      study began.

      While participants showed improved immune response no matter how large a dose of
      vitamin E they took, the optimal results were observed in the group taking the 200 mg
      supplements.

      Specifically, people consuming 200 mg of vitamin E had a 65% increase in DTH and a
      sixfold increase in antibody levels to hepatitis B compared with those taking the placebo.
      The DTH increases for 60 mg and 800 mg vitamin E were 41% and 49%, respectively.
      And the antibody increases were 3-fold and 2.5-fold. People taking 200 mg vitamin E
      also showed significant antibody increases in response to the tetanus vaccine.

      The improvement in antibody response associated with the antioxidant vitamin E did not
      come as a surprise to the researchers, says Meydani. But the optimal amount did.

      "The problem with a lot of studies in nutrition is that you find something, and people think
      more must be better," she says. "But what this points out is that you don't really have to
      go above 200 mg to see the results. What it's saying is there is an optimal level, and
      people shouldn't be thinking more is better."

      For most people, however, getting 200 mg of vitamin E a day probably requires taking a
      vitamin supplement, Meydani says. The vitamin is found in large amounts in oils and nuts,
      which means diets high in the nutrient also tend to be high in fat.

      "It is possible for a dietitian to put together a diet that includes this much vitamin E,"
      Meydani notes, "but it isn't easy." SOURCE: The Journal of the American Medical
      Association (1997;277(17):1380-1386)

      Copyright 1997 Reuters
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