Free standard shipping for orders over $340.
Menu
0 $0.00
0
0 $0.00

Blog

Anurag Pande

In Herbal Supplementsby

Stay Fit and Strong / Tribulus Evaluated for Efficacy in Treatment of Generalized Weakness

 

Tribulus terrestris Linn. (Small caltrops, puncture vine) belonging to the natural order Zygophyllaceae, is commonly found in the Indian sub-continent and in Africa. It thrives in well-irrigated black soil, growing at altitudes up to 10,000 feet above sea level. Charaka, the Ayurvedic physician in ancient India, recognized the diuretic and aphrodisiac properties of this plant, and recommended its use in rejuvenative formulations, particularly in the treatment of sexual deficiency. The ancient Greeks used this plant as a diuretic and mild laxative. In south-east Asia, the plant has been used in the treatment of post-partum hemorrhage, epistaxis and gastro-intestinal bleeding1. The fruit and seeds of Tribulus terrestris form a major part of several Ayurvedic formulations prescribed in urinary tract disorders including urolithiasis (urinary stones).

The fruit resembles the cloven hoof of a cow, and the Sanskrit name for the plant, “Gokshura” is derived from this analogy. Recent research in Eastern Europe has confirmed the aphrodisiac properties of this plant. The plant has also been widely used as a diuretic. The diuretic mechanism of action may be through stimulation of the renal blood supply.

 Chemistry

The extract obtained from the powdered root contains alkaloids (harmine, harmaline, harman and tetrahydroharmine) , resins, nitrates and fixed oils. The alkaloids are believed to be responsible for a slight increase in blood pressure and increase in renal perfusion1, with the consequent diuretic action. The fruit contains a semidrying oil (5%), the enzymes peroxidase and diastase, a glycoside resin, proteins and inorganic matter. Several steroidal sapogenins, steroidal saponins, (such as terrestrosins, dioscin, gracillin, kikuba saponin , protodioscin, neohecogenin glucoside and tribulosin) and three flavonoid glycosides have been isolated from the plant2,3.The saponins are obtained from the defatted plant material by extraction with ethyl alcohol3 and may be responsible for the aphrodisiac properties.

Terrestrosin (R : sugars)

Large quantities of potassium and nitrates are also present1. The lipolytic (urinary stone dissolving) properties of the plant have been attributed to the presence of aspartic and glutamic acids1.

 

Pharmacological Action

Preclinical studies:

The diuretic action of the water and alcoholic extracts of the seeds of Tribulus terrestris was studied in albino rats, by comparison of volume of urine collected during a five hour period from the group treated with Tribulus terrestris extract with that collected from a control (untreated) group. A significant diuretic effect was observed in the treated group.

The researchers attributed the diuretic action to the high potassium content of the plant. The aqueous extract of the plant material contained 180 mEq/L potassium. The extract lowered the specific gravity of the urine while the pH of urine increased4. Fig.1(a) compares the diuretic action of Tribulus terrestris with that of isotonic potassium chloride:

Figure 1(a)

Diuretic action = Urinary excretion in test group / Urinary excretion in control group

Fig.1(b) compares the characteristics of the urine in untreated animals with those of treated animals:

Figure 1(b)

The authors of this study postulate that the organic acid anions present in the crude drug are oxidized to bicarbonate in the body of the rat, resulting in the rise of urinary pH. Significant reduction in urinary stone weights was observed in rats with experimentally induced urolithiasis (urinary stones), when treated with different organic extracts of Tribulus terrestris5. Figure 2 shows the reduction in weight of urinary stones in rats treated with various fractions obtained from T. terrestris.

The fertility and aphrodisiac actions have been studied in rats. The steroidal saponins stimulated spermatogenesis and sexual activity in male rats. In female rats, the compound potentiated estrogens and increased fertility6. One study on boars with the standardized extract, at a dose of 70 mg/kg body weight for ten days, indicates the efficacy of T. terrestris in improving sexual functions of the animals 10.

 

Clinical Uses:

In Ayurveda, the plant has been used in treating genito-urinary troubles, and has been prescribed in treating impotence, urolithiasis, and as a geriatric tonic for centuries. An Ayurvedic preparation containing Tribulus terrestris, has been evaluated for efficacy in the treatment of generalized weakness. Fifty patients complaining of lethargy, fatigue and lack of interest in day to day activities, for periods ranging from two to six months were studied. An overall inprovement (45%) in symptoms of lethargy, fatigue and decreased mental alertness was observed7.

The standardized extract of Tribulus terrestris has been found to have a stimulating effect on the libido8. In one study, tests on healthy men demonstrated that a five day treatment with three tablets of the standardized extract (250 mg each) per day significantly increased the blood levels of testosterone by approximately 30%.10

In another study, a group of men suffering from a range of reproductive disorders (impotence, hypogonadism, infertility) were treated with the standardized extract of T. terrestris, administered in doses ranging from 750-1500 mg per day for thirty to sixty days. The results confirmed previous observations, and the treatment increased testosterone levels and improved libido without producing side effects10. Other positive changes observed in the long term study with a standardized extract of Tribulus terrestris, included reduction in blood cholesterol levels, improved mood and increased self confidence10. The reported increase in testosterone levels may be of particular interest in sports medicine, since testosterone belongs to a group of potent anabolic hormones.

Possible mechanism of action : The authors of the long term study cited above, postulate that T. terrestris probably produces its clinical effect through stimulation of secretion of leutenizing hormone (LH) produced by the pituitary gland in males. In women, follicle stimulating hormone, (FSH, but not LH) and the female hormone, estradiol (but not testosterone) were found to increase when treated with a standardized extract of Tribulus terrestris. According to the authors, T. terrestris may have particular potential in alleviating both the physiological and psychological symptoms accompanying menopause10.

 

Safety:

Clinical studies with the standardized extract of Tribulus terrestris revealed no adverse effects 10. The LD50 in rats, was found to be greater than 10 g per kg body weight. The standardized extract produced no adverse effects in rats fed oral doses of 150 mg per kg body weight per day, administered over an extended period up to 25 months.

References

  1. Selected Medicinal plants of India, CHEMEXIL (1992), 323-325.
  2. Mahato, S. et al.(1981) J. Chem. Soc., Perkin Trans. 1, 2405.
  3. Yan, W. et al. (1996) Phytochemistry, 42(5) 1417-1422.
  4. Santha kumari, G. and Iyer, G.S.N. (1967) Ind. J. Med. Res., 55(7), 714-716.
  5. Anand, R. et al. (1994). Indian Journal of Experimental Biology, 32, 548-552.
  6. Pramodkumar et al. (1980) J. Sci. Res. Plants Med. 1:9
  7. Jayaram, S.etal. (1993) Indian Drugs, 30(10), 498-500.
  8. Tomova, M. (1987) . Farmatsiya, 37(6), 40-42
  9. Milanov, Maleeva and Taskov (1981), cited in reference 8, page 142.
  10. Wright, J. (1996) Muscle and Fitness, September, 140-142, 224.

 

In Curcumin, Turmericby

Curcuminoids To Make A Difference in the Way You Feel

Curcuminoids are plant nutrients (also called phytonutrients) that are found in turmeric root (Curcuma longa) — the chief ingredient in curry powder that gives the mixture its yellowish-orange color. Curcuminoids are antioxidants; this means that they neutralize free radicals. The most prominent of the curcuminoids is curcumin.

Free radicals are reactive molecules that are produced by cell deterioration and accelerate the aging processes within the body. Think of them as tiny, invisible sharks zipping around in our cellular seas, taking small electrical bites out of muscle tissue, nerves, and glands. Curcuminoids act as nutritional “police” by deactivating these free radicals so they don’t wreak further havoc in our systems.

The Curcuminoids originate in a herbaceous plant, Curcuma longa that is a member of the ginger family (Zingiberaceae). The best source of this spice comes from Kerala, India. The underground root of turmeric is widely used in culinary dishes throughout the world. Only until very recently, have some of its main components been shown to have medicinal applications as well.


curcuminoids

The real strength in turmeric lays in the curcuminoids. There are basically three that we know of right now: curcumin, demethoxycurcumin and bisdemethoxycurcumin.

Besides their already mentioned antioxidants properties, these compounds also manifest anti-inflammatory, anti-mutagen, and anti-cancer activities as well. Inflammation is often due to physical trauma or disease. Numerous experiments conducted on animal models and human volunteers have repeatedly demonstrated wonderful anti-inflammatory action of these curcuminoids. The development of cancer, on the other hand, is a more complex, multifaceted process. Any number of environmental agents, dietary factors, and irregular social behavior initiate chemical stresses of different sorts within the human body. This commences on a cellular level, where such stresses trigger the production of abnormal cells. Curcuminoids have shown the ability to correct this production mistake and soon healthy cells are being formed again.

Curcuminoids have also manifested definite action within the liver several different ways. For one thing, they protect this vital organ from swelling, hardening, and infection. For another, they keep blood which constantly passes through it, flowing evenly which allows better detoxification of the entire organism. Bear in mind that the liver is our major detoxifying organ in the body.

The antibacterial, antiviral, and antiparasitic effects of turmeric root’s principal constituents have also been looked at as well. Interestingly enough, the main curcuminoid, curcumin, has its activities in these areas significantly enhanced with exposure to sunlight. Aflatoxins from ingested moldy food have been significantly neutralized by some of these curcuminoids before they could harm the liver. And intestinal parasites don’t like to stay around very long, on account of curcuminoids presence.

So, what may we deduce from all this information? Simply that curcuminoids help keep us young, cancer-free, and protect against inflammatory disorders like arthritis. Our vital organs, such as the heart and liver are reinvigorated with the strengthening properties of the curcuminoids.

Recent studies by Sabinsa Corporation at leading university in the US revealed that the unique composition of curcuminoids present in Sabinsa’s Curcumin C3 Complex product demonstrated the ability to not only scavenge and neutralize harmful existing free radicals, it was also able to prevent their formation in the first place. An ingredient with such capabilities should perhaps be thought of as more than just another antioxidant. Features such as these merit the term bioprotectant.

To keep your internal self in great shape, the inclusion of Curcumin C3 Complex into product formulations is recommended. Think of curcuminoids as giving your body a whole “new lease on life.” They are readily available, safe to use, and stronger in their effects than many of the other standard antioxidants. No human biological system should be without them.

Curcumin C3 Complex is a registered trademark of Sabinsa Corporation

Patent pending

Disclaimer:

This product overview was written for the sole purpose of giving a brief history along with educational insights into the product listed above. It is not designed, in whole or in part, as advice for self-diagnosis or self-treatment and should not be construed as such.

In Ginger Root Extractby

Management of Headache, Nervous Diseases, Nausea, and Vomiting Using Ginger Root Extract

Ginger is a well known spice and flavoring agent which has also been used in traditional medicine in many countries. This large seasonal plant is cultivated in Southeast Asia and China, India, and some parts of Africa. Ginger and turmeric plants have several similar characteristics – both possess pale green flowers and are surrounded by long lanceolate leaves.

Ginger, a source of valuable phytonutrients, is characterized as having an aromatic odor and a pungent taste1. The part of the ginger plant that is used is the root, which is botanically the rhizome. The flat surfaces of the rhizome are removed, leaving the remains of the underground stem2. Ginger contains essential oils including gingerol and zingiberene. It also contains pungent principles such as zingerone, gingerol and shogaol3.

For centuries, in Ayurvedic and Tibetan systems of medicine, ginger has been used in the management of headache, nervous diseases, nausea, and vomiting. Ginger has been noted to treat migraine headaches without side-effects4. In addition, it is also recommended in the management of rheumatic disorders and muscular pain5.

Chemistry

The ginger rhizome has the following chemical composition:

  • 60% starch,
  • 10% proteins,
  • 10% fats,
  • 5% fibers,
  • 6% inorganic material,
  • 10% residual moisture,
  • 1-4% essential oil5.

The percentage of essential oil varies with geographic origin. However, its chief elements, sesquiterpene hydrocarbons, remain constant. These include (-)-zingiberene, (+)-ar-curcumene, (-)-ß-sesquiphellandrene, E, E- a -farnesene, and b -bisabolene. These essential oils occur alongside monoterpene alcohols and aldehydes present as glycosides. A mixture of many terpenes and some non-terpenoid compounds make up the essential oil.1 It has been speculated that since there are a variety of chemical classes that these compounds can belong to, it is likely that ginger can eliminate symptoms associated with a variety of illnesses, such as arthritis, by interfering with the production and release of metabolic products from lipid membranes, peptides, proteins and amino acids.

Experimental data reveal that ginger may be a dual inhibitor of eicosanoid synthesis, inhibiting the synthesis of both prostaglandins and leukotrienes, which are inflammatory mediators produced from arachidonic acid5.

The rhizome contains a variety of chemicals called gingerols which provide its distinctive taste and characteristic pharmacological effects. The chemical constituents responsible for the pungent taste of ginger are 1-(3’ –methoxy –4’-hydroxypheny1)-5-hydroxyalkan- 3-ones, also known as [3-6]-,[8]-,[10]-,and [12]-gingerols.1

Biological Effects and Clinical Uses

In recent years, researchers have scientifically validated many of the therapeutic uses of ginger.

    • One study indicates that ginger is effective in reducing inflammation in arthritic conditions. In a study conducted with 56 patients experiencing either rheumatoid arthritis, osteoarthritis, or muscular discomfort, 75% experienced relief in pain and swelling after using powdered ginger. Furthermore, none of the patients complained of any side effects while using ginger to treat their symptoms. It is suggested that ginger works as an inhibitor of prostaglandin and leukotriene biosynthesis to produce its ameliorative effects.5

 

  • Another case study presented ginger as a preventive agent for migraine headache. In this application, one subject was given non-steroidal antiinflammatory medication to permit her migraine headaches to subside. However, even though her headache was eliminated in time, other side effects including depression and redness of the eyes appeared. The subject was then given ginger. With 500-600 mg of powdered ginger mixed with water, the migraine headaches ceased within 30 minutes. In addition, after the cessation of the migraine attack, the subject did not experience any side effects. Migraine headaches are an accumulation of pain syndromes.

Many anitihistamines are used to treat migraines. Ginger has been shown to contain antihistamine and antioxidant factors as well as possess anti-inflammatory action4.

    • The effect of ginger on stimulation of bile secretion was studied to identify the basis of its action as a metabolism enhancer. Results of this specific study reported that the acetone extracts of ginger, comprised of the essential oils and the pungent principles, produce an increase in bile secretion. The two pungent principles that were chiefly accountable for the cholagogic effect of ginger include [6]-gingerol and [10]-gingerol. Bile acids facilitate absorption of fat and electrolytes and peristalsis of the small intestine. Since ginger has been reported to increase bile secretion, it may be beneficial in the excretion of gallstones.3

 

    • Furthermore, a study was done on 20 healthy male individuals that were given 50 g of butter and 5g of ginger a day for seven days. Addition of five grams of ginger with a fatty meal inhibited the platelet aggregation induced by adenosine diphosphate and epinephrine to a large extent. Ginger has been reported to inhibit prostaglandin synthesis in It has been reported that dietary fat content affects platelet aggregation by modifying prostaglandin metabolism. Inhibiting the transformation of arachidonic acid to thromboxane and decreasing the sensitivity of platelets to many aggregating agents may be possible with the administration of ginger in a fatty diet.6

 

  • In view of the fact that ginger root has been used in several parts of the world in the management of motion sickness, researchers attempted to elucidate the mechanism of action. In one of the earlier studies, it was proposed that ginger constituents may increase gastric motility and prevent the accumulation of toxic substances, thereby blocking the gastrointestinal reactions which trigger the nausea feedback8. A more recent study addressed the role of ginger in preventing the nausea feedback at the nerve receptor level. In motion sickness, nausea and vomiting are mediated by specific receptors in the central and peripheral nervous system. These receptors are activated by the chemical messengers, acetylcholine and histamine. Ginger produces antimotion sickness action probably through anticholinergic and antihistaminic effects9.

The above studies indicate the inhibitory effects of ginger on synthesis of inflammatory mediators and the beneficial effects of powdered ginger as well as the isolated gingerols on digestion and metabolism. In view of these effects, ginger is a potential herbal alternative in the management of digestive disorders, migraine, painful arthritic conditions and motion sickness. The herb may be potentially useful in improving blood circulation as well, on account of its inhibitory effects on platelet aggregation. When used as a spice or therapeutically at the recommended levels, [for motion sickness: 300 mg of the extract (containing 5% gingerols) daily in divided doses; for digestive distress: (75 mg of the extract daily in divided doses)], ginger does not have any reported side effects7.

References

  1. Bruneton, Jean. (1995) Ginger. Pharmacognosy, Phytochemistry, Medicinal plants, Lavoisier publishing Co.Inc. 258-261.
  2. Bisset, N.G. (Ed.). Max Wichtl. Herbal Drugs and Phytopharmaceuticals: A Handbook for practice on a scientific basis. Stuttgart: Medpharm Scientific Publishers CRC, 1994,537-539.
2a. Mowrey, D.B., Clayson, D.E.(1982) Motion Sickness, ginger, and psychotropics.  Lancet: 655-657.
2b. Shoji, N. et al. (1982) Cardiotonic principles of ginger. Journal of Pharmaceutical Sciences 71 (10): 1174-1175,.
2c. Tyler, V. The Honest Herbal: A Sensible Guide to the Use of Herbs and Related Remedies. Birmingham, New york: Pharmaceutical products, Press,1993. 147-148.
  1. Yamahara, J. et al. (1985) Cholagogic Effect of Ginger and Its Active Constituents. Journal of Ethnopharmacology, 13: 217-225.
  2. Mustafa, T. and Srivastava K.T. (1990) Ginger (Zingiber Officinale) in Migraine Headache. Journal of Ethnopharmacology, 29: 267-273.
  3. Srivastava, K.C. and Mustafa, T. (1992) Ginger (Zingiber Officinale) in Rheumatism and Musculoskeletal Disorders. Medical Hypothesis, 39: 342-348.
  4. Verma, S.K. et al. (1993) Effect of Ginger on Platelet Aggregation in Indian Journal of Med Res, 98: 240-242.
  5. Zingiber officinale in Selected Medicinal Plants of India (A Monograph of Identity, Safety and Clinical Usage), CHEMEXIL, 1992,pp 362.
  6. Mowrey, D.B.(1982)Motion sickness, ginger and psychophysics. The Lancet, March 20, 656.
  7. Qian, DS and Liu ZS (1992) Pharmacologic Studies of Antimotion Sickness Actions of Ginger. Chung Ho Chung Hsi I Chieh Ho Tsa Chih, 12 (2): 95-8,70.

 

In Coleus Forskohliiby

Spectrum of Potential Therapeutic Activities of Forskolin – Glaucoma, Inflamation and Blood Pressure

Coleus forskohlii extract (standardized to contain 95% forskolin) is potentially useful in skin care formu-lations, particularly as a conditioning agent. Coleus forskohlii  belongs to the Natural Order Labiatae (Lamiaceae), a family of mints and
that grows wild in the warm sub-tropical temperate areas in India, Burma and Thailand.   In India, it is cultivated for use as a condiment1. In traditional Indian systems of medicine, the roots of Coleus forskohlii are used as a tonic.  Other therapeutically relevant properties include anthelmintic action and efficacy in the management of skin infections and eruptions.  The plant is also used traditionally in veterinary practice2.
 

Introduction

Coleus forskohlii  is the only known natural source of the unique adenylate cyclase activating phytonutrient, forskolin3.  Adenylate cyclase is the enzyme involved in the production of Cyclic Adenosine Monophosphate (cAMP), a significant biochemical agent in metabolic processes.  Cyclic AMP is a “second messenger” hormone signaling system. In many hormone sensitive systems the hormone itself does not enter the target cell but binds to a receptor and indirectly affects the production of another molecule within the cell which then diffuses intracellularly to the target enzymes or a receptor inside the cell to produce the response.  This intracellular mediator is called the second messenger.  cAMP and therefore forskolin have marked physiological effects through such “second messenger” actions on various biochemical processes in the body. A recently patented application includes the potentiation of lean body mass and benefits in the management of mood disorders4. Potential topical applications include its role as a skin-conditioning agent to support localized fat loss on topical application5.
 

Phytochemistry

Pharmacological effects

Research carried out over the last few decades has revealed the multi-faceted pharmacological effects of forskolin.  Most of these effects have been linked to the role of forskolin as an activator of adenylate cyclase7.

Adenylate cyclase is also involved in the regulation of lipolysis or enzymatic breakdown of fat in the adipocytes (fat cells).   Hormone sensitive lipase mediates lipolysis and this enzyme is activated through phosphorylation by protein kinase A that in turn is activated by cAMP.
 

Cosmeceutical applications

Topical fat reduction in specific areas of the body is a common concern for women. Ronsard8 popularized the term “cellulite” to describe the dimpling and “orange peel” external appearance of the thighs, the cause of which was attributed to the aging process by later researchers9.   The structure of subcutaneous adipose tissue accounts for the development of the “orange peel” appearance. Groups of fat cells are attached to the underside of the dermis by fibrous connective tissue. As fat cells enlarge, the fibers are stretched and pull down on the underlying skin.  This causes the indentation or dimpling of the skin called cellulite.

It has been demonstrated that adipose tissue metabolism varies from one region of the body to another, for example, in severely obese women losing weight after the jejuno-ileal bypass surgery, fat was seen to be absorbed more slowly in the thigh region than the abdominal region10.  These differences lead to the hypothesis that localized application of agents that trigger lipolysis or fat breakdown could help in cases of fat accumulation at specific subcutaneous sites4.  Forskolin accelerates lipolysis through the activation of hormone-sensitive lipase11

The adrenoreceptors play important roles in the regulation of lipolysis. Adrenoreceptors are neurons that are activated by adrenaline (epinephrine) or similar substances.  The relative number of b-2 and a-2 adrenoreceptors on the surface of the fat cells determine the  balance of lipolysis in those cells. Hormones such as estrogen influence the number of a-2 and b-2 adrenergic receptors in the fat cells.  Through the effects of estrogen, women more a-2 adrenergic receptors in fat cells in the hip and thigh region12.   The a-2 adrenoreceptors and the adenosine receptors in fat cells stimulate specific proteins [GTP inhibitory binding proteins (Gi proteins)] that inhibit adenylate cyclase thereby inhibiting lipolysis. A healthy balance of lipolysis is maintained through the simultaneous action of the b-2receptors that activate specific proteins [GTP binding proteins (Gs proteins)] which in turn activate adenylate cyclase (and thereby cAMP), stimulating lipolysis.    Due to the increased number of a-2 adrenergic receptors in the hip and thigh region in women, fat mobilizaton becomes more difficult from these areas5.  b-adrenergic stimulation and a-2-adrenergic inhibition has been reported to increase lipolysis from fat cells13.

Forskolin bypasses the adrenoreceptors, increasing cAMP levels directly, thereby stimulating lipolysis.  The beneficial effects of forskolin, therefore, do not depend upon the sensitivity of the adrenergic receptors, which can often decreases with age and other physiological factors. Forskolin has also been shown to counteract the decreased response of fat cells to epinephrine, associated with aging.
 

Clinical studies

:
A clinical study performed in 198713 established that regional fat loss from the thigh in obese women could be effected through adrenergic modulation. In this study, twenty eight obese women were placed on a calorie-restricted diet and subjected to one of five topical treatments to one thigh three to five times per week for four weeks: (1) isoproterenol injections; (2) cream containing forskolin, aminophylline, and yohimbine; (3) yohimbine cream; (4) forskolin cream; or (5) aminophylline cream. The opposite thigh was treated with a placebo (injection or cream), serving as the control. The treated thighs lost significantly more girth after treatment (both by injection and by cream). Additionally, no adverse reactions were observed that could be attributed to either the cream or the injections. The authors of this study concluded that local fat reduction from the thigh could be safely accomplished, using agents that affect the adrenergic mechanisms.

In a double–blind clinical trial5, five overweight women were treated with an ointment containing forskolin (1.2 X 10-5 mol/L), yohimbine (2.5 X 10-4 mol/L) and aminophylline (1.3 X 10-2 mol/L) in an aquaphor base on one thigh or the base alone (placebo) on the other thigh, for four weeks, five days per week. The subjects’ thighs were wrapped with warm 600 to 900 mOsm/L magnesium sulfate solutions for 30 minutes prior to each application to maximize transcutaneous absorption.  An occlusive plastic wrap was placed over the area to which the ointment was applied for the entire study period.

Measurements of girth two-thirds of the way between the knee and the greater trochanter were used to measure fat loss at the end of the study period.  Treated thighs showed significant decrease in girth fat loss as compared to untreated thighs with no significant changes in total body weight.
 

 Subjects after treatment with ointment containing forskolin, aminophylline and yohimbine or placebo

The decrease was attributed to the combined actions of forskolin, aminophylline and yohimbine that effected localized fat loss by different mechanisms – forskolin through cAMP and b-2 adrenoreceptor activation; aminophiline through adenosine receptor antagonistic action and inhibition of phosphodiesterase and yohimbine through a-2 adrenoreceptor antagonistic action.

A subsequent trial5 studied the effects of the individual components of the ointment.   Eighteen women were divided into three groups of six each, each group receiving one of the active compounds. The women were placed on a 800 kcal/day diet and encouraged to engage in a walking   program.  As before, the warm wraps with magnesium sulfate were applied, but the occlusive plastic wrap was not used.  Six women had one thigh treated with an ointment containing 25 X 10-5 mol/L forskolin in aquaphor base while the other thigh was treated with the base alone. Thigh girth measurements were taken as before. Four of the six women completed the study and showed significant decrease in treated thigh girth (p < 0.05)  as compared to the untreated thigh

The authors of this study concluded that  localized fat loss could be effected through topical  application of  substances like forskolin that stimulate lipolysis.

The subcutaneous fat cells are stimulated first, the dimpling on the skin of the thigh is lost as tension is relieved on the connective tissue that attached to the under surface of the dermis.

Based on these clinical studies reported in literature, Coleus forskohlii extract 95% is potentially useful in dislodging localized fat deposits immediately under the skin, when applied topically. The recommended levels of use as a skin conditioning agent : 0.1 to 0.5% of a topical formulation, such as an ointment, cream or lotion.   To improve transdermal penetration of the extract, 0.01-0.1% CosmoperineÒ (a standardized preparation derived from black pepper, a registered trademark of Sabinsa Corporation)14 may be added to the formulation.

 

References

  1. Bruneton, Jean.  (1995)  Coleus forskohlii. in  Pharmacognosy, Phytochemistry, Medicinal Plants, Lavoisier publishing Company, 521.
  2. Abraham, Z. In ” Glimpses of Indian Ethnobotany” , S.K. Jain, ed., Oxford & IBM Publishing Co., Bombay, 1981; 315.
  3. de Souza, N.J. (1991) Coleus forskohlii Briq.- The Indian plant source for forskolin. Recent Advances in Medicinal, Aromatic & Spice Crops, (ed: S..P. Raychaudhuri.) Today and Tomorrow’s printers and Publishers, New Delhi, India, Vol I: 83-91.
  4. U.S. Patent # 5, 804, 596. Method of preparing forskolin composition from forskolin extract and use of forskolin for promoting lean body mass and treating mood disorders, assigned to Sabinsa Corporation.
  5. Greenway, F.L. et al. (1995) Topical fat reduction. Obesity Res. 3 Suppl. 4: 561S-568S.
  6. Ammon, H.P.T. and Muller (1989) Forskolin: from an Ayurvedic Remedy to a Modern Agent Planta Medica. Vol 51, 475-476.
  7. Rupp, R.H. et al. ed. (1985) Forskolin: Its chemical biological and medical potential. Proc of the International Symposium, Hoechst India Ltd, Bombay.
  8. Ronsard, N. Cellulite: Those Lumps, Bumps and Bulges You Couldn’t Lose Before. New York: Beauty and Health Publishing Co. 1973.
  9. Bayard, E. The Thin Game: Dieting, Scams and Dietary Sense. New York Avon Books. 1979.
  10. Kral, G. et al. (1977) Body composition in adipose tissue cellularity before and after jejuno-ileostomy in several obese subjects. Eur. J. Clin. Invest. 7:414-419.
  11. Allen, D.O. et al. (1986) Relationships between cyclic AMP levels and lipolysis in fat cells after isoproterenol and  forskolin stimulation. The Journal of Pharmacology and Experimental Therapeutics. 238(2): 659-664.
  12. Arner, P. (1992) Adrenergic receptor function in fat cells. Am. J. Clin. Nutr. 55:228S-236S.
  13. Greenway, F.L. et al (1987) Regional fat loss from the thigh in obese women after adrenergic modulation. Clin. Ther. 9(6):663-669.
  14. Badmaev, V. and Majeed, M. (2001) Skin as a delivery system for nutrients, nutraceuticals and drugs. Tetrahydropiperine, (THP) a natural compound with potential to enhance bioavailability of drugs and nutrients throught he skin. Agro-Industry Hi-Tech. January-February, 6-10.
In Bacopa monnieraby

Memory At Its Best! With The Use Of Bacopa Monniera

Bacopin is botanically Bacopa monniera (syn. Herpestis monniera) or Brahmi, belonging to family Scrophulariaceae. Brahmi1,2,3,4,5 has been used by Ayurvedic medical practitioners in India since ancient times. The Ayurvedic physician, Charaka, in his treatise the Charaka Samhita, included Brahmi in formulations used in the management of mental conditions. According to Charaka, it acts as an effective brain tonic, boosting ones capabilities to think and reason. In India, it is a popular drug recognized as being effective in the treatment of mental illness and epilepsy. In the ancient Indian texts of Ayurveda, Brahmi has been described as sweet in taste, producing coolness. It also possesses the capacity to increase strength and endurance capabilities in individuals. Traditionally, Brahmi is attributed with detoxifying properties acting as a laxative and astringent. It is also described as “light” in digestion, attenuating brain functions and promoting longevity.

The name Brahmi is derived from the word “Brahma“, the mythical “creator” in the Hindu pantheon. According to Hindu concepts, the brain is the center for creative activity, and therefore the drug that improves this faculty of the brain is called Brahmi. Brahmi is also believed to promote fertility. Other Sanskrit names for this plant are “Bahuphene“, Atiphena” and “Phenavati“. The word “Phena” means “foaming property”. When mixed with water, Bacopa plant parts produce stable froth, as indicated in these synonyms. From the known pharmacological effects of the drug, it is understood that it has an unusual combination of constituents to combat mental inefficiency and illnesses as well as convulsive disorders, like epilepsy. The plant contains bacosides, the active principles responsible for improving memory related functions. These compounds are attributed with the capability to enhance the efficiency of transmission of nerve impulses, thereby strengthening memory and cognition.

BACOPA MONNIERA
 

The mechanism of memory

The hippocampus in the brain is the seat of the memory functions. It is located in the temporal (left and right) sides of the brain. The hippocampus processes signals sent to the brain by the senses into the templates of memory, which are then stored in other parts of the brain, creating a long term memory. Signals are triggered into electrical impulses in the nerve cells due to a rapid change in protein composition. These impulses are then conducted across neurons (nerve cells) and through synapses, which connect nerve cells. This process continues till the bonds between the nerve cells strengthen, and the memory is created.

Normal synaptic activity is a process mediated by neurotransmitters. Each neuron is a single nerve cell. It has one or more arms called axons that send signals (impulses) and one or more other arms called dendrites that receive signals. When a signal is transmitted through an axon terminal, spherical bodies called vesicles fuse with its membrane. Neurotransmitters are released when the vesicles burst open into the synaptic space, (a station to discharge “passengers”, the neurotransmitters) that is, the minute space between the sending and receiving cells. To end the signal, the axons reabsorb some neuro-transmitters and the enzymes in the synapse neutralize the other neurotransmitters 6. It is evident that a disruption in any part of this process would affect memory. This would occur with age and continuous electrical activity, resulting in the synapses getting worn out. New memory creation is thereby impaired and loss of memory occurs.

Chemical substances and plant extracts that are known to restore memory, work in different ways. The bacosides are the memory chemicals in Brahmi. According to scientists at the Central Drug Research Institute based in Lucknow, India, the bacosides help to repair damaged neurons by adding muscle to kinase, the protein involved in the synthesis of new neurons to replace the old ones7. Depleted synaptic activity is thus restored, leading to boosting of memory.

In this context, it is interesting to compare the mechanism of action of the bacosides with those of other plant extracts that possess neuropharmacological activity, (such as Ginkgo biloba), and the well known brain cell nutrient, phosphatidylserine. Ginkgo possesses efficacy in alleviating disturbances of the central nervous system of both the primary degenerative type (early stages of degenerative dementia) as well as those conditions of vascular origin. Several fractions in Ginkgo biloba extract have been proven to be the active components. They function through two major mechanisms8:

  1. a) Improvement of cerebral circulation, a function related to the anti-ischemic activity of the extract. Patients suffering from CNS insufficiency states or peripherial vascular and neurosensory disorders are thereby benefited.

  2. b) Protective effect of the extract on neural tissue (via free radical scavenging, increased energy metabolism or through inhibition of neurotransmitter degrading enzymes). Both these mechanisms indirectly contribute to enhancing alertness, awareness and cognition. However, direct effects on retention and memory are not indicated.

The well known brain cell nutrient, phosphatidylserine is a phospholipid that forms one of the large “lipid” molecules that hold the other large molecules in the cell’s membrane systems together. The cell membrane plays a vital role in the entry of nutrients into the cell, the exit of waste products, inter-cell communications, ion transport and cell movement. Being a vital part of the cell menbrane, phosphatidyl serine helps to attenuate these functions, thereby helping to maintain the cell’s internal environment , enhancing signal transduction mediated through protein kinase C and adenylate cyclase and promoting secretory vesicle release, a process essential for the release of neurotransmitters. All these effects contribute to the protective effect of phosphatidylserine on the hippocampus, the seat of memory. The loss of dendrite connections which normally occurs due to aging is thereby prevented9. Phosphatidylserine thus indirectly affects memory.

Controversy between Bacopa monniera and Centella asiatica.

In India Bacopa monniera is known as “brahmi” and the plant enjoys considerable reputation in the indigenous system of medicine as a nerve tonic. Early literature used the name brahmi to refer to another plant species known as Centella asiatica Linn. which is the Indian penniwort10. However, the name jala-brahmi or water- brahmi assigned to Bacopa monniera in ancient Sanskrit writings provides the differentiation10. The vernacular name “mandukaparni”, often confused with brahmi, in fact refers to Centella asiatica.

A critical study of the comparative phytochemistry, pharmacology and therapeutic properties of these two drugs also support the view that they are distinct:

  1. Charaka3 considers them both to be promoters of mental ability, but suggests that brahmi is superior to mandukaparni. brahmi is used to treat specific mental disorders such as insanity and epilepsy, while mandukaparni is a general rejuvenative tonic which improves mental health.

  2. Brahmi promotes fertility and sustains implantation of the embryo in the uterus, while mandukaparni tends to reject the embryo. This suggests that the plant materials have opposite effects on uterine functions.

 

References

  1. Chopra, R.N., Chopra, I.C. Handa K.K. and Kapur, L.D. (1994). Indigenous Drugs of India. Academic Publishers, Calcutta, India
  2. Kirtikar, K.R. and B.D. Basu, (1993). Indian Medicinal Plants. Periodical Experts Book Agency, New Delhi, India.
  3. 3. Nadkarni, A. K., (1954). Indian Materia Medica, Vol. 1, Popular Book Depot, Bombay.
  4. Chopra, R.N., (1958). Indigenous drugs of India, 2nd Edition, U.N. Dhur and Sons, Calcutta. P.341.
  5. Chopra, I.C., Handa, K.L. and. Sobti, S.N (1956). Indian J. Pharm. 18: 369
  6. Swerdlow, J.L., (1995) Quiet Miracles of the Brain, The National Geographic, June: 2.-21
  7. Chhachhi, V., (1996) Business Today, March 22- April 6 issue, page 18.
  8. DeFeudis, F.V. (1991) Ginkgo biloba Extract (EGb 761): Pharmacological activities and clinical applications. Elsevier. 13(3): 163- 167.
  9. Kidd, P.M. (1995) Phosphatidylserine (PS) a remarkable brain cell nutrient. Lucas Meyer, Inc.
  10. Satyawati, G., Gupta, A.K. and Tandon, N. (1987) in Medicinal plants of India, Vol. 2, (ICMR, New Delhi), 50.
In boswelliaby

An Ancient Indian Remedy For Joint Pain & Inflammation

“An Ancient Indian Remedy For Joint Pain and Inflammation”

Arthritis and gout are systemic disorders in that they affect an entire organ system. They are pretty well universal and affect the vast majority of mankind to some extent. There are two types of arthritis — osteoarthritis and rheumatoid arthritis — but only one kind of gout. Osteoarthritis is the gradual, age-related deterioration of joint cartilage, but without the usual inflammation that always characterizes rheumatoid arthritis. Both, however, carry with them a great amount of pain and joint deformities.

Arthritis and gout have been around since the dawn of civilization itself. Radiological and pathological examinations of some of the early pharaohs of ancient Egypt have revealed moderate to severe cases of arthritis even then. King Henry the VIII of England, known for his huge gluttony and murderous relations with unfortunate women, suffered terribly from gout in his big toes and ankles.

Through the ages, men and women have sought for remedies that could, hopefully, allay some of the physical misery attending such excruciating pains. Tree resins became a popular way to treat these symptoms naturally. Today, the medical approach is in the form of nonsteroidal anti-inflammatory drugs (NSAID’s) like Ibuprofen, Naproxen Sodium and Salicylic Acid. A second line of therapy for minor pain relief has been found in creams or lotions containing Capsaicin (the isolated active ingredient form Cayenne Pepper).

An old Ayurvedic remedy from India appears to hold noteworthy promise in dealing with the pain generally associated with arthritis. Boswellia serrata and related species are balsamiferous trees that secrete aromatic oleoresins which are then collected when they become solid or semi-solid. In ancient times they were almost worth their weight in gold. Witness the fact that two of the three presents presented by the Wise Men to the infant Christ were such exudations – Frankinscense (Boswellia serrata) and Myrrh (the other was gold).

The tapping of the oleogum from the Boswellia tree occurs in the late fall when transverse incisions are made in the trunk and the bark is removed in between these incisions to allow the sap to ooze out of the wound. Once exposed to air, though, the exudate becomes gum-like in consistency. The resinous material is sieved and sold as “Salai Guggal” in various commercial grades. These various grades are then sold in numerous Indian bazaars or market places to manufacturers of incense (Aggarbattis), local perfumes (attars) and medicinal products.

Sabinsa Corporation’s Boswellin®, starts out from the highest grade of “Salai Guggal” material available and is then further purified through an extraction process that yields a product standardized for a minimum 65% boswellic acids, the active constituents in Boswellin®.

Too bad that the pharaohs and kings of the distant past didn’t have some of this remarkable product to take care of their own gouty aches and arthritic pains. Perhaps the course of some history might have been changed for the better had Boswellin® been around then. Oh well, as they say, “better late than never.”

 

Boswellin® is a registered trademark of Sabinsa Corporation

 

Disclaimer:

This product overview was written for the sole purpose of giving a brief history along with educational insights into the product listed above. It is not designed, in whole or in part, as advice for self-diagnosis or self-treatment and should not be construed as such.

 

 

  • America’s Finest, Inc. 20 Lake Drive East Windsor NJ 08520, USA

(+1) 800 350 3305
(+1) 732 985 9851

Disclaimer

*The information provided on this site is for informational purposes only and should not be used as a substitute for advice from your healthcare professional or your physician. The product statements have not been evaluated by the U.S. Food and Drug Administration, and these products are not intended to diagnose, treat, cure, or prevent any disease. No medical or health claims are made with respect to treatment, prevention, mitigation or remediation of illness, diseases or medical conditions.

categories

contact

Please enable JavaScript in your browser to complete this form.

We accept

2024© America’s Finest, Inc. A­ll Rights Reserved
Select the fields to be shown. Others will be hidden. Drag and drop to rearrange the order.
  • Image
  • SKU
  • Rating
  • Price
  • Stock
  • Availability
  • Add to cart
  • Description
  • Content
  • Weight
  • Dimensions
  • Additional information
Click outside to hide the comparison bar
Compare
Shopping cart close