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Brindall Berry

Brindall Berry

Botanical Description & Habitat

Garcinia cambogia

Habitat
Asia, Australia

Medicinal Parts
The rind of the berry, extracted

Historical Properties & Uses

Brindall Berry is a relative new-comer to the ranks of Western herbalism, but was apparently used for thousands of years in China as a food supplement. It is used as an appetite suppressant and to inhibit the absorption and synthesis of fat, cholesterol and triglycerides. In other words, it is a dietary aid. It is sometimes combined with guar gum in proprietary packages.

Method of Action

The active principle in brindall berry is (-)-hydroxycitrate (or HCA). On a dry weight basis, HCA constitutes from 20-30% of the berry.

Brindall berry works in two ways

1. by suppressing appetite
2. by inhibiting lipid synthesis

This latter mechanism is based on the theory that inhibition of lipid biosynthesis or enhance lipid metabolism interfere with mechanisms that produce and maintain obesity.

At least seven animal studies, involving over 100 subjects have been reported. Normal oral dose was 3mgHCA/kg body weight. At this level, the product suppressed appetite by 43% at 6.5 hours, and 29% at 24 hours. No rebound eating ("pigging out") effect was observed. Time of administration was important, with greatest effect seen when given 30 - 60 minutes prior to eating. The effect is dose dependent.

HCA appears to work through peripheral, rather than central, sites. It works peripherally in the upper digestive tract and by suppression of fatty acid synthesis resulting in lower levels of body fat without altering body protein levels.

In the liver HCA alters metabolic processes by diverting carbohydrates from lipid biosynthesis to hepatic glycogen synthesis. This may partially explain how it reduces food intake.

Apparently HCA is a potent competitive inhibitor of citrate cleavage enzyme, a key enzyme involved in the production of acetyl coenzyme A which is necessary for lipid biosynthesis outside the mitochondria of hepatic cells.

Specifically, HCA prevents the enzyme from catalyzing the cleavage of citrate to acetyl coenzyme A and oxaloacetate. This inhibition significantly reduces the synthesis of triglycerides, cholesterol and body fat, without diminishing energy production. The result is significant loss of body weight in animals made obese genetically and by hypothalamic lesions.

Animal studies demonstrate that fatty acid and cholesterol synthesis in liver are significantly inhibited after oral administration of HCA.

Drug Interactions & Precautions

No information available.

Safety Factors & Toxicity

Toxicity tests have shown that brindall berry extract is nontoxic and safe. Unknown decades of use by Asians has also yielded no known side effects.

Research findings suggest that brindall berry does not interfere with energy production, nutrient metabolism, prostaglandin synthesis, or any other essential biochemical process.

Preparation & Administration

Exact doses and methods of the preparation have not been worked out for this product. Suggest following manufacturers' recommendations.

References

Lowenstein, J. Effect of (-)-hydroxycitrate on fatty acid synthesis by rat liver in vivo. The Journal of Biological Chemistry, 246(3), 629-632,1971.

Mowrey, Daniel B., Ph.D. Exper. Psych., Brigham Young University. Director of Nebo Institute of Herbal Sciences. Director of Behavior Change Agent Training Institute. Director of Research, Nova Corp.

Sullivan & Triscari. Novel pharmacological approaches to the treatment of obesity. in Recent Advances in Obesity Research, II, George Bray, Ed.

Sullivan, Hamilton, et. all. Inhibition of lipogenesis in rat liver by (-)-hydroxycitrate. Archives of Biochemistry and Biophysics, 150, 183,1972.

Sullivan & Triscari. Possible interrelationships between metabolite flux and appetite." in Hunger: Basic Mechanisms and Clinical Implications, D. Noven, w. Wyrwicka and G. Bray, eds., Raven Press, New York, pp. 115-125.

Sullivan, A.C., Triscari, J. & Hamilton, J.G. Hypolipidemic activity of (-)-hydroxycitrate, Lipids, 21(1), 1-9, 1976.

Sullivan, A.C., Guthrie, R.W. & Triscari, J. (-)-threo- chlorocitric acid <(-)-hydroxycitrate > - a novel anorectic agent with a peripheral site of action. Anorectic Agents: Mechanisms of Action and Tolerance, S. Garattini & R. Samanin, eds., Raven Press, New York, 1981, pp.143.

Sullivan, A.C., Triscari, J., et. al. Metabolic regulation as a control for lipid disorders. II. Influence of (-)- hydroxycitrate on genetically and experimental induced hypertriglyceridemia. American Journal of Clinical Nutrition, 30, 777-784, 1977.

Sullivan, A.C., Triscarie, et. al. Effect of (-)- hydroxycitrate upon the accumulation of lipid in the rat. 1. Lipogenesis. Lipids, 9(2), 121-128, 1973.

Watson, J.A., M. Fang & J. Lowenstein. Tricarballylate and hydroxycytrate: Substrate and inhibitor of ATP citrate oxaloacetatre lyase. Archives of Biochemistry and Biophysics, 135, 209-217, 1969.