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Alpha-Lipoic Acid: The Universal Antioxidant

by Hans R. Larsen, MSc ChE

Hans Larsen Vitamins C and E, beta-carotene and selenium are considered to be the most important dietary antioxidants. Vitamin-C is water-soluble and protects the cell fluid from free radical attacks while vitamin-E is fat-soluble and mainly involved in protecting the cell membrane. Several other antioxidants are needed to protect cells and tissue from oxidative damage. Lycopene, for example, is a carotenoid antioxidant which is more abundant in the human body than beta-carotene and is a far stronger antioxidant. Coenzyme Q10 (ubiquinone) is another very important fat-soluble antioxidant; it is particularly important in protecting the energy-producing parts of the cell (mitochondria) and is actually more effective than vitamin E.

Alpha-lipoic acid, also known as thioctic acid, is the newest kid on the antioxidant block. Alpha-lipoic acid (ALA) was first isolated in 1953 and was quickly discovered to be a very important cofactor in the Krebs cycle (citric acid cycle), the body's main process for converting carbohydrates into energy. ALA is a medium length (8 carbon atoms) fatty acid containing two sulfur atoms. It is readily synthesized in the body and is well absorbed from the diet through the stomach and intestines. Liver and yeast are especially good dietary sources of ALA. ALA is the oxidized form of dihydrolipoic acid (DHLA), is water-soluble, and is found in varying concentrations in all muscles and internal organs(1,2).

In 1959 it was discovered that both ALA and DHLA are powerful antioxidants. ALA scavenges hydroxyl radicals, singlet oxygen and hypochlorous acid, can remove heavy metals by chelation and regenerates other antioxidants like glutathione, vitamin C, ubiquinol (coenzyme Q10) and indirectly, vitamin E. DHLA has similar properties(1).

Researchers have found that administration of ALA (intravenously or orally) is effective in alleviating many of the problems accompanying diabetes. Animal experiments have shown that ALA can prevent the development of Type I (insulin-dependent) diabetes and enhances glucose uptake in Type II (non- insulin-dependent) diabetes. A recent clinical trial showed that intravenous administration of ALA (200 mg/day) for 21 days markedly reduces the pain caused by polyneuropathy (peripheral nerve disease) in diabetes patients(3). Another larger study of diabetics with polyneuropathy involved intravenous injection of 600 mg/day of ALA for three weeks followed by 12 weeks of oral supplementation (600 mg/day). Marked pain reduction was again evident and ALA is now approved in Germany for the treatment of diabetes neuropathy(1,4). Experiments have also shown that ALA supplementation can reduce the risk of cataract formation in diabetics(5-7). Diabetics taking ALA need close monitoring of their blood sugar levels as ALA supplementation may decrease the need for insulin and other drugs(2).

Heart attacks and strokes involve a disruption of the oxygen supply to the affected areas. When the oxygen supply is restored a burst of free radicals is produced which can cause additional tissue damage (ischemia-reperfusion injury). Animal experiments have shown that ALA and DHLA are effective in preventing or ameliorating ischemia-reperfusion injury(1).

HIV-infected patients are often antioxidant deficient and many researchers believe that oxidative stress (free radical reactions) play a major role in the initiation and progression of HIV infection and AIDS(8-10). Some very recent experiments have shown that ALA supplementation (150 mg three times per day) is effective in restoring antioxidant status in HIV patients(11). Oxidative stress also plays a major role in the development and progression of neurodegenerative diseases such as Alzheimer's and Parkinson's. Animal experiments have shown that ALA supplementation can reverse age-related memory loss and there is some evidence that ALA may be useful in the treatment of epilepsy(12,13).

A very recent study of children living in the area affected by the Chernobyl disaster showed that ALA prevents radiation damage(14). There is also evidence that ALA could play a role in minimizing the adverse effects of smoking and may be useful in the treatment of mercury and cadmium poisoning(1,15,16).

Alpha-lipoic acid and its cousin DHLA have justly been referred to as the "universal antioxidants". They are active in both cell fluids and membranes, they have no serious side effects, are non-carcinogenic and do not interfere with fetus development; however, until more data is available ALA supplementation is not recommended for pregnant women. Research into the beneficial effects of ALA is receiving increasing attention and there is already substantial experimental and clinical evidence to the effect that ALA may be useful in the prevention and treatment of such diverse conditions as diabetes, heart attack, stroke, HIV infection, AIDS, neurodegenerative diseases, heavy metal poisoning and radiation exposure. The recommended daily maintenance dose is 20 to 50 milligrams, but much higher doses are needed in the treatment of diseases such as diabetes and AIDS(2).

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  1. Cadenas, Enrique and Packer, Lester, eds. Handbook of Antioxidants, NY, Marcel Dekker, Inc., 1996, pp. 545-91
  2. Murray, Michael T. Encyclopedia of Nutritional Supplements, Rocklin, CA, Prima Publishing, 1996, pp. 343-46
  3. Sachse, G. and Willms, B. Efficacy of thioctic acid in the therapy of peripheral diabetic neuropathy. In: Gries, F.A., et al., eds. Aspects of Autonomic Neuropathy in Diabetes. Stuttgart, A. Thieme, 1980, pp. 105-8
  4. Ziegler, D., et al. Effeckte einer therapie mit alpha-liponsaure gegenuber vitamin B1 bei der diabetischen neuropathie. Diabet. Stoffwechs., Vol. 2, 1993, pp. 443-48
  5. Maitra, I., et al. Alpha-lipoic acid prevents buthionine sulfoximine- induced cataract formation in newborn rats. Free Rad. Biol. Med., Vol. 18, 1995, pp. 823-29
  6. Kilic, F., et al. Modeling cortical cataractogensis 17:in vitro effect of alpha-lipoic acid on glucose-induced lens membrane damage, a model of diabetic cataractogenesis. Biochem. Molec. Biol. Int. (in press)
  7. Packer, L. The role of anti-oxidative treatment of diabetes mellitus. Diabetologia, Vol. 36, 1993, pp. 1212-13
  8. Buhl, R., et al. Glutathione deficiency and HIV. Lancet, Vol. 335, March 3, 1990, p. 546
  9. Dworkin, B.M., et al. Dietary intake in patients with acquired immunodeficiency syndrome (AIDS), patients with AIDS-related complex, and serologically positive human immunodeficiency virus patients: correlations with nutritional status. Jpn. J. Parent Enteral. Nutr., Vol. 14, 1990, pp. 605-09
  10. Buhl, R., et al. Systemic glutathione deficiency in symptom-free HIV- seropositive individuals. Lancet, December 2, 1989, pp. 1294-98
  11. Fuchs, J., et al. Studies on lipoate effects on blood redox state in human immunodeficiency virus infected patients. Arzneimittelforsch., Vol. 43, 1993, pp. 1359-62
  12. Stoll, S., et al. The potent free radical scavenger alpha-lipoic acid improves memory in aged mice: putative relationship of NMDA receptor deficits. Pharmacol. Biochem. Behav., Vol. 46, 1993, pp. 799-805
  13. Dimpfel, et al. Wirkung von thioctsaure auf picrotoxin-induzierte epileptiforme entladungen in der CA1 -region des hippokampus in vitro. In: Borbe, H.O. and Ulrich, H., eds. Thioctsaure, Frankfurt, Verlag, 1989, pp. 237-47
  14. Korkina, L.G., et al. Antioxidant therapy in children affected by irradiation from the Chernobyl nuclear accident. Biochem. Soc. Trans., Vol. 21, 1993, p. 314S
  15. Grunert, R.R. The effect of DL-alpha-lipoic acid on heavy-metal intoxication in mice and dogs. Arch. Biochem. Biophys., Vol. 86, 1960, pp. 190-94
  16. Sumathi, R., et al. DL-alpha-lipoic acid protection against cadmium- induced tissue lipid peroxidation. Med. Sci. Res., Vol. 22, 1994, pp. 23-25

This article was first published in the November 1997 issue of International Health News

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