Beta-carotene is a provitamin A from plants and contains alpha, beta and gamma carotene. The main food sources are carrots, green leafy vegetables, sweet potatoes, squash and cantaloupe. About 33% of the ingested beta-carotene is absorbed and is then converted to retinol. Absorption requires bile and absorbable fat in the intestinal track. Low serum levels of beta-carotene are strongly associated with elevated risk of atherosclerosis. Beta-carotene can be expressed as retinol equivalent (RE), in mg or mcg of beta-carotene or in International Units. 1 RE = 6 mcg Beta-carotene = 10 IU. RDA of beta-carotene for adult women is 4.8 mg and men 6 mg. Supplementation of beta-carotene in adults greater than 6 mg should be based on Spectrox or similar intracellular test for oxidative potential.. Excessive intake of beta-carotene can result in hypercarotenemia. Hypervitaminosis does not develop because of limited conversion to retinol in high doses. Large doses of beta-carotene have prooxidant effect and accelerate oxidation of LDL. DRUG INTERACTIONS: ALCOHOL - competes with beta-carotene for dehydrogenases resulting in hepatotoxicity and increase risk of lung cancer and possibly promotion of CAD. SMOKING - in combination with beta-carotene promotes carcinogenesis possibly by acting as a prooxidant forming 4-nitro-beta carotene. IRON - oxidation of LDL may be inhibited by beta-carotene. ORLISTAT - inhibits absorption of beta carotene by 33%   STUDIES RELATED TO CARDIOVASCULAR DISEASE AND BETA CAROTENE ARE INCONSISTENT BUT THE CURRENT CONSCENOUS IS: Beta-carotene alone does not reduce oxidation of LDL. Beta-carotene in excess of physiological needs may act as a prooxidant on LDL and can cancel the protective effects of vitamin E. High serum levels of beta-carotene doubles the risk of subarachnoid hemorrhage. Apolipoprotein E (Apo-E) when deficient in animals results in the spontaneous atherosclerotic lesions and vitamin E and beta-carotene had no effect on Apo-E status. High doses of beta-carotene (30 mg) and 25,000 IU of vitamin A resulted in a 26% increase in cardiovascular mortality. Dietary supplementation of beta-carotene may have inhibitory effect on 3-hydroxy-3-mehtyl-glutaryl coenzyme A (HMGCoA) reductase and decrease the synthesis of cholesterol. John Hopkins study determined that optimal antioxidant dose in clinical trials was vitamin E 400 IU, vitamin C 500 mg and beta carotene 6 mg.   Dr. David Martin February 28, 2000