ATHEROSCLEROSIS UPDATE
ATHEROSCLEROSE: LE POINT Canadian Atherosclerosis Society/Societe canadienne d'atherosclerose
Alcohol consumption and plasma lipoproteins Sital Moorjani, PhD; Paul J. Lupien, MD, PhD, FRCPC E xcessive use of alcohol is associated with malnutrition, liver cirrhosis, pancreatitis, hypertension, cardiomyopathy, cardiac arrhythmia, and neurologic and behavioural problems. However, alcohol intake and coronary heart disease (CHD) are inversely associated; the CHD risk decreases with moderate drinking in both sexes, but this benefit disappears with higher consumption.' Alcohol's effects on plasma lipoproteins depend on dose, individual susceptibility, genetic variation and diet. Our knowledge comes mostly from studies of forced abstinence in people with chronic alcoholism, the short-term effects of alcohol in healthy volunteers2'3 and plasma lipoprotein levels in users and nonusers.4,5 In people with chronic alcoholism but normal liver function the plasma levels of very-low-density lipoprotein triglycerides (VLDL-TG) and low-density lipoprotein cholesterol (LDL-C) are normal or subnormal, whereas the levels of high-density lipoprotein cholesterol (HDL-C) and HDL2 and HDL3 are elevated. During alcohol withdrawal the HDL-C level returns to normal within 2 weeks. These effects have been attributed to stimulation of lipoprotein and hepatic lipase activity during alcohol intake.2 Alcohol intake also stimulates hepatic TG synthesis and VLDL secretion. Low to moderate alcohol consumption in nonalcoholic subjects causes a variable response in the plasma lipoprotein profile according to dose (32 to 90 g/d) and time (1 to 6 weeks).2'3 The VLDL-TG level is unchanged or increases, the HDL-C level usually increases, and the levels of the HDL subfractions are unchanged or increase. Since the level of apo A-I always increases, apo A-I synthesis may increase and so also the number of HDL3 particles. The plasma TG level is normal or slightly increased in people with low to moderate alcohol
consumption, the LDL-C level is normal or slightly reduced, and the HDL-C level is usually increased.",4'5 Both HDL subfractions contribute to the elevated HDL-C level,4'5 which varies directly with alcohol consumption4 up to 90 g/d. The increase in the level of HDL3-C plateaus at 40 g of alcohol per day, whereas that of HDL2-C continues.4 Since HDL-C protects against CHD, and since alcohol increases HDL-C levels, is alcohol's effect on CHD mediated through its effect on HDL-C? Yes, in part: about 50% of alcohol's protective effect is mediated by HDL. ' Obviously it would not be wise to recommend moderate consumption of alcohol to nonusers; however, one or two drinks daily has not been found to harm healthy adults.7
References 1. Criqui MH: The roles of alcohol in the epidemiology of cardiovascular diseases. Acta Med Scand Suppl 1987; 717: 7385 2. Taskinen MT, Nikkila EA, Valimaki M et al: Alcohol-induced changes in serum lipoproteins and in their metabolism. Am Heart J 1987; 113: 458-464 3. Hartung GH, Foreyt JP, Reeves RS et al: Effect of alcohol dose on plasma lipoprotein subfractions and lipolytic enzyme activity in active and inactive men. Metabolism 1990; 39: 81-86 4. Lupien PJ, Moorjani S, Jobin J et al: Smoking, alcohol consumption, lipid and lipoprotein levels. Can J Cardiol 1988; 4: 102-107 5. Miller NE, Bolton CH, Hayes TM et al: Associations of alcohol consumption with plasma high density lipoprotein cholesterol and its major subfractions. J Epidemiol Community Health 1988; 42: 220-225 6. Stampfer MS, Colditz GA, Willet WE et al: A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. N Engl J Med 1988; 319: 267-273 7. Nutrition and Your Health: Dietary Guidelines for Americans, 2nd ed, US Dept of Agriculture and US Dept of Health and Human Services, Washington, 1985: 1-24
Dr. Moorjani is clinical professor ofbiochemistry and chiefof laboratory, Lipid Research Centre, and Dr. Lupien is professor ofmedicine and director, Lipid Research Centre, Laval University Hospital, Sainte-Foy, PQ.
The opinions expressed in this article are those of the authors and not necessarily those of the Canadian Atherosclerosis Society. Reprint requests to: Dr. Sital Moorjani, CHUL/S-102, 2705, boulevard Laurier, Sainte-Foy, PQ GJ V 4G2 CAN MED ASSOC J 1990; 142 (10)
1089
ATHEROSCLEROSE: LE POINT Canadian Atherosclerosis Society/Societe canadienne d'atherosclerose
Alcohol consumption and plasma lipoproteins Sital Moorjani, PhD; Paul J. Lupien, MD, PhD, FRCPC E xcessive use of alcohol is associated with malnutrition, liver cirrhosis, pancreatitis, hypertension, cardiomyopathy, cardiac arrhythmia, and neurologic and behavioural problems. However, alcohol intake and coronary heart disease (CHD) are inversely associated; the CHD risk decreases with moderate drinking in both sexes, but this benefit disappears with higher consumption.' Alcohol's effects on plasma lipoproteins depend on dose, individual susceptibility, genetic variation and diet. Our knowledge comes mostly from studies of forced abstinence in people with chronic alcoholism, the short-term effects of alcohol in healthy volunteers2'3 and plasma lipoprotein levels in users and nonusers.4,5 In people with chronic alcoholism but normal liver function the plasma levels of very-low-density lipoprotein triglycerides (VLDL-TG) and low-density lipoprotein cholesterol (LDL-C) are normal or subnormal, whereas the levels of high-density lipoprotein cholesterol (HDL-C) and HDL2 and HDL3 are elevated. During alcohol withdrawal the HDL-C level returns to normal within 2 weeks. These effects have been attributed to stimulation of lipoprotein and hepatic lipase activity during alcohol intake.2 Alcohol intake also stimulates hepatic TG synthesis and VLDL secretion. Low to moderate alcohol consumption in nonalcoholic subjects causes a variable response in the plasma lipoprotein profile according to dose (32 to 90 g/d) and time (1 to 6 weeks).2'3 The VLDL-TG level is unchanged or increases, the HDL-C level usually increases, and the levels of the HDL subfractions are unchanged or increase. Since the level of apo A-I always increases, apo A-I synthesis may increase and so also the number of HDL3 particles. The plasma TG level is normal or slightly increased in people with low to moderate alcohol
consumption, the LDL-C level is normal or slightly reduced, and the HDL-C level is usually increased.",4'5 Both HDL subfractions contribute to the elevated HDL-C level,4'5 which varies directly with alcohol consumption4 up to 90 g/d. The increase in the level of HDL3-C plateaus at 40 g of alcohol per day, whereas that of HDL2-C continues.4 Since HDL-C protects against CHD, and since alcohol increases HDL-C levels, is alcohol's effect on CHD mediated through its effect on HDL-C? Yes, in part: about 50% of alcohol's protective effect is mediated by HDL. ' Obviously it would not be wise to recommend moderate consumption of alcohol to nonusers; however, one or two drinks daily has not been found to harm healthy adults.7
References 1. Criqui MH: The roles of alcohol in the epidemiology of cardiovascular diseases. Acta Med Scand Suppl 1987; 717: 7385 2. Taskinen MT, Nikkila EA, Valimaki M et al: Alcohol-induced changes in serum lipoproteins and in their metabolism. Am Heart J 1987; 113: 458-464 3. Hartung GH, Foreyt JP, Reeves RS et al: Effect of alcohol dose on plasma lipoprotein subfractions and lipolytic enzyme activity in active and inactive men. Metabolism 1990; 39: 81-86 4. Lupien PJ, Moorjani S, Jobin J et al: Smoking, alcohol consumption, lipid and lipoprotein levels. Can J Cardiol 1988; 4: 102-107 5. Miller NE, Bolton CH, Hayes TM et al: Associations of alcohol consumption with plasma high density lipoprotein cholesterol and its major subfractions. J Epidemiol Community Health 1988; 42: 220-225 6. Stampfer MS, Colditz GA, Willet WE et al: A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. N Engl J Med 1988; 319: 267-273 7. Nutrition and Your Health: Dietary Guidelines for Americans, 2nd ed, US Dept of Agriculture and US Dept of Health and Human Services, Washington, 1985: 1-24
Dr. Moorjani is clinical professor ofbiochemistry and chiefof laboratory, Lipid Research Centre, and Dr. Lupien is professor ofmedicine and director, Lipid Research Centre, Laval University Hospital, Sainte-Foy, PQ.
The opinions expressed in this article are those of the authors and not necessarily those of the Canadian Atherosclerosis Society. Reprint requests to: Dr. Sital Moorjani, CHUL/S-102, 2705, boulevard Laurier, Sainte-Foy, PQ GJ V 4G2 CAN MED ASSOC J 1990; 142 (10)
1089
