Elsevier

Atherosclerosis

Volume 88, Issue 1, May 1991, Pages 49-59
Atherosclerosis

Research paper
Effect of drinking pattern on plasma lipoproteins and body weight

https://doi.org/10.1016/0021-9150(91)90256-3Get rights and content

Abstract

The effect of drinking pattern on plasma lipoproteins and body weight was examined in three groups of squirrel monkeys: (1) controls fed isocaloric liquid diet; (2) regular drinkers given liquid diet containing ethanol (EtOH) substituted isocalorically for carbohydrate at 12% of calories daily; and (3) binge drinkers fed 6% EtOH calories daily for a four-day period followed by three days of 20% EtOH to mimic a weekend bout drinking cycle. The number of calories offered per day was the same for all groups, and the average weekly EtOH consumption (12% calories) was identical for the two alcohol treatments. The entire study lasted six months. There were no significant differences in plasma cholesterol, triglyceride or liver function tests. Regular drinkers had the highest high density lipoprotein2/high density lipoprotein3 (HDL2HDL3) protein and apolipoprotein A-IB ratios of any group and exhibited a significant elevation in the molar plasma lecithin: cholesterol acyltransferase (LCAT) rate (nmol/min/ml). Binge drinking produced a selective increase in low density lipoprotein (LDL) cholesterol and apolipoprotein B, and a depression in the fractional LCAT rate (% esterified/min). During the course of the study, controls ate 92% of their diet while the alcohol groups each consumed 95% of the liquid diet. Despite this difference, body weight and Quetelet index (weight/height2)decreased progressively in the order controls > regular drinkers > binge drinkers. Results from our study indicate that moderate, regular daily consumption of EtOH at 12% of calories causes a modest reduction in body weight and produces a coronary protective lipoprotein profile (↑HDL2HDL3, T apolipoprotein A-IB, low LDL cholesterol). By contrast, when this same average weekly dose is concentrated in a binge cycle, unfavorable alterations in lipoprotein composition (↑ LDL cholesterol, ↑ apolipoprotein B) and metabolism (↑ LCAT activity) occur along with weight loss and depletion of body fat. These studies point to the value of the squirrel monkey model in evaluating both favorable and pathophysiological effects of chronic EtOH intake.

References (62)

  • M. Taskinen et al.

    Sequence of alcohol-induced initial changes in plasma lipoproteins (VLDL and HDL) and lipolytic enzymes in humans

    Metabolism

    (1985)
  • N.A. Pikaar et al.

    Effects of moderate alcohol consumption on platelet aggregation, fibrinolysis, and blood lipids

    Metabolism

    (1987)
  • N.A. Frimpong et al.

    Effects of moderate alcohol intake in fixed or variable amounts on concentration of serum lipids and liver enzymes in healthy young men

    Am. J. Clin. Nutr.

    (1989)
  • S.K. Witzgall et al.

    Plasma lipoprotein alterations in squirrel monkeys (Saimiri sciureus) during ethanol administration and abstinence

    Atherosclerosis

    (1988)
  • J.F. Oram

    Effects of high density lipoprotein subfractions on cholesterol homeostasis in human fibroblasts and arterial smooth muscle cells

    Arteriosclerosis

    (1983)
  • P. Swetnam et al.

    High density lipoprotein subclasses as coronary heart disease risk factors in British men: the Speedwell study

    Circulation

    (1989)
  • J.L. Marx

    The HDL: the good cholesterol carriers?

    Science

    (1979)
  • J. Mulligan et al.

    Ethanol dose and plasma low density lipoproteins

    Clin. Res.

    (1987)
  • J. Babiak et al.

    Lecithin: cholesterol acyltransferase-induced modifications of liver perfusate discoidal high density lipoproteins from African green monkeys

    J. Lipid Res.

    (1986)
  • D. Reichl et al.

    Pathophysiology of reverse cholesterol transport

    Arteriosclerosis

    (1989)
  • M.H. Criqui

    Alcohol consumption, blood pressure, lipids and cardiovascular mortality

    Clin. Exp. Res.

    (1986)
  • J. Hojnacki et al.

    Effect of ethanol dose on low density lipoproteins and high density lipoprotein subfractions

    Alcoholism Clin. Exp Res.

    (1988)
  • W.B. Kannel

    Alcohol and cardiovascular disease

  • J.J. Barboriak et al.

    Alcohol consumption and the diet-heart controversy

    Alcoholism Clin. Exp. Res.

    (1983)
  • H.W. Gruchow et al.

    Apolipoproteins and alcohol intake patterns, CVD Epidemiol

    Newsletter

    (1987)
  • H.K. Naito

    The clinical significance of apolipoprotein measurements

    J. Clin. Immunoassay

    (1986)
  • D.F. Williamson et al.

    Alcohol and body weight in United States adults

    Am. J. Publ. Health

    (1987)
  • M.C. Mitchell et al.

    Alcohol and nutrition; Caloric value, bioenergetics, and relationship to liver damage

    Annu. Rev. Nutr.

    (1986)
  • P. Avogaro et al.

    HDL-cholesterol, apolipoproteins Al and B

    Atherosclerosis

    (1986)
  • C.J. Glueck et al.

    Plasma high-density lipoprotein cholesterol: association with measurements of body mass

    Circulation

    (1980)
  • A.J. Anderson et al.

    Body fat distribution, plasma lipids, and lipoproteins

    Arteriosclerosis

    (1988)
  • Cited by (35)

    • Associations between heavy alcohol drinking and lipid-related indices in middle-aged men

      2013, Alcohol
      Citation Excerpt :

      A recent meta-analysis study revealed a 45% increase in the risk of ischemic heart disease as an effect of episodic heavy drinking, while controlling for volume of alcohol consumed (Roerecke & Rehm, 2010). However, there is limited knowledge regarding the relationships between pattern of drinking and blood lipid levels, and results of previous studies on the effects of binge drinking on HDL cholesterol and LDL cholesterol levels are inconsistent (Gruchow, Hoffmann, Anderson, & Barboriak, 1982; Hojnacki et al., 1991; Peasey et al., 2005; Rakic, Puddey, Dimmitt, Burke, & Beilin, 1998; Taskinen, Välimäki, Nikkilä, Kuusi, & Ylikahri, 1985). The ratio of LDL cholesterol to HDL cholesterol (LDL-C/HDL-C), a classic atherogenic index (Kannel, 1985), has been reported to decrease as alcohol intake increases (Wakabayashi, 2012a).

    • Effects of regular and abusive intake of alcohol at weekends on physiological parameters in Spanish young

      2012, Public Health
      Citation Excerpt :

      However, in our study no significant change in HDL-C was observed amongst weekend drinkers. In this way, alterations in serum lipoprotein levels following different patterns of alcohol suggested that ingestion of regular small doses of alcohol increased HDL-C significantly, while binge drinking had no favorable influence on HDL-C.26 In addition, the young people who drink abusive quantities of alcohol two days a weekend showed a significantly higher systolic blood pressure than non-drinkers.

    • Dietary omega-3 polyunsaturated fatty acid intake is related to a protective high-density lipoprotein subspecies profile independent of genetic effects: A monozygotic twin pair study

      2011, Atherosclerosis
      Citation Excerpt :

      In the current study, alcohol intake, as calculated from the 3-days food diaries, was unrelated to HDL-C and associated with reduced percentages of HDL2b if it replaced carbohydrates in a multivariate nutrient density model. Earlier studies have reported that the pattern of alcohol drinking may be of major importance, suggesting that regular light to moderate ethanol intake is associated with an increase in HDL-C, but heavy episodic drinking (binge drinking), which is common among the young Finnish population, is not associated with HDL-C in animals or humans [44,45]. Previous studies have reported associations between individual HDL subspecies and cardiovascular risk factors.

    • The French paradox: Possible involvement of ethanol in the protective effect against cardiovascular diseases

      2002, Nutrition
      Citation Excerpt :

      Alcohol can act directly on the liver by increasing apoAI, apoAII, and HDL-C synthesis,53–55 decreasing lipoprotein catabolism,56,57 or modifying the activity of the enzymes that act on lipoprotein metabolism.47 Lipoprotein lipase activity generally is not modified with moderate doses of alcohol46,58 but may be increased,47 leading to enhanced formation of HDL-C. Hepatic lipase is inhibited by alcohol,38 and no change was observed in lecithin:cholesterol acyltransferase activity47 but that activity can be increased38 or decreased59 with moderate alcohol intake. Alternatively, cholesterol ester transfer protein (CETP) activity, which transfers cholesteryl esters from HDL2 to very-LDL and LDL and, reciprocally, triacylglycerol from these lipoproteins to HDL, may be significantly reduced due to alcohol consumption, as shown in studies in moderate drinkers.60,61

    View all citing articles on Scopus
    View full text