For citation purposes: Gupta S, Figueredo VM. Alcohol and lipids. OA Alcohol 2014 Feb 10;2(1):3.

Review

 
Biomedical

Alcohol and lipids.

V Figueredo1*,2*, S Gupta1
 

Authors affiliations

(1) Institute for Heart & Vascular Health, Einstein Medical Center, Philadelphia, USA

(2) Jefferson Medical College, Philadelphia, USA

* Corresponding author Email: figueredov@einstein.edu

Abstract

Introduction

The effects of moderate alcohol consumption on the lipid profile are well-documented, showing an association between alcohol-induced increases in HDL-C levels and cardioprotection (though there remains some debate). Whereas prior research was focused on alcohol-induced changes in lipoprotein levels, the paradigm has shifted to the composition of lipoproteins, with emphasis on smaller lipid molecules such as sphingolipids. The benefits of red wine over other forms of alcohol have not been proven clinically, especially in terms of effects on the lipid profile. This review discusses the effects of alcohol on lipoprotein levels and function as related to atherosclerosis and CVD risk.

Conclusion

Direct evidence to recommend drinking alcohol in moderation for decreasing cardiovascular risk is still lacking, and presents another avenue for clinical research.

Introduction

Large scale epidemiologic studies suggest a protective effect of low to moderate alcohol consumption against cardiovascular disease (CVD) events. In a pooled analysis of eight prospective studies from North America and Europe, including 192,067 women and 74,919 men free of CVD and diabetes (Figure 1), there was an inverse association between alcohol and CVD risk in all age groups[1]. This cardioprotective effect of alcohol has been attributed largely to its effect of raising high density lipoprotein cholesterol (HDL-C)[2,3,4]. However, some recent evidence has disputed this paradigm[5]. In addition, the effects of alcohol on cholesterol metabolism have been better elucidated at the molecular level. This review discusses the effects of alcohol on lipoprotein levels and function as related to atherosclerosis and CVD risk.

Relative risk functions (95% CI) describing the dose-response relation between alcohol intake and risk of CVD. *After adjusting for year of baseline questionnaire, education, smoking, BMI, physical activity, total energy intake, polyunsaturated fat, monounsaturated fat, saturated fat, fibre, and cholesterol intake. Reproduced with permission from: Hvidtfeldt U A et al. Circulation 2010;121:1589-1597.

Discussion

Impact of Alcohol Intake on the Lipid Profile

In a meta-analysis of experimental studies that assessed the effects of moderate alcohol intake on biological markers of CVD, consumption of 30 grams of alcohol per day increased concentrations of HDL-C by 3.99 mg/dl (95% confidence interval 3.25 to 4.73), apolipoprotein A-1 by 8.82 mg/dl (7.79 to 9.86), and triglycerides by 5.69 mg/dl (2.49 to 8.89), in addition to affecting several haemostatic parameters (Figure 2). The authors concluded on the basis of published data that 30 g of alcohol a day would cause an estimated reduction of 24.7% in the CVD risk[6].

Percentage change in biomarkers associated with intake of 30 g of alcohol per day based on a meta-analysis of 42 studies. Reproduced with permission from: Rimm E B et al. Br Med J 1999;319(7224):1523-1528.

In a pooled analysis of forty four human intervention studies on the effects of alcohol on CVD biomarkers, alcohol significantly increased levels of HDL-C and apolipoprotein A-1. Furthermore, alcohol showed a dose-response relationship with HDL-C increases. Intake of 30 g (approximately 2 drinks) of alcohol a day increased HDL-C concentration approximately 0.1 mmol/l (3.8 mg/dl; Figure 3 and Table 1). Alcohol consumption did not significantly alter total cholesterol, LDL-C, triglycerides, or lipoprotein(a). Pooled analysis of the impact of alcohol on triglycerides did demonstrate a significant increase at the highest doses of alcohol (>60 g/day) in two studies reporting such high doses[7].

Forest plot of meta-analysis (random effects) of effect of alcohol consumption on levels of high density lipoprotein cholesterol (HDL-C). Reproduced with permission from: Brien SE et al. BMJ 2011;342:d636

Table 1

Summary of pooled mean difference in lipid biomarker level after alcohol use in a meta-analysis of 44 studies. *Indicates significant (P<0.01) change in biomarker level after alcohol use compared with a period of no alcohol use. †Heterogeneity detected across pooled studies, where Q statistic P<0.10. Modified, with permission from: Brien SE et al. BMJ 2011;342:d636

Alcohol and HDL-Cholesterol

The synthesis and metabolism of HDL-C is summarized in Figure 4. Alcohol increases HDL-C by raising transport rates of the major HDL apolipoproteins apoA-I and apoA–II[8]. Apo A-I takes up cellular cholesterol, thus eliminating excess tissue cholesterol, initiating reverse cholesterol transport. Alcohol increases apoA-I secretion[9]. During reverse cholesterol transport, free cholesterol is removed from peripheral cells (cholesterol efflux) by the interaction between serum lipoproteins and cells. Free cholesterol released from the cell is esterified by lecithin:cholesterol acyltransferase and incorporated into the HDL particle. The cardioprotective effect of HDL-C is largely attributed to its role in reverse cholesterol transport[10]. Alcohol increases cellular cholesterol efflux and plasma cholesterol esterification (the first two steps of reverse cholesterol transport) after regular consumption for 3 weeks in a study of middle-aged men, independent of the type of alcoholic beverage; thus enhancing the reverse cholesterol transport process[11].

HDL metabolism and reverse cholesterol transport. Precursors of HDL (nascent HDL or pre-HDL) are disc-shaped particles that are secreted by the liver and the gut. They are converted to spherical HDL particles by the action of LCAT, which further converts smaller HDL-3 particles to larger HDL-2 particles. Cholesterol efflux occurs to apo-A1 particles via ABCA-1 and to mature HDL particles via ABCG-1 and ABCG-4. Alcohol consumption increases cholesterol efflux by both these pathways and by stimulating apo-A1 synthesis (red arrows). ABCA1, ATP binding cassette transporter A1; ABCG1, ATP binding cassette transporter G1; ABCG 4, ATP binding cassette transporter G4; LCAT, lecithin:cholesterol acyltransferase; CETP, cholesteryl ester transfer protein; VLDL, very low density lipoproteins; LDL, low density lipoproteins; apo E, apolipoprotein E, apo A-1, apolipoprotein A1.

The extent to which the increase in HDL-C with alcohol contributes to reduced incidence of CVD is unclear. Several articles using multiple regression analyses in observational cohort studies suggested a significant contribution from this effect: 50% in the Honolulu Heart Program study; 36% in women in the Nurses Health Study and 50% in men in the Health Professionals Follow-Up Study; and 16% in the Helsinki Heart Study[2,3,4]. However, in a large, population-based Norwegian cohort study (Cohort of Norway-CONOR), even though alcohol intake was related to a reduced risk of CVD death, this association did not change substantially when taking the serum level of HDL-C into account, contrary to findings from other published studies[5]. This raises the possibility that raising HDL-C may simply be a biochemical side-effect of alcohol consumption, and the effect of alcohol on CVD mortality may be unrelated. However, this study examined only fatal CVD, and it is plausible that the effect of alcohol on fatal and non-fatal CVD may be different.

Recent evidence suggests the composition of the HDL particle, rather than the HDL-C concentration, may be responsible for the HDL cardioprotective effect. In addition to free and esterified cholesterol, the HDL particle is composed of phospholipids, free and esterified fatty acids, and sphingolipids. Alcohol causes phospholipid enrichment of HDL particles and a shift from the HDL-3 subfraction to the lipid rich HDL-2 subfraction (which indicates enhanced reverse cholesterol transport). Both of these processes may contribute to HDL anti-atherogenic effects. The increase of phospholipids may reduce inflammation in the vessel wall, as HDL particles reconstituted with phospholipids have been shown to inhibit the cytokine-induced activation of endothelial cells in vitro. In addition, phospholipids [12].

In a study performed in both rats and humans, long-term heavy ethanol intake (rats fed 14 gm/kg body weight of ethanol daily for 8 weeks; human subjects consuming > 80 grams of alcohol per day for a mean period of 21 years) led to depletion of sphingomyelin from plasma HDL particles, which was accompanied by a decreased ability of sphingomyein-depleted HDL to carry out reverse cholesterol transport; both the cholesterol efflux and the cholesterol uptake. This effect of heavy ethanol consumption was more pronounced in alcoholic individuals, with or without liver disease, who had dramatically reduced plasma HDL sphingomyelin content with concomitant impaired reverse cholesterol transport capacity of their HDL-C[13]. This could contribute to elevated mortality risk with heavy alcohol consumption, despite the observed increases in HDL-C levels.

Alcohol and LDL-Cholesterol

Data regarding the effect of alcohol on LDL-C are conflicting, with a meta-analysis of pooled human intervention studies showing a trend (not statistically significant) of ethanol-induced LDL-C lowering (Table 1). However, in the Cardiovascular Health Study of subjects over 65 years of age, a U-shaped relationship was observed between LDL and alcohol consumption. Alcohol intake was associated with less total LDL particles, lower levels of small LDL, HDL, and very-low-density lipoprotein (VLDL) particles, and higher levels of large LDL and medium- and large-sized HDL particles, as measured by nuclear magnetic resonance spectroscopy[14]. Small LDL particles tend to be more atherogenic, and the shift towards larger LDL particles could account for part of the anti-atherogenic activity of alcohol. However, heavy long term alcohol intake reduces the total mass of LDL-C and all is components. As one LDL particle contains one apoB-100 molecule, the lower concentration of apoB in alcohol abusers indicates a lower number of LDL particles[15]. One possible mechanism for the reduced LDL-C levels may be the formation of acetaldehyde adducts of apoB leading to reduced conversion of VLDL to LDL and increased clearance of LDL[16].

Alcohol and Non-HDL Cholesterol

Non-HDL cholesterol, defined as total cholesterol minus HDL-C, contains particles of all atherogenic apolipoprotein B-containing lipoproteins such as VLDL, intermediate-density lipoprotein (IDL), LDL and lipoprotein(a). Non-HDL cholesterol has been reported to be superior to LDL-C in predicting CVD events[17]. In a study of healthy Japanese men and women aged 35 to 55 years, non-HDL cholesterol levels and prevalence of high non-HDL cholesterol were found to be lower with increasing alcohol intake; the effect being more pronounced in women[18]. The relationship of alcohol consumption with serum non-HDL cholesterol appeared to depend mainly on LDL-C, and not on triglycerides.

Alcohol and Triglycerides

Recent studies demonstrate a biphasic relationship between alcohol consumption and triglyceride concentrations. Moderate alcohol intake (2-3 drinks per day) may lower triglycerides, while high alcohol intake has been consistently related to elevated triglycerides[19]. In one study, low alcohol intake (<10 gm/day) was associated with a decrease in diurnal triglyceridemia in males after adjustment for age, BMI and smoking, while moderate to high alcohol intake (10-30 and >30 gm/day respectively) were associated with increased postprandial triglycerides after dinner and at bedtime[20].

Alcoholic Beverage Type

In a French population sample, total alcohol intake showed a significant positive association with both HDL-C and triglycerides (TG) in men and women (median daily alcohol intake 24 g for men and 4 g for women)[21]. In multivariate analysis, wine was positively associated with HDL-C. Beer was positively associated with HDL-C in men and with triglycerides in men and women. Wine drinkers had higher HDL-C levels than non-wine drinkers, but this difference lost its significance after adjustment for confounders, particularly socio-economic status, as wine drinkers were likely to have a higher socio-economic status and a healthier lifestyle[21].

Red wine contains abundant polyphenolic compounds (notably resveratrol and anthocyanins) in addition to alcohol, which some have suggested provide additional benefit in lowering CVD risk. However, in a study comparing the effects of moderate consumption of red wine, dealcoholized red wine, and gin on glucose metabolism and the lipid profile, the mean adjusted lipoprotein(a) was reduced by 12% after red wine (ethanol plus polyphenols) but not after the other two interventions (Table 2)[22]. Further, moderate consumption of red wine and gin, but not dealcoholized red wine, increased plasma HDL-C and ApoA-I and ApoA-II concentrations, and decreased the LDL/HDL ratio, suggesting that the alcohol component is responsible for these changes[22].

Table 2

Comparison of changes in lipid profile after intervention with red wine (RW), dealcoholized red wine (DRW) and gin for 4 weeks in 67 subjects. Adapted with permission from: Chiva-Blanch G, et al. Clin Nutr 2013;32(2):200-206.

Demographic Factors

In a substudy of the Atherosclerosis Risk in Communities (ARIC) study[23], both low-to-moderate and heavy alcohol consumption, regardless of the type of alcoholic beverage consumed, resulted in significantly greater levels of HDL-C, HDL-3 cholesterol (a major HDL fraction), and apo A-I in both white and African-American males and females. However, significantly lower levels of LDL-C, apolipoprotein B, and triglycerides were observed only in white females, whereas significantly higher triglyceride levels were observed only in African-Americans (Figure 5). HDL-2 cholesterol levels were significantly associated with low to moderate and heavy drinking in both white males and females, but not in African- Americans. These differences could partially account for the positive correlation between alcohol consumption and coronary artery disease observed in African-Americans in the ARIC study[24]. Apart from race, body mass index greater than 25 kg/m[2] was found to attenuate the association of alcohol intake with lower LDL-C and higher HDL-C[25].

Mean lipid levels in Atherosclerosis Risk in Communities (ARIC) participants according to alcohol intake stratified by race and gender. Alcohol consumption defined as: for men, low-moderate ≤210 grams/week, heavy >210 grams/week; for women, low-moderate ≤105 grams/week, heavy >105 grams/week. WM = white male; AAM = African-American male; WF = white female; and AAF = African-American female. Adapted with permission from: Volcik KA, et al. Ann Epidemiol 2008;18(2):101-107

Genetic Polymorphisms

Genetic polymorphisms and their interaction with alcohol consumption have been implicated in modulating serum lipid levels. A polymorphism in the gene for alcohol dehydrogenase type 3 (ADH3) alters the rate of alcohol metabolism. In the Physician Health Study, moderate drinkers who were homozygous for the slow-oxidizing ADH3 allele (Figure 6) had higher HDL levels and a substantially decreased risk of myocardial infarction[26]. Carriers of the X447 allele (gain of function polymorphism) of lipoprotein lipase were found to have higher HDL-C concentrations and lower cardiovascular risk than those with the wild type allele. A study from Korea found that carriers of this allele benefited from moderate alcohol consumption in terms of higher HDL-C concentrations[27]. Polymorphisms of the ApoA5 gene leading to differential interactions of apoA with alcohol may account for differences in lipid parameters between drinkers and non-drinkers[28]. Of note, data from the Cohorte Lausannoise (CoLaus) study did not find an association between alcohol consumption on HDL-C mediated by polymorphisms of ApoA5, cholesteryl ester transfer protein, hepatic lipase or lipoprotein lipase genes[29].

Figure 6a: Adjusted high-density lipoprotein levels according to the level of alcohol consumption and the ADH3 genotype in 385 patients with myocardial infarction and 385 controls in the physicians' health study (panel a) and 325 postmenopausal women in the nurses' health study who were not receiving hormone-replacement therapy (panel b). Reproduced with permission from: Hines LM et al. N Engl J Med 2001;344:549-555.

In a cross-sectional study derived from the Framingham Offspring Study, the effects of alcohol intake on LDL-C were modulated in part by variability at the APOE locus in men (Figure 7). A negative association was noted between alcohol and LDL-C in men with the E2 allele, but a positive association in men with the E4 allele. No significant associations were observed in men or women with the E3 allele[30].

Mean (±SEM) plasma LDL-cholesterol concentrations by APOE genotype and alcohol intake status in men and women. Mean (±SEM) plasma LDL-cholesterol concentrations by APOE genotype and alcohol intake status in men and women. ANOVA: in men, NS for nondrinkers and P <0.001 for drinkers; in women, P <0.001 for both nondrinkers and drinkers. There was a significant interaction (P <0.01) between alcohol intake and the effect of APOE allele type on LDL-cholesterol concentrations in men, but not in women. For analytical purposes, genotypes E2/E2 and E2/E3 were grouped as E2, genotypes E3/E4 and E4/E4 as E4, and genotype E3/E3 as E3. Subjects with the E2/E4 genotype were excluded from the analysis. Reproduced with permission from: Corella D et al. Am J Clin Nutr 2001;73:736-745

Conclusion

The effects of moderate alcohol consumption on the lipid profile are well-documented, showing an association between alcohol-induced increases in HDL-C levels and cardioprotection (though there remains some debate). The mechanism of this potential cardioprotective effect of alcohol is fertile ground for research. Whereas prior research was focused on alcohol-induced changes in cholesterol and triglycerides levels, the paradigm has shifted to the composition of lipoproteins, with emphasis on smaller lipid molecules such as sphingolipids. These molecules may impact the endothelium by their interaction with cell membranes and ultimately be responsible for the potential atheroprotection afforded by alcohol. The benefits of red wine over other forms of alcohol have not been proven clinically, especially in terms of effects on the lipid profile. Finally, direct evidence to recommend drinking alcohol in moderation for decreasing cardiovascular risk is still lacking, and presents another avenue for clinical research.

Conflict of interests

None declared.

Competing interests

None declared

References

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    Licensee to OAPL (UK) 2014. Creative Commons Attribution License (CC-BY)

    Summary of pooled mean difference in lipid biomarker level after alcohol use in a meta-analysis of 44 studies. *Indicates significant (P<0.01) change in biomarker level after alcohol use compared with a period of no alcohol use. †Heterogeneity detected across pooled studies, where Q statistic P<0.10. Modified, with permission from: Brien SE et al. BMJ 2011;342:d636

     

    Biomarker

    Number of pooled studies

    Number of pooled participants

    Pooled mean difference in

    biomarker level (95% CI)

    HDL-C (mmol/L)

    33

    796

    0.094 (0.064 to 0.123)*†

    LDL-C (mmol/L)

    24

    513

    −0.11 (−0.22 to 0.006)†

    Total-C (mmol/L)

    26

    596

    0.00 (0.066 to 0.067)

    Triglycerides (mmol/L)

    31

    752

    0.016 (0.018 to 0.051)

    Apolipoprotein A1 (g/L)

    16

    374

    0.101 (0.073 to 0.129)*†

    Lp(a) lipoprotein (mg/dL)

    3

    114

    0.80 (4.17 to 5.76)

    Comparison of changes in lipid profile after intervention with red wine (RW), dealcoholized red wine (DRW) and gin for 4 weeks in 67 subjects. Adapted with permission from: Chiva-Blanch G, et al. Clin Nutr 2013;32(2):200-206.

     

    mg/dL

    Mean±SD

     

     

     

    P value

     

    Baseline

    RW

    DRW

    Gin

     

    Total cholesterol

    204±33

    202±34

    196±32

    199±35

    0.16

    Triglycerides

    128±60

    131±60

    125±58

    124±61

    0.28

    LDL-cholesterol

    133±32

    127±28

    130±25

    128±28

    0.64

    HDL-cholesterol

    43±7

    46±9

    43±10

    45±10

    0.002

    LDL/HDL ratio

    3.08±0.10

    2.86±0.09

    3.10±0.09

    2.94±0.10

    0.001

    Lipoprotein (a)

    54.4±10.6

    50.2±11.9

    57.2±11.4

    57.4±11.4

    0.012

    Apolipoprotein A-I

    754±18

    802±17

    713±17

    803±16

    0.009

    Apolipoprotein A-II

    0.032±0.0

    0.035±0.0

    0.031±0.0

    0.033±0.0

    0.013

    Keywords