In this pooled cohort of eight prospective studies, we observed a lower risk of coronary heart disease among men and women with a light to moderate alcohol intake compared with non-drinkers, and this finding was consistent across different age groups without significant variations in dose-response.
The current knowledge on the effect of alcohol on CHD in younger adults is sparse. In a study based on the Honolulu Heart Program, the authors compared CHD risk according to conventional risk factors in middle-aged and older men (45–93 years). Compared with non-drinkers, they observed a lower risk of CHD among drinkers in middle-aged but not among older participants (75+ years), and concluded accordingly that the relation between alcohol and CHD weakened with age. The study, however, was limited by the simple categorisation of alcohol intake into drinkers versus non-drinkers and included men only.10
Several plausible explanations for the lowered risk of CHD among moderate drinkers exist. Among those explanations, the evidence is probably strongest for a mechanism involving alcohol increasing high-density lipoprotein (HDL) cholesterol and reducing plasma fibrinogen levels, thereby reducing platelet aggregability.7;34
The hypothesised J-shaped relation between alcohol intake and diabetes could also explain some of the benefit from alcohol intake.35;36
Also, alcohol has an effect on PAI-1 that would tend to reduce thrombosis.37
Previous studies have suggested that the causes of CHD in younger adults differ from the mechanisms involved with CHD in older persons. Results from the Honolulu Heart Program indicated that the effect of hypertension, body mass index (BMI), and cholesterol on CHD differed according to age. For instance, the relative risk of CHD in hypertensive men declined from 3.7 in those aged 45–54 years to 1.7 in those aged 75 years or more. Similarly, associations between BMI and total cholesterol weakened with advancing age.10
The Coronary Artery Risk in Young Adults (CARDIA) study of men and women aged 33–45 years found that alcohol intake was associated with expected dose-response between alcohol and HDL cholesterol levels and an inverse relation between alcohol and fibrinogen levels.9
They also observed an increased risk of coronary calcification with greater alcohol consumption. Since coronary calcification is a marker of atherosclerosis this result in young adults is not consistent with the results of the present study.9
Another aspect of alcohol consumption related to age is drinking patterns. Younger adults may tend to binge-drink more often than older persons, and this may increase their risk of CHD;5;7;9
however, findings from the CARDIA study mentioned above did not indicate a protective effect of alcohol intake on coronary calcification in younger adults even after excluding binge-drinkers.9
Our findings suggest a J-shaped curve in women; but in men, the risk did not increase significantly at high amounts of alchohol. Biomarkers that mediate the association between alcohol and decreased risk of CHD, such as high-density lipoprotein and fibrinogen, are found to explain a larger proportion of the association among men than among women which may indicate that alcohol has specific effects on such mediators according to sex.7
Other biological explanations for sex-specific associations include differences in alcohol pharmacokinetics (i.e. processing and elimination of alcohol in the body), which depend largely on body composition.38;39
However, as the risk curves of this study were modelled separately for the genders comparisons between the two are not straight forward.
The present study is one of few existing studies focusing on the effects of alcohol on CHD according to age. Our work was based on a large body of data with thorough measurements of alcohol intake and relevant covariates. A strength was the availability of diet data in the Pooling Project of Diet and Coronary Disease that enabled adjustment for potential dietary confounders. The size of the study population allowed us to perform subset analyses exploring the association between alcohol and CHD in strata of younger men and women – aspects even large individual cohorts do not have the power to address. The findings of the present study are strengthened by the prospective design, which provided information on the sequence of events allowing for conclusions on causality – assuming proper confounding control. Potential confounders of the association between alcohol and CHD were carefully selected on basis of Directed Acyclic Graphs, ensuring a minimally sufficient set of covariates. Further, the inclusion criteria of the Pooling Project of Diet and Coronary Disease enabled adjustment for relevant dietary factors, for which most previous studies did not control. The pooled analyses included both cohorts and intervention studies from North America and Europe, and similar effects were observed across the studies. Finally, an advantage of the Pooling Project is the inclusion of previously unpublished results thereby reducing the risk of publication bias.
However, several limitations of the study should also be considered. We focused on the importance of amount of alcohol consumed; however, other aspects of patterns of alcohol intake may be equally important and were not addressed. Our study only included information on current alcohol consumption and confounders at baseline. For this reason, the reference category of abstainers may contain former drinkers who quit because of existing illness, which could cause a moderate alcohol intake to appear more protective than it is. Although several studies including only lifelong or long-term abstainers in this category have confirmed a protective effect of alcohol even among healthy individuals,6;40
the “sick-quitter” hypothesis is relevant in the present context, as older age groups may include more abstainers who stopped drinking due to illness, e.g. hypertension.
As mentioned above, patterns of alcohol consumption (e.g. choice of alcohol type and frequency of consumption) may differ considerably with age which we did not account for. Our findings of protective effects of alcohol on CHD in all examined age-groups may indicate that neither type of alcohol or frequency of consumption modify the influence of alcohol on CHD considerably. However, future research based on observational studies should place emphasis on other measures of alcohol intake such as frequency of alcohol consumed. Further, cohort studies with information on lifetime alcohol intake or repeated measurements of alcohol intake and potential confounders could contribute with valuable insight, as changes in alcohol intake over a given period may be of great importance. Additional experimental studies are also needed in order to expand the knowledge on biological mechanisms.
Further, this study only focused on CHD events. Overall effects of alcohol on all-cause morbidity and mortality must be considered in order to be able to optimize alcohol guidelines for different age groups of the population. The lower risk of all-cause mortality is mainly expected to be caused by the effects of alcohol on CHD. In this study, a lower risk of CHD was observed in all examined age-groups in moderate alcohol consumers compared to abstainers; however, the absolute risk of CHD was rather low in the youngest age group. Thus, considering the increasing contribution of CHD to all-cause mortality with age, it is reasonable to assume that the protective effect of alcohol on all-cause mortality is mostly pronounced in older age-groups. This issue has been addressed in a few previuos studies indicating that the protective effect of alcohol consumption on mortality in general is confined to middle-aged and older individuals.4;41;42
Unfortunately, information on all-cause mortality was not collected in the database of the Pooling Project on Diet and CHD.
In summary, this study supports current knowledge that alcohol in moderate amounts protects against coronary heart disease in both men and women. Our findings further suggest that this effect is also present in younger age groups. However, younger adults are at low risk for CHD and the beneficial effects obtained by a moderate alcohol intake may be negligible compared to the increased risk of for instance traffic accidents and cancer. Recommendations on alcohol intake among younger adults should consider all-cause mortality and morbidity.