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Mental disorders remain one of the world's major international public health problems, and mental disorders may also interact with the progress and development of many physical diseases [1].

Mental health status (MHS) plays a central role in influencing the behaviours of individuals, especially those related to physical health [1]. Given this, MHS has the potential to confound observational research studies which seek to understand associations between physical health problems and behaviour factors. Two such health problems are coronary heart disease (CHD) and ischaemic stroke [1,2].

Many cohort studies from the medical epidemiology literature have observed a ‘J-shaped’ association between alcohol consumption and risk of CHD and stroke for middle-aged and older people [3–5]. Non-drinkers appear to have a higher risk of CHD and stroke than regular moderate drinkers. The direct implication is that moderate drinking is cardioprotective, but the veracity of the J-shaped curve is being scrutinized increasingly [e.g. 4].

As well as research concerned with cardiovascular health, studies have emerged recently which show consistently that the prevalence of depression is significantly higher among non-drinkers compared to moderate drinkers [6–8]. It is arguable that adjustment for socio-economic factors may mitigate some MHS effects; however, the large-scale cohort study by Skogen et al. [8] adjusted for confounders typically controlled for in alcohol–CHD studies and the effects of MHS on cardiovascular health remained.

Three alternative hypotheses explicate the association observed between mental disorders and alcohol consumption, as follows.

  • 1Better MHS leads to drinking at moderate levels.
  • 2Moderate alcohol consumption leads to lower risk of mental disorders (i.e. depression).
  • 3There is no causal relation between MHS and alcohol consumption, and the association is due to unknown confounding factors.

If hypothesis 3 is true, hypotheses 1 and 2 must be rejected and if hypotheses 1 and 2 are true, hypothesis 3 must be rejected. However, hypotheses 1 and 2 are not mutually exclusive.

Bringing the observations from the mental health and cardiovascular literature together: if hypothesis 2 is true, then moderate regular alcohol consumption may protect against cardiovascular disease via its positive effect on MHS (i.e. lower risk of depression). Alternatively, the action of drinking and/or the constituents of the beverage (e.g. alcohol) may produce a desirable effect on MHS and thereby a protective effect on CHD.

Conversely, if hypothesis 2 is not true, the apparent cardioprotective effect of moderate drinking may be due, in fact, to the better MHS of moderate drinkers. It is not currently possible to determine whether or not this might be the case, as MHS is rarely investigated using reliable psychiatric measurements by cohort studies [2,3,5,9]. It is not feasible to test hypothesis 2 with animal studies; however, it would be useful to test how MHS may change among moderate drinkers who stop drinking or switch to lower-strength alcoholic beverages in a randomized controlled trial. Attempts to test this outside a randomized setting would be prone to bias, as people who cease alcohol consumption often do so because of failing health and/or increasing age [4].

The adjusted likelihood of depression among abstainers compared to moderate drinkers was 38% higher [8]—about 10% higher than the comparative likelihood of CHD among abstainers (1.25) [3]. We argue that a concerted effort to adjust for MHS with reliable, comprehensive measures will bring the apparent association between moderate alcohol consumption and CHD substantially closer to 1. Until such efforts are made, apparent cardioprotective effects of moderate drinking from observational studies will be questionable.

Changing MHS over the life-span and its association with drinking behaviours may be key to understanding the true nature of the apparent cardioprotective effects of moderate alcohol consumption on older populations.

Declarations of interest