Those health benefits have since been shown in numerous epidemiological studies which show a U- or J-shaped curve for alcohol consumption and mortality, with a very clear protective effect for cardiovascular disease in particular. These findings cannot be explained by the "sick quitter" hypothesis.
Today, as in the nineteenth century, those who ignore or dispute the medicinal benefits of moderate alcohol consumption usually have a temperance axe to grind. As Eric Crampton and Dick Puddlecote have both noticed, one such fellow is Tim Stockwell of the University of Victoria's Centre for Addictions Research. This is the man who led the media to believe that a 10% increase in British Columbia's minimum alcohol price led to a 32% reduction in alcohol-related deaths, despite the fact that there has been no 10% increase in price and there was no reduction at all in alcohol-related deaths.
Stockwell wrote to the journal Addiction after yet another study showed the cardiovascular health benefits of alcohol consumption. His argument was basically "confounding factors, confounding factors, confounding factors" even though the confounding factors he mentions have been repeatedly examined and discounted as explanations. He then calls for randomised control trials, though he must know that such experiments can never be conducted since they would require thousands of people to be force fed different quantities of alcohol for decades.
The authors of the study have replied with what Crampton calls "a beautiful glove slap", noting the tendency of neo-temperance folk to accept any old epidemiological association if it indicts alcohol while setting the bar impossibly high when it comes to benefits.
Epidemiology is only one of several pillars of evidence. Basic research on pathways in animals and humans constitute the other pillars. Together, the meta-analyses of both the epidemiology and the two most important biological causal pathways, which can be examined using randomized controlled trials (more rigorous evidence), coincide with the conclusions that regular and moderate alcohol consumption is associated with a lower risk of ischaemic disease.
Given the above points and further points made in , it seems that some researchers in the ﬁeld may be using different standards in assessing the cardioprotective effect of alcohol vs. its detrimental effect. Consider two examples. One is the effects of alcohol on colon cancer. Would the same arguments used to judge the relationship between alcohol and ischaemic heart disease not hold for this relation as well? The other example is the more than 200 other risk relations between alcohol and disease and injury outcomes.
Of course, this is not a good argument against scrutinizing the cardioprotective effect of alcohol, but we sense a desire by some in the ﬁeld to apply tough standards on protective effects and more lenient standards on other effects, where sometimes the responses to very simple survey questions such as ‘Did your partner’s alcohol consumption contribute to your marriage problems?’ are accepted as causal evidence.
Touché. Alas, this lesson in epidemiology may be wasted on the psychologist Stockwell, who neglects to include such basics as control groups in his own studies and whose own data are at odds with those of his own institute.
Speaking of which, it is worth noting that Stockwell's stomping ground, the University of Victoria's Centre for Addiction Research, mentions that it does not include several major diseases in its estimates of alcohol-related mortality...
Alcohol-attributed numbers do not include the following conditions: diabetes, ischemic heart disease, cerebrovascular disease, ischemic stroke, and haemorrhagic stroke (female only)
And why is that?
Alcohol has a net protective effect on these conditions and it is not possible to separate the number of alcohol-attributed and prevented deaths and hospitalizations