 Where did we get this idea that light to moderate drinking was beneficial for health? Are there any benefits? Watch to find out. Why do we not see the corporate interests of the alcohol industry as clearly we see those of the tobacco industry? Well, the alcohol industry has waged a sophisticated and successful campaign of the last few decades undermining perceptions of the extent of alcohol-related harm to health by framing the argument as a balance of benefits and harms. Yes, alcohol may be an intoxicated carcinogen increase in cancer risk, but what about reducing heart disease risk? Policymakers hesitate to introduce effective alcohol policies or even to support the addition of warning labels for fear they might undermine or contradict any possible health benefits of alcohol use. After all, alcohol consumption clearly raises HDL, the supposed good cholesterol. But sadly, as I've already explored, HDL is no longer considered protective, based on part of so-called Mendelian randomization studies where having a high HDL your whole life doesn't appear to help. Whereas a lifelong reduction of bad cholesterol, LDL, just thanks to luck-of-the-draw genetics, does indeed decrease heart disease risk. So the boost in HDL from alcohol may not matter, and if you look at subclinical markers of atherosclerosis like the thickening of the wall of your crudded arteries in your neck, those that abstain from alcohol completely seem to be at the lowest risk, in the same with coronary calcium scores, where in general the lower the alcohol consumption, the lower the risk. And alcohol bumps our blood pressure up a bit as well, which would be expected to raise, not lower our cardiac risk. So where do we get this idea that alcohol was good for us? From the famous J-curve. Check it out. If you follow large populations of people over time in general, the more people drink, the higher their risk of dying prematurely, but the lowest risk, those who tend to live the longest, were not those who drank zero, the abstainers, but those who drank moderately like one drink a day. That's why you get some folks recommending that physicians should counsel lifelong non-drinkers to take up the habit. Sure, there are statin drugs, but alcoholic beverages don't require a prescription or far cheaper, and certainly more enjoyable. Is moderate drinking really protective, or is there just something about people who abstain completely from alcohol that puts them in a higher risk category? The reason we suspect something fishy is going on is that abstainers seem to be at higher risk of a whole swath of diseases, including, ironically, liver cirrhosis. Compared to lifelong abstainers, those who have never touched the stuff, men and women drinking a little appear to have less liver cirrhosis. Wait, what? How could a little drinking be linked to lower rates of liver cirrhosis? Well, let's think about it. What makes more sense that drinking led to less liver cirrhosis or liver cirrhosis led to less drinking? In other words, reverse causation, the so-called sick quitter effect. If you look at studies of smokers, sometimes you see higher mortality rates among those who quit smoking compared to those who continue smoking. Why? Because the reason they quit smoking is because they got sick. So, of course, sick people die more often than less sick people. That's why when you classify someone as a non-smoker in a study, you have to make sure they're a lifelong non-smoker, not just a non-smoker since last Tuesday. Yet, unbelievably, that's not what they do in most alcohol studies, where instead they misclassify former drinkers as if they were lifelong abstainers. And look, individuals with poorer health are more likely to cut down or stop drinking completely, thereby making current drinkers look good in comparison to those who drink zero, because some of the abstainers are just abstaining because they got sick and stopped. Okay, so what if you went back to all those studies and corrected the misclassifications, separate out the former drinkers from the lifelong abstainers? We didn't know until now. They indeed found a drinker, misclassification errors all too common, plaguing three-quarters of the studies, and when they controlled for that, the J-curve disappeared. The death versus alcohol relationship became more consistent with a straight-line, you know, linear dose response, meaning more alcohol, more death, no protection at low levels of consumption. So no apparent benefit of life-to-matter drinking after all when you use better comparison groups. Although these results are not what the majority of drinking adults may desire to believe, the public deserves to hear and to read in a more complete and balanced detail the ever-growing evidence that drinking alcohol is very unlikely to improve their health. Once you remove from studies on alcohol and mortality the systematic error of misclassifying former drinkers as if they were lifelong abstainers, moderate alcohol consumption, like a glass and wine a day, does not appear to be protective after all. The immediate implication from this new research is that clinicians need to be highly skeptical about the hypothesized health benefits of alcohol consumption and should not advise their patients to drink to improve their life expectancy. This is especially important, given increasing awareness of cancer risk from even moderate alcohol use. Given the cancer risk, if there's just harms and no benefits, then the ideal alcohol intake on a routine day-to-day basis should really be zero, potentially making it a red-light beverage. The problem was that many of these population types classified those that quit drinking in response to ill health as non-drinkers. This is the problem of reverse causation. Instead of abstaining leading to poor health, poor health may have led to abstaining. As like when studies show those who sit around and watch TV have worse health, is more TV leading to illness, or is illness leading to more TV on the couch? That's one of the reasons why if you look at the hierarchy of evidence, where higher on the period means stronger evidence, interventional trials, like randomized control trials, tend to offer better evidence than observational studies of populations which can suffer from both reverse causation and confounding factors. For example, light drinkers as a group may be more likely to drink their glass of wine with a salad than a cheeseburger, and that's why the wine appeared protective. But sometimes it's hard to do randomized control trials, like you can't randomize people to smoke a pack a day for a few decades, and so sometimes you have to base your decisions on observational studies. But now we have a new tool, Mendelian randomization. In cases where randomized control trials are not feasible or practical, this new tool can provide reliable evidence on the cause-and-effect relationship between exposures and risks of disease. It's like the HDL story. Alcohol does raise your HDL good cholesterol levels, but unfortunately it seems good cholesterol isn't any good at lowering heart disease risk after all, based in part on Mendelian randomization studies, where people who are randomly assigned higher HDL levels genetically from birth don't appear to be protected. Is there any way to study people who are randomly assigned since conception to not drink as much? Remarkably, yes. Alcohol is detoxified and delivered to carbon dioxide and water by two enzymes, but in the process a toxic intermediate metabolite is produced called acid aldehyde, which can cause unpleasant nausea and flushing sensation. So if people are born with a slow variant of this enzyme or a superfast variant of this enzyme, acid aldehyde can build up, making alcohol drinking and these people a relatively unpleasant experience throughout their lives. So they're just born less likely to drink as much. So do they have increased risk of heart disease, like the original observational studies would suggest? No, they have reduced risk of heart disease. This suggests that reduction of alcohol consumption, even for light to moderate drinkers, is beneficial for cardiovascular health. So this just sheds further doubt on the protective association between moderate alcohol consumption and heart disease, which was already plagued with the confounding and bias, and now the scientific pillars on which it's based appear increasingly shaky, leading some to suggest the leaning tower of presumed health benefits from moderate alcohol use has finally collapsed. Given the harms attributed to alcohol use, it's not surprising that reports suggesting benefits attracted enthusiasm among consumers, the media, and of course the alcohol industry. But these apparent benefits are now evaporating. What conclusion should we draw from this emerging evidence? First, in health as elsewhere, if something looks too good to be true, like butter is back, it should be treated with great caution. Secondly, health professionals should discourage drinking. Thirdly, health advice should come from health authorities, not from the alcohol industry, which will remove all misleading references to reported health benefits, which are increasingly looking more like a triumph of spin doctoring than good science. As contrived as the alleged split among scientists over climate change advanced by the petroleum industry. As an intoxicating addictive toxic carcinogenic drug, alcohol is not a great choice as a therapeutic agent, even if it did help. There are better ways to prevent heart attacks, namely diet and exercise and drugs when necessary. In contrast to that of alcohol, effectiveness of lifestyle interventions has been demonstrated, and as a bonus has no abuse potential. There's a reason there's no apple-holics anonymous.