Friday Favorites: Is It Better to Drink Little Alcohol Than None? Do Any Benefits of Alcohol Outweigh the Risks?

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Even if alcohol causes cancer and there is no “French paradox,” what about the famous J-shaped curve, where excessive drinking is bad, but light drinkers appear to have lower mortality than abstainers?

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

“Why do we not see the corporate interests of the alcohol industry as clearly as we see those of the tobacco industry?” Well, the alcohol industry has “waged a sophisticated and successful campaign [over the last few decades] undermin[ing] perceptions of the extent of alcohol-related harms to health by [framing the argument as] a balance of benefits and harms.” Yes, alcohol may be an “intoxicating carcinogen,” increasing cancer risk, but what about reducing heart disease risk? “[P]olicymakers 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 already explored, HDL is no longer considered protective, based in part on 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 carotid arteries in your neck, those that abstain from alcohol completely seem to be at the lowest risk. And, 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 did 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—are not those who drink zero, the abstainers, but those who drink moderately, like one drink a day.

That’s why you get some folks recommending that “physicians should counsel lifelong nondrinkers” to take up the habit. Sure, there are statin drugs, but “alcoholic beverages [don’t] require a prescription, are 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 leads to less liver cirrhosis, or liver cirrhosis leads 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 that 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 nonsmoker” and 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, separated out the former drinkers from the lifelong abstainers? We didn’t know… until now.

They, indeed, found “drinker misclassification errors” all too common, plaguing three quarters of the studies, and when they controlled for that, the J-shaped curve disappeared. The death versus alcohol relationship became more consistent with a straight line, “linear dose response,” meaning more alcohol, more death: no protection at low levels of consumption.

So: “No [apparent] benefit of light to moderate 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 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 of 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 sceptical 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 risks 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 studies classified those that quit drinking in response to ill-health as nondrinkers. This is the problem of reverse causation: instead of abstaining leading to poor health, poor health may have lead to abstaining. It’s 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? That’s one of the reasons why, if you look at the “hierarchy of evidence,” where higher on the pyramid means stronger evidence, interventional trials—like randomized, controlled 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, controlled trials—like, you can’t randomize people to smoke a pack a day for a few decades. So, sometimes you have to base your decisions on observational studies. But now, we have a new tool: “Mendelian randomization.”

“In cases where [randomized, controlled 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 were randomly assigned higher HDL levels genetically from birth don’t appear to be protected. Is there any way to study people who were randomly assigned since conception to not drink as much? Remarkably, yes.

Alcohol is detoxified in the liver to carbon dioxide and water by two enzymes. But, in the process, a toxic intermediate metabolite is produced, called acetaldehyde, which can cause unpleasant nausea and flushing sensations. So, if people are born with a slow variant of this enzyme, or a superfast variant of this enzyme, acetaldehyde can build up, making alcohol drinking for these people a relatively unpleasant experience throughout their lives. So, they are born less likely to drink as much. So, do they have an increased risk of heart disease, like the original observational studies would suggest? No, they have a 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. “…[N]ow the scientific pillars on which it is 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 is not surprising that reports [suggesting] benefits attracted enthusiasm among consumers, the media, and [of course] the alcohol industry. [But] [t]hese apparent benefits are now evaporating.”

“What conclusions should we draw from this emerging evidence…? Firstly, 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] should remove [all] misleading references to [purported] 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 does 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, these interventions have] no abuse potential.” There’s a reason there’s no Appleholics Anonymous.

Please consider volunteering to help out on the site.

Image credit: Joel Herzog via Unsplash. Image has been modified.

Motion graphics by Avocado Video.

Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

“Why do we not see the corporate interests of the alcohol industry as clearly as we see those of the tobacco industry?” Well, the alcohol industry has “waged a sophisticated and successful campaign [over the last few decades] undermin[ing] perceptions of the extent of alcohol-related harms to health by [framing the argument as] a balance of benefits and harms.” Yes, alcohol may be an “intoxicating carcinogen,” increasing cancer risk, but what about reducing heart disease risk? “[P]olicymakers 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 already explored, HDL is no longer considered protective, based in part on 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 carotid arteries in your neck, those that abstain from alcohol completely seem to be at the lowest risk. And, 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 did 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—are not those who drink zero, the abstainers, but those who drink moderately, like one drink a day.

That’s why you get some folks recommending that “physicians should counsel lifelong nondrinkers” to take up the habit. Sure, there are statin drugs, but “alcoholic beverages [don’t] require a prescription, are 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 leads to less liver cirrhosis, or liver cirrhosis leads 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 that 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 nonsmoker” and 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, separated out the former drinkers from the lifelong abstainers? We didn’t know… until now.

They, indeed, found “drinker misclassification errors” all too common, plaguing three quarters of the studies, and when they controlled for that, the J-shaped curve disappeared. The death versus alcohol relationship became more consistent with a straight line, “linear dose response,” meaning more alcohol, more death: no protection at low levels of consumption.

So: “No [apparent] benefit of light to moderate 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 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 of 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 sceptical 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 risks 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 studies classified those that quit drinking in response to ill-health as nondrinkers. This is the problem of reverse causation: instead of abstaining leading to poor health, poor health may have lead to abstaining. It’s 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? That’s one of the reasons why, if you look at the “hierarchy of evidence,” where higher on the pyramid means stronger evidence, interventional trials—like randomized, controlled 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, controlled trials—like, you can’t randomize people to smoke a pack a day for a few decades. So, sometimes you have to base your decisions on observational studies. But now, we have a new tool: “Mendelian randomization.”

“In cases where [randomized, controlled 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 were randomly assigned higher HDL levels genetically from birth don’t appear to be protected. Is there any way to study people who were randomly assigned since conception to not drink as much? Remarkably, yes.

Alcohol is detoxified in the liver to carbon dioxide and water by two enzymes. But, in the process, a toxic intermediate metabolite is produced, called acetaldehyde, which can cause unpleasant nausea and flushing sensations. So, if people are born with a slow variant of this enzyme, or a superfast variant of this enzyme, acetaldehyde can build up, making alcohol drinking for these people a relatively unpleasant experience throughout their lives. So, they are born less likely to drink as much. So, do they have an increased risk of heart disease, like the original observational studies would suggest? No, they have a 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. “…[N]ow the scientific pillars on which it is 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 is not surprising that reports [suggesting] benefits attracted enthusiasm among consumers, the media, and [of course] the alcohol industry. [But] [t]hese apparent benefits are now evaporating.”

“What conclusions should we draw from this emerging evidence…? Firstly, 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] should remove [all] misleading references to [purported] 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 does 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, these interventions have] no abuse potential.” There’s a reason there’s no Appleholics Anonymous.

Please consider volunteering to help out on the site.

Image credit: Joel Herzog via Unsplash. Image has been modified.

Motion graphics by Avocado Video.

Doctor's Note

Hold on. HDL isn’t “good” cholesterol anymore? Check out my ashtray and gym shoes analogies in reference to causal risk factors in my Coconut Oil and the Boost in HDL “Good” Cholesterol video.

How much cancer does alcohol really cause, though? You might have missed the first video of this series: Can Alcohol Cause Cancer?.

What about resveratrol and the French paradox? See The Best Source of Resveratrol and What Explains the French Paradox?.

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