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So, the raise in HDL from alcohol may not matter.

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And, in case you have a look at subclinical markers of atherosclerosis, just like the thickening of the wall of your carotid arteries in your neck, those who abstain from alcohol absolutely seem to be at the bottom risk. And, the equal with coronary calcium scores, wherein, in wellknown, the decrease the alcohol consumption, the lower the chance.

And, alcohol bumps our blood stress up a piece as nicely, which might be anticipated to raise, not decrease, our cardiac danger.

So, Where Did We Get This Idea That Alcohol Was Good For Us?

From the famous J curve.

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Check it out.

If you observe huge populations of human beings over time, in trendy, the extra people drink, the higher their hazard of dying in advance. But the lowest danger—those who generally tend to live the longest—aren't people who drink zero, the abstainers, however folks who drink fairly, like one drink a day.

That’s why you get some oldsters recommending that “physicians must recommend lifelong nondrinkers” to take up the habit.

Sure, there are statin pills, however “alcoholic beverages [don’t] require a prescription, are a ways cheaper, and really extra fun.” Is slight ingesting virtually shielding?

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Or, is there simply something about individuals who abstain absolutely from alcohol that places them in a higher danger category?

The motive we suspect some thing fishy is going on is that abstainers seem to be at higher hazard of an entire swath of sicknesses such as, ironically, liver cirrhosis.

Compared to lifelong abstainers—the ones who have by no means touched the stuff—males and females drinking a little seem to have much less liver cirrhosis. Wait—what?

How could a touch drinking be connected to lower shares of liver cirrhosis?

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Well, let’s reflect onconsideration on it. What makes greater feel, that drinking results in much less liver cirrhosis, or liver cirrhosis ends in much less ingesting?

In different words, reverse causation:

the so-called “sick quitter impact.” If you have a look at reports of smokers, now and again you notice better mortality shares amongst those who stop smoking, in comparison to people who continue smoking.

Why?

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Because the purpose they end smoking is due to the fact they were given sick.

So, of route, sick people die extra frequently than less sick humans. That’s why while you classify someone as a non-smoker in a study, you need to make sure they’re a “lifelong nonsmoker” and not only a non-smoker…for the reason that remaining Tuesday.

Yet, unbelievably, that’s now not what they do in most alcohol studies, in which rather they misclassify former drinkers as if they were lifelong abstainers.

And, look, “individuals with poorer health are more likely to reduce down or stop drinking absolutely,” thereby making contemporary drinkers “‘look precise’ [in] assessment” to folks who drink zero, because a number of the “abstainers” are just abstaining because they were given unwell and stopped.

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Okay.

So, what if you went again to all those reviews and corrected the misclassifications, split out the former drinkers from the lifelong abstainers?

We didn’t know… till now. They, indeed, observed “drinker misclassification errors” all too not unusual, plaguing three quarters of the experiences, and when they managed for that, the J-fashioned curve disappeared.

The loss of life versus alcohol relationship became more constant with a straight line, “linear dose response,” meaning greater alcohol, greater death:

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no safety at low levels of consumption. So: