Whether You Have One or Two Shots of Whiskey Occasionally, It Affects Your Health
The latest news? Do not drink.
A shot of anything is generally 1.50 fluid ounces, which is 41.7 grams. Whiskey can range in proof, starting at 80 proof. Simple math and using 80 proof whisky (40% alcohol) yields 16.68 grams of alcohol. I am going to guess Bourbon is similar.
I got tired of reading the NYT article which is also on Yahoo and printed twice in the same column. I do not have leeway to current NYT articles. This JAMA Network Open study which also includes author Tim Stockwell is similar to what the NYT article is. It is stating the same thing. If you drink any form of liquid being whiskey or wine there is a of risk all-cause mortality. An increased health risk among female drinkers who drank 25 or more grams per day and among male drinkers who drank 45 or more grams of ethanol per day. It does not matter if you have one shot or two shots. You are at risk.
This is not the complete study. I narrowed it down to the main points leaving behind some of the information leading to their conclusions.
~~~~~~~~
The Study: Association Between Daily Alcohol Intake and Risk of All-Cause Mortality
by Jinhui Zhao, Tim Stockwell, and Tim Naimi
JAMA Network Open March 2023
This systematic review and meta-analysis of 107 cohort studies involving more than 4.8 million participants found no significant reductions in risk of all-cause mortality for drinkers who drank less than 25 g of ethanol per day (about 2 Canadian standard drinks compared with lifetime nondrinkers) after adjustment for key study characteristics such as median age and sex of study cohorts. The study showed there is a significantly increased risk of all-cause mortality among female drinkers who drank 25 or more grams per day and among male drinkers who drank 45 or more grams per day.
Meaning: Low-volume alcohol drinking was not associated with protection against death from all causes.
Introduction
The proposition that low-dose alcohol use protects against all-cause mortality in general populations continues to be controversial.1 Observational studies tend to show that people classified as “moderate drinkers” have longer life expectancy and are less likely to die from heart disease than those classified as abstainers.2 Systematic reviews and meta-analyses of this literature3 confirm J-shaped risk curves (protective associations at low doses with increasing risk at higher doses).
However, mounting evidence suggests these associations might be due to systematic biases that affect many studies. For example, light and moderate drinkers are systematically healthier than current abstainers on a range of health indicators unlikely to be associated with alcohol use eg, dental hygiene, exercise routines, diet, weight, income4; and lifetime abstainers may be systematically biased toward poorer health5.
Studies fail to control for biases in the abstainer reference group, in particular failing to remove “sick quitters” or former drinkers. Many of whom cut down or stop for health reasons2; and most studies have nonrepresentative samples leading to an overrepresentation of older White men. Adjustment of cohort samples to make them more representative has been shown to eliminate apparent protective associations.6 Mendelian randomization studies controlling for the confounding effects of socio-demographic and environmental factors find no evidence of cardioprotection.7
The present study updates our earlier systematic review and meta-analysis for all-cause mortality and alcohol use,8 including studies published up to July 2021 (ie, 6.5 years of additional publications). The study also investigated the risk of all-cause mortality for alcohol consumption according to:
(1) median ages of the study populations (younger than 56 years or 56 years and older), replicating the methods of Zhao et al9;
(2) the sex distribution of the study populations, and
(3) studies of cohorts recruited before a median age of 51 years of age and followed up in health records until a median age of at least 60 years (ie, with stricter rules to further minimize lifetime selection biases).
Because younger cohorts followed up to an age at which they may experience heart disease are less likely to be affected by lifetime selection biases,9 we hypothesized that such studies would be less likely to show reduced mortality risks for low-volume drinkers. Finally, we reran the analyses using occasional drinkers (<1 drink per week) as the reference, for whom physiological health benefits are unlikely. Occasional drinkers are a more appropriate reference group, given evidence demonstrating that lifetime abstainers may be biased toward ill health.10
Discussion
In fully adjusted, prespecified models that accounted for effects of sampling, between-study variation, and potential confounding from former drinker bias and other study-level covariates, our meta-analysis of 107 studies found:
(1) no significant protective associations of occasional or low-volume drinking (moderate drinking) with all-cause mortality; and
(2) an increased risk of all-cause mortality for drinkers who drank 25 g or more and a significantly increased risk when drinking 45 g or more per day.
Several meta-analytic strategies were used to explore the role of abstainer reference group biases caused by drinker misclassification errors and also the potential confounding effects of other study-level quality covariates in studies.2 Drinker misclassification errors were common. Of 107 studies identified, 86 included former drinkers and/or occasional drinkers in the abstainer reference group, and only 21 were free of both these abstainer biases. The importance of controlling for former drinker bias/misclassification is highlighted once more in our results which are consistent with prior studies showing that former drinkers have significantly elevated mortality risks compared with lifetime abstainers.
In addition to presenting our fully adjusted models, a strength of the study was the examination of the differences in relative risks according to unadjusted and partially adjusted models, including the effect of removing individual covariates from the fully adjusted model. We found evidence that abstainer biases and other study characteristics changed the shape of the risk relationship between mortality and rising alcohol consumption, and that most study-level controls increased the observed risks from alcohol, or attenuated protective associations at low levels of consumption such that they were no longer significant. The reduced RR estimates for occasional or moderate drinkers observed without adjustment may be due to the misclassification of former and occasional drinkers into the reference group, a possibility which is more likely to have occurred in studies of older cohorts which use current abstainers as the reference group. This study also demonstrates the degree to which observed associations between consumption and mortality are highly dependent on the modeling strategy used and the degree to which efforts are made to minimize confounding and other threats to validity.
It also examined risk estimates when using occasional drinkers rather than lifetime abstainers as the reference group. The occasional drinker reference group avoids the issue of former drinker misclassification that can affect the abstainer reference group, and may reduce confounding to the extent that occasional drinkers are more like low-volume drinkers than are lifetime abstainers.2,8,132 In the unadjusted and partially adjusted analyses, using occasional drinkers as the reference group resulted in nonsignificant protective associations and lower point estimates for low-volume drinkers compared with significant protective associations and higher point estimates when using lifetime nondrinkers as the reference group. In the fully adjusted models, there were nonsignificant protective associations for low-volume drinkers whether using lifetime abstainers or occasional drinkers as the reference group, though this was only a RR of 0.97 for the latter.
Across all studies, there were few differences in risk for studies when stratified by median age of enrollment above or below age 56 years in the fully adjusted analyses. However, in the subset of studies who enrolled participants aged 50 years or younger who were followed for at least 10 years, occasional drinkers and medium-volume drinkers had significantly increased risk of mortality and substantially higher risk estimates for high- and higher-volume consumption compared with results from all studies. This is consistent with our previous meta-analysis for CHD,9 in which younger cohorts followed up to older age did not show a significantly beneficial association of low-volume consumption, while older cohorts, with more opportunity for lifetime selection bias, showed marked, significant protective associations.
Our study also found sex differences in the risk of all-cause mortality. A larger risk of all-cause mortality for women than men was observed when drinking 25 or more grams per day, including a significant increase in risk for medium-level consumption for women that was not observed for men. However, mortality risk for mean consumption up to 25 g per day were very similar for both sexes.
Footnotes and references can be found at the article’s References.
Drinking a Little Alcohol Won’t Kill You Before Someone Who Never Drank, WSJ
Quantifying Alcohol’s Death Risk; NDAs Hide Docs’ Mistakes; H5N1 Pandemic Prep, MedPage Today
In every animal that’s been tested, the single most reliable intervention to increase longevity is caloric restriction. IOW, if you want to live longer, you need to decrease caloric intake by about 40%. Is that really “living?”
As for alcohol, let’s let Ben Franklin have the last word:
“Behold the rain which descends from heaven upon our vineyards; there it enters the roots of the vines, to be changed into wine; a constant proof that God loves us, and loves to see us happy.”
It’s a poison, we all know it. Like oil, go to great lengths to convince ourselves otherwise
Did any of these studies also control for fructose consumption as a variable? It’s nearly as hepatotoxic as alcohol and in fact, overconsumption leads to your own body turning it into alcohol via the aldehyde pathway. So, any discussion about human biology and alcohol needs to properly account for all the sources of alcohol, not just from a bottle, but also from a plate.
@Pitcher,
Also sucrose consumption, which is a disaccharide of glucose and fructose. HFCS is only somewhat enriched for fructose compared to sucrose.
time for someone to post an anecdote about their grandpa who drank whiskey every night and live to 98
David:
Time for 1 out of 10 million anecdote for sure
Remember the news articles from some years ago about the extraordinarily healthy, long lived Italian country people who had their daily bottle of red wine? A whole generation of drinkers switched to red wine. Ever any follow up to those reports?
jack:
It would be interesting too, for this half-breed Italian.
@Jack,
Here’s an update:
Thanks; looks like there’s hope for red wine drinkers, especially old ones who need whatever pleasures they can get.
@David,
LOL!
But seriously, there *are* genetic variants that affect alcohol metabolism, with attendant effects on alcohol abuse and alcohol-related cancers. Anecdotally, I have a variant at the ADH1B locus that is annotated on ClinVar as protective against addictive alcohol use and aerodigestive tract alcohol-related squamous cell cancer. OTOH, I have blue eyes, and studies have found a statistically significant association between blue eye color and alcohol dependency among Americans of European ancestry.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6139948/
article is , eventually, a good example of why a person should take scientific studies with a grain of salt. sure, science eventually gets there, but there are many pitfalls along the way.
i have seen people poison themselves with alcohol…assuming they were not already on their way to ill health for other reasons. ugly enough to encourage abstinence (which does not make the heart grow fonder). but even the temporary high from very occasional drinking is a manifestation of at least temporary brain damage. my body tells me so.
My father was encouraged by his doctor to have a drink a day for blood thinning – at least that was his claim and I have no reason to doubt it. I don’t think he quite got up to that, but 3 martinis per week might have been his regimen. He passed, but not young and not of heart or vascular disease.
@Eric,
People often confuse physicians with scientists, and assume that their doctor is relying on the latest science.
Shortly after I joined the faculty at my medical school, I found myself in a meeting of the “curriculum management committee” in which some of the faculty mentioned a new trend called “evidence-based medicine.” I asked one of the MDs in attendance (sotto voce): Evidence-based medicine as opposed to what? Fantasy-based medicine? Isn’t all medicine supposed to be evidence-based? He explained: No, the alternative to evidence-based medicine is tradition-based medicine. Most physicians are *not* scientists and don’t keep up with the scientific evidence. They practice according to the traditions they’ve learned.
If you’ve been told something by your doctor, you can’t assume that s/he is relying on current science. Similarly, if someone tells you a story about their medical condition on the internet, you shouldn’t take it at face value. The plural of anecdote isn’t data.
Eric
many years ago I got a lab report that said I had high cholesterol. I did not start a regimen of statins or stop eating eggs. I am fairly sure I have outlived all the doctors who advised me to worry about cholesterol. Were they wrong? I think “the science” has changed since then. But science has it fads as much as any theory of everything that people latch on to.
It turns out that sometimes “anecdotes” are as useful as “data.”
It sounds like the problem in the earlier study was that the non-drinkers group actually contained former drinkers. They weren’t drinking anymore, but they had already suffered negative health effects of alcohol. Never drinkers as opposed to non-drinkers were much healthier, so they provided a new basis for comparison. Roughly, MODERATE > Combined(NEVER, FORMER) but MODERATE < NEVER.
@Kaleberg,
Correct. The problem wasn’t the science, it was taxonomy.
“taxonomy” (the naming of things?)
as in everything, a problem that plagues even the best hopes of science.
unless you define “science” as “that which now appears to work.”
or, as Isaac Asimov once pointed out, “the most thrilling words heard in a laboratory are not ‘Eureka!’, but, That’s odd…’ “
If you set yourself up to be an authority, and “science” to be a god, you are not being “scientific.”