Introduction
Alcohol has been used for thousands of years for various purposes: In ceremony, during celebrations, and as a general social lubricant amongst other uses. We know alcohol is a toxin in nature, and there have been many claims thrown around as far as its health benefits and detriments.
While we’ll touch on the fact that moderate alcohol use is fine in many circumstances, we can’t ignore the fact that alcohol is one of the most used and abused substances in the United States. It is the third leading cause of preventable death here and as far as substances, it is the number one killer next to tobacco, leading even over opiates.
Heavy alcohol drinking increases the risk of cardiovascular and liver disease, metabolic disturbances, nutritional deficiencies, cancers (i.e. mouth, stomach, colon, liver and breast cancer), neurological disorders and fetal abnormalities.
In contrast to heavy alcohol use, light to moderate drinking, especially of alcoholic beverages rich in polyphenols such as red wine, was reported to lower the risk of coronary heart disease, stroke, type 2 diabetes, cognitive decline, and osteoporosis. Heavy alcohol use will obviously hurt body recomposition and fat loss efforts through a variety of different mechanisms, but light to moderate may not be as deleterious as we may think (with some exceptions that we’ll get into).
Definitions
You’ll be reading a lot of references to “moderate alcohol use” or “heavy alcohol use” as we go further. In scientific literature, moderate drinking is defined as 1 drink per night for women and 2 drinks per night for men. Heavy drinking for women is defined as more than 3 drinks in any given sitting or more than 8 drinks per week and for men that goes to more than 4 drinks in any given sitting or more than 15 drinks per week. There is a third level, dubbed “High intensity drinking” in studies, which we won’t mention very much, but this is defined as 8+ drinks in a sitting for women, and 10+ drinks in a sitting for men.
Before we dive into health effects, to fully grasp those effects, its important to understand how alcohol is processed in the body.
The Metabolism of Alcohol in the Body
A fact that a lot of people don’t realize is that alcohol is it’s own macronutrient. I hear a lot of people in the general population saying something like “alcohol all turns to sugar!” or “all alcohol is loaded with sugar!”. The former isnt true and the latter isn’t necessarily true depending on what you’re drinking, but alcohol is it’s own separate macronutrient. We know protein and carbs have around 4 calories per gram, fat has 9 calories, and alcohol has 7 calories per gram.
My Friend and I Are the Exact Same Size, But he/she Can Tolerate More Alcohol!
There are many factors that affect how much alcohol reaches your blood and stays there, but one seeming mystery is how alcohol differentially affects folks with the same exact body size. One reason contributing to this is that the same dose of alcohol per unit of body weight can produce very different blood alcohol concentrations in different individuals because of the large variations in proportions of fat and water in their bodies.
The higher the body fat of an individual, the lower their body water content vs. someone who is the same weight but much lower bodyfat percentage and higher lean mass percentage. Alcohol is not distributed through bodyfat after consumption, and if we have more lean tissue and less bodyfat, there’s simply more tissue that alcohol can be distributed across, resulting in dilution of the alcohol.
Women generally have a smaller volume of tissue distribution for alcohol than men because of their higher percentage of body fat, and again, alcohol cannot diffuse into body fat, but will diffuse into tissues that hold significant water. Women will have higher peak blood alcohol levels than men when given the same dose of alcohol as g per kg body weight but no differences occur when given the same dose per liter of body water.
In other words, if you took two 180lb males with one at 25% bodyfat but the other at 12% bodyfat and gave them the same amount of alcohol, the guy with 25% body fat will probably have higher blood alcohol content due to less water-rich tissues for the alcohol to diffuse to. There are, however, many other factors determining blood alcohol content (BAC).
First Pass at the Stomach
Both enzymes necessary for alcohols complete metabolism are present in the stomach, although this contributes a very small amount to overall alcohol metabolism. Some alcohol is broken in the stomach by alcohol dehydrogenase (ADH), and what’s broken down there goes all the way through to acetate (the end product).
Interestingly, people exhibit many different genetic isoforms of ADH, with some associated with significantly less alcohol toxicity while others more.
Gastric emptying rate affects this portion as well. If you have food in your stomach when you drink, this slows down gastric emptying and gives ADH more time to act on alcohol, which means less alcohol will reach the blood.
This is one reason you require more alcohol to feel a buzz when you’re eating or have just eaten a big meal. If consumed on an empty stomach, almost no metabolism of alcohol occurs in the stomach due to fast gastric emptying.
This is also another reason why women have a lower tolerance than men; they naturally have lower ADH activity in both the stomach and liver than men do.
Liver and Other Tissues
Alcohol can first be metabolized by 3 different pathways. Alcohol can be converted to acetaldehyde (first step) by:
- Alcohol dehydrogenase
- Catalase (This is one of the body’s endogenous antioxidant systems – so if you’re a heavier drinker, this is hurting your antioxidant defenses)
- CYP2E1
The first two can occur in a variety of tissues, while CYP2E1 metabolism occurs only in the liver. The majority of alcohol processing happens in the liver regardless. In conditions of light drinking, ADH and catalase do most of the heavy lifting, but with heavier drinking, CYP2E1 steps it up.
When you get more of a tolerance to alcohol, this is due to highly increased CYP2E1 expression in the liver; the other two pathways aren’t inducible or changeable by alcohol consumption.
The second step is acetaldehyde to acetic acid (vinegar) and acetate by acetaldehyde dehydrogenase (ALDH)
Acetaldehyde is the main component that we should worry about when we consume alcohol. It is 10 to 15 times more toxic than ethanol itself and highly reactive, having the ability to cause free radical generation and damage other tissues.
A high proportion of Asians have an ALDH isoform that significantly reduces it’s activity, which results in the “Asian glow” as its colloquially referred to in society. This manifests as a very flushed red face and upper chest after consuming a decent amount of alcohol.
This is actually significantly more damaging. Individuals that experience this have a much higher risk of certain types of cancer (esophageal being the main one) as well as increased risk of many other diseases with heavy drinking.
From there, acetate gets converted to Acetyl CoA, which is the energy-producing intermediate that glucose, fatty acids, ketones, etc get converted to in the process of creating ATP.
Other Factors Influencing Alcohol Elimination Rate
Race: Higher proportions of African Americans and Native Americans have an ADH isoform that eliminates alcohol at a faster rate, leading to less buildup of blood alcohol content. However, this may also result in faster build-up of acetaldehyde since thats the product of the first step of alcohol metabolism, resulting in more potential damage or worse hangovers even if their BAC doesnt reach high levels.
Age: Fetal alcohol syndrome that occurs when pregnant mothers consume too much alcohol happens because the fetus’ liver is not equipped to process even small amounts of alcohol. Conversely, older individuals may have less of a tolerance due to reduced body water content and/or less liver mass.
Food: Alcohol metabolism is sped up in the fed state in several ways. More alcohol metabolism in the stomach via reduced gastric emptying, higher levels of ADH present in the liver after consumption of food, and increased shuttling of reducing equivalents into mitochondria.
In other words, if your goal is to feel a bit of a buzz on the least calories possible, consume alcohol on an empty stomach or with a small amount of food. However, BE CAREFUL if doing more than 1 or 2 drinks as you can get to dangerous blood levels significantly faster.
Circadian Rhythm: Alcohol elimination is actually the highest or fastest at the end of the biological night, so in the very early hours of the morning, and begins to slow when people normally drink (after 5PM). However the magnitude of change is fairly minimal.
Hormonal and Physiological Effects of Alcohol Consumption
The general theme that we’re going to be seeing here is that alcohol consumption exhibits a U-shaped curve depending on amount ingested. For a lot of these outcomes, specifically more health-related outcomes, moderate amounts of alcohol show no or beneficial effects, whereas heavier drinking always exhibits negative effects.
Sleep
The first thing we’ll talk about is sleep, since we know that poor sleep has a trickle-down effect on hurting the entirety of our physiology and everything we’ll talk about following.
Moderate drinking: Results are mixed. A 2006 study with a smaller sample size (10 people – 5 men and 5 women) looked at raising BAC to 0.03% (1-2 drinks) right before bed as well as to 0.1% (4-6 drinks) and looked at sleep stages with polysomnography. No change in sleep stages were detected in any of the individuals who raised their BAC to 0.03%.
A 2013 review that claims to be the most comprehensive review on alcohol and sleep up to that point quotes: “The effects on rapid eye movement (REM) sleep in the first half of sleep appear to be dose related with low and moderate doses showing no clear trend on REM sleep in the first half of the night…” and when looking at entire-night REM %, they say the majority of studies saw less total REM% in heavy drinking, but no clear trend in moderate drinking. Slow wave sleep was actually increased with moderate doses.
Heavy drinking: The same 2006 study mentioned above saw significant decreases in REM density in the first half of the night and interrupted sleep in the second half of the night when BAC was 0.1% before bed.
The 2013 review mentioned above quotes “… At high doses, total REM % was significantly reduced”. They then go on to state that “the majority of studies, regardless of low, moderate, or heavy drinking, age and gender, confirm an increase in slow wave sleep (SWS) in the first half of the night relative to baseline values without alcohol. The impact of alcohol on (increasing) SWS in the first half of night appears to be more robust than the (reduction) effect on REM sleep and does not appear to be an epiphenomenon of REM sleep reduction.”
Sleep apnea: It’s well known that alcohol has the potential to exacerbate or induce sleep apnea, which increases inflammatory signaling and raises risk of insulin resistance and cardiovascular disease, as well as imparting significant daytime fatigue.Studies on moderate drinking with sleep apnea are mixed. Heavy drinking can severely exacerbate sleep apnea by causing relaxation and easier collapse of the soft palate.
With moderate drinking, one study looked at raising BAC to 0.07% directly before bed in young men with moderate sleep apnea (averaging 7 apnea events per night) and with alcohol administration, this rose to 9 apnea events per night. However, blood oxygenation was not affected and they also did polysomnography and in this study none of the sleep stages were significantly affected compared to their baseline, even with 2 more apnea events.
Translation and takeaway: Heavy drinking obviously wrecks sleep with many night wakeups and significantly reduced REM sleep but with seemingly increased slow-wave sleep. However, light to moderate drinking seems to be very variable and totally individual.
Many studies saw some effect with mild to moderate total REM% reduction, while others saw no effect. Regardless, light to moderate drinking increases slow wave sleep beyond baseline, especially in the first half of the night. So what this tells me is that when it comes to REM reduction and night wakeups with low-moderate drinking, it’s going to come down to the individual.
If we look at the known functions of REM vs. slow wave sleep; REM seems to be more important for keeping the brain sharp and has functions for memory consolidation and learning, and REM deprived individuals experience higher blood pressure as well amongst other deleterious cognitive effects including anxiety.
SWS also has functions in the brain; more glymphatic drainage of the brain happens during SWS, so basically more “clean-up”. SWS is also when 95% of growth hormone is made, and in studies looking at selectively depriving REM vs. SWS, testosterone decreases more in those that are deprived of SWS signifying that SWS has more functions in growth and repair of tissues than REM sleep.
Therefore, moderate drinking, if it reduces REM in that specific individual, may hurt them cognitively over the long run moreso than from a muscle recovery, growth hormone, and testosterone standpoint.
This is going to come down to you, individually, when it comes to moderate consumption. Test yourself with an Oura ring or similar to see if you have more night wake-ups or altered sleep stages when it comes to 1-2 drinks in the evening.
Inflammatory Markers
There’s robust data that has been repeated many times showing that alcohol consumption moderates inflammatory markers in a U shaped fashion, with moderate amounts associated with the lowest hs-CRP and others.
For example, one 2008 study looked at 636 individuals and found that hs-CRP and fibrinogen were the lowest at intakes of 20-70g daily (1 – 4 drinks daily).
Another study looked at around 1400 subjects and assessed hs-CRP, TNF-a, and IL-6. The authors conclude: “Compared to non-drinkers, both men and women who consumed 1-2 drinks/day had significantly lower sTNF-R1 (-9% in men, -6% in women) and sTNF-R2 (-7% in men, -6% in women) levels as well as lower CRP (-10% in men, -32% in women) and IL-6 (-45% in men, -27% in women) levels”. Shorter term RCTs also mimic this effect.
Metabolic Effects and Insulin Resistance
Once again, we have a U-shaped curve in terms of the risk of metabolic syndrome/insulin resistance/type 2 diabetes.
From the authors of a review study: “Low or moderate alcohol consumption shows protective effects against type 2 diabetes in patients through enhanced peripheral insulin sensitivity. A 30% reduced risk of type 2 diabetes was observed in patients with moderate alcohol consumption, whereas no risk reduction was observed in consumers of amounts of alcohol equal to or over 48 g/day (a little over 3 drinks). Whether moderate alcohol consumption affects insulin secretion is still very controversial. Some studies show that moderate alcohol consumption improves insulin action without affecting its secretion, whereas others show a reduced basal insulin secretion rate associated with a lower fasting plasma glucagon concentration. Avogaro et al. have also shown, in the same study, that the enhanced insulin sensitivity observed may be in part due to the inhibitory effect of alcohol on lipolysis. The beneficial metabolic effects of moderate alcohol consumption on insulin sensitivity and glucose tolerance may explain the significant reduction in the development of type 2 diabetes and the risk of cardiovascular disorders reported in several epidemiological studies.”
Heavy alcohol consumption, (>48g/day) on the other hand, is an independent risk factor for the development of Type 2 diabetes mellitus. In addition to its effects on peripheral tissues, such as adipose tissue and liver, where it induces insulin resistance, heavy alcohol consumption was also proposed to negatively impact pancreatic ß-cell function.
HPG Axis and Sex Hormones
Testosterone
With sex hormones, many of the studies we are looking at break things into looking at acute effects, meaning levels of hormones directly after alcohol consumption, and others are looking more at long term effects. I’ll delineate which is which as we go through. Let’s start with moderate drinking.
Moderate drinking:
Acutely after exercise: Rojdmark et al. used a dose of 0.45 g/kg on three separate pulses (this would be 3 drinks every pulse for a 100kg man), 90 minutes apart and noted that there was a trend for testosterone to decrease slightly.
Conversely, a slightly lower intake (0.5 g/kg) has been shown to increase circulating testosterone from 13.6 nmol/L to 16 nmol/L (+17%) 2 hours after ingestion. This increase in testosterone after 0.5 g/kg has also been noted in premenopausal women previously, and suggested to act vicariously through the increased NADH/NAD + ratio in the liver after these doses. I found 3-4 other studies with very similar results.
Longer term: A study in non-resistance trained individuals had men consume 3 beers every night and women consume 2 beers every night for 3 weeks. Plasma testosterone level decreased in men by 6.8% after 3 beers per night for 3 weeks, but no effect was found in women.
Translation and takeaway for moderate drinking: It doesn’t seem that having a few drinks a week, or even one day where you’re drinking a little more than moderately will have any effect on testosterone levels. 3 beers every night saw a small decrease in testosterone in non-resistance trained men, but this is also more than moderate drinking (7 drinks per week more).
Heavy Drinking:
Multiple studies show that chronic heavy alcohol consumption (one study used 1.5g/kg/day for 2 weeks – this would be the equivalent of 10 (!) drinks for a 100kg person) significantly decreased testosterone production with a range of 23-76%.
All the studies that analyzed testosterone using a dose lower than 1.5 g/kg show an increase or no change (except for the single 3 beers a night study that showed the 6.8% reduction) in the circulating levels of the hormone.
Conversely all those using higher dosages (1.5 g/kg ) show a significant decrease. It also seems that the decrease can only be seen in men while an increase is evident in women. The increase in testosterone in women that is seen across the board has to be thought about contextually; for a woman with PCOS this could be very deleterious and may exacerbate their androgenic symptoms.
Gonadotropins, Estradiol, Progesterone
Moderate drinking in women:
Jensen et al., in a study on 430 healthy women aged 20 to 35 years who were trying to conceive for the first time, found that alcohol intake, even as few as five or less drinks per week, was associated with decreased fertility and potential cycle disruptions. In another study, 50% of “social drinkers” (4-6 drinks/week – so low to moderate drinking) saw significantly increased estradiol and prolactin, and some had irregular menstrual cycles (controlled for lifestyle and exclusion criteria was strict enough for them to be healthy otherwise). Progesterone did not seem to be affected in moderate drinking.
In men: In the same study above giving men 3 beers per night for 3 weeks; no change in estradiol levels were detected. Other studies mirror this. In other studies, progesterone also did not change due to moderate drinking.
Heavy drinking:
The typical profile of a chronic heavy drinking male or female is significantly increased FSH, LH, and estrogen levels, whereas progesterone is significantly decreased. In men, prolactin seems to remain unchanged, but hyperprolactinemia is present in heavy drinking women.
HPA Axis and Cortisol
This one’s fairly interesting and a little nuanced.
Moderate drinking: A review that pooled results showing that moderate drinking (reaching BAC levels of 0.04 – 0.06 – basically equivalent to our previous definitions) does not increase CRH, ACTH, or cortisol, and two studies even showed a decrease in cortisol. However, the interesting portion is that this was highly dependent on family history of alcoholism.
If an individual had a family history of alcoholism, they experienced an increase in all of the HPA axis hormones even with moderate drinking, and had significantly more acute-stress related alcohol cravings than those without a family history of alcoholism, so it seems to be genetically or at least epigenetically mediated.
Heavy drinking: Chronic heavy drinking, at first, will highly increase CRH, ACTH, and cortisol. After a significant time period of heavy drinking to the point of alcohol dependence, all of the aforementioned hormones are significantly lowered below baseline when someone isn’t under the influence of alcohol, and come back up to “normal levels” under intoxication, and the very low CRH levels were associated with extreme alcohol cravings. This is indicating a dependence on alcohol for the release of cortisol.
Translation: We all know by now that chronically elevated cortisol has deleterious effects on body transformation and disease risk, but it looks like moderate drinking in those that don’t have a family history of alcoholism won’t really hurt one in this regard. Heavy drinking most certainly will.
HPT Axis and Thyroid
Moderate drinking: Studies were pretty scarce on moderate consumption and thyroid hormone. One study I could find was associational in nature, meaning they monitored groups who then reported their daily alcohol consumption.
Men on average consumed 2 drinks an evening and women consumed 1. The trend was slightly lower free T4 levels with TSH and free T3 unchanged.
Heavy drinking: Significant decreases in circulating TSH, T4, and T3 are consistently observed in chronic heavy drinking.
Translation: Moderate drinking doesn’t appear to affect thyroid hormone levels, but heavy drinking most certainly will.
Gut and Autoimmune Disease
A great review summarized both the effects of low-moderate and heavy doses on multiple gut metrics as well as autoimmune diseases. The summary is that low-moderate doses do not affect gut permeability or gut dysbiosis in normal healthy individuals, or even those with autoimmune disease.
Low-moderate doses may actually have positive effects on gut bacteria (see image and caption below – From Caslin et al 2021 “Alcohol as friend or foe in autoimmune diseases: a role for gut microbiome?”). Recent evidence actually points toward alcohol’s protective effects in several autoimmune diseases, including autoimmune thyroid disease, autoimmune diabetes, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and multiple sclerosis (MS) in both human and animal studies.
Chronic, heavier doses, however, cause significant increases in gut permeability, gut-associated inflammation, deleterious dysbiosis, etc, also exacerbating autoimmune conditions.
It’s important to know that even small-moderate doses of alcohol may exacerbate or effect individuals with pre-existing IBS; so it’s still one of the first things to eliminate it when doing an elimination diet.
Acute Effects on Appetite-Related Hormone Leptin
We’ve all heard about and probably have experienced “drunk munchies”, but are there hormonal fluctuations during drinking to back that statement? Let’s look at the data.
Leptin is our primary satiety hormone, but it also has a role in controlling daily energy expenditure as well as our sex and thyroid hormones. With leptin, when we’re looking at moderate amounts of alcohol (15-30g/day – equivalent to 1-2 drinks), we can look at a study done on postmenopausal women. The women were divided into 0 alcohol, 15g/day, and 30g/day. Younger women (49-54) experienced a 24% increase in leptin levels and older women (55-79) experienced a 12% increase in leptin when consuming 30g/day. This may be good or bad depending on the context; for someone with very low leptin levels, this may be beneficial, but if someone has high levels of leptin and leptin resistance, this is going to add to the problem.
Conversely, a study done on 14 young, healthy subjects (7 male, 7 female) gave them 3 drinks with 0.45g of alcohol per kg in each drink over 6 hours (this would be equivalent to roughly 8 drinks over 6 hours for a 180lb man). In this case of heavier drinking, we saw leptin decrease significantly: the leptin area under the curve was 53 +/- 18 after alcohol and 113 +/- 15 after water (control). As serum alcohol levels began to fall, leptin concentrations began to rise again, so the effect was acute.
Translation: Yes, the acute and rather severe decrease in leptin with heavier drinking may be contributing to your drunk munchies!
TDEE Note: This acute decrease in leptin doesn’t acutely affect energy expenditure as alcohol itself is thermogenic and raises resting energy expenditure because of how hard the body has to work to process it. One study gave individuals 2 alcoholic drinks at every meal, and their energy expenditure was 5.5% greater over a 24h period vs. a control day (many other variables were controlled for).
No – This doesn’t mean that alcohol is going to help you lose fat, it just shows that the TEF of alcohol is roughly the same as protein (calculated in the same study as 23-28%), but not near as satiating and mostly nutritionally devoid otherwise. However, used in moderation and intelligently, it probably wouldn’t hurt fat loss efforts.
Muscle Protein Synthesis and Exercise Recovery
A great review looked at various measures of recovery, from hormones to actual force production, reps completed, RPE, etc. It included 10 studies. Most of the studies used doses of alcohol that would be considered heavier (average around 1g/kg (6.5 drinks for a 180lb man), and 3 studies tested 0.45-0.6g/kg which is more along the lines of moderate drinking) after either resistance exercise or a sports event/game of some sort.
Recovery markers like creatine kinase, heart rate, lactate, blood glucose, estradiol, sex hormone binding globulin, leukocytes and cytokines, C-reactive protein and calcium do not seem to be modified following moderate alcohol consumption in the recovery phase of exercise.
Only in the studies using >1g/kg (heavy drinking) was cortisol increased; conversely, testosterone, plasma amino acids, and rates of muscle protein synthesis decreased at this level. No effects on the latter were found with moderate doses, except for small increases in testosterone.
In terms of performance; usually performance is measured by measures of force production compared to a completely recovered baseline. In that vein, only one study showed that following alcohol consumption, the levels of isometric, concentric and eccentric torque decreased, while other studies in this review that measured force production showed no differences between the alcohol and no-alcohol groups during recovery following resistance training, and that was even with doses bordering on heavy drinking.
The huge caveat here is that I couldn’t find a single study that was more long term in nature, such as looking at the effects of moderate consumption on hypertrophy/strength gains over say, 8 weeks or 12 weeks. All of the above were very short term in nature, looking at recovery from one acute bout of resistance training. It’s very possible and even likely that if carried out over a longer period of time, recovery would be hurt.
Longer Term Health Outcomes
The Brain and CNS
There’s some evidence that low-moderate consumption can increased glymphatic system drainage or “brain cleaning”. The glymphatic system is basically our internal system that deals with junk removal in our central nervous system (CNS), and is critical in both the prevention and development of various neurological and CNS disease.
Recent studies (in mice) showed that daily low-dose alcohol exposure (equivalent to the “moderate” drinking doses in humans) significantly increased glymphatic activity. However, at higher doses (equivalent to the “heavy” drinking doses), glymphatic activity was significantly reduced below baseline.
Epidemiological and observational studies show that moderate consumers have lower risk of Alzheimer’s or Parkinson’s disease and this could be one potential mechanism.
The Rancho Bernardo study sought to look at cognitively healthy longevity and alcohol use. The study looked at 1344 older, community dwelling adults and assessed alcohol habits over several years. They defined cognitively healthy longevity as reaching 85 years of age without any cognitive impairment. The authors adjusted for all lifestyle and health factors they could to isolate alcohol’s effects.
Surprisingly, near-daily moderate drinkers had 2–3 fold higher adjusted odds of cognitively healthy longevity (reaching 85 with no cognitive impairment) versus abstainers.
Cardiovascular and Lipids
Most studies that look at cardiovascular outcomes show better outcomes with moderate intakes vs. not; generally a 20-25% lowered risk of any CVD outcome. We have the decreased inflammatory markers talked about earlier that may be contributing. Moderate alcohol intake also increases HDL; the figure across many studies ranges from 11% – 18%. Studies estimate that a higher HDL concentration could explain ∼50% of the coronary heart disease preventive effect of alcohol consumption.
Bringing it All Together: Integration and Summary
Now that we’ve gone over the data, let’s summarize and integrate what we’ve laid out so far. We’ll also talk about alcohol-related damage control strategies when it comes to wanting to drink MORE THAN MODERATELY (not recommended/advocating, but most people do this every now and then) but not wanting to hurt your body recomposition efforts.
At the moderate drinking level (again 1 drink/night for women, 2 for men), most things do not seem to be affected, but this should be thought about contextually. Starting with sleep since this is close to the top of the hierarchy: you have to test this individually for yourself when it comes to moderate drinking. Studies show a very individualized response, with many subjects showing no change in sleep architecture at low-moderate doses, while others showed reduction in total REM% as well as more night wakeups even with low-moderate doses. If you’re one of the individuals where sleep is hurt, this could potentially be a detractor from all of the other metrics.
After all, I did not see any study that showed measures of hypertrophy/strength gains with alcohol consumption over the longer term, there were only acute studies of ingestion of alcohol post resistance training and measuring subsequent recovery. If we go by the acute studies, then moderate drinking after exercise may not affect recovery, but heavy drinking absolutely does. However, that may change with moderate consumption over the longer term, say, if sleep is affected. We don’t have that data, but common sense and putting together 2 + 2 says it most likely would.
Another thing to remember is the HPA axis effects in those with a family history of alcoholism; even small and moderate doses increased all HPA axis hormones in these folks. However, if you have a family history and you know you’re more predisposed to alcoholism, you’re probably not drinking very much anyway (hopefully).
HPG hormones in men with moderate levels didn’t seem to be affected, except in the one 3 drink/night study which saw slightly lower testosterone. However, it is concerning that some studies saw deleterious effects in women’s HPG axis with even small-moderate amounts of alcohol; including the increased estradiol, prolactin, and higher rates of anovulatory and irregular menstrual cycles. As a reminder that was even with 4-6 drinks per week. Again, this is going to come down to you and your individuality. Be honest with yourself about your menstrual status and alcohol intake, and if you think there’s an issue there, abstain for 1-2 months to see if this makes a difference in how you feel, PMS symptoms, and other aspects of cycle health.
Getting Ready for a Big Night Out
As far as moderate drinking goes, if you’re just fitting 1-2 drinks into your daily macros every now and then, it would be safe to subtract those from either carbs or fat; doesn’t make too much of a difference here. If you’re an athlete, serious bodybuilder or strength sport athlete, you’re probably not doing this on a daily basis anyway, but if you have a lifestyle client that’s just looking to lose fat and wants to have 1 drink per night or every other night, you can advise them to subtract from either fat or carbs when fitting these in. Keep in mind this is for a generally healthy individual, those with IBS may not do well with this level of moderate intake.
Pure spirits are going to be the lowest calorie count, coming in at 98 – 110 calories per drink (1.5 oz), dry red and white wines are going to be next at 120 – 135 calories per drink (about the same with some light beers although with significantly less alcohol content), and beers come last with 150-180 per average beer, going all the way up to 350 calories per beer for craft beers that are a little higher gravity.
If you’re going for the least amount of calories, think gin/vodka/whiskey and soda water with lime or just neat, or go with a dry red or white wine. You can actually make some pretty tasty/low calorie vodka and gin drinks with all the flavored soda waters that are out there these days.
Now, if you KNOW you’re going to be going to an event or have some other circumstance where you’re going to be consuming a heavier amount of alcohol, here’s a little guide:
If you don’t want to accelerate or induce de novo lipogenesis (the creation of fat from carbs), and, at the same time, get more bang for your calorie buck (aka drink less for more of a buzz), I would go in with at least slightly depleted liver glycogen levels as well as on an empty stomach. This would mean eating light during the day; mostly protein and veggies and some fats.
Heavier alcohol consumption induces oxidative stress, and nicotinic acid (niacin or nicotinamide riboside) and zinc play large roles in alcohol’s metabolism. Therefore, a decent little cocktail prior to a heavy night of drinking would be vitamin C, NAC or glutathione, zinc, and nicotinamide riboside or niacin; NR would be better than niacin. Indeed, studies show that people who had higher dietary nicotinic acid and zinc content had less hangover severity.
There is also a newer product on the market, called Z-Biotics, that is a probiotic drink that specifically metabolizes excess acetaldehyde, preventing it from reaching the bloodstream and causing a worse hangover. Anecdotally, many people swear by this product to lessen or eliminate hangovers if taken prior to a night of drinking.
After the first drink or two, you probably want to consume a little food to hedge against getting too drunk too fast (or you can just stop drinking when you feel it). Ideally, you don’t want to eat a huge meal; the old adage of “eating to absorb the alcohol” is not true.
The liver has to process the alcohol as well as whatever you eat, so if you over-indulge on the food side, depending on what you’re consuming, you could be stressing your liver out even more. This is especially true if you eat a lot of fructose and unsaturated fatty acids along with alcohol; fructose has to be directly metabolized by the liver, and the increased oxidative stress during periods of heavier drinking increases lipid peroxidation of unsaturated fatty acids.
Indeed, studies in alcoholics actually show reversal of their fatty liver if they completely cut unsaturated fatty acids out while drinking and only drink with saturated fats. If you don’t want to remain on an empty stomach, which I wouldn’t advise, just dont overdo the food, and get some protein and polyphenols (to help with oxidative stress) in, but watch the fructose and unsaturated fatty acids. The dose of fructose gotten from a piece of fruit or two wouldnt pose an issue, but drinking excess fruit juices/sodas/eating desserts would. Obviously, we want to stay hydrated and make sure we’re consuming enough water alongside as well.
Be careful! After a few drinks and a buzz, you can easily stop paying as much attention to how much alcohol you’re consuming, and since your body is low on food, you can go from buzzed to drunk quite fast without realizing it.
“Hair of the Dog”
A common “hangover cure” is drinking a small amount of alcoholic beverage the morning of a hangover. This actually works, although I’m not condoning drinking a half glass of wine with breakfast, I just think its an interesting piece of information.
A hangover arises, in part, through deficiency in oxidizable substrates for energy metabolism in the brain (resulting in the headaches and foggyness). When the levels of alcohol and acetate fall too quickly for regulation to fully compensate by switching back to the usual energy sources such as carbohydrate and/or fatty acids, the deficiency can be overcome by providing some alcohol. This temporarily relieves the deficiency in energy metabolism, and thereby the hangover, as well as providing additional time for metabolic regulation to compensate for lack of ethanol/acetate. Again, I’m not condoning this, just thought it was an interesting piece of information. Alternatively, replenishing electrolytes and eating a solid meal will help more than staying fasted in the morning.
Conclusion
The TL;DR of this whole thing is that basically, moderate drinking (2 drinks a night for men, 1 for women) doesn’t seem to hurt much of physiology. The exceptions are potential sex hormone and cycle dysregulation for females, cortisol in those with a family history of alcoholism, and potential sleep architecture disruption depending on the individual. There may be potential benefits with it for cardiovascular outcomes, insulin resistance, and autoimmune disease.
Since studies report averages, however, and people are individuals, I’d highly recommend assessing these things for you. These also doesn’t speak much to how these people feel on a daily basis or quality of life; it could be that moderate drinking may cause a bit of fatigue if sleep is impaired. So the main take home is assess how YOU personally feel and how it personally affects your labwork, but if you fall into the “average”, moderate drinking is probably okay.
References
Cederbaum AI. Alcohol metabolism. Clin Liver Dis. 2012 Nov;16(4):667-85. doi: 10.1016/j.cld.2012.08.002. PMID: 23101976; PMCID: PMC3484320.
David F. Wilson, Franz M. Matschinsky. Ethanol metabolism: The good, the bad, and the ugly. Medical Hypotheses, Volume 140, 2020, 109638, ISSN 0306-9877, https://doi.org/10.1016/j.mehy.2020.109638.
Röjdmark S, Calissendorff J, Brismar K. Alcohol ingestion decreases both diurnal and nocturnal secretion of leptin in healthy individuals. Clin Endocrinol (Oxf). 2001 Nov;55(5):639-47. doi: 10.1046/j.1365-2265.2001.01401.x. PMID: 11894976.
Calissendorff, J., Danielsson, O., Brismar, K., & Röjdmark, S. (2005). Inhibitory effect of alcohol on ghrelin secretion in normal man, European Journal of Endocrinology eur j endocrinol, 152(5), 743-747. Retrieved Nov 21, 2021
Rachdaoui N, Sarkar DK. Effects of alcohol on the endocrine system. Endocrinol Metab Clin North Am. 2013 Sep;42(3):593-615. doi: 10.1016/j.ecl.2013.05.008. PMID: 24011889; PMCID: PMC3767933.
Health risks and benefits of alcohol consumption. Alcohol Res Health. 2000;24(1):5-11. PMID: 11199274; PMCID: PMC6713002.
Levitt DE, Idemudia NO, Cregar CM, Duplanty AA, Hill DW, Vingren JL. Alcohol After Resistance Exercise Does Not Affect Muscle Power Recovery. J Strength Cond Res. 2020 Jul;34(7):1938-1944. doi: 10.1519/JSC.0000000000002455. PMID: 29385007.
Lakićević N. The Effects of Alcohol Consumption on Recovery Following Resistance Exercise: A Systematic Review. J Funct Morphol Kinesiol. 2019 Jun 26;4(3):41. doi: 10.3390/jfmk4030041. PMID: 33467356; PMCID: PMC7739274.
El-Sayed MS, Ali N, El-Sayed Ali Z. Interaction between alcohol and exercise: physiological and haematological implications. Sports Med. 2005;35(3):257-69. doi: 10.2165/00007256-200535030-00005. PMID: 15730339.
Duplanty, Anthony A.1,2,3; Budnar, Ronald G.1; Luk, Hui Y.1,2; Levitt, Danielle E.1,2; Hill, David W.1; McFarlin, Brian K.1,2; Huggett, Duane B.2; Vingren, Jakob L.1,2 Effect of Acute Alcohol Ingestion on Resistance Exercise–Induced mTORC1 Signaling in Human Muscle, Journal of Strength and Conditioning Research: January 2017 – Volume 31 – Issue 1 – p 54-61
doi: 10.1519/JSC.0000000000001468
Bianco, A., Thomas, E., Pomara, F. et al. Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review. Nutr Metab (Lond) 11, 26 (2014). https://doi.org/10.1186/1743-7075-11-26’
Sarkola T, Eriksson CJ. Testosterone increases in men after a low dose of alcohol. Alcohol Clin Exp Res. 2003 Apr;27(4):682-5. doi: 10.1097/01.ALC.0000060526.43976.68. PMID: 12711931.
Engen PA, Green SJ, Voigt RM, Forsyth CB, Keshavarzian A. The Gastrointestinal Microbiome: Alcohol Effects on the Composition of Intestinal Microbiota. Alcohol Res. 2015;37(2):223-36. PMID: 26695747; PMCID: PMC4590619.
Blaine Caslin, Kailey Mohler, Shreya Thiagarajan & Esther Melamed (2021)
Alcohol as friend or foe in autoimmune diseases: a role for gut microbiome?, Gut Microbes, 13:1, 1916278, DOI: 10.1080/19490976.2021.1916278
Caruana M, Cauchi R, Vassallo N. Putative Role of Red Wine Polyphenols against Brain Pathology in Alzheimer’s and Parkinson’s Disease. Front Nutr. 2016 Aug 12;3:31. doi: 10.3389/fnut.2016.00031. PMID: 27570766; PMCID: PMC4981604.
Richard EL, Kritz-Silverstein D, Laughlin GA, Fung TT, Barrett-Connor E, McEvoy LK. Alcohol Intake and Cognitively Healthy Longevity in Community-Dwelling Adults: The Rancho Bernardo Study. J Alzheimers Dis. 2017;59(3):803-814. doi: 10.3233/JAD-161153. PMID: 28671111; PMCID: PMC5939941.
Brust JC. Ethanol and cognition: indirect effects, neurotoxicity and neuroprotection: a review. Int J Environ Res Public Health. 2010 Apr;7(4):1540-57. doi: 10.3390/ijerph7041540. Epub 2010 Apr 4. PMID: 20617045; PMCID: PMC2872345.
Lundgaard, I., Wang, W., Eberhardt, A. et al. Beneficial effects of low alcohol exposure, but adverse effects of high alcohol intake on glymphatic function. Sci Rep 8, 2246 (2018). https://doi.org/10.1038/s41598-018-20424-y
Wang JJ, Tung TH, Yin WH, Huang CM, Jen HL, Wei J, Young MS. Effects of moderate alcohol consumption on inflammatory biomarkers. Acta Cardiol. 2008 Feb;63(1):65-72. doi: 10.2143/AC.63.1.2025334. PMID: 18372583.
Stote KS, Tracy RP, Taylor PR, Baer DJ. The effect of moderate alcohol consumption on biomarkers of inflammation and hemostatic factors in postmenopausal women. Eur J Clin Nutr. 2016 Apr;70(4):470-4. doi: 10.1038/ejcn.2015.182. Epub 2015 Nov 11. PMID: 26554758.
Pai JK, Hankinson SE, Thadhani R, Rifai N, Pischon T, Rimm EB. Moderate alcohol consumption and lower levels of inflammatory markers in US men and women. Atherosclerosis. 2006 May;186(1):113-20. doi: 10.1016/j.atherosclerosis.2005.06.037. Epub 2005 Aug 1. PMID: 16055129.
Steiner JL, Crowell KT, Lang CH. Impact of Alcohol on Glycemic Control and Insulin Action. Biomolecules. 2015 Sep 29;5(4):2223-46. doi: 10.3390/biom5042223. PMID: 26426068; PMCID: PMC4693236.
Barve S, Chen SY, Kirpich I, Watson WH, Mcclain C. Development, Prevention, and Treatment of Alcohol-Induced Organ Injury: The Role of Nutrition. Alcohol Res. 2017;38(2):289-302. PMID: 28988580; PMCID: PMC5513692.
Scott DM, Taylor RE. Health-related effects of genetic variations of alcohol-metabolizing enzymes in African Americans. Alcohol Res Health. 2007;30(1):18-21. PMID: 17718396; PMCID: PMC3860436.
Forsyth CB, Voigt RM, Burgess HJ, Swanson GR, Keshavarzian A. Circadian rhythms, alcohol and gut interactions. Alcohol. 2015 Jun;49(4):389-98. doi: 10.1016/j.alcohol.2014.07.021. Epub 2014 Nov 14. PMID: 25499101; PMCID: PMC4431951.
Kang, H., Park, YK. & Lee, JY. Nicotinamide riboside, an NAD+ precursor, attenuates inflammation and oxidative stress by activating sirtuin 1 in alcohol-stimulated macrophages. Lab Invest 101, 1225–1237 (2021). https://doi.org/10.1038/s41374-021-00599-1
Roth MJ, Baer DJ, Albert PS, Castonguay TW, Dorgan JF, Dawsey SM, Brown ED, Hartman TJ, Campbell WS, Giffen CA, Judd JT, Taylor PR. Relationship between serum leptin levels and alcohol consumption in a controlled feeding and alcohol ingestion study. J Natl Cancer Inst. 2003 Nov 19;95(22):1722-5. doi: 10.1093/jnci/djg090. PMID: 14625264.
Suter PM, Jéquier E, Schutz Y. Effect of ethanol on energy expenditure. Am J Physiol. 1994 Apr;266(4 Pt 2):R1204-12. doi: 10.1152/ajpregu.1994.266.4.R1204. PMID: 8184963.
Blaine SK, Milivojevic V, Fox H, Sinha R. Alcohol Effects on Stress Pathways: Impact on Craving and Relapse Risk. Can J Psychiatry. 2016 Mar;61(3):145-53. doi: 10.1177/0706743716632512. Epub 2016 Feb 9. PMID: 27254089; PMCID: PMC4813419.
Feige, B., Gann, H., Brueck, R., Hornyak, M., Litsch, S., Hohagen, F. and Riemann, D. (2006), Effects of Alcohol on Polysomnographically Recorded Sleep in Healthy Subjects. Alcoholism: Clinical and Experimental Research, 30: 1527-1537. https://doi.org/10.1111/j.1530-0277.2006.00184.x
Ebrahim, I.O., Shapiro, C.M., Williams, A.J. and Fenwick, P.B. (2013), Alcohol and Sleep I: Effects on Normal Sleep. Alcohol Clin Exp Res, 37: 539`-549. https://doi.org/10.1111/acer.12006
Park SY, Oh MK, Lee BS, Kim HG, Lee WJ, Lee JH, Lim JT, Kim JY. The Effects of Alcohol on Quality of Sleep. Korean J Fam Med. 2015 Nov;36(6):294-9. doi: 10.4082/kjfm.2015.36.6.294. Epub 2015 Nov 20. PMID: 26634095; PMCID: PMC4666864.
Scanlan MF, Roebuck T, Little PJ, Redman JR, Naughton MT. Effect of moderate alcohol upon obstructive sleep apnoea. Eur Respir J. 2000 Nov;16(5):909-13. doi: 10.1183/09031936.00.16590900. PMID: 11153591.
Sierksma A, Sarkola T, Eriksson CJ, van der Gaag MS, Grobbee DE, Hendriks HF. Effect of moderate alcohol consumption on plasma dehydroepiandrosterone sulfate, testosterone, and estradiol levels in middle-aged men and postmenopausal women: a diet-controlled intervention study. Alcohol Clin Exp Res. 2004 May;28(5):780-5. doi: 10.1097/01.alc.0000125356.70824.81. PMID: 15166654.
Parr EB, Camera DM, Areta JL, Burke LM, Phillips SM, Hawley JA, Coffey VG. Alcohol ingestion impairs maximal post-exercise rates of myofibrillar protein synthesis following a single bout of concurrent training. PLoS One. 2014 Feb 12;9(2):e88384. doi: 10.1371/journal.pone.0088384. PMID: 24533082; PMCID: PMC3922864.
Verster JC, Vermeulen SA, Loo AJAEV, Balikji S, Kraneveld AD, Garssen J, Scholey A. Dietary Nutrient Intake, Alcohol Metabolism, and Hangover Severity. J Clin Med. 2019 Aug 27;8(9):1316. doi: 10.3390/jcm8091316. PMID: 31461972; PMCID: PMC6780234.
Elizabeth R. De Oliveira e Silva , MD , David Foster , PhD , Monnie McGee Harper , PhD , Cynthia E. Seidman , MS, RD , Jonathan D. Smith , PhD , Jan L. Breslow , MD , and Eliot A. Brinton , MD. Alcohol Consumption Raises HDL Cholesterol Levels by Increasing the Transport Rate of Apolipoproteins A-I and A-II. 7 Nov 2000. https://doi.org/10.1161/01.CIR.102.19.2347Circulation. 2000;102:2347–2352
Huang S, Li J, Shearer GC, Lichtenstein AH, Zheng X, Wu Y, Jin C, Wu S, Gao X. Longitudinal study of alcohol consumption and HDL concentrations: a community-based study. Am J Clin Nutr. 2017 Apr;105(4):905-912. doi: 10.3945/ajcn.116.144832. Epub 2017 Mar 1. PMID: 28251934; PMCID: PMC5366050.
