ArchiveSee matrix →ES
Food

Alcohol

There is no level of alcohol that improves health; the supposed benefit of red wine has been debunked. The less, the better.
Category
Scientific evidence
Very high
Number of findings
1
Sources
Our own summaries · Cited studies
Recommended dose and how to use
The healthiest approach is to not drink or to drink very little; no amount is 'good for the heart'.

In practice

The healthiest approach is to not drink or to drink very little; no amount is 'good for the heart'.

Precautions

Increases the risk of several cancers, damages the liver and brain, and worsens sleep. Zero alcohol in pregnancy.

Effect by goal · level of evidence

Risk of several cancers

harms Very high meta-analysis (AAA)

Huge meta-analysis (572 studies, 486,538 cases): high alcohol consumption multiplies the risk of cancer of the mouth and pharynx (×5.1), esophagus (×5.0), larynx (×2.7), colorectum (×1.4) and breast (×1.6), among others. Clear dose-response relationship: the more alcohol, the more risk.

View the study (meta-analysis) →

In depth

⏱ 7 min read

Alcohol is one of the most widely consumed and, at the same time, most abused drugs on the planet, and its relationship with human health is far more complex and nuanced than popular culture usually acknowledges: there is both genuine confusion and unresolved scientific debate, and understanding the difference between what we know with certainty and what remains a matter of controversy is fundamental to making informed decisions about something so omnipresent in modern social life.

A standard drink in the United States equals 14 grams of ethanol: a 350 ml beer, 150 ml of wine, or 45 ml of 40 percent distilled spirits; these equivalences matter because most people systematically underestimate how much alcohol they consume when they lack these reference numbers, and that underestimation has direct consequences for the risks they take on without knowing it.

How your body metabolizes alcohol

Alcohol metabolism occurs in three steps: first, the enzyme alcohol dehydrogenase converts ethanol into acetaldehyde; second, the enzyme aldehyde dehydrogenase converts acetaldehyde into acetate; third, that acetate enters the circulation and is converted into acetyl coenzyme A to generate energy in the citric acid cycle; both ethanol and acetaldehyde are responsible for the neurotoxic and behavioral effects of alcohol.

Not everyone metabolizes alcohol at the same rate, and the reasons are largely genetic: variants in the ALDH2 and ADH1B genes can cause acetaldehyde to accumulate after drinking, raising oxidative stress and producing the intolerance symptoms known as flushing syndrome, which include facial redness, nausea, and tachycardia; these variants are common in people of East Asian ancestry, with a prevalence of between 21 and 69 percent.

Alcohol and gut health

Just 20 grams of alcohol, equivalent to a glass and a half of beer, is enough to disrupt two critical tight-junction proteins in the intestine: zonulin-1 and occludin; when these proteins are affected, the intestinal barrier loses integrity and allows bacterial toxins, in particular lipopolysaccharide or LPS, to migrate from the gut into the bloodstream, where they trigger a systemic inflammatory response linked to type 2 diabetes, cardiovascular disease, and liver damage.

A single episode of heavy drinking raises blood LPS levels for up to three hours; chronic heavy drinking is associated with higher circulating levels of that endotoxin compared with people who drink less; and, in the other direction, just 19 days of abstinence reduce intestinal permeability in adults with alcohol dependence to levels comparable to those of someone who has a single drink a day, which speaks to the gut's capacity for recovery when given the chance.

Alcohol and the brain

Alcohol crosses the blood-brain barrier because it is soluble in both water and fat, and once in the brain it acts on multiple neurotransmitter systems: it activates GABA receptors, the brain's main inhibitory system, and reduces levels of the excitatory glutamate, which explains both alcohol's initial anxiolytic effect and the phenomenon of "hangxiety," the anxiety that appears when those receptors are upregulated during metabolism and the brain swings in the opposite direction.

Drinking one or two drinks a day has been associated in some studies with a lower risk of cognitive decline and dementia, with reductions of up to 26 or 28 percent for Alzheimer's; however, much of that evidence is confounded by the "sick quitter" effect, that is, by the fact that many nondrinkers are former drinkers who gave up alcohol precisely because of health problems, which artificially inflates the risk of the reference group and makes moderate drinkers look healthier than their consumption justifies.

For carriers of the APOE e4 allele, the best-known genetic risk factor for Alzheimer's, the relationship with alcohol is especially worrying: even drinking less than once a month raises dementia risk 2.3-fold compared with people who never drink; two or more drinks a day raise that risk 3.6-fold, and five or more drinks a day boost it by as much as 730 percent, according to some studies, which makes alcohol an especially relevant risk factor for those who know their genetic profile.

Alcohol and sleep

Alcohol shortens the time it takes you to fall asleep, an effect many people mistake for a sleep aid, but at the same time it suppresses REM sleep during the first half of the night, increases nighttime awakenings, and delays the onset of the first REM period; the net result is biologically less restorative sleep, even though it may subjectively feel deep, especially in the first few hours.

The effects on REM sleep are minimized when alcohol is consumed four or more hours before bedtime compared with drinking it 90 minutes or less before sleep, although even with that time gap residual effects persist, such as lower sleep efficiency, more total time awake, and less REM in the second half of the night; for people with sleep apnea, the risk is 25 percent higher if they drink alcohol, since it relaxes the muscles that keep the airway open.

Alcohol and cancer

Alcohol is recognized as a Group 1 carcinogen by the International Agency for Research on Cancer, the same group that includes asbestos, ionizing radiation, and tobacco; it is associated with a higher risk of oropharyngeal, laryngeal, esophageal, liver, colorectal, and breast cancer, and this risk rises proportionally with dose, with no threshold identified below which it disappears completely.

Light drinking of approximately seven drinks per week is associated with a 4 to 9 percent increase in the risk of breast and colorectal cancer, a 13 to 17 percent increase in oral and pharyngeal cancer, and a 26 to 44 percent increase in esophageal cancer; drinking three or more drinks a day raises the risk of esophageal, pharyngeal, and oral cancers by 300 to 400 percent; these figures put the idea that "a glass of wine a day is good for your health" in a very different perspective.

One study estimated that consuming five standard drinks per week, roughly the equivalent of a bottle of wine, carries a cancer risk comparable to smoking four to five cigarettes per week in men and ten cigarettes per week in women; what most people call "moderate drinking" has an impact on cancer risk that the alcohol industry has systematically worked to minimize in public communication.

Alcohol and cardiovascular health

The popular narrative about red wine and heart health rests on evidence that is mostly confounded by the sick-quitter effect and by healthy-user bias: when these factors are properly controlled for, the cardiovascular protection attributed to moderate drinking shrinks or disappears, and what remains is a far more nuanced relationship in which the type of cardiovascular disease matters as much as the amount of alcohol consumed.

The most robust analyses suggest that the lowest risk of ischemic heart disease occurs at less than one standard drink per week, with increases of 6 to 24 percent in the risk of stroke, heart failure, hypertension, and aortic aneurysm for every additional 100 grams of weekly alcohol; myocardial infarction is the only exception where a modest risk reduction is observed with moderate drinking, although that reduction does not offset the increases in other types of cardiovascular disease.

Alcohol and fertility

Alcohol affects the hypothalamic-pituitary-gonadal axis, which regulates hormone production and fertility: light drinking may raise testosterone levels while heavy drinking lowers them in men; in women, drinking even one drink a day increases the risk of premenstrual syndrome by 79 percent, and light drinking is associated with an 11 percent lower chance of achieving pregnancy, while moderate drinking reduces that chance by 23 percent.

Paternal alcohol consumption also has epigenetic consequences for offspring: in animal studies, binge-equivalent levels of drinking before conception produce offspring with lower birth weight, compromised brain development, and cognitive and motor alterations reminiscent of the symptoms of fetal alcohol syndrome, a finding that underscores that the responsibility for protecting the future baby does not fall on the mother alone.

Harm-reduction strategies

If you are going to drink alcohol, the evidence suggests that one or two drinks per week represents the lowest-risk level for most types of cancer, whereas one or two drinks a day offers the lowest-risk profile for cardiovascular disease and diabetes; those two ranges are not compatible with each other, which means that the cardioprotective effect of moderate daily drinking does not offset the increase in cancer risk associated with that same level of intake.

Regular physical exercise is the most powerful intervention available to someone who drinks occasionally: it reduces all-cause mortality associated with alcohol consumption and almost completely cancels out the association between alcohol consumption and cancer mortality, which speaks eloquently of the power of movement as medicine and as a biological counterweight to the adverse effects of this substance.

References

  1. Scott, D.M.; Taylor, R.E. (2007). Health-related effects of genetic variations of alcohol-metabolizing enzymes in African Americans. Alcohol Res Health 30, 1.
  2. Ramchandani, V.A. et al. (2010). A Genetic Determinant Of The Striatal Dopamine Response To Alcohol In Men. Molecular Psychiatry 16, 8.
  3. Kegeles, L.S. et al. (2018). Enhanced Striatal Dopamine Release To Expectation Of Alcohol: A Potential Risk Factor For Alcohol Use Disorder. Biol Psychiatry Cogn Neurosci Neuroimaging 3, 7.
  4. Cederbaum, A.I. (2012). Alcohol Metabolism. Clinics In Liver Disease 16, 4.
  5. Uzuegbu, U.E.; Onyesom, I. (2009). Fructose-induced Increase In Ethanol Metabolism And The Risk Of Syndrome X In Man. C R Biol 332, 6.
  6. Bagnardi, V. et al. (2015). Alcohol consumption and site-specific cancer risk: A comprehensive dose-response meta-analysis. Br J Cancer 112, 3.
  7. Rehm, J. et al. (2010). The relation between different dimensions of alcohol consumption and burden of disease. Addiction 105, 5.
  8. Ronksley, P.E. et al. (2011). Association of alcohol consumption with selected cardiovascular disease outcomes. BMJ 342.
  9. Anstey, K.J. et al. (2009). Alcohol consumption as a risk factor for dementia and cognitive decline. Am J Geriatr Psychiatry 17, 7.
  10. Roerecke, M.; Rehm, J. (2014). Alcohol consumption, drinking patterns, and ischemic heart disease. Eur Heart J 35, 7.
  11. Lim, S.S. et al. (2012). A comparative risk assessment of burden of disease and injury attributable to 67 risk factors. Lancet 380, 9859.
  12. Fillmore, K.M. et al. (2006). Moderate alcohol use and reduced mortality risk: Systematic error in prospective studies. Addict Res Theory 14, 2.
  13. Room, R. et al. (2005). Alcohol and public health. Lancet 365, 9458.
  14. Sacks, J.J. et al. (2015). 2010 National and State Costs of Excessive Alcohol Consumption. Am J Prev Med 49, 5.
  15. Griswold, M.G. et al. (2018). Alcohol use and burden for 195 countries and territories, 1990-2016 (GBD 2016 Alcohol Collaborators). Lancet 392, 10152.

Information, not medical advice. Scientific evidence reflects the quality of the studies.

Loading assistant…