Alcohol

The idea that a drink or two a day is good for you has not survived better methods: nobody has found a level of drinking below which cancer risk stops rising, and the apparent heart benefit largely dissolves once you account for the fact that many "non-drinkers" quit because they were already ill. For a healthy adult the lowest-risk amount is at or near zero.

The scientific consensus on alcohol has shifted substantially over the past decade. The historical "J-curve" — a few drinks per day appearing protective for cardiovascular events and all-cause mortality — has largely collapsed under more rigorous methods, particularly Mendelian randomization (using inherited genetic differences as a natural experiment) and meta-analyses that correct for "abstainer bias."

What survives is narrower and more contested than the headlines on either side suggest. The cancer evidence is genuinely strong, and rises across every dose anyone has measured. The cardiovascular picture is a live argument between observational data that still shows a benefit and genetic data that does not — and, as the sections below show, the genetic data is not uniformly damning either.

Where official guidance now stands

Evidence rating: Caution — documented harm signal at commonly consumed doses, which is what has driven guidance down. Note that official guidance and the evidence have recently moved in opposite directions.

World Health Organization, January 2023: "No level of alcohol consumption is safe for our health."^[1]
Canada, 2023: the Canadian Centre on Substance Use and Addiction (CCSA) replaced its 2011 limits with a continuum of risk — 2 standard drinks per week or fewer is low risk, 3–6 is moderate, and more than 6 is "increasingly high," with every additional drink adding risk. Those cut-points are anchored to accepted mortality thresholds: the report puts the limit associated with a 1-in-1,000 lifetime chance of dying from an alcohol-related cause at two drinks per week, and the 1-in-100 limit at six.^[2]
US Surgeon General, January 2025: an advisory on alcohol and cancer identifying alcohol as the third leading preventable cause of cancer in the US, after tobacco and obesity. It attributes about 100,000 cancer cases and 20,000 cancer deaths a year to alcohol — "greater than the 13,500 alcohol-associated traffic crash fatalities per year" — notes that less than half of Americans know alcohol raises cancer risk, and calls for updated warning labels.^[3]

The 2026 reversal

That trend broke in January 2026. The 2025–2030 Dietary Guidelines for Americans dropped the previous numeric limits — no more than two drinks a day for men and one for women — along with the distinction between the sexes, replacing them with an unquantified instruction to consume less alcohol for better health.^[4] The guidelines are also silent on the cancer link that the Surgeon General's advisory had highlighted a year earlier. The American Association for the Study of Liver Diseases objected to the removal of evidence-based guidance,^[5] and The Lancet Gastroenterology & Hepatology called it a step backwards.^[6]

So the honest summary is not "limits keep falling everywhere." It is that the scientific case for lower limits has strengthened while the largest national guidance in the field moved the other way — a policy divergence, not an evidentiary one.

The one surviving dissent: the National Academies review

Evidence rating: Moderate (observational only).

The strongest remaining pro-moderate-drinking signal comes from a congressionally mandated review by the US National Academies of Sciences, Engineering, and Medicine (NASEM). Pooling eight eligible studies, it found that people who drank moderately had about 16% lower all-cause mortality than people who never drank — a relative risk (RR) of 0.84, with a 95% confidence interval of 0.81 to 0.87, graded moderate certainty.^[7]

That bracketed range is a confidence interval: the span within which the true effect most plausibly lies. When it sits entirely below 1.0, as here, the result is unlikely to be chance alone; when it crosses 1.0, the finding is compatible with no effect at all. Confidence intervals appear throughout this article and are read the same way each time.

Three caveats keep this from overturning the "no safe level" picture. The finding is observational; NASEM reached no conclusion at high certainty, noting that none of its 34 included articles was a randomized trial. The comparison hinges on the never-drinker reference group — the same group vulnerable to sick-quitter contamination. And when the review compared higher versus lower amounts within the moderate range, the mortality difference vanished: a 4% difference well inside the range expected from chance (RR 0.96, 95% CI 0.87 to 1.06), graded low certainty. A parallel federal review the following month reached the opposite conclusion — that at no age was there a significant net mortality benefit — and both reports drew conflict-of-interest accusations from opposite directions. The live frontier is the tension between these observational signals and the genetic evidence below, which finds no protective threshold.

Cancer: the strongest harm signal

Evidence rating: Strong.

The International Agency for Research on Cancer (IARC) has classified alcoholic beverages as a Group 1 carcinogen since 1988, and added acetaldehyde — the first product the body makes from alcohol — in 2009. Group 1 is the same category as tobacco and asbestos. There is sufficient evidence that alcohol causes seven cancers: mouth, pharynx, larynx, oesophagus (squamous cell), liver, colorectum, and female breast.

About 4% of cancers worldwide — roughly 741,000 cases in 2020 — are attributable to alcohol. Most of that burden comes from heavy drinking (346,400 cases) and risky drinking (291,800), but moderate drinking, defined as under 20 g of alcohol a day, still accounted for 103,100 cases, of which 41,300 arose at 10 g a day or less.^[8] In other words, roughly one alcohol-attributable cancer in seven occurs at intakes most people would not call heavy drinking.

Dose-response

A landmark dose-response meta-analysis of 572 studies and 486,538 cancer cases found clear monotonic curves — risk climbing steadily with dose, with no protective dip at the bottom.^[9] At light drinking (about one drink a day, ~12.5 g of alcohol), risk is already measurably raised: about 13% higher for mouth and pharyngeal cancer (RR 1.13), 26% higher for squamous-cell oesophageal cancer (RR 1.26), and 4% higher for female breast cancer (RR 1.04).

At moderate drinking — here about 25 g/day, a higher band than the under-20 g/day Rumgay used above, because the word is not standardised across studies — the same cancers rise further — oral and pharyngeal risk roughly doubles (RR 1.83), oesophageal squamous-cell risk more than doubles (RR 2.23), breast cancer runs about a quarter higher (RR 1.23), and colorectal about a fifth higher (RR 1.21). Among heavy drinkers, oral and pharyngeal cancer risk is more than five times that of non-drinkers (RR 5.13) and oesophageal squamous-cell cancer nearly five times (RR 4.95).

Breast cancer specifically

Evidence rating: Moderate (consistent, but observational).

The breast-cancer dose-response is the cleanest refutation of the J-curve anywhere in this literature: it is a straight line that starts below one drink a day. NASEM's meta-analysis put the increase at about 5% for every 10–14 g of alcohol per day (RR 1.05, 95% CI 1.04 to 1.06, moderate certainty) and concluded there is no evidence of a J-shaped association — the relationship appears linear, with increased risk at every amount. Comparing moderate drinkers with never-drinkers, the same review found about 10% higher risk (RR 1.10, 95% CI 1.02 to 1.19, moderate certainty).^[10]

For scale in absolute terms: the US National Cancer Institute estimates that about 18,500 of 297,790 new American breast-cancer cases are attributable to alcohol, and that roughly 5,000 of those arise at low levels of consumption.^[11] Estimates of this burden vary several-fold between research groups depending on how intake is measured, so treat the exact count as approximate and the direction as settled.

Mechanisms

Acetaldehyde — the first product of alcohol metabolism; it binds to DNA and interferes with repair, and is itself a Group 1 carcinogen.
Oxidative damage — an alternative alcohol-processing pathway in the liver generates reactive molecules that damage DNA.
Hormonal effects — alcohol raises circulating oestrogens, the leading explanation for the breast-cancer dose-response.
Disrupted folate metabolism — impairing the chemical tagging that regulates which genes are switched on.
Impaired absorption of protective nutrients (vitamins A, D and E, folate, carotenoids).

The natural experiment that closes the causal loop. Roughly 540 million people, mostly of East Asian descent, carry a variant of the enzyme that clears acetaldehyde; it works poorly, so acetaldehyde accumulates and the face flushes. Carriers who drink have markedly higher rates of cancers of the mouth, throat and oesophagus than non-carriers drinking the same amount, and the gap widens sharply with heavier drinking. Because the variant is inherited at random and affects nothing except acetaldehyde clearance, this is about as close to a controlled experiment as the field gets — and the flushing reaction is a reliable stand-in for the genotype, making it a simple and actionable warning sign.^[12]

Cardiovascular: the J-curve has mostly collapsed

Evidence rating: Strong (for harm to blood pressure and stroke); Moderate (for the absence of coronary benefit).

For three decades observational studies showed a J-shape: light drinkers appeared healthier than abstainers. The protective hypothesis rested on alcohol raising HDL ("good") cholesterol and mildly reducing blood clotting.

What the genetic evidence shows

Mendelian randomization exploits the fact that people inherit, at random, gene variants that strongly influence how much they drink — most importantly in the two enzymes that metabolise alcohol. Because those variants are fixed at conception, they cannot be confounded by wealth, diet or illness, which makes them a natural experiment for lifetime alcohol exposure.

The China Kadoorie Biobank enrolled 512,715 adults and genotyped 161,498 men. Genetically predicted alcohol intake had a continuously positive association with stroke — about 58% higher risk of brain haemorrhage and 27% higher risk of ischaemic stroke per 280 g a week, about 20 US standard drinks (RR 1.58, 95% CI 1.36–1.84; RR 1.27, 95% CI 1.13–1.43) — and raised blood pressure, with no protective threshold anywhere. Notably, it found no significant effect on heart attack (RR 0.96, 95% CI 0.78–1.18), a result compatible with no effect at all; the authors concluded alcohol "appears in this one study to have little net effect on the risk of myocardial infarction."^[13]
A 94-variant analysis found roughly 27% higher stroke risk and a three-fold higher risk of peripheral artery disease among people whose genes predispose them to drink substantially more (odds ratios, OR, of 1.27, 95% CI 1.12–1.45, and 3.05, 95% CI 1.92–4.85, per standard-deviation increase in predicted drinking).^[14]
In UK Biobank, each additional daily drink was causally associated with +2.65 mmHg systolic blood pressure, roughly double the risk of haemorrhagic stroke (OR 2.25) and about 26% higher atrial fibrillation risk (OR 1.26). The authors' summary is blunt: alcohol "was not protective for any disease outcome with any analysis method, dataset, or strata."^[15]
A Million Veteran Program analysis reproduced the U-shaped observational curve and then found no causal benefit at moderate intake in the genetic analysis — the signature of confounding.^[16]

A systematic review of 24 Mendelian randomization studies found null associations between genetically predicted alcohol and cardiovascular disease in 67% of studies and diabetes in 75%, with the single study of all-cause mortality reporting harm. Its authors were careful, though: given how much the methodological quality varied, they judged it "not yet possible to draw conclusions on the causal role of moderate alcohol consumption on cardiometabolic health." (Moderate)^[17] That is weaker than "genetics proves harm" — but it is fatal to "genetics proves benefit," which is what the J-curve needed.

Specific outcomes

Hypertension — an almost perfectly linear dose-response with no safe floor. Against a 12 g/day reference, risk runs about 11% higher at 24 g/day, 22% at 36 g/day and 33% at 48 g/day; drinking nothing at all is associated with 11% lower risk than the 12 g/day reference (RR 0.89, 95% CI 0.84–0.94). (Strong)^[18]
Atrial fibrillation — pooling 13 studies and over 10 million participants, each additional daily drink raised risk about 6% (RR 1.06, 95% CI 1.03–1.08). The relationship was linear in men (about 8% per drink) but J-shaped in women, whose pooled estimate did not reach significance (RR 1.05, 95% CI 0.96–1.14). Binge drinking can also trigger acute "holiday heart" episodes in otherwise healthy hearts. (Moderate)^[19]
Stroke — rises with intake, and the genetic evidence supports causation, most strongly for bleeding strokes.
Cardiomyopathy — heavy chronic drinking causes dilated cardiomyopathy, a weakening and enlargement of the heart muscle.

The residual protective signal in some cohorts appears to be confounded by the socioeconomic and lifestyle advantages that travel with moderate drinking in Western populations. The one endpoint where the genetic evidence genuinely does not show harm is heart attack — which is exactly the endpoint the J-curve was built on, and exactly why this argument has not ended.

All-cause mortality and global burden

Evidence rating: Strong (harm above roughly 45 g/day); Moderate (absence of benefit at low intakes).

Bias-corrected meta-analysis. A systematic review of 107 cohort studies — 4,838,825 people and 425,564 deaths — reproduced the classic J-curve in naïve estimates. But once it corrected for the sick-quitter problem (former drinkers, many of whom quit because they were ill, landing in the abstainer reference group) and for study quality, the apparent low-dose protection disappeared. Occasional drinkers showed no meaningful mortality difference from lifetime non-drinkers — a 4% gap well within the range expected from chance (RR 0.96, 95% CI 0.86–1.06) — and low-volume drinkers (1.3–24 g/day) likewise fell short of significance. Risk turned significantly upward at 45–64 g/day (about 19% higher) and at 65 g/day or more (about 35% higher). The threshold at which risk became significant was lower for women than men: the review found significantly raised mortality in women drinking 25 g a day or more, against 45 g a day or more in men — about 22% higher than female lifetime non-drinkers (RR 1.22). (Strong)^[20]

Global burden modelling. The Global Burden of Disease study found that "the level of alcohol consumption that minimised harm across health outcomes was zero" standard drinks per week. Alcohol was the seventh leading risk factor for death worldwide in 2016 and the leading risk factor for people aged 15–49, where it accounted for 12.2% of male and 3.8% of female deaths. (Moderate — modelled estimate, now superseded)^[21]

The same collaboration replaced that single global figure in 2022 with age- and region-specific thresholds. For people aged 15–39 the harm-minimising level is essentially zero everywhere, with injury dominating. For adults 40 and over the burden-weighted risk curve was J-shaped in every region, with a harm-minimising level ranging from about 0.1 to 1.9 drinks a day depending on background disease rates. That "older adults may benefit" element is a relative-risk statement inside an age band, says nothing about an individual's absolute benefit, and is the single most-quoted line in industry communications. (Moderate — modelled estimate; supersedes the 2018 "zero" figure)^[22]

The US toll. Excessive drinking accounted for an estimated 12.9% of all deaths among US adults aged 20 to 64 between 2015 and 2019 — about 89,700 deaths a year, or one in eight — rising to 20.3%, one in five, among adults aged 20 to 49.^[23]

Why no definitive trial exists

The one large randomized trial designed to settle the question — the Moderate Alcohol and Cardiovascular Health Trial, testing about one drink a day against abstention — collapsed in 2018. Of 390 people who consented, only 32 had been randomized before the National Institutes of Health withdrew funding.^[24]^[25]

The reason it ended matters as much as the fact. Roughly two-thirds of the trial's $100 million budget had been raised from five alcohol producers — Anheuser-Busch InBev, Carlsberg, Diageo, Heineken and Pernod Ricard — and an NIH advisory working group found that officials appeared "to intentionally bias the framing of the scientific premise in the direction of demonstrating a beneficial health effect," while the design lacked sufficient patients and follow-up time to detect cancer harms.^[26] This is why genetic and bias-corrected observational evidence, rather than a trial, carry the weight here — and why conflict-of-interest flags recur throughout this field, on the advocacy side as well as the industry side.

Liver

Evidence rating: Strong (heavy drinking); Moderate (interaction with fatty liver disease).

Alcohol produces a direct dose-response for fatty liver, alcoholic hepatitis and cirrhosis, and is a dominant cause of cirrhosis worldwide alongside the hepatitis viruses. Pooling 44 studies and 5.1 million people, drinking 25 g a day — under two US standard drinks — was associated with roughly 1.8 times the risk of developing cirrhosis and 2.7 times the risk of dying from it, rising to about 8-fold and 16-fold at 100 g a day. The curve has no threshold below which risk stops rising, and mortality accelerates faster than illness does.^[27]

The clinically useful numbers now come from the 2023 renaming of fatty liver disease. Metabolic dysfunction–associated steatotic liver disease (MASLD, formerly non-alcoholic fatty liver disease) plus drinking of 140–350 g per week for women or 210–420 g per week for men — roughly 20–50 and 30–60 g a day — is reclassified as MetALD, a combined metabolic-and-alcohol disease; above that range it becomes alcohol-related liver disease outright.^[28] The practical reading: if you already have fatty liver, amounts well inside what most guidelines call moderate are enough to change your diagnosis. See bile and metabolism for the wider liver picture.

Brain

Evidence rating: Strong (heavy drinking); Moderate (structural changes at moderate intake); Weak (clinical significance of those changes).

Alcohol use disorder clearly causes brain atrophy and cognitive decline.
Even moderate drinking tracks with reduced grey-matter volume. In 25,378 UK Biobank participants, alcohol intake was negatively and linearly associated with global grey matter with no safe threshold.^[29] A separate analysis of 36,678 people found the negative associations with both grey-matter volume and white-matter structure "already apparent in individuals consuming an average of only one to two daily alcohol units," strengthening with intake.^[30]
The 2024 Lancet Commission on dementia lists excessive alcohol among its modifiable risk factors — see dementia prevention.
The older "moderate alcohol protects against dementia" finding has not held up: it appears in observational analyses and not in genetic ones, the pattern expected when people already declining cognitively drink less.

What these imaging studies do not establish is how much a few percent of grey-matter volume matters for how you think and function. Treat the structural signal as a reason not to be reassured, not as a diagnosis.

Biological aging

Evidence rating: Moderate (telomeres); Weak (gut–liver axis).

Telomeres. (Moderate) Alcohol appears to accelerate one measurable marker of cellular aging. A UK Biobank study of 245,354 people paired with Mendelian randomization found genetically predicted alcohol use disorder causally associated with shorter telomeres — the protective caps on chromosome ends. To scale it: in the observational data, drinking more than 29 UK units a week — a UK unit is 8 g, so roughly 17 US standard drinks — versus fewer than 6 was equivalent to 1–2 years of age-related telomere change, while the genetic estimate came out larger, at about 3 years per standard-deviation increase in predicted drinking. The genetic association appeared only in current drinkers and not in never- or former-drinkers, which is the test the authors used to confirm the gene variants act on telomeres through alcohol rather than by some other route. Two honest caveats: the non-linear analysis suggested a threshold rather than a straight line, and telomere length is an imperfect aging marker — treat this as suggestive.^[31]
Gut–liver axis. (Weak) Chronic drinking disrupts the gut microbiome and increases intestinal permeability, letting bacterial fragments cross into the blood draining the gut, where they activate liver immune cells and drive inflammation and scarring. A plausible mechanistic bridge to the low-grade systemic inflammation associated with biological aging, but not demonstrated as a pathway in humans at moderate intakes.

Sleep

Evidence rating: Moderate — consistent laboratory findings, but on sleep-architecture measures rather than hard endpoints.

Alcohol shortens the time it takes to fall asleep and then degrades the rest of the night. Across all doses it delays the onset of the first REM (rapid eye movement, or dreaming) period; total REM across the night falls at moderate and high doses, with no clear trend at low ones.^[32] The second half of the night becomes fragmented, and snoring and sleep apnoea worsen — see sleep-disordered breathing.

The trap for anyone using a sleep tracker: alcohol reliably increases deep (slow-wave) sleep in the first half of the night — a finding that holds across doses, ages and sexes, and one the reviewers describe as more robust than its REM suppression.^[33] So a nightcap can produce a flattering deep-sleep score while degrading the night in every way that matters. It is the clearest single demonstration that the deep-sleep number is not a health metric — see sleep architecture.

Practical: if you drink, finish at least 3 hours before bed, or skip it on nights when sleep matters.

Mental health

Evidence rating: Moderate.

The relationship between alcohol and both depression and anxiety runs in both directions and reinforces itself: distress prompts drinking, and drinking worsens distress through disrupted sleep, rebound anxiety the following day, and stress-hormone effects. Alcohol is pharmacologically a depressant, and even moderate use degrades sleep quality enough to feed the loop.

The hardest endpoint here is suicide. Pooling 24 studies covering 37.9 million people, alcohol use disorder was associated with roughly two and a half times the risk of dying by suicide in longitudinal studies, and the association was similar in men and women (odds ratios 2.68, 95% CI 1.86–3.87, and 2.39, 95% CI 1.50–3.81).^[34] If drinking has become something you would describe as a problem, this is the reason to treat it as urgent rather than gradual.

Sex differences

Evidence rating: Moderate.

Women reach a higher blood-alcohol concentration than men from the same drink — the standard explanation is lower total body water and less first-pass breakdown of alcohol in the stomach — and the outcome data broadly track that. Women crossed into significantly raised all-cause mortality at 25 g a day against 45 g a day in men, as above,^[35] the hypertension dose-response was steeper in women at high intake,^[36] cirrhosis develops at lower exposures, and breast cancer is a large alcohol-attributable burden with no threshold that applies almost entirely to women.

The pattern is not universal, which is worth stating plainly: the atrial-fibrillation dose-response was linear in men but J-shaped and non-significant in women.^[37] The 2025–2030 US Dietary Guidelines removed the sex distinction from national advice; the evidence for keeping it, on balance, got stronger rather than weaker.

Pregnancy

Evidence rating: Strong (harm); Caution (no threshold established).

No safe level is established. Fetal alcohol spectrum disorders are dose-dependent, and individual susceptibility varies widely enough that no threshold can be identified as safe. These conditions are also more common than most people assume: a population-based screening study of Canadian schoolchildren estimated a prevalence of 2–3%, exceeding that of Down syndrome, spina bifida and autism spectrum disorder in the same country.^[38] The recommendation across every major authority is complete avoidance during pregnancy, and ideally from the point of trying to conceive.

What's overrated

Evidence rating: Moderate — these are claims the evidence has moved away from, not claims never tested.

Red wine and resveratrol. A 150 mL (5 oz) glass of red wine contains 0.3–1 mg of resveratrol; the research showing benefits uses 100–500 mg. You would need hundreds of glasses to reach a studied dose. The "wine drinkers live longer" cohorts are overwhelmingly explained by confounding — wine drinkers in those studies were wealthier, better educated, more active and ate better. There is no special protective effect of wine over other alcohol that survives rigorous methods.
The HDL story. Alcohol does causally raise HDL cholesterol. But a Mendelian randomization study found that genetic variants which raise HDL do not lower heart-attack risk, concluding that these data "challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction"; HDL-raising drugs have likewise failed in trials.^[39] That removes the mechanism the J-curve was resting on — see lipid management.
Type 2 diabetes protection. This is the second-strongest surviving benefit claim and it is real in observational data: across three US cohorts totalling 200,969 people and 20,551 diabetes cases over three decades, light-to-moderate drinking was associated with lower risk, driven mainly by drinking frequency rather than amount — those drinking 5–6 days a week had roughly a quarter lower risk than those drinking 1–2 days (hazard ratios, HR, of 0.73–0.76 across cohorts).^[40] But the genetic analyses do not reproduce it, and a benefit that appears only when you compare people who differ in a hundred other ways is the exact pattern that abstainer bias and lifestyle confounding produce. (Moderate for the association; Weak for causation.)
"A drink helps me relax." True acutely, and it is a real reason people drink. It is also not a health benefit, and the same effect is available from things that do not carry a Group 1 carcinogen classification.

Quantifying "a drink"

Standard drinks differ by country, so grams are the only stable unit. A US standard drink is 14 g of pure alcohol — about 350 mL (12 oz) of 5% beer, 150 mL (5 oz) of 12% wine, or 45 mL (1.5 oz) of 40% spirits. A UK unit is 8 g; a Canadian standard drink is 13.45 g; an Australian one is 10 g. When comparing studies, always convert to grams.

Where the thresholds sit now:

Level	Amount
Lowest risk	0 drinks/week
Low risk (Canada 2023)	2 or fewer/week
Moderate risk (Canada 2023)	3–6/week
Increasingly high risk	more than 6/week
Binge (single occasion)	4+ for women, 5+ for men in about 2 hours

The shift from "moderate is fine" to "less is better, ideally zero" reflects better methods, not new puritanism — and note that the two are separable: the case for lower limits strengthened in the same period that US federal guidance dropped its numbers.

Practical guidance

If you don't drink, don't start for health benefits — none survive rigorous methods.
If you drink, less is better. Treat each drink as an exposure with a dose, not a category you are either in or out of.
Count in grams, not glasses. Home and bar pours routinely exceed a standard drink.
Avoid binge drinking (defined in the table above). It adds acute risks for the liver, brain and heart rhythm on top of your average intake.
Don't drink within 3 hours of bed if sleep matters, and expect your tracker to disagree with you.
Family history of breast cancer: the dose-response is a straight line from the lowest intakes that have been measured, with no threshold below which it flattens, so this is one of the few places where the difference between zero and "a small glass most nights" is worth taking seriously.
Flushing reaction, or East Asian heritage: flushing marks the poor-acetaldehyde-clearing variant, and drinking with it carries sharply raised risk of mouth, throat and oesophageal cancer. Avoidance is the appropriate response.
Fatty liver, hepatitis, or any liver disease: amounts inside conventional "moderate" limits are enough to reclassify your diagnosis. Talk to your clinician before drinking at all.
Pregnancy, trying to conceive, or breastfeeding: abstain.
Use periods of abstinence to check your own dependency. Finding it hard to stop is the signal, not the inconvenience.
Screening doesn't undo the exposure. Screening finds cancers earlier; it does not remove the cause. Reducing intake and screening are complements, not substitutes.