L20 Metabolism Alcohol

Overview

This lecture covers alcohol (ethanol) as a non-essential but energy-yielding substance: its chemistry and fermentation origin, digestion/absorption, the three metabolic pathways that clear it from the body, the factors that alter metabolic rate, and the concept of a “standard drink” and its relation to blood alcohol concentration (BAC). It then moves from individual metabolism to population and policy level: NZ drinking statistics, current and proposed recommended intakes (NZ, Canada, Ireland), and a critical evaluation of the evidence linking alcohol to cardiovascular disease and cancer, concluding that the “French paradox” and moderate-drinking-is-protective narrative have not held up under genetic (Mendelian randomisation) analysis, and that current major health bodies (WHO, NZ Heart Foundation, GBD 2016) hold that no level of alcohol consumption is safe.

Alcohol: definition, chemistry and nutrient status

Definition: alcohol is a colourless, volatile, flammable liquid produced by the natural fermentation of sugars, and is the intoxicating constituent of wine, beer, spirits and other drinks. Chemically, it is an organic substance formed when a hydroxyl group is substituted for a hydrogen atom in a hydrocarbon. The alcohol in alcoholic beverages is Ethanol (ethyl alcohol), formula $C_2{H}_{5}OH$, derived from fermenting sugar with yeast.

Nutrient classification:

• Macronutrients: required in the diet in large (gram) quantities. Water provides no energy; carbohydrate, fat and protein provide energy.
• Micronutrients: vitamins and minerals, required in small amounts.
• Alcohol is not considered a nutrient, but it does provide energy: Atwater factor of 29 kJ/gram, compared with 17 kJ/g for protein/carbohydrate and 37 kJ/g for fat.

Alcohol has no essential physiological function: it is not an essential nutrient, and is classed as a drug and a toxin. Its only nutritional contribution is energy.

Fermentation (in the source beverage, not human metabolism): certain yeasts contain pyruvate decarboxylase (PD) and alcohol dehydrogenase (ADH). Glucose (from grapes/barley/rice) → pyruvate → [PD] → acetaldehyde → [ADH] → ethanol.

Digestion and absorption

Alcohol does not require digestion. Absorption:

• 20% absorbed in the stomach (food in the stomach slows this).
• 80% absorbed in the small intestine.
• Moves easily between cells and distributes throughout total body water.

Worked example of distribution: 10 g of alcohol (= one standard drink) distributed across 40 L of total body water = 0.25 g/L = 0.025 g/dL. The legal driving limit for adults 21+ is 0.05 g/dL (50 mg/100 mL).

Metabolism of alcohol

A small amount is metabolised in the stomach (first pass), but the majority is metabolised in the liver. A small unmetabolised fraction leaves the body via urine (detectable 12–80 hours after a drink), breath (≈250 microg/L breath), and breast milk.

Three metabolic pathways:

1. Alcohol dehydrogenase (ADH) — an interconversion reaction occurring in stomach, liver, pancreas and brain. This is the major pathway in most people, and ADH is the rate-limiting step of alcohol metabolism.
2. Microsomal ethanol-oxidising system (MEOS) — activated in long-term heavy drinkers.
3. Catalase, acting in the presence of hydrogen peroxide, converts ethanol to acetaldehyde; probably accounts for <2% of ethanol metabolism.

Pathway sequence (liver): Alcohol (ethanol) → [alcohol dehydrogenase; NAD⁺ → NADH + H⁺] → Acetaldehyde → [acetaldehyde dehydrogenase; NAD⁺ → NADH + H⁺] → Acetate → (+ CoA) → Acetyl CoA.

From Acetyl CoA, two routes are possible:

• Normal route: into the TCA cycle for energy.
• Alternative route (when NADH is high): Acetyl CoA is blocked from entering the TCA cycle by the elevated NADH level, and instead becomes a building block for fatty acids → fat (triglycerides).

Factors affecting alcohol metabolism

1. Quantity of alcohol consumed — since ADH is rate-limiting, the liver can only process about 5–10 grams of alcohol per hour.
2. Sex (male vs female) — women have smaller livers, a lower percentage of total body water, less stomach ADH, and higher absorption than men.
3. Body size.
4. Genetics — Chinese, Korean and Japanese populations carry a different ADH variant; a resulting build-up of acetaldehyde causes flushing and headaches.

A dose-response graph (BAC after rapid consumption of 1, 2, 3 or 4 drinks in fasting male subjects) shows BAC rising rapidly within the first hour post-consumption (peak height increasing with number of drinks, up to ~85 mg% for four drinks), then declining gradually back toward zero by 6–8 hours; more drinks produce both a higher peak and a slower return to baseline. Reference points: 100 mg% is the legal level of intoxication in most US states; 50 mg% is the level at which driving-skill deterioration begins.

Standard drinks and alcohol content

10 grams of alcohol = one standard drink. Alcohol content by beverage type (volume providing 10 g alcohol, vs typical serving size):

Type of drink	% alcohol	Volume providing 10 g alcohol	Typical serving size
Low alcohol beer	2–3%	~500 mL	330 mL
Average beer	4–5%	285 mL	330 mL
Wine	10%	120 mL	150 mL
Wine	13%	100 mL	120 mL
Sherry, port	20%	60 mL	60 mL
Spirits (whisky, vodka)	30%	30 mL	30 mL

Effects of excess alcohol consumption

Three mechanisms of harm from consuming too much alcohol:

1. Effects of acetaldehyde — short-lived but toxic (cell-damaging) effects on the liver, GIT, brain (marked with a query in the slide), and pancreas. Long term, this leads to cirrhosis of the liver and cancers.
2. Elevated NADH:NAD⁺ ratio — NAD⁺ becomes unavailable for other pathways (e.g. gluconeogenesis, TCA cycle, electron transport chain); H⁺ accumulates, affecting acid–base balance; lipid synthesis increases (fatty liver); fatty acid oxidation is inhibited (elevated triglycerides).
3. Induced metabolic tolerance — the MEOS pathway produces many toxic metabolites.

Chronic heavy drinking shifts alcohol metabolism onto the MEOS pathway, which both reflects and reinforces tolerance, while generating additional toxic metabolites.

Effect on the brain (dose–response)

Blood alcohol (g/dL)	Stage	Effects
Up to 0.05	Feeling of well-being	Relaxed, talkative
0.05–0.08	Risky state	Judgement and fine movements affected
0.08–0.15	Dangerous state	Slow speech, balance affected, blurred eyesight, sleepy, likely to vomit, needs help walking
0.20–0.40	Drunken stupor	Dead drunk, no bladder control, heavy breathing, unconscious
0.45–0.60	Death	Shock and death

Alcohol and weight gain

Alcoholic drinks provide substantial hidden energy. Examples given (kJ-equivalence to food):

• 375 mL can of full-strength beer (580 kJ) ≈ 3 chicken nuggets; 570 mL pint of full-strength beer (880 kJ) ≈ 1 slice of pizza.
• 150 mL glass of wine (460 kJ) ≈ 1 chocolate paddle pop; 2 × 375 mL cans of rum and cola (2240 kJ) ≈ 1 cheeseburger + 1 chocolate bar.
• 330 mL bottle of pre-mixed spirits (870 kJ) ≈ 1 slice of pizza; 2 × 330 mL bottles of cider (1260 kJ) ≈ 1 cheeseburger.

[slide does not elaborate further on whether NZ/Australian alcoholic beverages carry a mandatory Nutrition Information Panel — this is posed as an open question on the slide, not answered]

NZ drinking patterns (population data)

Slide 19 (NZ Adult Nutrition Survey 2008/09, Table 3.27, alcohol intake by age/sex): the table is cut off at the bottom of the slide, so rows beyond "Females Total" (including ethnic-group breakdown referenced in the table title) are not captured. One printed value ("20.0.6" for Males 31–50 mean alcohol grams) appears to be a typo/OCR artefact, likely intended as 20.6.

Key figures captured from Table 3.27: total population mean alcohol intake 14.0 g/day (90th percentile 35.1 g), 3.8% of energy from alcohol on average. Males consume more than females at every age band (e.g. Males 19–30 mean 19.3 g/day vs Females 19–30 mean 11.9 g/day); intake and %energy from alcohol are highest in the 19–70 year age bands for both sexes and lowest in the youngest (15–18) and oldest (71+) bands.

Slide 20 (NZ Adult Nutrition Survey 2008/09, Table 3.28, alcohol source by food group): the right edge of the table (Females 71+ and Females Total columns) is cut off and not visible.

Table 3.28 (proportion of alcohol intake from each beverage type, among drinkers): nationally, wine contributes the largest share (42.0%), followed by beer (36.0%), spirits (10.6%), other/RTDs (7.5%), and liqueurs/cocktails (1.6%). By sex, beer dominates for men (e.g. 69.4% of alcohol source in males 15–18) while wine dominates for women, increasing with age (e.g. 78.1% of alcohol source in females 51–70).

Current NZ drinking prevalence (NZ Health Survey, 2024/25): 74.9% of adults (an estimated 3,250,000 people) drank alcohol in the past year, a figure that has stayed in the roughly 75–83% range over the survey’s time series with a slight peak around 2019/20 and slight decline toward 2024/25. By age, prevalence is lowest in 15–17 year olds (~48%) and highest in 18–24 year olds (~79%), staying broadly similar (~70–78%) across older age bands.

Slide 22 (Our World in Data world maps on alcohol consumption per person and share of adults who drank in the last year, 2020): specific NZ numeric values are not legible on the choropleth maps at the resolution available.

Recommended alcohol intakes

Current NZ recommendations (three-panel guidance):

• To reduce long-term health risks: no more than 2 standard drinks/day for women, 3/day for men, and no more than 10/week (women) or 15/week (men), with at least 2 alcohol-free days per week.
• To reduce injury risk: no more than 4 standard drinks (women) or 5 (men) on any single occasion.
• Pregnant women: no alcohol — 0 standard drinks. There is no known safe level of alcohol use at any stage of pregnancy.

There is no known safe level of alcohol use at any stage of pregnancy.

Alcohol and pregnancy warning labels: mandatory, visible pregnancy health warnings (“PREGNANCY WARNING — Alcohol can cause lifelong harm to your baby”) are now required on alcohol products in Australia and New Zealand, following more than 20 years of advocacy from people with Fetal Alcohol Spectrum Disorder (FASD), their families, and groups such as NOFASD.

Ireland (2026, proposed world-first policy): labels to warn of calories, cancer risk, liver disease risk, and dangers of drinking while pregnant, plus injury and driving risk and harm to the developing brain. Example wording caps safe drinking at 14 UNITS/week on a regular basis, and advises avoiding alcohol when pregnant or trying to conceive.

Canada (2023, revised recommendations) — “drinking less is better”: no amount or kind of alcohol is considered good for health. Risk ladder by drinks/week:

• 0 drinks = no risk (during pregnancy, none is the only safe option).
• 1–2 standard drinks/week = low risk.
• 3–6 standard drinks/week = moderate risk (increased risk of several cancers, including breast and colon).
• 7+ standard drinks/week = increasingly high risk (increased risk of heart disease/stroke, each additional drink further raising risk).

A Canadian standard drink is defined as: beer 341 mL (12 oz) at 5%; cooler/cider/RTD 341 mL (12 oz) at 5%; wine 142 mL (5 oz) at 12%; spirits 43 mL (1.5 oz) at 40%. The new Canadian guidance (2 drinks/week maximum for low risk) is a steep drop from the 2011 guidelines (up to 10/week for women, 15/week for men).

Future NZ recommendations (proposed): framed as “weighing up the evidence” with the balance tipping toward harm rather than benefit; proposed guideline cards mirror the Canadian approach with “no more than 0” daily for both long-term risk reduction and injury-risk reduction, retaining the pregnancy guidance of 0 standard drinks.

Slide 45 duplicates the content of Slide 27 exactly (a recap slide in the source deck).

The “French paradox” and the case against moderate drinking

The French paradox refers to the historical observation that France had the highest saturated fat intake and the lowest rates of coronary heart disease (CHD) among 41 European countries (1998 WHO/FAO data), which was used to argue that moderate red wine consumption might be cardioprotective. The slide frames this as a myth.

The classic J/U-shaped curve (relative cardiovascular risk vs drinks/day, with lowest risk at 1–2 drinks/day and higher risk at abstinence or >2 drinks/day) is explicitly rejected in the lecture material. Reasons the earlier “moderate drinking is protective” research is now considered flawed:

• Light drinkers in those studies tended to be better educated, wealthier, more physically active, better insured, and had better diets (confounding).
• The French also walked more and ate more healthily.
• More recent research adjusting for these factors found no protective effect of alcohol on longevity, and found elevated risk of hypertension and coronary artery disease with each progressive drink.
• Studies showing positive health impacts were often low-level-of-evidence studies.

Resveratrol and red wine: red wine contains 0.4–2 mg of resveratrol per litre, whereas supplement pills contain 250–1,600 mg. A person would need to drink 833 to 5,333 glasses of wine to match the resveratrol dose in a single supplement pill, so any antioxidant benefit from red wine is negligible in practice.

Global Burden of Disease evidence (GBD 2016)

The GBD 2016 Alcohol Collaborators study (Lancet, 2018) generated estimates of alcohol use and alcohol-attributable deaths and DALYs for 195 locations, 1990–2016.

Slide 32 has no visible title bar in the source; it is a direct continuation of the GBD 2016 discussion begun on slides 30–31.

Figure 5 of the study (weighted relative risk of alcohol for all attributable causes, by standard drinks/day) shows relative risk starting near 1.0 at zero drinks and rising steadily to approximately 3.0 at 15 drinks/day, with a widening confidence band (~2.25–4.75 at 15 drinks/day) — i.e. risk increases continuously with intake, with no dip at low/moderate intake.

Slide 33 also has no visible title bar; it continues the GBD 2016 conclusion.

GBD 2016 conclusion: "Our results show that the safest level of drinking is none." Alcohol use accounts for nearly 10% of global deaths among populations aged 15–49, in conflict with health guidelines that espouse benefits of consuming up to two drinks per day. Policies reducing population-level consumption are the most effective way to reduce alcohol-related health loss.

Alcohol and cardiovascular disease: conventional vs genetic evidence

The China Kadoorie Biobank study (Millwood, Walters, et al., Lancet 2019) compared conventional epidemiology (self-reported drinking) against genetic epidemiology (Mendelian randomisation, using genotype-predicted alcohol intake) in ~500,000 Chinese adults, to test whether the apparent cardioprotective effect of moderate drinking is causal.

Method: 512,715 adults enrolled 2004–2008 across ten areas of China, followed for ~10 years (to 2017) for cardiovascular disease (ischaemic stroke, intracerebral haemorrhage, myocardial infarction). 161,498 participants were genotyped for two variants that alter alcohol metabolism, ALDH2-rs671 and ADH1B-rs1229984, allowing Mendelian randomisation.

Slide 36 also has no visible title bar; it continues the CVD/Mendelian randomisation results from slides 34–35.

Findings (in men):

• Conventional analyses (self-reported drinking) found the classic U-shaped association: lowest risk of stroke and myocardial infarction at moderate intake. For total coronary heart disease, RR 1.12 (95% CI 1.04–1.21) per 280 g/week (p=0.003).
• Genetic analyses (genotype-predicted intake) found no U-shape: risk rose steadily and near-linearly with genotype-predicted intake across the full range (near zero to ~4 drinks/day), and was strongly positively associated with blood pressure, ischaemic stroke, and haemorrhagic stroke throughout.

Genetic evidence indicates the apparently protective effect of moderate alcohol intake against stroke seen in conventional (self-report) studies is largely an artefact of reverse causation and confounding, not a true causal effect. Increasing mean alcohol intake uniformly increases blood pressure and stroke incidence. In this cohort, alcohol was responsible for about 8% of ischaemic strokes and 16% of intracerebral haemorrhages; effects on myocardial infarction were less certain.

Alcohol and cancer

The 2020 population-based Global Burden of Cancer study (Rumgay et al., Lancet Oncology 2021) estimated the global cancer burden attributable to alcohol.

Findings: globally, an estimated 741,300 (4.1% of all new cancer cases) in 2020 were attributable to alcohol. Males accounted for 76.7% (568,700 cases) of the total, with oesophageal (189,700), liver (154,700) and breast (98,300) cancers contributing the most cases. Population attributable fractions (PAFs) were lowest in northern Africa (0.3%) and western Asia (0.7%), and highest in eastern Asia (5.7%) and central/eastern Europe (5.6%). By drinking category, heavy drinking contributed the largest share of cases (346,400; 46.7%), followed by risky drinking (291,800; 39.4%), then moderate drinking (103,100; 13.9%) — with drinking up to 10 g/day alone contributing 41,300 cases.

By region, PAFs were largest for males in eastern Asia and central/eastern Europe (~7–8%) and smallest in northern Africa and western Asia (<1%). Choropleth maps show the highest alcohol-attributable cancer incidence rates concentrated in Eastern Europe/Russia, Mongolia and parts of East Asia for both sexes, with absolute rates generally lower in females than males.

Current position of major health bodies

WHO (2023): "No level of alcohol consumption is safe for our health." Alcohol is a toxic, psychoactive, dependence-producing substance, classified as a Group 1 carcinogen by the International Agency for Research on Cancer (the same risk category as asbestos, radiation and tobacco). Alcohol causes at least seven types of cancer, including bowel and female breast cancer. Notably, half of all alcohol-attributable cancers in the WHO European Region are caused by "light" and "moderate" consumption (less than 1.5 L wine, 3.5 L beer, or 450 mL spirits per week) — this pattern accounts for the majority of alcohol-attributable cancers in women.

NZ Heart Foundation: "No amount of alcohol is good for your heart"; the Foundation does not recommend drinking alcohol to improve heart health. Every 10 g increase in daily pure alcohol intake (= 1 standard drink) raises the risk of high blood pressure by 6%. Alcohol also increases risk of atrial fibrillation and haemorrhagic stroke, and may increase risk of heart failure and ischaemic heart disease. Conclusion: there is no safe level of alcohol consumption; non-drinkers should not start, and drinkers should drink less.

Alcohol and young people: alcohol is considered more dangerous for younger people, even past the legal drinking age, for several reasons —

• Body size/shape: teenagers do not reach adult height until 21 and may lack adult bulk even after vertical growth stops, so a given drink produces a higher BAC in young people than in adults.
• A higher head-to-body ratio in adolescents also affects the intoxication experienced.
• Alcohol reaches the brain within five minutes of drinking, crossing the blood-brain barrier that normally protects the brain from harmful substances; a relatively large proportion of the alcohol reaches young people’s brains, contributing to a higher likelihood of alcohol poisoning.
• The adolescent brain undergoes complex rewiring that continues until at least age 25, later than previously thought (neural development was once believed to stop in the early teens).

Alcohol policy and industry influence

The lecture closes on alcohol as a public-health “big business” alongside big tobacco and big food, citing: exposure of the alcohol industry’s track record of undermining science and evidence-based policy for profit (“Big Alcohol Exposed”); investigative reporting on alcohol lobbyists being given input on NZ health policy; and continued alcohol-industry sponsorship of major sporting and community events (e.g. a major NZ marathon, and long-standing beer-brand sponsorship of a professional rugby team).

Slide 46: the final bullet in the "Big business / Big tobacco / Big food / Big alcohol" list is truncated to a single period in the source slide — it is not possible to confirm from the rendered image whether text is missing or this is an intentional trailing marker.

Self-test

1. Why is alcohol not classified as a nutrient, despite providing energy?
2. What is alcohol’s Atwater energy factor (kJ/gram), and how does it compare with protein, carbohydrate and fat?
3. Give the molecular formula of ethanol.
4. What percentage of ingested alcohol is absorbed in the stomach versus the small intestine, and what slows stomach absorption?
5. How many grams of alcohol are in a standard drink?
6. List the three metabolic pathways for alcohol and state which is the major pathway in most people and which enzyme step is rate limiting.
7. Approximately how many grams of alcohol per hour can the liver metabolise, and why is this rate fixed?
8. Describe, in order, the steps from ethanol to Acetyl CoA in liver metabolism, naming the enzymes and cofactor changes involved.
9. Why does excess alcohol consumption promote fat (triglyceride) synthesis rather than energy production from Acetyl CoA?
10. List the factors that make women reach a higher blood alcohol concentration than men for the same alcohol intake.
11. Why do some East Asian populations experience flushing and headaches after drinking?
12. A patient at 0.10 g/dL blood alcohol has slurred speech, impaired balance and blurred vision. Which stage of intoxication is this, and what BAC range does the legal driving limit fall within relative to it?
13. By what three mechanisms does excess alcohol cause tissue damage and metabolic disturbance? Name the mechanism relating to NAD⁺ availability specifically.
14. Distinguish the conventional (self-report) epidemiological findings from the genetic (Mendelian randomisation) findings on alcohol and coronary heart disease in the China Kadoorie Biobank study.
15. Why does Mendelian randomisation provide stronger evidence than self-reported drinking studies for whether moderate alcohol intake is protective against cardiovascular disease?
16. According to the GBD 2016 study, what is the shape of the relative-risk curve for alcohol against standard drinks/day, and what does this imply about “safe” moderate drinking?
17. Give three explanations for why earlier research (e.g. the French paradox) appeared to show a protective effect of moderate drinking that more recent research has not confirmed.
18. Why is red wine’s resveratrol content unlikely to provide a meaningful health benefit in practice?
19. What cancer types contributed the most alcohol-attributable cases globally in 2020, and which drinking category (moderate/risky/heavy) contributed the largest share of cases?
20. Why does the WHO classify alcohol in the same carcinogen risk group as asbestos and tobacco, and what proportion of alcohol-attributable cancers in the WHO European Region are due to light/moderate drinking?
21. State the current NZ recommended intakes to (a) reduce long-term health risk and (b) reduce injury risk, for both men and women.
22. What is the recommended level of alcohol consumption during pregnancy, and why?
23. Give three reasons why alcohol is considered more dangerous for young people than for adults, even past the legal drinking age.
24. Close the note. From memory, write out the full alcohol metabolism pathway from ethanol to Acetyl CoA, including enzymes, cofactor changes, and the two possible fates of Acetyl CoA, then check against Metabolism of alcohol.

Answers

Reveal answers

1. Alcohol is not required in the diet and has no essential physiological function (not a macro- or micronutrient), even though it does supply energy.
2. 29 kJ/gram, compared with 17 kJ/g for protein and carbohydrate, and 37 kJ/g for fat.
3. $C_2{H}_{5}OH$.
4. 20% absorbed in the stomach, 80% in the small intestine; food in the stomach slows stomach absorption.
5. 10 grams.
6. Alcohol dehydrogenase (ADH; occurs in stomach, liver, pancreas, brain — major pathway, ADH is rate-limiting), microsomal ethanol-oxidising system (MEOS; activated in long-term heavy drinkers), and catalase (in the presence of hydrogen peroxide; <2% of metabolism).
7. About 5–10 grams per hour, because ADH is the rate-limiting enzyme and cannot be sped up by drinking more.
8. Ethanol → (alcohol dehydrogenase; NAD⁺ → NADH + H⁺) → Acetaldehyde → (acetaldehyde dehydrogenase; NAD⁺ → NADH + H⁺) → Acetate → (+ CoA) → Acetyl CoA.
9. High NADH levels (produced during alcohol metabolism) block Acetyl CoA from entering the TCA cycle, so it is instead diverted to fatty acid synthesis and stored as triglyceride.
10. Smaller livers, lower percentage of total body water, less stomach ADH, and higher absorption in women compared to men.
11. They carry a different variant of ADH, leading to a build-up of acetaldehyde, which causes flushing and headaches.
12. This is the “dangerous state” (BAC 0.08–0.15 g/dL). The legal driving limit (0.05 g/dL) is below this range, within the “risky state” band (0.05–0.08 g/dL).
13. (1) Toxic effects of acetaldehyde on liver, GIT, brain and pancreas, leading long-term to cirrhosis and cancers; (2) elevated NADH:NAD⁺ ratio, which makes NAD⁺ unavailable for gluconeogenesis, the TCA cycle and the electron transport chain, causes H⁺ accumulation affecting acid-base balance, increases lipid synthesis (fatty liver) and inhibits fatty acid oxidation (raised triglycerides); (3) induced metabolic tolerance via MEOS, which produces toxic metabolites.
14. Conventional (self-report) analyses showed a U-shaped association, with lowest cardiovascular risk at moderate self-reported intake. Genetic (Mendelian randomisation) analyses, using genotype-predicted intake, showed no U-shape — risk rose steadily and near-linearly across the full range of intake, with no protective dip at moderate levels.
15. Because self-reported drinking is confounded by lifestyle and health factors (e.g. moderate drinkers tend to be healthier for other reasons), whereas genotype is fixed at birth and unrelated to those confounders, so Mendelian randomisation isolates the causal effect of alcohol itself.
16. Relative risk rises steadily from near 1.0 at zero drinks to about 3.0 at 15 drinks/day, with no dip at low intake — implying there is no “safe” moderate level; risk increases continuously with any amount consumed.
17. Light/moderate drinkers in earlier studies tended to be better educated, wealthier, more physically active, better insured and had better diets (confounding); the French additionally walked more and ate more healthily; many of the original studies showing benefit were low-level-of-evidence studies.
18. Red wine contains only 0.4–2 mg of resveratrol per litre, while a single supplement pill contains 250–1,600 mg — a person would need to drink 833 to 5,333 glasses of wine to match one supplement dose.
19. Cancers of the oesophagus, liver and breast contributed the most cases; heavy drinking contributed the largest share of alcohol-attributable cancer cases (46.7%), followed by risky drinking (39.4%).
20. Alcohol is classified as a Group 1 carcinogen because it causes cancer through biological mechanisms as ethanol breaks down in the body, regardless of beverage type, price or quality; about half of alcohol-attributable cancers in the WHO European Region are due to light/moderate drinking.
21. To reduce long-term health risk: no more than 2 standard drinks/day for women (max 10/week) and 3/day for men (max 15/week), with at least 2 alcohol-free days/week. To reduce injury risk: no more than 4 standard drinks (women) or 5 (men) on any single occasion.
22. No alcohol — 0 standard drinks — because there is no known safe level of alcohol use at any stage of pregnancy.
23. Smaller body size/bulk (even after reaching adult height) produces a higher BAC per drink; a higher head-to-body ratio affects intoxication; alcohol reaches the brain within 5 minutes and a relatively larger share ends up in young people’s brains, increasing poisoning risk; the adolescent brain continues complex rewiring until at least age 25.
24. See Metabolism of alcohol for the full pathway to self-check against.