Around 80% of Asian people (less common in Thailand, Laos and the Indian subcontinent) have a variant of the gene coding for the enzyme alcohol dehydrogenase called "ADH1B", whereas almost all Japanese, Korean and Chinese people have a variant of the gene called "ADH1C", both resulting in an alcohol dehydrogenase enzyme that converts alcohol to toxic acetaldehyde at a much higher efficiency than other gene variants (40- to 100-fold in case of ADH1B).

In about 50% of Asians, the increased acetaldehyde accumulation is worsened by another gene variant, the mitochondrial ALDH2 allele, which results in a less functional acetaldehyde dehydrogenase enzyme, responsible for the breakdown of acetaldehyde. The result is that affected people may be better at metabolizing alcohol, often not feeling the alcohol "buzz" to the same extent as others, but show far more acetaldehyde-based side effects while drinking.

Since the mutation is a genetic issue, there is currently no cure for the flush reaction. Clinicians and the East Asian public generally know about the alcohol flushing response. Prevention would include not drinking alcohol.

Having a particular genetic variant (A-allele of ADH1B rs1229984) is associated with non-drinking and lower alcohol consumption. This variant is also associated with favorable cardiovascular profile and a reduced risk of coronary heart disease compared to those without the genetic variant, but it is unknown whether this may be caused by differences in alcohol consumption or by additional confounding effects of the genetic variant itself.

Regular consumption of alcohol is associated with an increased risk of gouty arthritis and a decreased risk of rheumatoid arthritis. Two recent studies report that the more alcohol consumed, the lower the risk of developing rheumatoid arthritis. Among those who drank regularly, the one-quarter who drank the most were up to 50% less likely to develop the disease compared to the half who drank the least.

The researchers noted that moderate alcohol consumption also reduces the risk of other inflammatory processes such as cardiovascualar disease. Some of the biological mechanisms by which ethanol reduces the risk of destructive arthritis and prevents the loss of bone mineral density (BMD), which is part of the disease process.

A study concluded, "Alcohol either protects from RA or, subjects with RA curtail their drinking after the manifestation of RA". Another study found, "Postmenopausal women who averaged more than 14 alcoholic drinks per week had a reduced risk of rheumatoid arthritis..."

Research has found that drinking reduces the risk of developing gallstones. Compared with alcohol abstainers, the relative risk of gallstone disease, controlling for age, sex, education, smoking, and body mass index, is 0.83 for occasional and regular moderate drinkers (< 25 ml of ethanol per day), 0.67 for intermediate drinkers (25-50 ml per day), and 0.58 for heavy drinkers. This inverse association was consistent across strata of age, sex, and body mass index." Frequency of drinking also appears to be a factor. "An increase in frequency of alcohol consumption also was related to decreased risk. Combining the reports of quantity and frequency of alcohol intake, a consumption pattern that reflected frequent intake (5-7 days/week) of any given amount of alcohol was associated with a decreased risk, as compared with nondrinkers. In contrast, infrequent alcohol intake (1-2 days/week) showed no significant association with risk."

A large self-reported study published in 1998 found no correlation between gallbladder disease and multiple factors including smoking, alcohol consumption, hypertension, and coffee consumption. A retrospective study from 1997 found vitamin C (ascorbic acid) supplement use in drinkers was associated with a lower prevalence of gallbladder disease, but this association was not seen in non-drinkers.

While little detailed genetic research has been done, it has been shown that alcoholism tends to run in families with possible involvement of differences in alcohol metabolism and the genotype of alcohol-metabolizing enzymes.

Research has shown that moderate levels of alcohol consumed with meals does not have a substantial impact on blood sugar levels. A 2005 study presented to the American Diabetes Association suggest that moderate consumption may lower the risk of developing Type 2 diabetes.

The tolerance to alcohol is not equally distributed throughout the world's population, and genetics of alcohol dehydrogenase indicate resistance has arisen independently in different cultures. In North America, Native Americans have the highest probability of developing alcoholism compared to Europeans and Asians.

Higher body masses and the prevalence of high levels of alcohol dehydrogenase in an individual increase alcohol tolerance.

Not all differences in tolerance can be traced to biochemistry. Differences in tolerance levels are also influenced by socio-economic and cultural difference including diet, average body weight and patterns of consumption.

An estimated one out of twenty people have an alcohol flush reaction. It is not in any way an indicator for the drunkenness of an individual. It is colloquially known as "face flush", a condition where the body metabolizes alcohol nearly 100-times less efficiently into acetaldehyde, a toxic metabolite. Flushing, or blushing, is associated with the erythema (reddening caused by dilation of capillaries) of the face, neck, and shoulder, after consumption of alcohol.

The International Agency for Research on Cancer of the World Health Organization has classified alcohol as a Group 1 carcinogen.

Alcohol-induced respiratory reactions, also termed alcohol-induced asthma and alcohol-induced respiratory symptoms, are increasingly recognized as a pathological bronchoconstriction response to the consumption of alcohol that afflicts many people with a "classical" form of asthma, the airway constriction disease evoked by the inhalation of allergens. Alcohol-induced respiratory reactions reflect the operation of different and often racially related mechanisms that differ from those of classical, allergen-induced asthma.

Direct alcohol tolerance is largely dependent on body size. Large-bodied people will require more alcohol to reach insobriety than lightly built people. Thus men, being larger than women on average, will have a higher alcohol tolerance. The alcohol tolerance is also connected with activity of "alcohol dehydrogenases" (a group of enzymes responsible for the breakdown of alcohol) in the liver, and in the bloodstream.

High level of alcohol dehydrogenase activity results in fast transformation of ethanol to more toxic acetaldehyde. Such atypical alcohol dehydrogenase levels are less frequent in alcoholics than in nonalcoholics and, alongside other symptoms, can indicate various forms of liver disease. Furthermore, among alcoholics, the carriers of this atypical enzyme consume lower ethanol doses, compared to the individuals without the allele.

Conditions of fatigue correlate positively with increased alcohol consumption.

In 1973, Breslin et al. tested the effects of alcoholic beverage consumption on the respiratory symptoms of 11 asthmatic subjects who gave a history of asthma attacks following certain alcoholic beverages. In response to ingesting the type of beverage that the subjects reported to provoke their symptoms, six developed the asthmatic symptom of chest tightness, two developed a symptom often associated with asthma, rhinitis, and one subject developed both chest tightness and rhinitis. Symptoms developed almost immediately after ingestion, inhalation of fumes from the beverages did not precipitate symptoms, and bronchoconstriction in response to the ingestion was confirmed in the three patients evaluated by pulmonary function tests. The study suggested that these reactions were induced by non-alcoholic allergens that were contained in or contaminated the beverages. In 1978 a non-asthmatic female of Japanese descent with a history of moderately severe bronchoconstriction responses to various alcoholic beverages and in 1981 an asthmatic Japanese male with a similar history beer or 95% pure ethanol were studied and found to develop bronchoconstriction after drinking apple juice but not after drinking apple juice per se; intravenous infusion or inhalation of ethanol also caused bronchospasm responses in the male subject. These studies suggested that alcohol itself caused the asthmatic symptoms triggered by alcoholic beverages. A subsequent study in 1986 found that 9 of 18 patients with a history of red wine-induced asthma symptoms showed bronchoconstriction in response to ingesting red wine; the response correlated positively with the amount of sulfur dioxide contained in the provocative wine. The study suggested that the reaction was not allergen-induced but rather triggered by sulfur dioxide, a sulfur dioxide-related agent, or an agent whose levels in alcohol beverages correlated positively with those of sulfur dioxide. Finally, a questionnaire survey of 366 asthmatic patients conducted in 2000 found that 33% reported asthma symptoms in response to alcoholic beverages; there was a significant association between wine-induced asthma and asthma triggered by sulfite-containing foods, by aspirin, and by nonsteroidal anti-inflammatory drugs (NSAID) other than aspirin. The study suggested the salicylate-"contaminates" in wine may contribute to these responses. In other studies, D.P. Agarwal and colleagues associated race-based variations in the activity alcohol-metabolizing enzymes with the occurrence of alcohol flush reactions to alcohol and alcoholic beverages in certain Asian populations. This early work is the basis for further studies that have defined not only many alcohol-induced flush reactions but also many alcohol-induced respiratory reactions as due to racially associated genetic differences in alcohol-metabolizing enzymes.

Many wines contain a warning label about sulfites, and some people believe that sulfites are the cause of RWH and other allergic and pseudoallergic reactions. However, this may not be the case. Dried fruit and processed foods like lunch meat have more sulfites than red wine. Reactions to sulfites are not considered a "true allergy" and reactions more commonly occur in persons with asthma and may manifest themselves in difficulty breathing or skin reactions, rather than headache. It is unclear if consuming alcohol in combination with sulfites may have a different effect.

Some wines may be exempt from including a sulfite warning. Wines that have under 10mg/l of sulfites do not need to be labeled that they contain sulfites. This includes added and natural sulfites, like sulfites that come from the soil, or those produced by yeasts during alcoholic fermentation. Wines labeled "100% Organic", "Organic", "Made With Organic Grapes", "Made With Organic and Non-Organic Grapes" or without organic certification may contain sulfites, and must disclose this on the label. This also means that the so called "Natural" wine can also contain sulfites. Different rules might apply in different continents.

Tyramine may well be a major player in RWH syndrome. Tyramine is an amine that is produced naturally from the breakdown of protein as food ages. More specifically it is formed by the decarboxylation of the amino acid tyrosine. It is found in aged, fermented, and spoiled foods. Everyday foods we consume including aged cheeses, overripe and dried fruit, sauerkraut, soy, and many processed foods contain high levels of tyramine. Tyramine is suspected of inducing migraine headaches in about 40% of migraine sufferers, according to F.G.Freitag of Diamond Headache Clinic in Chicago.

Moderate alcohol consumption 30–60 minutes before sleep, although decreasing, disrupts sleep architecture. Rebound effects occur once the alcohol has been largely metabolized, causing late night disruptions in sleep maintenance. Under conditions of moderate alcohol consumption where blood alcohol levels average 0.06–0.08 percent and decrease 0.01–0.02 percent per hour, an alcohol clearance rate of 4–5 hours would coincide with disruptions in sleep maintenance in the second half of an 8-hour sleep episode. In terms of sleep architecture, moderate doses of alcohol facilitate "rebounds" in rapid eye movement (REM) following suppression in REM and stage 1 sleep in the first half of an 8-hour sleep episode, REM and stage 1 sleep increase well beyond baseline in the second half. Moderate doses of alcohol also very quickly increase slow wave sleep (SWS) in the first half of an 8-hour sleep episode. Enhancements in REM sleep and SWS following moderate alcohol consumption are mediated by reductions in glutamatergic activity by adenosine in the central nervous system. In addition, tolerance to changes in sleep maintenance and sleep architecture develops within 3 days of alcohol consumption before bedtime.

A few studies have indicated an increased risk of neuroblastoma with use of alcohol during pregnancy.

Extensive epidemiological studies have demonstrated the cardioprotective effect of alcohol consumption. However the mechanism by which this occurs is not fully understood. Research has suggested several possible mechanisms, including the following.

There is a lack of medical consensus about whether moderate consumption of beer, wine, or distilled spirits has a stronger association with heart disease. Studies suggest that each is effective, with none having a clear advantage. Most researchers now believe that the most important ingredient is the alcohol itself.

The American Heart Association has reported that "More than a dozen prospective studies have demonstrated a consistent, strong, dose-response relation between increasing alcohol consumption and decreasing incidence of CHD (coronary heart disease). The data are similar in men and women in a number of different geographic and ethnic groups. Consumption of one or two drinks per day is associated with a reduction in risk of approximately 30% to 50%".

Heart disease is the largest cause of mortality in the United States and many other countries. Therefore, some physicians have suggested that patients be informed of the potential health benefits of drinking alcohol in moderation, especially if they abstain and alcohol is not contraindicated. Others, however, argue against the practice in fear that it might lead to heavy or abusive alcohol consumption. Heavy drinking is associated with a number of health and safety problems.

Alcohol consumption at any quantity is a risk factor for cancers of the mouth, esophagus, pharynx and larynx. The U.S. National Cancer Institute states "Drinking alcohol increases the risk of cancers of the mouth, esophagus, pharynx, larynx, and liver in men and women, … In general, risks increases above baseline with any alcohol intake (mild; <2 glass of wine per week) and increases significantly with moderate alcohol intake (one glass of wine per day) with highest risk in those with greater than 7 glasses of wine per week. (A drink is defined as 12 ounces of regular beer, 5 ounces of wine, or 1.5 ounces of 80-proof liquor.) … Also, using alcohol with tobacco is riskier than using either one alone, because it further increases the chances of getting cancers of the mouth, throat, and esophagus." The federal government’s Dietary Guidelines for Americans 2010 defines moderate alcohol drinking as up to one drink per day for women and up to two drinks per day for men. Heavy alcohol drinking is defined as having more than three drinks on any day or more than seven drinks per week for women and more than four drinks on any day or more than 14 drinks per week for men.

The International Head and Neck Cancer Epidemiology (INHANCE) Consortium co-ordinated a meta-study on the issue. A study looking at laryngeal cancer and beverage type concluded, "This study thus indicates that in the Italian population characterized by frequent wine consumption, wine is the beverage most strongly related to the risk of laryngeal cancer."

A review of the epidemiological literature published from 1966 to 2006 concluded that:

- The risk of esophageal cancer nearly doubled in the first two years following alcohol cessation, a sharp increase that may be due to the fact that some people only stop drinking when they are already experiencing disease symptoms. However, risk then decreased rapidly and significantly after longer periods of abstention.

- Risk of head and neck cancer only reduced significantly after 10 years of cessation.

- After more than 20 years of alcohol cessation, the risks for both cancers were similar to those seen in people who never drank alcohol.

A study concluded that for every additional drink regularly consumed per day, the incidence of oral cavity and pharynx cancers increases by 1 per 1000. The incidence of cancers of the esophagus and larynx increase by 0.7 per 1000.

A 2008 study suggests that acetaldehyde (a breakdown product of alcohol) is implicated in oral cancer.

A complex mixture of genetic and environmental factors influences the risk of the development of alcoholism. Genes that influence the metabolism of alcohol also influence the risk of alcoholism, and may be indicated by a family history of alcoholism. One paper has found that alcohol use at an early age may influence the expression of genes which increase the risk of alcohol dependence. Individuals who have a genetic disposition to alcoholism are also more likely to begin drinking at an earlier age than average. Also, a younger age of onset of drinking is associated with an increased risk of the development of alcoholism, and about 40 percent of alcoholics will drink excessively by their late adolescence. It is not entirely clear whether this association is causal, and some researchers have been known to disagree with this view.

Severe childhood trauma is also associated with a general increase in the risk of drug dependency. Lack of peer and family support is associated with an increased risk of alcoholism developing. Genetics and adolescence are associated with an increased sensitivity to the neurotoxic effects of chronic alcohol abuse. Cortical degeneration due to the neurotoxic effects increases impulsive behaviour, which may contribute to the development, persistence and severity of alcohol use disorders. There is evidence that with abstinence, there is a reversal of at least some of the alcohol induced central nervous system damage. The use of cannabis was associated with later problems with alcohol use. Alcohol use was associated with an increased probability of later use of tobacco, cannabis, and other illegal drugs.

Based on combined data from SAMHSA's 2004–2005 National Surveys on Drug Use & Health, the rate of past-year alcohol dependence or abuse among persons aged 12 or older varied by level of alcohol use: 44.7% of past month heavy drinkers, 18.5% binge drinkers, 3.8% past month non-binge drinkers, and 1.3% of those who did not drink alcohol in the past month met the criteria for alcohol dependence or abuse in the past year. Males had higher rates than females for all measures of drinking in the past month: any alcohol use (57.5% vs. 45%), binge drinking (30.8% vs. 15.1%), and heavy alcohol use (10.5% vs. 3.3%), and males were twice as likely as females to have met the criteria for alcohol dependence or abuse in the past year (10.5% vs. 5.1%).

An alcohol enema is a faster method of alcohol intoxication since the alcohol is absorbed directly into the bloodstream. The lower gastrointestinal tract lacks the alcohol dehydrogenase enzyme present in the stomach and liver that breaks down ethanol into acetylaldehyde, which is actually more toxic than ethanol (drinking alcohol) and is responsible for most chronic effects of ethanol. When rectally absorbed, ethanol will still eventually arrive at the liver, but the high alcohol content could overwhelm the organ. Additionally, consuming the alcohol rectally neutralizes the body's ability to reject the toxin by vomiting.

Two reported alcohol enema techniques are via an alcohol-soaked tampon or a funnel, such as a beer bong, inserted into the rectum.

When exposure to toluene occurs there is usually simultaneous exposure to several other chemicals. Often toluene exposure occurs in conjunction with benzene and since they are to some degree metabolised by the same enzymes, the relative concentrations will determine their rate of elimination. Of course the longer it takes for toluene to be eliminated the more harm it is likely to do.

The smoking and drinking habits of those exposed to toluene will partially determine the elimination of toluene. Studies have shown that even a modest amount of acute ethanol consumption can significantly decrease the distribution or elimination of toluene from the blood resulting in increased tissue exposure. Other studies have shown that chronic ethanol consumption can enhance toluene metabolism via the induction of CYP2E1. Smoking has been shown to enhance the elimination rate of toluene from the body, perhaps as a result of enzyme induction.

The diet can also influence toluene elimination. Both a low-carbohydrate diet and fasting have been shown to induce CYP2E1 and as a result increase toluene metabolism. A low protein diet may decrease total CYP content and thereby reduce the elimination rate of the drug.

Alcohol abuse is said to be most common in people aged between 15 and 24 years, according to Moreira 2009. However, this particular study of 7275 college students in England collected no comparative data from other age groups or countries.

Causes of alcohol abuse are complex and are likely the combination of many factors, from coping with stress to childhood development. The US Department of Health & Human Services identifies several factors influencing adolescent alcohol use, such as risk-taking, expectancies, sensitivity and tolerance, personality and psychiatric comorbidity, hereditary factors, and environmental aspects. Studies show that child maltreatment such as neglect, physical, and/or sexual abuse, as well as having parents with alcohol abuse problems, increases the likelihood of that child developing alcohol use disorders later in life. According to Shin, Edwards, Heeren, & Amodeo (2009), underage drinking is more prevalent among teens that experienced multiple types of childhood maltreatment regardless of parental alcohol abuse, putting them at a greater risk for alcohol use disorders. Genetic and environmental factors play a role in the development of alcohol use disorders, depending on age. The influence of genetic risk factors in developing alcohol use disorders increase with age ranging from 28% in adolescence and 58% in adults.