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The long-term effects of alcohol consumption on health are predominantly detrimental, with the severity and range of harms generally increasing with the cumulative amount of alcohol consumed over a lifetime. The extent of these effects varies depending on several factors, including the quantity and frequency of alcohol intake, as well as individual genetic and lifestyle factors. Alcohol is recognized as a direct cause of several diseases, including cancer. The International Agency for Research on Cancer (IARC) classifies alcohol as a Group 1 carcinogen, meaning it is capable of causing cancer in humans. Research shows a causal link between alcohol consumption and at least seven types of cancer, including cancers of the oropharynx (mouth and throat), esophagus, liver, colorectum, and female breast. The risk begins with any level of consumption and goes up with higher intake—even light or moderate drinking adds to the risk. No level of alcohol consumption has been identified as completely safe in terms of cancer risk. The biological mechanisms include the damage caused by acetaldehyde, a toxic byproduct of alcohol metabolism, which can alter DNA, and the generation of oxidative stress.
Beyond cancer, chronic and excessive alcohol use—as seen in alcohol use disorder—is capable of damaging nearly every part of the body.
Such use is linked to alcoholic liver disease, which can progress to cirrhosis and chronic pancreatitis; various forms of cardiovascular disease, including hypertension, coronary heart disease, heart failure, and atrial fibrillation; and digestive conditions such as gastritis and . Alcohol also interferes with how the body absorbs nutrients, which can lead to malnutrition. Long-term use can cause alcohol-related dementia and damage to the peripheral nervous system, leading to conditions like painful peripheral neuropathy. Drinkers are also more likely to get injured in accidents, including traffic accidents and falls, and may age faster.Children and fetuses are especially at risk. Alcohol consumption during pregnancy can result in fetal alcohol spectrum disorders (FASDs), a range of lifelong physical, behavioral, and intellectual disabilities. In response to these risks, some countries now require alcohol packaging warning messages that mention cancer risks and pregnancy dangers.
Although some studies have proposed potential health benefits of light alcohol consumption—such as reduced risk of cardiovascular disease, type 2 diabetes, gastritis, and cholelithiasis— experts, including the World Health Organization (WHO), have questioned the validity of these studies, and say these possible benefits are small and uncertain when weighed against the well-known risks, especially cancer. While alcohol may provide short term effects of temporary stress reduction, mood elevation, or increased sociability, experts emphasize that, in the long run, the significant and cumulative health consequences of alcohol use outweigh these perceived psychosocial benefits.
]] The level of ethanol consumption that minimizes the risk of disease, injury, and death is subject to some controversy. Several studies have found a J-shaped relationship between alcohol consumption and health, meaning that risk is minimized at a certain (non-zero) consumption level, and drinking below or above this level increases risk, with the risk level of drinking a large amount of alcohol greater than the risk level of abstinence. Other studies have found a dose-response relationship, with lifetime abstention from alcohol being the optimal strategy and more consumption incurring more risk. The studies use different data sets and statistical techniques so they cannot be directly compared. Some older studies included former and occasional drinkers in the "abstainers" category, which obscures the benefits of lifetime abstention as former drinkers often are in poor health. However, the J-curve was reconfirmed by studies that took the mentioned confounders into account. Nonetheless, some authors remain suspicious that the apparent health benefits of light alcohol use are in large part due to various Selection bias and competing risks. Mendelian randomization studies have been inconsistent regarding the risk curve, with three studies finding linear dose-response risks overall and two studies finding a J-shape for lipid profiles. The variance in alcohol consumption that is explained by genetics is small, requiring large sample sizes and potentially violating assumptions of the analysis.
As one reviewer noted, "Despite the wealth of observational data, it is not absolutely clear that alcohol reduces risk, because no randomized controlled trials have been performed." The National Institute on Alcohol Abuse and Alcoholism (NIAAA) announced a randomized controlled trial in 2017, but the National Institutes of Health (NIH) cancelled it in 2018 due to irregular interactions by the program staff with the alcohol industry. A trial in Spain is expected to complete in 2028.
In 2013, Norwegian psychiatrist Hans Olav Fekjær compared the situation to those of hormone replacement therapy (HRT), vitamin E, and β-carotene; similarly to alcohol, observational studies for each of these treatments showed significantly reduced risk of coronary heart disease, but initial randomized trials of these treatments failed to replicate the effect. For HRT, pooling multiple randomized control trials and stratifying the data by age and time since menopause showed the benefits were limited to treatment soon after menopause. For vitamin E, trials have shown that the benefits are limited to certain populations such as those with diabetes and a specific genotype. For β-carotene, the randomized trials have shown that β-carotene increases cardiovascular disease risk when supplemented, with all beneficial effects due to other vitamins in foods providing β-carotene.
In light of the conflicting evidence, many have cautioned against recommendations for the use of alcohol for health benefits. At a symposium in 1997, Dr. Peter Anderson of the World Health Organization (WHO) labeled such alcohol promotion as "ridiculous and dangerous". It has been argued that the health benefits from alcohol have been exaggerated by the alcohol industry, with industry participation in the wording of messages and warnings. The debate is not purely scientific, with groups such as the International Scientific Forum on Alcohol Research (ISFAR) critiquing anti-alcohol studies as distorting the evidence, scientists in turn accusing these groups of bias due to industry funding, and members of the groups responding that these are false and misleading assertions. Studies with industry funding find less risk of stroke, and industry-linked systematic reviews consistently find cardioprotective effects, compared to reviews with no associations being 54% positive.
Considered as a treatment for cardiovascular disease, alcohol is addictive, has greater risk of adverse effects, and is less effective than other interventions such as heart medications, exercise, or good nutrition.
Globally, assuming the J-shaped curve is correct, the age-standardised, both-sexes consumption that minimizes risk is about 5 grams of ethanol per day, and an average individual would cause themselves harm by drinking more than 17 grams per day. However, the average intake among current drinkers in 2016 was approximately 40 grams of ethanol per day. 1.03 billion males (35.1% of the male population aged ≥15 years, ~2/3 of male drinkers) and 312 million females (10.5% of the female population aged ≥15 years, ~1/3 of female drinkers) consumed harmful amounts of alcohol. The proportion of the population consuming harmful amounts of alcohol has stayed at approximately the same level over the past three decades.
Estimates of the worldwide number of deaths per year caused by alcohol vary. The 2016 Global Burden of Disease (GBD) study estimated 2.8 million, while the 2020 GBD study estimated 1.78 million. The WHO estimates 3 million deaths per year from harmful use of alcohol, representing 5.3% of all deaths across the globe. All of these numbers are net deaths, subtracting deaths prevented from deaths caused. Professor Tim Stockwell, former director of the Canadian Institute for Substance Use Research argues that alcohol may not prevent any deaths and guesses that as many as 6 million deaths may be caused by alcohol. Besides this, the WHO attributes 5.1% of the global burden of disease and injury to alcohol, as measured in disability-adjusted life years (DALYs). The WHO does not list alcohol in its 2019 list of the top 20 leading causes of DALYs, but alcohol use disorder (AUD) would rank around #39, combining AUD with alcohol-related cirrhosis and liver cancer would rank between malaria (#19) and refractive errors (#20), and all alcohol-attributed DALYs would rank between stroke (#3) and lower respiratory infections (#4). Similarly the number of alcohol-attributed deaths would rank between chronic obstructive pulmonary disease (#3) and lower respiratory infections (#4).
Research of Western cultures has consistently shown increased survival associated with light to moderate alcohol consumption.Di Castelnuovo A, Costanzo S, Bagnardi V, Donati MB, Iacoviello L, de Gaetano G. Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies. Arch Intern Med. 2006 Dec 11–25;166(22) 2437-45. Australasia and Europe are also the locations with the highest levels of harmful alcohol consumption. Researchers have investigated cultures with different alcohol consumption norms and found conflicting results.
The risks of alcohol consumption are age-dependent. Risk is greatest among males aged 15–39 years, due to binge drinking which may result in violence or traffic accidents. It is less risky and potentially more beneficial for an older individual to consume a given amount of alcohol, compared to a similar younger individual, as they are less likely to develop cancer during their remaining lifespan, less likely to be involved in accidents, and more likely to benefit from alcohol's cardiovascular effects. Taking the lower bound of the confidence intervals, the GBD 2020 study suggests that people do not need to drink until age 25, and in many regions, the study did not find any significant benefit for drinking over abstinence even as late as ages 45 or 60. Other studies have found similar patterns.
A UK report came to the result that the effects of low-to-moderate alcohol consumption on mortality are age-dependent. Low-to-moderate alcohol use increases the risk of death for individuals aged 16–34 (due to increased risk of cancers, accidents, liver disease, and other factors), but decreases the risk of death for individuals ages 55+ (due to decreased risk of ischemic heart disease).
A study in the United Kingdom found that alcohol causes about 4% of cancer cases in the UK (12,500 cases per year).
Frequent drinking of alcoholic beverages is a major contributing factor in cases of elevated blood levels of .
Alcohol can cause neurotoxicity, Wernicke's encephalopathy and alcoholic Korsakoff syndrome which frequently occur simultaneously, known as Wernicke–Korsakoff syndrome. Brain lesion, or brain abnormalities, are typically located in the diencephalon which result in anterograde and retrograde amnesia, or memory loss.
Wernicke–Korsakoff syndrome is a manifestation of thiamine deficiency, usually as a secondary effect of alcohol misuse. The syndrome is a combined manifestation of two eponymous disorders, Korsakoff's psychosis and Wernicke's encephalopathy. Wernicke's encephalopathy is the acute presentation of the syndrome and is characterised by a state while Korsakoff's psychosis main are amnesia and executive dysfunction. "", intravenous fluid containers containing vitamins and minerals (bright yellow due to the vitamins), can be used to mitigate these outcomes.
Ethanol is known to activate aminobutyric acid type A (GABAA) and inhibit N-methyl-D-aspartate (NMDA) glutamate receptors, which are both implicated in essential tremor pathology and could underlie the ameliorative effects. Additionally, the effects of ethanol have been studied in different animal essential tremor models. (For more details on this topic, see Essential tremor).
Social skills are significantly impaired in people that have alcoholism due to the neurotoxic effects of alcohol on the brain, especially the prefrontal cortex area of the brain. The social skills that are impaired by alcohol use disorder include impairments in perceiving facial emotions, prosody perception problems and theory of mind deficits; the ability to understand humor is also impaired in people with an alcohol use disorder.
Studies have shown that alcohol dependence relates directly to cravings and irritability. Another study has shown that alcohol use is a significant predisposing factor towards antisocial behavior in children. Depression, anxiety and panic disorder are disorders commonly reported by alcohol dependent people. Alcoholism is associated with dampened activation in brain networks responsible for emotional processing ( e.g. the amygdala and hippocampus). Evidence that the mental health disorders are often induced by alcohol misuse via distortion of brain neurochemistry is indicated by the improvement or disappearance of symptoms that occurs after prolonged abstinence, although problems may worsen in early withdrawal and recovery periods. Psychosis is secondary to several alcohol-related conditions including acute intoxication and withdrawal after significant exposure. Chronic alcohol misuse can cause psychotic type symptoms to develop, more so than with other illicit substances. Alcohol misuse has been shown to cause an 800% increased risk of psychotic disorders in men and a 300% increased risk of psychotic disorders in women which are not related to pre-existing psychiatric disorders. This is significantly higher than the increased risk of psychotic disorders seen from cannabis use making alcohol misuse a very significant cause of psychotic disorders. Approximately 3 percent of people who are alcohol dependent experience psychosis during acute intoxication or withdrawal. Alcohol-related psychosis may manifest itself through a kindling mechanism. The mechanism of alcohol-related psychosis is due to distortions to neuronal membranes, gene expression, as well as thiamin deficiency. It is possible in some cases that excessive alcohol use, via a kindling mechanism, can cause the development of a chronic substance-induced psychotic disorder, i.e., schizophrenia. The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as psychosocial impairments. However, moderate wine drinking has been shown to lower the risk for depression.
While ethanol initially helps social phobia or panic symptoms, with longer term alcohol misuse can often worsen social phobia symptoms and can cause panic disorder to develop or worsen, during alcohol intoxication and especially during the alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines, which are sometimes prescribed as tranquilizers to people with alcohol problems. Approximately half of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia have alcohol or benzodiazepine dependence. It was noted that every individual has an individual sensitivity level to alcohol or sedative hypnotic drugs and what one person can tolerate without ill health another will have very ill health and that even moderate drinking can cause rebound anxiety syndromes and sleep disorders. A person who is experiencing the toxic effects of alcohol will not benefit from other therapies or medications as they do not address the root cause of the symptoms.
Addiction to alcohol, as with any addictive substance tested so far, has been correlated with an enduring reduction in the expression of GLT1 (EAAT2) in the nucleus accumbens and is implicated in the drug-seeking behavior expressed nearly universally across all documented addiction syndromes. This long-term dysregulation of glutamate transmission is associated with an increase in vulnerability to both relapse-events after re-exposure to drug-use triggers as well as an overall increase in the likelihood of developing addiction to other reinforcing drugs. Drugs which help to re-stabilize the glutamate system such as N-acetylcysteine have been proposed for the treatment of addiction to cocaine, nicotine, and alcohol.
The effect on depression and returning to drinking among individuals with alcohol dependence has always been controversial. Studies show that after doing a study on men and women hospitalized for alcohol dependence the likelihood of returning to drinking with depression is extremely high. A diagnosis of major depression at entry into an inpatient treatment for alcohol dependence showed shorter times to first drink and also relapse in both women and men.
Alcohol use increases the risk of chronic gastritis (stomach inflammation);
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.
Alcoholic liver disease is a major public health problem. For example, in the United States up to two million people have alcohol-related liver disorders. Chronic heavy alcohol consumption can cause fatty liver, cirrhosis, and alcoholic hepatitis. Treatment options are limited and consist of most importantly discontinuing alcohol consumption. In cases of severe liver disease, the only treatment option may be a liver transplant from alcohol abstinent donors. Research is being conducted into the effectiveness of . Certain complementary medications, e.g., milk thistle and silymarin, appear to offer some benefit. Alcohol is a leading cause of liver cancer in the Western world, accounting for 32-45% of hepatic cancers. Up to half a million people in the United States develop alcohol-related liver cancer.
Alcohol consumption has frequently been associated with an increased risk of oral cancer in current literature. Studies have found that people that consume alcohol were two times more likely to develop oral cancer in comparison to people who did not. The mechanisms in which alcohol acts as a carcinogen within the oral cavity are currently not fully understood. It is thought to be a multifactorial disease which then gives rise to a cancerous lesion. Many theories have become apparent in research, including alcohol being responsible for high estrogen and androgen levels, specifically in women, which may facilitate the alcohol-related immunodeficiency and/or immunosuppression that causes carcinogenesis. Therefore, immediate cessation of the habit of alcohol consumption can aid in decreasing the risk of oral cancer.
Alcohol-based mouthwashes used to be very common and can still be purchased for use today. Correlation in the presence of alcohol in mouthwashes with development of oral and pharyngeal cancer is unknown due to lack of evidence. However, it has been suggested that acetaldehyde, the first metabolite of ethanol, plays a role in the carcinogenesis of alcohol in oral cancer. Acetaldehyde, has been found to increase when in the salivary medium after an alcoholic beverage has been consumed and could possibly occur with alcohol-based mouthwashes as well, posing as a possible risk factor for oral cancer. However, more research must be conducted regarding these theories.
Men's sexual behaviors can be affected dramatically by high alcohol consumption. Both chronic and acute alcohol consumption have been shown in most studies (but not all ) to inhibit testosterone production in the testes. This is believed to be caused by the metabolism of alcohol reducing the NAD+/NADH ratio both in the liver and the testes; since the synthesis of testosterone requires NAD+, this tends to reduce testosterone production.
Long term excessive intake of alcohol can lead to damage to the central nervous system and the peripheral nervous system resulting in loss of sexual desire and impotence in men. This is caused by reduction of testosterone from ethanol-induced testicular atrophy, resulting in increased feminisation of males and is a clinical feature of alcohol abusing males who have cirrhosis of the liver.
The way in which alcohol is consumed (i.e., with meals or binge drinking) affects various health outcomes. It may be the case that the risk of diabetes associated with heavy alcohol consumption is due to consumption mainly on the weekend as opposed to the same amount spread over a week. In the United Kingdom "advice on weekly consumption is avoided". A twenty-year twin study from Finland reported that moderate alcohol consumption may reduce the risk of type 2 diabetes in men and women. However, binge drinking and high alcohol consumption was found to increase the risk of type 2 diabetes in women.
The researchers noted that moderate alcohol consumption also reduces the risk of other inflammatory processes such as cardiovascular 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..."
A 2010 study concluded, "Nonlight beer intake is associated with an increased risk of developing psoriasis among women. Other alcoholic beverages did not increase the risk of psoriasis in this study."
Another study concluded, "Findings suggest that wine intake, especially red wine, may have a protective effect against common cold. Beer, spirits, and total alcohol intakes do not seem to affect the incidence of common cold."
It was estimated in 2006 that "3.6% of all cancer cases worldwide are related to alcohol drinking, resulting in 3.5% of all cancer deaths." A European study from 2011 found that one in 10 of all cancers in men and one in 33 in women were caused by past or current alcohol intake.BBC News Drinking over recommended limit 'raises cancer risk' 8 April 2011 The World Cancer Research Fund panel report Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective finds the evidence "convincing" that alcoholic drinks increase the risk of the following cancers: mouth, pharynx and larynx, oesophagus, colorectum (men), breast (pre- and postmenopause).WCRF World Cancer Research Fund / American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR, 2007
Even light and moderate alcohol consumption increases cancer risk in individuals, especially with respect to squamous cell carcinoma of the esophagus, oropharyngeal cancer, and breast cancer.
Acetaldehyde is the major metabolite when one drinks alcohol, produced in the liver, and it is known to be carcinogenic. Agents Classified by the IARC Monographs, Volumes 1–111 . monographs.iarc.fr It is suspected that this metabolite is the main reason alcohol promotes cancer. Typically the liver eliminates 99% of acetaldehyde produced. However, liver disease and certain genetic enzyme deficiencies result in high acetaldehyde levels. Heavy drinkers who are exposed to high acetaldehyde levels due to a genetic defect in alcohol dehydrogenase have been found to be at greater risk of developing cancers of the upper gastrointestinal tract and liver. A review in 2007 found "convincing evidence that acetaldehyde... is responsible for the carcinogenic effect of ethanol... owing to its multiple mutagenic effects on DNA." Acetaldehyde can react with DNA to create DNA adducts including the Cr-PdG adduct. This Cr-PdG adduct "is likely to play a central role in the mechanism of alcoholic beverage related carcinogenesis."
Children of alcoholics often incorporate behaviors learned as children into their marital relationships. These behaviors lead to poor parenting practices. For example, adult children of alcoholics may simultaneously express love and rejection toward a child or spouse. This is known as insecure attachment. Insecure attachment contributes to trust and bonding issues with intimate partners and offspring. In addition, prior parental emotional unavailability contributes to poor conflict resolution skills in adult relationships. Evidence shows a correlation between alcoholic fathers who display harsh and ineffective parenting practices with adolescent and adult alcohol dependence.
Children of alcoholics are often unable to trust other adults due to fear of abandonment. Further, because children learn their bonding behaviors from watching their parents' interactions, daughters of alcoholic fathers may be unable to interact appropriately with men when they reach adulthood. Poor behavior modeling by alcoholic parents contributes to inadequate understanding of how to engage in opposite gender interactions.
Sons of alcoholics are at risk for poor self-regulation that is often displayed in the preschool years. This leads to blaming others for behavioral problems and difficulties with impulse control. Poor decision-making correlates to early alcohol use, especially in sons of alcoholics. Sons often demonstrate thrill-seeking behavior, harm avoidance, and exhibit a low level of frustration tolerance.
Alcohol dependence has a far reaching impact on health outcomes. A study conducted in Germany in 2016 found the economic burden for those dependent on alcohol was 50% higher than those who were not. In the study, over half of the economic cost was due to lost productivity, and only 6% was due to alcohol treatment programs. The economic cost was mostly borne by individuals between 30 and 49 years old. In another study conducted with data from eight European countries, 77% of alcohol dependent patients had psychiatric and somatic co-morbidity, which in turn increased systematic healthcare and economic cost. Alcohol consumption can also affect the immune system and produce complications in people with HIV, pneumonia, and tuberculosis.
Indirect costs due to alcohol dependence are significant. The biggest indirect cost comes from lost productivity, followed by premature mortality. Men with alcohol dependence in the U.S. have lower labor force participation by 2.5%, lower earnings by 5.0%, and higher absenteeism by 0.5–1.2 days. Female binge drinkers have higher absenteeism by 0.4–0.9 days. Premature mortality is another large contributor to indirect costs of alcohol dependence. In 2004, 3.8% of global deaths were attributable to alcohol (6.3% for men and 1.1% for women). Those under 60 years old have much higher prevalence in global deaths attributable to alcohol at 5.3%.
In general, indirect costs such as premature mortality due to alcohol dependence, loss of productivity due to absenteeism and presenteeism, and cost of property damage and enforcement, far exceed the direct health care and law enforcement costs. Aggregating the economic cost from all sources, the impact can range from 0.45 to 5.44% of a country's gross domestic product (GDP). The wide range is due to inconsistency in measurement of economic burden, as researchers in some studies attributed possible positive effects from long term alcohol consumption.
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