Long-term effects of alcohol#Cardiovascular system

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The level of ethanol consumption that minimizes the risk of disease, injury, and death is subject to some controversy.{{cite journal |last1=Tsai |first1=MK |last2=Gao |first2=W |last3=Wen |first3=CP |title=The relationship between alcohol consumption and health: J-shaped or less is more? |journal=BMC Medicine |date=3 July 2023 |volume=21 |issue=1 |pages=228 |doi=10.1186/s12916-023-02911-w |pmid=37400823 |pmc=10318728 |doi-access=free }} Several studies have found a J-shaped relationship between alcohol consumption and health,{{Cite journal|last1=Di Castelnuovo|first1=A.|last2=Costanzo|first2=S.|last3=Bagnardi|first3=V.|last4=Donati|first4=MB.|last5=Iacoviello|first5=L.|last6=de Gaetano|first6=G.|title=Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies|journal=Arch Intern Med|volume=166|issue=22|pages=2437–45|doi=10.1001/archinte.166.22.2437|pmid=17159008|year=2006}}{{cite journal |vauthors=Stockwell T, Zhao J, Panwar S, Roemer A, Naimi T, Chikritzhs T |title=Do "Moderate" Drinkers Have Reduced Mortality Risk? A Systematic Review and Meta-Analysis of Alcohol Consumption and All-Cause Mortality |journal=J Stud Alcohol Drugs |volume=77 |issue=2 |pages=185–198 |date=2016 |pmid=26997174 |pmc=4803651 |doi= 10.15288/jsad.2016.77.185}}{{cite journal |last1=Tian |first1=Y |last2=Liu |first2=J |last3=Zhao |first3=Y |last4=Jiang |first4=N |last5=Liu |first5=X |last6=Zhao |first6=G |last7=Wang |first7=X |title=Alcohol consumption and all-cause and cause-specific mortality among US adults: prospective cohort study. |journal=BMC Medicine |date=7 June 2023 |volume=21 |issue=1 |pages=208 |doi=10.1186/s12916-023-02907-6 |pmid=37286970 |pmc=10249162 |doi-access=free }} 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.{{cite journal |vauthors=((GBD 2016 Alcohol Collaboration)) |title=Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016 |journal=The Lancet |date=September 2018 |volume=392 |issue=10152 |pages=1015–1035 |doi=10.1016/S0140-6736(18)31310-2|pmid=30146330 |pmc=6148333}} The studies use different data sets and statistical techniques so 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.{{cite journal |last1=O'Keefe |first1=JH |last2=Bhatti |first2=SK|last3=Bajwa|first3=A|last4=DiNicolantonio|first4=JJ|last5=Lavie|first5=CJ|title=Alcohol and cardiovascular health: the dose makes the poison...or the remedy.|journal=Mayo Clinic Proceedings|date=March 2014|volume=89|issue=3|pages=382–393|pmid=24582196|doi=10.1016/j.mayocp.2013.11.005|doi-access=free}} However, the J-curve was reconfirmed by studies that took the mentioned confounders into account.{{cite journal |author1=Klatsky Arthur L. |author2=Udaltsova Natalia | year = 2007 | title = Alcohol Drinking and Total Mortality Risk | journal = Ann Epidemiol | volume = 17 | issue = 5| page = 555 |doi=10.1016/j.annepidem.2007.01.014 }}{{Cite journal|last1=Lee|first1=SJ.|last2=Sudore|first2=RL.|last3=Williams|first3=BA.|last4=Lindquist|first4=K.|last5=Chen|first5=HL.|last6=Covinsky|first6=KE.|title=Functional limitations, socioeconomic status, and all-cause mortality in moderate alcohol drinkers|journal=J Am Geriatr Soc|volume=57|issue=6|pages=955–62|date=Jun 2009|doi=10.1111/j.1532-5415.2009.02184.x|pmid=19473456|pmc=2847409}}{{Cite journal|last1=Arriola|first1=L.|last2=Martinez-Camblor|first2=P.|last3=Larrañaga|first3=N.|last4=Basterretxea|first4=M.|last5=Amiano|first5=P.|last6=Moreno-Iribas|first6=C.|last7=Carracedo|first7=R.|last8=Agudo|first8=A.|last9=Ardanaz|first9=E.|title=Alcohol intake and the risk of coronary heart disease in the Spanish EPIC cohort study|journal=Heart|volume=96|issue=2|pages=124–30|date=Jan 2010|doi=10.1136/hrt.2009.173419|pmid=19933099|s2cid=10125924|doi-access=free|hdl=10668/316|hdl-access=free}}{{Cite journal|last1=Holahan|first1=CJ.|last2=Schutte|first2=KK.|last3=Brennan|first3=PL.|last4=Holahan|first4=CK.|last5=Moos|first5=BS.|last6=Moos|first6=RH.|title=Late-life alcohol consumption and 20-year mortality|journal=Alcohol Clin Exp Res|volume=34|issue=11|pages=1961–71|date=Nov 2010|doi=10.1111/j.1530-0277.2010.01286.x|pmid=20735372}} Nonetheless, some authors remain suspicious that the apparent health benefits of light alcohol use are in large part due to various selection biases and competing risks.{{cite journal |last1=Stockwell |first1=Tim |last2=Zhao |first2=Jinhui |last3=Clay |first3=James |last4=Levesque |first4=Christine |last5=Sanger |first5=Nitika |last6=Sherk |first6=Adam |last7=Naimi |first7=Timothy |title=Why do only some cohort studies find health benefits from low volume alcohol use? A systematic review and meta-analysis of study characteristics that may bias mortality risk estimates |journal=Journal of Studies on Alcohol and Drugs |date=30 January 2024 |volume=85 |issue=4 |pages=441–452 |doi=10.15288/jsad.23-00283|pmid=38289182 }} 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.{{cite journal |last1=van de Luitgaarden |first1=IAT |last2=van Oort |first2=S |last3=Bouman |first3=EJ |last4=Schoonmade |first4=LJ |last5=Schrieks |first5=IC |last6=Grobbee |first6=DE |last7=van der Schouw |first7=YT |last8=Larsson |first8=SC |last9=Burgess |first9=S |last10=van Ballegooijen |first10=AJ |last11=Onland-Moret |first11=NC |last12=Beulens |first12=JWJ |title=Alcohol consumption in relation to cardiovascular diseases and mortality: a systematic review of Mendelian randomization studies. |journal=European Journal of Epidemiology |date=July 2022 |volume=37 |issue=7 |pages=655–669 |doi=10.1007/s10654-021-00799-5 |pmid=34420153|pmc=9329419 }}

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."{{Cite journal|last1=Vogel|first1=RA|title=Alcohol, heart disease, and mortality: a review.|journal=Rev Cardiovasc Med|volume=3|issue=1|pages=7–13|year=2002|pmid=12439349}} 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.{{cite journal |last1=DeJong |first1=William |title=The Moderate Alcohol and Cardiovascular Health Trial: Public health advocates should support good science, not undermine it |journal=European Journal of Preventive Cardiology |date=29 December 2021 |volume=28 |issue=15 |pages=e22–e24 |doi=10.1177/2047487320915802|pmid=33611427 }}{{cite journal |last1=Oppenheimer |first1=Gerald M. |last2=Bayer |first2=Ronald |title=Is Moderate Drinking Protective Against Heart Disease? The Science, Politics and History of a Public Health Conundrum |url=https://www.milbank.org/quarterly/articles/is-moderate-drinking-protective-against-heart-disease-the-science-politics-and-history-of-a-public-health-conundrum/ |journal=The Milbank Quarterly |date=5 December 2019 |volume=98 |issue=1 |pages=39–56 |doi=10.1111/1468-0009.12437|pmid=31803980 |pmc=7077768 }} A trial in Spain is expected to complete in 2028.{{cite journal |last1=Martínez-González |first1=Miguel A. |title=UNATI - A non-inferiority randomized trial testing an advice of moderate drinking pattern versus advice on abstention on major disease and mortality |journal=CORDIS {{!}} European Commission |doi=10.3030/101097681 |url=https://www.unav.edu/documents/16089811/16155256/unati-research-plan.pdf}}

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.{{cite journal |last1=El Khoudary |first1=Samar R. |last2=Aggarwal |first2=Brooke |last3=Beckie |first3=Theresa M. |last4=Hodis |first4=Howard N. |last5=Johnson |first5=Amber E. |last6=Langer |first6=Robert D. |last7=Limacher |first7=Marian C. |last8=Manson |first8=JoAnn E. |last9=Stefanick |first9=Marcia L. |last10=Allison |first10=Matthew A. |title=Menopause Transition and Cardiovascular Disease Risk: Implications for Timing of Early Prevention: A Scientific Statement From the American Heart Association |journal=Circulation |date=22 December 2020 |volume=142 |issue=25 |pages=e506–e532 |doi=10.1161/CIR.0000000000000912|doi-access=free |pmid=33251828 }} For vitamin E, trials have shown that the benefits are limited to certain populations such as those with diabetes and a specific genotype.{{cite journal |last1=Vardi |first1=Moshe |last2=Levy |first2=Nina S. |last3=Levy |first3=Andrew P. |title=Vitamin E in the prevention of cardiovascular disease: the importance of proper patient selection |journal=Journal of Lipid Research |date=September 2013 |volume=54 |issue=9 |pages=2307–2314 |doi=10.1194/jlr.R026641|doi-access=free |pmid=23505320 |pmc=3735930 }} 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.{{cite journal |last1=Yang |first1=Jiaqi |last2=Zhang |first2=Yulin |last3=Na |first3=Xiaona |last4=Zhao |first4=Ai |title=β-Carotene Supplementation and Risk of Cardiovascular Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials |journal=Nutrients |date=18 March 2022 |volume=14 |issue=6 |pages=1284 |doi=10.3390/nu14061284|doi-access=free |pmid=35334942 |pmc=8950884 }}

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".{{cite journal|author=Abdulla S|title=Is alcohol really good for you?|journal=J R Soc Med|volume=90|issue=12|page=651|date= 1997 |pmid=9496287|pmc=1296731|doi=10.1177/014107689709001204}}{{cite journal |vauthors=Naimi TS, Brown DW, Brewer RD, etal |title=Cardiovascular risk factors and confounders among nondrinking and moderate-drinking U.S. adults|journal=Am J Prev Med|volume=28|issue=4|pages=369–373|date=2005|pmid=15831343|doi=10.1016/j.amepre.2005.01.011}} 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.{{Cite journal |last=Casswell |first=Sally |date=April 2013 |title=Vested interests in addiction research and policy. Why do we not see the corporate interests of the alcohol industry as clearly as we see those of the tobacco industry?: Alcohol corporate interests compared with tobacco |url=https://onlinelibrary.wiley.com/doi/10.1111/add.12011 |journal=Addiction |language=en |volume=108 |issue=4 |pages=680–685 |doi=10.1111/add.12011|pmid=23496067 }}{{Cite journal|last1=Sellman|first1=D|last2=Connor|first2=J|last3=Robinson |first3=G |last4=Jackson|first4=R |title=Alcohol cardio-protection has been talked up.|journal=N Z Med J|volume=122|issue=1303|pages=97–101|year=2009|pmid=19851424|url=https://nzmj.org.nz/media/pages/journal/vol-122-no-1303/4a415421eb-1696469507/vol-122-no-1303.pdf#page=97}} 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,{{cite web |title=New perspectives on how to formulate alcohol drinking guidelines |url=https://alcoholinmoderation.com/articles/moderate-drinking/new-perspectives-on-how-to-formulate-alcohol-drinking-guidelines/ |website=Alcohol in Moderation |publisher=ISFAR |access-date=30 May 2024 |date=December 2023}}{{cite journal |last1=Stockley |first1=Creina S. |last2=Hendriks |first2=Henk F.J. |last3=Ellison |first3=R. Curtis |title=ISFAR reiterates its defence of moderate alcohol consumption's health benefits |journal=Journal of Studies on Alcohol and Drugs |date=12 December 2023 |volume=85 |issue=1 |pages=136–140 |doi=10.15288/jsad.23-00293|pmid=38095176 }} scientists in turn accusing these groups of bias due to industry funding,{{cite journal |last1=Stockwell |first1=Tim |last2=Chikritzhs |first2=Tanya |last3=Naimi |first3=Timothy |last4=Zhao |first4=Jinhui |title=ISFAR Doth Protest Too Much: Another Attempt From Industry Sympathizers to Marginalize Scientific Skepticism About Alcohol's Hypothesized Health Benefits? |journal=Journal of Studies on Alcohol and Drugs |date=September 2016 |volume=77 |issue=5 |pages=839–841 |doi=10.15288/jsad.2016.77.839|pmid=27588546 }}{{cite news |title=Alcohol Research Awash in Industry Money |url=https://alcoholjustice.org/news-2/blog/1330-alcohol-research-awash-in-industry-money |access-date=29 May 2024 |work=Alcohol Justice |date=2018}} and members of the groups responding that these are false and misleading assertions.{{cite journal |last1=Conibear |first1=Helena |title=Response to Babor & Miller Editorial 'McCarthyism, conflict of interest and Addiction's new transparency declaration procedures' |journal=Addiction |date=August 2014 |volume=109 |issue=8 |pages=1382–1383 |doi=10.1111/add.12625|pmid=25041207 }} Studies with industry funding find less risk of stroke,{{cite journal |last1=McCambridge |first1=J |last2=Hartwell |first2=G |title=Has industry funding biased studies of the protective effects of alcohol on cardiovascular disease? A preliminary investigation of prospective cohort studies. |journal=Drug and Alcohol Review |date=January 2015 |volume=34 |issue=1 |pages=58–66 |doi=10.1111/dar.12125 |pmid=24602075|pmc=4441279 }} and industry-linked systematic reviews consistently find cardioprotective effects, compared to reviews with no associations being 54% positive.{{cite journal |last1=Golder |first1=S |last2=McCambridge |first2=J |title=Alcohol, cardiovascular disease and industry funding: A co-authorship network analysis of systematic reviews. |journal=Social Science & Medicine |date=November 2021 |volume=289 |pages=114450 |doi=10.1016/j.socscimed.2021.114450 |pmid=34607052|pmc=8586735 }}

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.{{Cite journal|last1=Sinkiewicz|first1=W|last2=Weglarz|first2=M |title=Alcohol and wine and cardiovascular diseases in epidemiologic studies|journal=Przegl Lek |volume=66 |issue=5 |pages=233–238 |year=2009 |pmid=19739580}}

The available evidence is in agreement that current drinking levels are too high. The WHO has emphasized the need to revise alcohol control policies worldwide in order to reduce overall alcohol consumption.

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.{{efn|Calculated as {{math|(1.5*1.7/0.39+0.9*0.87/0.25)/(1.5+0.9)}}, with figures from {{harvtxt|GBD 2016 Alcohol Collaboration|2018}}. See also [https://www.who.int/data/gho/data/indicators/indicator-details/GHO/alcohol-average-daily-intake-in-grams-among-drinkers-with-95-ci WHO figures by country]}} 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.{{efn|The fraction of current drinkers is estimated using [https://databank.worldbank.org/source/population-estimates-and-projections/preview/on WorldBank 2016 population numbers] and combining the GBD 2016 and GBD 2020 analyses based on the statement that "Since 1990, the global proportion of drinkers consuming alcohol in excess of the NDE has not changed significantly." For example, GBD 2016 states there were 1.5 billion male current drinkers in 2016, WorldBank states there were 3,770,341,364 males and 1,018,695,045 males under 15, and we can assume based on GBD 2020 that 35.1% of males 15+ were drinking harmful amounts, so we calculate {{math|1= .351*(3770341364-1018695045)/1.5e9≈2/3}}}} 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.{{cite web |last1=Stockwell |first1=Tim |title=How Several Hundred Lancet Co-Authors Lost a Million Global Alcohol-Caused Deaths |url=https://movendi.ngo/blog/2022/08/04/how-several-hundred-lancet-co-authors-lost-a-million-global-alcohol-caused-deaths/ |website=Movendi International |date=4 August 2022}} 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).{{Cite web |title=Alcohol |url=https://www.who.int/news-room/fact-sheets/detail/alcohol |access-date=2024-03-18 |website=www.who.int |language=en}} 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).{{cite web |title=Global health estimates 2020: Leading causes of DALYs |url=https://www.who.int/data/gho/data/themes/mortality-and-global-health-estimates/global-health-estimates-leading-causes-of-dalys |website=World Health Organization|date=2020 |language=en}} Similarly the number of alcohol-attributed deaths would rank between chronic obstructive pulmonary disease (#3) and lower respiratory infections (#4).{{cite web |title=Global health estimates 2020: Leading causes of death |url=https://www.who.int/data/gho/data/themes/mortality-and-global-health-estimates/ghe-leading-causes-of-death |website=World Health Organization|date=2020 |language=en}}

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.{{Cite journal|vauthors=Wood AM, Kaptoge S, Butterworth AS, Willeit P, et al |date=2018-04-14|title=Risk thresholds for alcohol consumption: combined analysis of individual-participant data for 599 912 current drinkers in 83 prospective studies|url= |journal=The Lancet|language=en|volume=391|issue=10129|pages=1513–1523|doi=10.1016/S0140-6736(18)30134-X|pmid=29676281|pmc=5899998|issn=0140-6736}} 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.{{cn|date=May 2024}}

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.{{cite journal |last1=White |first1=Ian R. |last2=Altmann |first2=Dan R. |last3=Nanchahal |first3=Kiran |title=Alcohol consumption and mortality: modelling risks for men and women at different ages |journal=BMJ |date=27 July 2002 |volume=325 |issue=7357 |pages=191 |doi=10.1136/bmj.325.7357.191|pmid=12142306 |pmc=117446 }}

===India===

A study of 4,465 subjects in India confirmed the association of alcohol consumption with coronary risk in men. Compared to lifetime abstainers, alcohol users had higher blood sugar (2 mg/dl), blood pressure (2 mm Hg) levels, and the high-density lipoprotein cholesterol (HDL-C) levels (2 mg/dl) and significantly higher tobacco use (63% vs. 21%). Indians who consume alcohol had a 60% higher risk of heart attack, which was greater with local spirits (80%) than branded spirits (50%).{{cite journal|author1=Roy, A.|author2=Prabhakaran, D.|author3=Jeemon, P.|author4=Thankappan, K.R.|author5=Mohan, V.|author6=Ramakrishnan, L.|author7=Joshi, P.|author8=Ahmed, F.|author9=Mohan, B.V.|author10=Saran, R.K.|author11=Sinha, N.|author12=Reddy, K.S.|title=Impact of alcohol on coronary heart disease in Indian men|journal=Atherosclerosis|date=26 February 2010|volume=210|issue=2|pages=531–535|pmid=20226461|doi=10.1016/j.atherosclerosis.2010.02.033}} The harm was observed in alcohol users classified as occasional as well as regular light, moderate, and heavy consumers. Five percent of all cancers diagnosed in Indians in 2021 were attributed to alcohol consumption, with cancers of the esophagus, liver, and breast accounting for the most number of cases.{{Cite news |date=2021-07-15 |title=Alcohol drinking linked to over 62,000 new cancer cases in India last year: Lancet study |url=https://economictimes.indiatimes.com/industry/healthcare/biotech/healthcare/alcohol-drinking-linked-to-over-62000-new-cancer-cases-in-india-last-year-lancet-study/articleshow/84436113.cms?from=mdr |access-date=2025-01-18 |work=The Economic Times |issn=0013-0389}}

{{Main|Alcoholism in Russia}}

As of 2014, male life expectancy was lower in Russia than other countries. For example, at 2005 mortality rates, only 7% of UK men but 37% of Russian men would die before the age of 55 years.{{cite journal |last1=Zaridze |first1=David |last2=Lewington |first2=Sarah |last3=Boroda |first3=Alexander |last4=Scélo |first4=Ghislaine |last5=Karpov |first5=Rostislav |last6=Lazarev |first6=Alexander |last7=Konobeevskaya |first7=Irina |last8=Igitov |first8=Vladimir |last9=Terechova |first9=Tatiyana |last10=Boffetta |first10=Paolo |last11=Sherliker |first11=Paul |last12=Kong |first12=Xiangling |last13=Whitlock |first13=Gary |last14=Boreham |first14=Jillian |last15=Brennan |first15=Paul |last16=Peto |first16=Richard |title=Alcohol and mortality in Russia: prospective observational study of 151 000 adults |journal=The Lancet |date=April 2014 |volume=383 |issue=9927 |pages=1465–1473 |doi=10.1016/S0140-6736(13)62247-3|doi-access=free|pmid=24486187 |pmc=4007591 }} A study by Zaridze et al. in 2009 found that "excessive alcohol consumption in Russia, particularly by men, has in recent years caused more than half of all the deaths at ages 15–54 years."IARC [http://www.iarc.fr/en/media-centre/iarcnews/2009/IARCLancet270709.pdf Alcohol causes more than half of all the premature deaths in Russian adults] The study used 43,802 deaths linked to alcohol or tobacco but only 5475 other deaths as controls. Further studies have confirmed that heavy drinking and smoking are the main cause of high death rates in Russia as of 2014. The high consumption of vodka in the context of binge drinking is a significant factor.{{cite journal |last1=Rehm |first1=Jürgen |title=Russia: lessons for alcohol epidemiology and alcohol policy |journal=The Lancet |date=April 2014 |volume=383 |issue=9927 |pages=1440–1442 |doi=10.1016/S0140-6736(14)60038-6|doi-access=free |pmid=24486186 }} For smokers aged 35-54, the 20-year risk of death was 35% for men who had reported drinking three or more bottles of vodka a week and 16% for men who had reported consuming less than one bottle a week.

The landmark INTERHEART Study has revealed that alcohol consumption in South Asians was not protective against CAD in sharp contrast to other populations who benefit from it.{{cite journal|author1=Joshi, Prashant|author2=Islam, Shofiqul|author3=Pais, Prem|author4=Reddy, Srinath|author5=Dorairaj, Prabhakaran|author6=Kazmi, Khawar|author7=Pandey, Mrigendra Raj|author8=Haque, Sirajul|author9=Mendis, Shanthi|author10=Rangarajan, Sumathy|author11=Yusuf, Salim|title=Risk Factors for Early Myocardial Infarction in South Asians Compared With Individuals in Other Countries|journal=JAMA|date=17 January 2007|volume=297|issue=3|pages=286–294|pmid=17227980|doi=10.1001/jama.297.3.286}}

A governmental report from Britain has found that "There were 8,724 alcohol-related deaths in 2007, lower than 2006, but more than double the 4,144 recorded in 1991. The alcohol-related death rate was 13.3 per 100,000 population in 2007, compared with 6.9 per 100,000 population in 1991."{{cite web|url=http://www.statistics.gov.uk/cci/nugget.asp?id=1091 |title=Alcohol Deaths: Rates stabilise in the UK |publisher=Statistics.gov.uk |access-date=2014-04-22}} In Scotland, the NHS estimate that in 2003 one in every 20 deaths could be attributed to alcohol.BBC [http://news.bbc.co.uk/1/hi/scotland/8126129.stm Alcohol 'kills one in 20 Scots'] 30 June 2009 A 2009 report noted that the death rate from alcohol-related disease was 9,000, a number three times that of 25 years previously.Sam Lister [https://www.thetimes.com/uk/science/article/the-price-of-alcohol-an-extra-6000-early-deaths-a-year-8k0sjc2nkvh The price of alcohol: an extra 6,000 early deaths a year] The Times, 19 October 2009

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).{{cite web|title='Optimal' levels of alcohol consumption for men and women at different ages, and the all-cause mortality attributable to drinking.|vauthors=White IR, Altmann DR, Nanchahal K|publisher=London School of Hygiene and Tropical Medicine. Technical report.|date=2000|url=http://alcoholresearchuk.org/downloads/finalReports/AERC_FinalReport_0015.pdf|access-date=2014-04-25|archive-url=https://web.archive.org/web/20140426232641/http://alcoholresearchuk.org/downloads/finalReports/AERC_FinalReport_0015.pdf|archive-date=2014-04-26|url-status=dead}}

A study in the United Kingdom found that alcohol causes about 4% of cancer cases in the UK (12,500 cases per year).{{cite web|title=Alcohol and cancer |url=http://info.cancerresearchuk.org/healthyliving/alcohol/ |publisher=Cancer Research UK|date=2013-08-22 }}

Excessive alcohol use was the 3rd leading behavioral cause of death for people in the United States in the year 2000.{{cite journal |last1=Mokdad |first1=Ali H. |title=Actual Causes of Death in the United States, 2000 |journal=JAMA |date=10 March 2004 |volume=291 |issue=10 |pages=1238 |doi=10.1001/jama.291.10.1238|pmid=15010446}} In 2001, an estimated 75,766 deaths were attributable to alcohol.{{cite journal |last1=Centers for Disease Control and Prevention |title=Alcohol-attributable deaths and years of potential life lost--United States, 2001. |journal=Morbidity and Mortality Weekly Report |date=24 September 2004 |volume=53 |issue=37 |pages=866–70 |pmid=15385917 |url=https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5337a2.htm}} From 2006 through 2010, there were approximately 87,798 deaths on average attributable to alcohol occurred in the United States each year.{{cite journal |last1=Stahre |first1=Mandy |last2=Roeber |first2=Jim |last3=Kanny |first3=Dafna |last4=Brewer |first4=Robert D. |last5=Zhang |first5=Xingyou |title=Contribution of Excessive Alcohol Consumption to Deaths and Years of Potential Life Lost in the United States |journal=Preventing Chronic Disease |date=26 June 2014 |volume=11 |pages=E109 |doi=10.5888/pcd11.130293 |pmid=24967831 |url=https://www.cdc.gov/pcd/issues/2014/13_0293.htm|pmc=4075492 }} Alcohol-related deaths among Americans about doubled from 1999 to 2020. In 2020, alcohol was linked to nearly 50,000 deaths among adults aged 25 to 85, a sharp rise from just under 20,000 in 1999. All age groups experienced increases, with the most significant rise occurring in individuals aged 25 to 34, where death rates nearly quadrupled during this period.{{Cite journal |last1=Matarazzo |first1=Alexandra |last2=Hennekens |first2=Charles H. |last3=Dunn |first3=John |last4=Benson |first4=Katerina |last5=Willett |first5=Yanna |last6=Levine |first6=Robert S. |last7=Mejia |first7=Maria Carmenza |last8=Kitsantas |first8=Panagiota |date=2024-11-10 |title=New Clinical and Public Health Challenges: Increasing Trends in United States Alcohol Related Mortality |url=https://linkinghub.elsevier.com/retrieve/pii/S0002934324007046 |journal=The American Journal of Medicine |language=English |volume=0 |doi=10.1016/j.amjmed.2024.10.024 |issn=0002-9343 |pmid=39532247}} In 2025, the US Surgeon General advocated for cancer risk warnings on alcoholic beverages.{{cite news |title=US top doctor calls for cancer warnings on alcohol |url=https://www.bbc.com/news/articles/cj90x3np0zpo |agency=BBC|date=3 January 2025}}

{{main|Alcohol and cardiovascular disease}}

Alcohol has been found to have anticoagulant properties.{{cite journal|vauthors=Mennen LI, Balkau B, Vol S, Cacès E, Eschwège E|title=Fibrinogen: a possible link between alcohol consumption and cardiovascular disease? DESIR Study Group|journal=Arterioscler Thromb Vasc Biol|volume=19|issue=4|pages=887–892|date=1999|pmid=10195914|url=http://atvb.ahajournals.org/cgi/pmidlookup?view=long&pmid=10195914|doi=10.1161/01.atv.19.4.887|access-date=2009-01-10|archive-date=2013-01-12|archive-url=https://archive.today/20130112121432/http://atvb.ahajournals.org/cgi/pmidlookup?view=long&pmid=10195914|url-status=dead}} Thrombosis is lower among moderate drinkers than abstainers.{{cite journal |vauthors=Pahor M, Guralnik JM, Havlik RJ, et al |title=Alcohol consumption and risk of deep venous thrombosis and pulmonary embolism in older persons|journal=J Am Geriatr Soc|volume=44|issue=9|pages=1030–1037|date=1996|pmid=8790226|doi=10.1111/j.1532-5415.1996.tb02933.x|s2cid=11553439}} A meta-analysis of randomized trials found that alcohol consumption in moderation decreases serum levels of fibrinogen, a protein that promotes clot formation, while it increases levels of tissue type plasminogen activator, an enzyme that helps dissolve clots.{{Cite journal|last1=Rimm|first1=EB|last2=Williams|first2=P|last3=Fosher|first3=K|last4=Criqui|first4=M|last5=Stampfer|first5=MJ|title=Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors.|journal=BMJ|volume=319|issue=7224|pages=1523–1528|date=1999|pmid=10591709 |pmc=28294|doi=10.1136/bmj.319.7224.1523}} These changes were estimated to reduce coronary heart disease risk by about 24%. Another meta-analysis in 2011 found favorable changes in HDL cholesterol, adiponectin, and fibrinogen associated with moderate alcohol consumption.{{cite journal |vauthors=Brien Susan E, Ronksley Paul E, Turner Barbara J, Mukamal Kenneth J, Ghali William A | year = 2011 | title = Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies | journal = BMJ |volume = 342 |page = d636 | doi = 10.1136/bmj.d636 | pmid = 21343206 | pmc = 3043110 }} A systematic review based on 16,351 participants showed J-shaped curve for the overall relationship between cardiovascular mortality and alcohol intake. Maximal protective effect was shown with 5–10 g of alcohol consumption per day and the effect was significant up to 26 g/day alcohol consumption.{{cite journal |vauthors=Costanzo S, Di Castelnuovo A, Donati MB, Iacoviello L, de Gaetano G |title=Alcohol consumption and mortality in patients with cardiovascular disease: a meta-analysis |journal=J. Am. Coll. Cardiol. |volume=55 |issue=13 |pages=1339–1347 |date=2010 |pmid=20338495 |doi=10.1016/j.jacc.2010.01.006 }} Serum levels of C-reactive protein (CRP), a putative marker of inflammation and predictor of CHD (coronary heart disease) risk, are lower in moderate drinkers than in those who abstain from alcohol, suggesting that alcohol consumption in moderation might have anti-inflammatory effects.{{Cite journal|last1=Albert|first1=MA|last2=Glynn|first2=RJ|last3=Ridker|first3=PM|title=Alcohol consumption and plasma concentration of C-reactive protein|journal=Circulation|volume=107|issue=3|pages=443–447|date=2003|doi=10.1161/01.CIR.0000045669.16499.EC|pmid=12551869|s2cid=323583|doi-access=free}}{{Cite journal|last1=Stewart|first1=SH|last2=Mainous|first2=AG|last3=Gilbert|first3=G|title=Relation between alcohol consumption and C-reactive protein levels in the adult US population|url=http://www.jabfm.org/cgi/reprint/15/6/437.pdf|journal=J Am Board Fam Pract|volume=15|issue=6|pages=437–442|year=2002|pmid=12463288}}{{Cite journal|last1=Imhof|first1=A|last2=Froehlich|first2=M|last3=Brenner|first3=H|last4=Boeing|first4=H|last5=Pepys|first5=MB|last6=Koenig|first6=W.|title=Effect of alcohol consumption on systemic markers of inflammation|journal=Lancet|volume=357|issue=9258|pages=763–767|date=2001|doi=10.1016/S0140-6736(00)04170-2|pmid=11253971|s2cid=8046780}} Data from one prospective study suggest that, among men with initially low alcohol consumption ({{cite journal |vauthors=Sesso HD, Stampfer MJ, Rosner B, Hennekens CH, Manson JE, Gaziano JM |title=Seven-Year Changes in Alcohol Consumption and Subsequent Risk of Cardiovascular Disease in Men |journal=Arch Intern Med |volume=160 |issue=17 |pages=2605–2612 |year=2000 |doi=10.1001/archinte.160.17.2605 |pmid=10999974}}

A prospective study published in 1997 found "moderate alcohol consumption appears to decrease the risk of PAD in apparently healthy men."{{cite journal |vauthors=Camargo CA, Stampfer MJ, Glynn RJ, etal |title=Prospective study of moderate alcohol consumption and risk of peripheral arterial disease in US male physicians |journal=Circulation |volume=95 |issue=3 |pages=577–580 |date=1997 |pmid=9024142 |url=http://www.circ.ahajournals.org/cgi/content/full/95/3/577 |doi=10.1161/01.cir.95.3.577 |access-date=2006-07-25 |archive-date=2011-02-12 |archive-url=https://web.archive.org/web/20110212015931/http://www.circ.ahajournals.org/cgi/content/full/95/3/577 |url-status=dead }} In a large population-based study, moderate alcohol consumption was inversely associated with peripheral arterial disease in women but not in men. But when confounding by smoking was considered, the benefit extended to men. The study concluded "an inverse association between alcohol consumption and peripheral arterial disease was found in nonsmoking men and women."{{cite journal |vauthors=Vliegenthart R, Geleijnse JM, Hofman A, et al |title=Alcohol consumption and risk of peripheral arterial disease: the Rotterdam study|journal=Am J Epidemiol|volume=155|issue=4|pages=332–338|date=2002|pmid=11836197|doi=10.1093/aje/155.4.332|doi-access=free|hdl=1765/9842|hdl-access=free}}{{cite journal |vauthors=Mingardi R, Avogaro A, Noventa F, et al |title=Alcohol intake is no longer associated with a lower prevalence of peripheral vascular disease in non-insulin dependent diabetic women|journal=Nutrition Metabolism and Cardiovascular Disease|volume=7|issue=4|pages=301–308|year=1997}}

A study found that moderate consumption of alcohol had a protective effect against intermittent claudication. The lowest risk was seen in men who drank 1 to 2 drinks per day and in women who drank half to 1 drink per day.{{cite journal|vauthors=Djoussé L, Levy D, Murabito JM, Cupples LA, Ellison RC |title=Alcohol consumption and risk of intermittent claudication in the Framingham Heart Study|journal=Circulation|volume=102|issue=25|pages=3092–3097|date=2000|pmid=11120700 |doi=10.1161/01.cir.102.25.3092|s2cid=1586122|doi-access=free}}

Drinking in moderation has been found to help those who have had a heart attack survive it.{{cite journal|vauthors=Muntwyler J, Hennekens CH, Buring JE, Gaziano JM |title=Mortality and light to moderate alcohol consumption after myocardial infarction|journal=Lancet|volume=352|issue=9144|pages=1882–1885|date=1998|pmid=9863785 |doi=10.1016/S0140-6736(98)06351-X|s2cid=54365788}}{{cite journal|vauthors=Mukamal KJ, Maclure M, Muller JE, Sherwood JB, Mittleman MA |title=Prior alcohol consumption and mortality following acute myocardial infarction|journal=JAMA|volume=285|issue=15|pages=1965–1970|date=2001|pmid=11308432|doi=10.1001/jama.285.15.1965}}{{cite web|url=http://www.newswise.com/articles/view/506828/ |title=Alcohol helps reduce damage after heart attacks |publisher=Newswise.com |date=2004-08-30 |access-date=2014-04-22}} However, excessive alcohol consumption leads to an increased risk of heart failure.{{cite journal|vauthors=Djoussé L, Gaziano JM |title=Alcohol consumption and heart failure: a systematic review|journal=Curr Atheroscler Rep|volume=10|issue=2|pages=117–120|date=2008|pmid=18417065|doi=10.1007/s11883-008-0017-z|pmc=2365733}} At present there have been no randomised trials to confirm the evidence which suggests a protective role of low doses of alcohol against heart attacks.{{cite journal|vauthors=Kloner RA, Rezkalla SH |title=To drink or not to drink? That is the question|journal=Circulation|volume=116|issue=11|pages=1306–1317|date=2007|pmid=17846344 |doi=10.1161/CIRCULATIONAHA.106.678375 |doi-access=free}} There is an increased risk of hypertriglyceridemia, cardiomyopathy, hypertension, and stroke if three or more standard drinks of alcohol are taken per day.{{cite journal |vauthors=Saremi A, Arora R |title=The cardiovascular implications of alcohol and red wine|journal=Am J Ther|volume=15|issue=3|pages=265–277|year=2008 |pmid=18496264 |doi=10.1097/MJT.0b013e3180a5e61a|s2cid=7243756}} A systematic review reported that reducing alcohol intake lowers blood pressure in a dose-dependent manner in heavy drinkers. There is no safe amount of alcohol without having a negative effect on blood pressure. Even individuals who consume only one drink per day show a link to higher blood pressure.{{Cite web |title=Even just 1 alcoholic drink a day may increase blood pressure |url=https://www.heart.org/en/news/2023/07/31/even-just-1-alcoholic-drink-a-day-may-increase-blood-pressure |access-date=2025-01-18 |website=www.heart.org |language=en}}

Frequent drinking of alcoholic beverages is a major contributing factor in cases of elevated blood levels of triglycerides.{{cite web|url=http://americanheart.org/presenter.jhtml?identifier=4778|title=Triglycerides

| access-date=4 September 2007|publisher=American Heart Association|archive-url=https://web.archive.org/web/20070827102812/http://www.americanheart.org/presenter.jhtml?identifier=4778 |archive-date=27 August 2007}}

Large amounts of alcohol over the long term can lead to alcoholic cardiomyopathy. Alcoholic cardiomyopathy presents in a manner clinically identical to idiopathic dilated cardiomyopathy, involving hypertrophy of the musculature of the heart that can lead to congestive heart failure.{{Cite journal |last1=Awtry|first1=EH |last2=Philippides |first2=GJ|title=Alcoholic and cocaine-associated cardiomyopathies.|journal=Prog Cardiovasc Dis|volume=52|issue=4|pages=289–299|year=2010 |doi=10.1016/j.pcad.2009.11.004|pmid=20109599}}

Alcoholics may have anemia from several causes;{{cite journal|vauthors=Savage D, Lindenbaum J |title=Anemia in alcoholics|journal=Medicine (Baltimore) |volume=65|issue=5|pages=322–338|year=1986|pmid=3747828|doi=10.1097/00005792-198609000-00005|s2cid=25790752|doi-access=free}} they may also develop thrombocytopenia from direct toxic effect on megakaryocytes, or from hypersplenism.{{Cite journal|last=Ballard|first=Harold S.|date=1997|title=The Hematological Complications of Alcoholism|url=https://pubs.niaaa.nih.gov/publications/arh21-1/42.pdf|journal=Alcohol Health & Research World|volume=21|issue=1|pages=44|pmid=15706762|pmc=6826798|access-date=2020-10-22|archive-date=2021-09-14|archive-url=https://web.archive.org/web/20210914183420/https://pubs.niaaa.nih.gov/publications/arh21-1/42.pdf|url-status=dead}}

Alcohol consumption increases the risk of atrial fibrillation, a type of abnormal heart rhythm that increases the risk of stroke and heart failure.{{Cite web |title=Atrial fibrillation - Symptoms and causes |url=https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624#:~:text=Atrial%20fibrillation%20(AFib)%20is%20an,and%20other%20heart-related%20complications. |access-date=2025-01-18 |website=Mayo Clinic |language=en}} This remains true even at moderate levels of consumption.{{cite journal |last1=Larsson |first1=SC|last2=Drca|first2=N|last3=Wolk|first3=A|title=Alcohol Consumption and Risk of Atrial Fibrillation|journal=Journal of the American College of Cardiology|date=2014|volume=64|issue=3|pages=281–289|doi=10.1016/j.jacc.2014.03.048|pmid=25034065|s2cid=22236791 |doi-access=free}}

Chronic heavy alcohol consumption impairs brain development, causes alcohol dementia, brain shrinkage, physical dependence, alcoholic polyneuropathy (also known as 'alcohol leg'), increases neuropsychiatric and cognitive disorders and causes distortion of the brain chemistry. At present, due to poor study design and methodology, the literature is inconclusive on whether moderate alcohol consumption increases the risk of dementia or decreases it.{{cite journal |vauthors=Panza F, Capurso C, D'Introno A, etal |title=Vascular risk factors, alcohol intake, and cognitive decline|journal=J Nutr Health Aging|volume=12|issue=6|pages=376–81|year=2008|pmid=18548174|doi=10.1007/BF02982669|s2cid=3123226|doi-access=free}} Evidence for a protective effect of low to moderate alcohol consumption on age-related cognitive decline and dementia has been suggested by some research; however, other research has not found a protective effect of low to moderate alcohol consumption.{{Cite journal|last1=Panza|first1=F.|last2=Capurso|first2=C.|last3=D'Introno|first3=A.|last4=Colacicco|first4=AM.|last5=Frisardi|first5=V.

|last6=Lorusso|first6=M.|last7=Santamato|first7=A.|last8=Seripa|first8=D.|last9=Pilotto|first9=A.| display-authors = 8|title=Alcohol drinking, cognitive functions in older age, predementia, and dementia syndromes.|journal=J Alzheimers Dis|volume=17|issue=1|pages=7–31|date=May 2009|doi=10.3233/JAD-2009-1009|pmid=19494429}} Some evidence suggests that low to moderate alcohol consumption may speed up brain volume loss.{{Cite journal|last1=Verbaten|first1=MN.|title=Chronic effects of low to moderate alcohol consumption on structural and functional properties of the brain: beneficial or not?|journal=Hum Psychopharmacol|volume=24|issue=3|pages=199–205|date=Apr 2009|doi=10.1002/hup.1022|pmid=19330800|s2cid=205924421}} Chronic consumption of alcohol may result in increased plasma levels of the toxic amino acid homocysteine;{{cite journal|pmid=11373253|volume=36|issue=3|title=Moderate alcohol consumption in social drinkers raises plasma homocysteine levels: a contradiction to the 'French Paradox'?|year=2001 |vauthors=Bleich S, Bleich K, Kropp S, etal |journal=Alcohol Alcohol.|pages=189–92|doi=10.1093/alcalc/36.3.189|doi-access=free}}{{cite journal|pmid=15770107|volume=29|issue=3|title=Evidence of increased homocysteine levels in alcoholism: the Franconian alcoholism research studies (FARS)|date=March 2005 |vauthors=Bleich S, Carl M, Bayerlein K, etal |journal=Alcohol. Clin. Exp. Res.|pages=334–6|doi=10.1097/01.alc.0000156083.91214.59}} which may explain alcohol withdrawal seizures,{{cite journal|pmid=10976956|volume=11|issue=12|title=Plasma homocysteine is a predictor of alcohol withdrawal seizures|date=August 2000|vauthors=Bleich S, Degner D, Bandelow B, von Ahsen N, Rüther E, Kornhuber J |journal=NeuroReport|pages=2749–52|doi=10.1097/00001756-200008210-00028|s2cid=20270541}} alcohol-induced brain atrophy{{cite journal|pmid=12531462|volume=335|issue=3|title=Hyperhomocysteinemia as a new risk factor for brain shrinkage in patients with alcoholism|date=January 2003 |vauthors=Bleich S, Bandelow B, Javaheripour K, etal |journal=Neurosci. Lett.|pages=179–82|doi=10.1016/S0304-3940(02)01194-1|s2cid=33032529}} and alcohol-related cognitive disturbances.{{cite journal|pmid=15997414|doi=10.1007/s00702-005-0333-1|volume=113|issue=3|title=Short-term cognition deficits during early alcohol withdrawal are associated with elevated plasma homocysteine levels in patients with alcoholism|date=March 2006 |vauthors=Wilhelm J, Bayerlein K, Hillemacher T, etal |journal=J Neural Transm|pages=357–63|s2cid=11980558}} Alcohol's impact on the nervous system can also include disruptions of memory and learning (see Effects of alcohol on memory), such as resulting in a blackout phenomenon.

Epidemiological studies of middle-aged populations generally find the relationship between alcohol intake and the risk of stroke to be either U- or J-shaped.{{Cite journal|last1=Di Castelnuovo|first1=A.|last2=Costanzo|first2=S.|last3=di Giuseppe|first3=R.|last4=de Gaetano|first4=G.|last5=Iacoviello|first5=L.|title=Alcohol consumption and cardiovascular risk: mechanisms of action and epidemiologic perspectives.|journal=Future Cardiol|volume=5|issue=5|pages=467–77|date=Sep 2009|doi=10.2217/fca.09.36|pmid=19715411}}{{Cite journal|last1=Klatsky|first1=AL.|title=Alcohol and cardiovascular diseases.|journal=Expert Rev Cardiovasc Ther|volume=7|issue=5|pages=499–506|date=May 2009|doi=10.1586/erc.09.22|pmid=19419257|s2cid=23782870}}{{Cite journal|last1=Galimanis|first1=A.|last2=Mono|first2=ML.|last3=Arnold|first3=M.|last4=Nedeltchev|first4=K.|last5=Mattle|first5=HP.|title=Lifestyle and stroke risk: a review.|journal=Current Opinion in Neurology|volume=22|issue=1|pages=60–8|date=Feb 2009|doi=10.1097/WCO.0b013e32831fda0e|pmid=19155763|s2cid=22619761}}{{Cite journal|last1=O'Keefe|first1=JH.|last2=Bybee|first2=KA.|last3=Lavie|first3=CJ.|title=Alcohol and cardiovascular health: the razor-sharp double-edged sword|journal=J Am Coll Cardiol|volume=50|issue=11|pages=1009–14|date=Sep 2007|doi=10.1016/j.jacc.2007.04.089|pmid=17825708|s2cid=42462804 |doi-access=free}} There may be very different effects of alcohol based on the type of stroke studied. The predominant form of stroke in Western cultures is ischemic, whereas non-western cultures have more hemorrhagic stroke. In contrast to the beneficial effect of alcohol on ischemic stroke, consumption of more than two drinks per day increases the risk of hemorrhagic stroke. The National Stroke Association estimates this higher amount of alcohol increases stroke risk by 50%.{{cite web|url=http://www.stroke.org/site/PageServer?pagename=Alcohol |title=Stroke Risk Reduction – Alcohol Use – National Stroke Association |publisher=Stroke.org |access-date=2014-04-22}} "For stroke, the observed relationship between alcohol consumption and risk in a given population depends on the proportion of strokes that are hemorrhagic. Light-to-moderate alcohol intake is associated with a lower risk of ischemic stroke which is likely to be, in part, causal. Hemorrhagic stroke, on the other hand, displays a log-linear relationship with alcohol intake."{{Cite journal|last1=Emberson|first1=JR.|last2=Bennett|first2=DA.|title=Effect of alcohol on risk of coronary heart disease and stroke: causality, bias, or a bit of both?|journal=Vasc Health Risk Manag|volume=2|issue=3|pages=239–49|year=2006|pmid=17326330|pmc=1993990|doi=10.2147/vhrm.2006.2.3.239 |doi-access=free }}

{{Main|Alcohol-related brain damage|Long-term impact of alcohol on the brain}}

Alcohol misuse is associated with widespread and significant brain lesions. Alcohol related brain damage is not only due to the direct toxic effects of alcohol; alcohol withdrawal, nutritional deficiency, electrolyte disturbances, and liver damage are also believed to contribute to alcohol-related brain damage.{{Cite journal|doi=10.1111/j.1530-0277.1998.tb04389.x|last1=Neiman|first1=J.|title=Alcohol as a risk factor for brain damage: neurologic aspects|journal=Alcohol Clin Exp Res|volume=22|issue=7 Suppl|pages=346S–351S|date=Oct 1998|pmid=9799959}}

Alcohol can cause brain damage, Wernicke's encephalopathy and Alcoholic Korsakoff syndrome which frequently occur simultaneously, known as Wernicke–Korsakoff syndrome.{{cite journal | vauthors = Arts NJ, Walvoort SJ, Kessels RP | title = Korsakoff's syndrome: a critical review | journal = Neuropsychiatric Disease and Treatment | volume = 13 | pages = 2875–2890 | date = 2017-11-27 | pmid = 29225466 | pmc = 5708199 | doi = 10.2147/NDT.S130078 | doi-access = free }} Lesions, or brain abnormalities, are typically located in the diencephalon which result in anterograde and retrograde amnesia, or memory loss.

Excessive alcohol intake is associated with impaired prospective memory. This impaired cognitive ability leads to increased failure to carry out an intended task at a later date, for example, forgetting to lock the door or to post a letter on time. The higher the volume of alcohol consumed and the longer consumed, the more severe the impairments.{{Cite journal|doi=10.2174/1874473710801010036|last1=Heffernan|first1=TM|title=The impact of excessive alcohol use on prospective memory: a brief review.|journal=Curr Drug Abuse Rev|volume=1|issue=1|pages=36–41|date=2008|pmid=19630703}} One of the organs most sensitive to the toxic effects of chronic alcohol consumption is the brain. In the United States approximately 20% of admissions to mental health facilities are related to alcohol-related cognitive impairment, most notably alcohol-related dementia. Chronic excessive alcohol intake is also associated with serious cognitive decline and a range of neuropsychiatric complications. The elderly are the most sensitive to the toxic effects of alcohol on the brain.{{cite journal|vauthors=Pierucci-Lagha A, Derouesné C |title=Alcoholism and aging. 2. Alcoholic dementia or alcoholic cognitive impairment?|language=fr|journal=Psychol Neuropsychiatr Vieil|volume=1|issue=4|pages=237–249|date=2003|pmid=15683959}} There is some inconclusive evidence that small amounts of alcohol taken in earlier adult life is protective in later life against cognitive decline and dementia.{{cite journal|vauthors=Peters R, Peters J, Warner J, Beckett N, Bulpitt C |title=Alcohol, dementia and cognitive decline in the elderly: a systematic review|journal=Age Ageing|volume=37|issue=5|pages=505–512|date=2008|pmid=18487267 |doi=10.1093/ageing/afn095 |doi-access=free}} However, a study concluded, "Our findings suggest that, despite previous suggestions, moderate alcohol consumption does not protect older people from cognitive decline."{{cite journal |vauthors=Cooper C, Bebbington P, Meltzer H, Jenkins R, Brugha T, Lindesay J, Livingston G | year = 2009| title = Alcohol in moderation, premorbid intelligence and cognition In Older Adults: results from the Psychiatric Morbidity Survey | url = http://jnnp.bmj.com/cgi/content/abstract/jnnp.2008.163964v1 | journal = J Neurol Neurosurg Psychiatry | volume = 80| issue = 11| pages = 1236–1239| doi = 10.1136/jnnp.2008.163964 | pmid = 19620140| s2cid = 9226226}}

Wernicke–Korsakoff syndrome is a manifestation of thiamine deficiency, usually as a secondary effect of alcohol misuse.{{cite journal|vauthors=Martin PR, Singleton CK, Hiller-Sturmhöfel S |title=The role of thiamine deficiency in alcoholic brain disease|journal=Alcohol Res Health|volume=27|issue=2|pages=134–142|year=2003|pmid=15303623|pmc=6668887}} 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 confusional state while Korsakoff's psychosis main symptoms are amnesia and executive dysfunction.{{cite journal|author=Butters N|title=The Wernicke-Korsakoff syndrome: a review of psychological, neuropathological and etiological factors|journal=Curr Alcohol|volume=8|pages=205–232|year=1981|pmid=6806017}} "Banana bags", intravenous fluid containers containing vitamins and minerals (bright yellow due to the vitamins), can be used to mitigate these outcomes.{{cite book|title=Principles of Psychopharmacology for Mental Health Professionals|author1=Jeffrey E Kelsey |author2=D Jeffrey Newport |author3=Charles B Nemeroff |name-list-style=amp |chapter=Alcohol Use Disorders|pages=196–197|publisher=Wiley-Interscience|year=2006|isbn= 978-0-471-79462-2}}{{cite book|title=Introduction to Emergency Medicine|editor1=Elizabeth Mitchell |editor2=Ron Medzon |publisher=Lippincott Williams & Wilkins|year=2005|isbn= 978-0-7817-3200-0|chapter=Acute and Chronic Alcohol Intoxication|author1=Merle A. Carter |author2=Edward Bernstein |name-list-style=amp |page=272}}

Essential tremors—or, in the case of essential tremors on a background of family history of essential tremors, familial tremors—can be temporarily relieved in up to two-thirds of patients by drinking small amounts of alcohol.

{{cite journal |vauthors=Bain PG, Findley LJ, Thompson PD, etal |title=A study of hereditary essential tremor|journal=Brain|volume=117|issue=Pt 4|pages=805–24|date=August 1994|pmid=7922467|doi=10.1093/brain/117.4.805}}

{{cite journal|vauthors=Lou JS, Jankovic J |title=Essential tremor: clinical correlates in 350 patients|journal=Neurology|volume=41|issue=2 (Pt 1)|pages=234–8|date=February 1991|pmid=1992367|doi=10.1212/WNL.41.2_Part_1.234|s2cid=20531450}}

{{cite journal|doi=10.1002/mds.870131316|vauthors=Wasielewski PG, Burns JM, Koller WC |title=Pharmacologic treatment of tremor|journal=Mov. Disord.|volume=13|issue=Suppl 3|pages=90–100|year=1998|pmid=9827602|s2cid=21004382 }}

{{cite journal |vauthors=Boecker H, Wills AJ, Ceballos-Baumann A, etal |title=The effect of ethanol on alcohol-responsive essential tremor: a positron emission tomography study|journal=Annals of Neurology|volume=39|issue=5|pages=650–8|date=May 1996|pmid=8619551|doi=10.1002/ana.410390515|s2cid=11083928}}

{{cite journal|title=Setting a steady course for benign essential tremor|journal=Johns Hopkins Med Lett Health After 50|volume=11|issue=10|page=3|date=December 1999|pmid=10586714}}

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{{Cite journal

| last1 = Mostile | first1 = G.

| last2 = Jankovic | first2 = J.

| doi = 10.1002/mds.23240

| title = Alcohol in essential tremor and other movement disorders

| journal = Movement Disorders

| volume = 25

| issue = 14

| pages = 2274–2284

| year = 2010

| pmid = 20721919

| s2cid = 39981956

}} and could underlie the ameliorative effects.{{Cite journal

| last1 = Iseri | first1 = P. K.

| last2 = Karson | first2 = A.

| last3 = Gullu | first3 = K. M.

| last4 = Akman | first4 = O.

| last5 = Kokturk | first5 = S.

| last6 = Yardýmoglu | first6 = M.

| last7 = Erturk | first7 = S.

| last8 = Ates | first8 = N.

| doi = 10.1016/j.neuropharm.2011.05.015

| title = The effect of memantine in harmaline-induced tremor and neurodegeneration

| journal = Neuropharmacology

| volume = 61

| issue = 4

| pages = 715–723

| year = 2011

| pmid = 21640732

| s2cid = 16296043

}}{{Cite journal

| last1 = Miwa | first1 = H.

| doi = 10.1080/14734220601016080

| title = Rodent models of tremor

| journal = The Cerebellum

| volume = 6

| issue = 1

| pages = 66–72

| year = 2007

| pmid = 17366267

| s2cid = 24179439

}} Additionally, the effects of ethanol have been studied in different animal essential tremor models. (For more details on this topic, see Essential tremor).

{{main|Alcohol use and sleep}}

Chronic use of alcohol used to induce sleep can lead to insomnia: frequent moving between sleep stages occurs, with awakenings due to headaches and diaphoresis. Stopping chronic alcohol misuse can also lead to profound disturbances of sleep with vivid dreams. Chronic alcohol misuse is associated with NREM stage 3 and 4 sleep as well as suppression of REM sleep and REM sleep fragmentation. During withdrawal REM sleep is typically exaggerated as part of a rebound effect.{{Cite book|last1=Lee-chiong|first1=Teofilo|title=Sleep Medicine: Essentials and Review|date=24 April 2008|publisher=Oxford University Press, USA|url=https://books.google.com/books?id=s1F_DEbRNMcC&pg=PT105|isbn=978-0-19-530659-0|page=105}}

High rates of major depressive disorder occur in heavy drinkers. Whether it is more true that major depressive disorder causes self-medicating alcohol use, or the increased incidence of the disorder in people with an alcohol use disorder is caused by the drinking, is not known though some evidence suggests drinking causes the disorder.{{cite journal |vauthors=Fergusson DM, Boden JM, Horwood LJ |title=Tests of causal links between alcohol abuse or dependence and major depression |journal=Arch. Gen. Psychiatry |volume=66 |issue=3 |pages=260–6 |date=March 2009 |pmid=19255375 |doi=10.1001/archgenpsychiatry.2008.543}} Alcohol misuse is associated with a number of mental health disorders and alcoholics have a very high suicide rate.{{cite journal |vauthors=Chignon JM, Cortes MJ, Martin P, Chabannes JP |title=Tentative de suicide et dépendance alcoolique : résultats d'une enquête épidémiologique |trans-title=Attempted suicide and alcohol dependence: results of an epidemiologic survey |language=fr |journal=Encephale |volume=24 |issue=4 |pages=347–54 |year=1998 |pmid=9809240}} A study of people hospitalized for suicide attempts found that those who were alcoholics were 75 times more likely to go on to successfully commit suicide than non-alcoholic suicide attempts.{{Cite book|last1=Ayd|first1=Frank J.|title=Lexicon of psychiatry, neurology, and the neurosciences|url=https://books.google.com/books?id=ea_QVG2BFy8C|date=31 May 2000|publisher=Lippincott-Williams Wilkins|location=Philadelphia|isbn=978-0-7817-2468-5|page=349}} In the general alcoholic population the increased risk of suicide compared to the general public is 5-20 times greater. About 15 percent of alcoholics commit suicide, the most common methods being overdosing and cutting/scratching. There are high rates of suicide attempts, self-harm, suicidal ideation, and self-harm ideation in people with substance dependence who have been hospitalized.{{Cite journal |last1=Harned |first1=Melanie S. |last2=Najavits |first2=Lisa M. |last3=Weiss |first3=Roger D. |date=January 2006 |title=Self-Harm and Suicidal Behavior in Women with Comorbid PTSD and Substance Dependence |url=http://doi.wiley.com/10.1080/10550490600860387 |journal=American Journal on Addictions |language=en |volume=15 |issue=5 |pages=392–395 |doi=10.1080/10550490600860387 |pmid=16966196 |issn=1055-0496}} Use of other illicit drugs is also associated with an increased risk of suicide. About 33 percent of suicides in the under 35s are correlated with alcohol or other substance misuse.{{Cite book|last1=Appleby|first1=Louis|last2=Duffy|first2=David|last3=Ryan|first3=Tony|date=25 Aug 2004|title=New Approaches to Preventing Suicide: A Manual For Practitioners|url=https://books.google.com/books?id=d6Kw9GaJdzEC|publisher=Jessica Kingsley Publishers|isbn=978-1-84310-221-2|pages=31–32}}

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.{{cite journal|vauthors=Uekermann J, Daum I |title=Social cognition in alcoholism: a link to prefrontal cortex dysfunction?|journal=Addiction|volume=103|issue=5|pages=726–35|date=May 2008|pmid=18412750|doi=10.1111/j.1360-0443.2008.02157.x}}

Studies have shown that alcohol dependence relates directly to cravings and irritability.{{cite journal|vauthors=Jasova D, Bob P, Fedor-Freybergh P |title=Alcohol craving, limbic irritability, and stress|journal=Med. Sci. Monit.|volume=13|issue=12|pages=CR543–7|date=December 2007|pmid=18049433|url=http://www.medscimonit.com/fulltxt.php?ICID=563763|access-date=2008-05-13}} Another study has shown that alcohol use is a significant predisposing factor towards antisocial behavior in children.{{cite journal |vauthors=Young R, Sweeting H, West P |title=A longitudinal study of alcohol use and antisocial behaviour in young people |journal=Alcohol Alcohol. |volume=43 |issue=2 |pages=204–14 |year=2008 |pmid=17977868 |doi=10.1093/alcalc/agm147 |pmc=2367698}} 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).{{cite journal|author=Marinkovic K|author2=Oscar-Berman M |author3=Urban T |author4=O'Reilly CE |author5=Howard JA |author6=Sawyer K |author7=Harris GJ |date=November 2009|title=Alcoholism and dampened temporal limbic activation to emotional faces|journal=Alcohol Clin Exp Res|volume=33|issue=11|pages=1880–92|pmid=19673745|doi=10.1111/j.1530-0277.2009.01026.x|pmc=3543694}} 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.{{cite journal|author=Wetterling T|author2=Junghanns K |date=December 2000|title=Psychopathology of alcoholics during withdrawal and early abstinence|journal=Eur Psychiatry|volume=15|issue=8|pages=483–8|pmid=11175926|doi=10.1016/S0924-9338(00)00519-8|s2cid=24094651 }}{{cite journal|author=Cowley DS|date=24 January 1992|title=Alcohol abuse, substance abuse, and panic disorder|journal=Am J Med|volume=92|issue=1A|pages=41S–8S|pmid=1346485|doi=10.1016/0002-9343(92)90136-Y}}{{cite journal|author=Cosci F|author2=Schruers KR |author3=Abrams K |author4=Griez EJ |date=June 2007|title=Alcohol use disorders and panic disorder: a review of the evidence of a direct relationship|journal=J Clin Psychiatry|volume=68|issue=6|pages=874–80|pmid=17592911|doi=10.4088/JCP.v68n0608}} Psychosis is secondary to several alcohol-related conditions including acute intoxication and withdrawal after significant exposure.{{EMedicine|med|3113|Alcohol-Related Psychosis}} 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.{{cite journal|vauthors=Tien AY, Anthony JC |title=Epidemiological analysis of alcohol and drug use as risk factors for psychotic experiences|journal=J. Nerv. Ment. Dis.|volume=178|issue=8|pages=473–80|date=August 1990|pmid=2380692|doi=10.1097/00005053-199017880-00001}} 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.{{cite web|url=https://www.sciencedaily.com/releases/2013/08/130829214354.htm |title=A wine a day ... keeps the psychiatrist away? Light drinking linked to lower risk of depression |publisher=ScienceDaily |access-date=2014-04-22}}

While alcohol 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.{{cite journal |vauthors=Terra MB, Figueira I, Barros HM |title=Impact of alcohol intoxication and withdrawal syndrome on social phobia and panic disorder in alcoholic inpatients |journal=Rev Hosp Clin Fac Med Sao Paulo |volume=59 |issue=4 |pages=187–92 |date=August 2004 |pmid=15361983 |doi=10.1590/S0041-87812004000400006|doi-access=free }} 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.{{cite journal|author=Cohen SI|title=Alcohol and benzodiazepines generate anxiety, panic and phobias|journal=J R Soc Med|volume=88|issue=2|pages=73–7|date=February 1995|pmid=7769598|pmc=1295099}}

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.{{cite journal | vauthors = McClure EA, Gipson CD, Malcolm RJ, Kalivas PW, Gray KM | title = Potential role of N-acetylcysteine in the management of substance use disorders | journal = CNS Drugs | volume = 28 | issue = 2 | pages = 95–106 | year = 2014 | pmid = 24442756 | pmc = 4009342 | doi = 10.1007/s40263-014-0142-x }}

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.{{Cite journal |last1=Greenfield |first1=Shelly F. |last2=Weiss |first2=Roger D. |last3=Muenz |first3=Larry R. |last4=Vagge |first4=Lisa M. |last5=Kelly |first5=John F. |last6=Bello |first6=Lisa R. |last7=Michael |first7=Jacqueline |date=1998-03-01 |title=The Effect of Depression on Return to Drinking: A Prospective Study |url=https://doi.org/10.1001/archpsyc.55.3.259 |journal=Archives of General Psychiatry |volume=55 |issue=3 |pages=259–265 |doi=10.1001/archpsyc.55.3.259 |pmid=9510220 |issn=0003-990X}}

{{see also|Alcohol and weight|Alcoholic liver disease|Alcoholic hepatitis|Fatty liver|Cirrhosis}}

The impact of alcohol on weight-gain is contentious: some studies find no effect,{{cite journal|vauthors=Cordain L, Bryan ED, Melby CL, Smith MJ |title=Influence of moderate daily wine consumption on body weight regulation and metabolism in healthy free-living males |journal=J Am Coll Nutr |volume=16 |issue=2 |pages=134–9 |date=1 April 1997 |pmid=9100213 |url=http://intl.jacn.org/cgi/content/abstract/16/2/134 |doi=10.1080/07315724.1997.10718663 |url-status=dead |archive-url=https://web.archive.org/web/20070223161851/http://intl.jacn.org/cgi/content/abstract/16/2/134 |archive-date=23 February 2007 }} others find decreased{{cite journal|vauthors=Arif AA, Rohrer JE |title=Patterns of alcohol drinking and its association with obesity: data from the Third National Health and Nutrition Examination Survey, 1988–1994|journal=BMC Public Health|volume=5|page=126|year=2005|pmid=16329757|pmc=1318457|doi=10.1186/1471-2458-5-126|issue=1 |doi-access=free }} or increased effect on weight gain.

Alcohol use increases the risk of chronic gastritis (stomach inflammation);{{cite book|author=National Institute on Alcohol Abuse and Alcoholism (NIAAA)|title=Health risks and benefits of alcohol consumption|journal=Alcohol Res Health|volume=24|issue=1|pages=5–11|year=2000|pmid=11199274|pmc=6713002|url=http://pubs.niaaa.nih.gov/publications/arh24-1/05-11.pdf|doi=10.4135/9781412963855.n839|isbn=9781412941860|access-date=2006-07-31|archive-date=2020-11-11|archive-url=https://web.archive.org/web/20201111230707/https://pubs.niaaa.nih.gov/publications/arh24-1/05-11.pdf|url-status=dead}}{{cite journal|vauthors=Bode C, Bode JC|title=Alcohol's role in gastrointestinal tract disorders|journal=Alcohol Health Res World|volume=21|issue=1|pages=76–83|year=1997|pmid=15706765|pmc=6826790|url=https://webapps.ou.edu/alcohol/docs/12EtohGastroinstestinalTractDisorders76.pdf|url-status=dead|archive-url=https://web.archive.org/web/20060902085657/https://webapps.ou.edu/alcohol/docs/12EtohGastroinstestinalTractDisorders76.pdf|archive-date=2006-09-02}} it is one cause of cirrhosis, hepatitis, and pancreatitis in both its chronic and acute forms.

A national survey (NHANES) conducted in the U.S. concluded, "Mild to moderate alcohol consumption is associated with a lower prevalence of the metabolic syndrome, with a favorable influence on lipids, waist circumference, and fasting insulin. This association was strongest among whites and among beer and wine drinkers."{{cite journal|vauthors=Freiberg MS, Cabral HJ, Heeren TC, Vasan RS, Curtis Ellison R |title=Alcohol consumption and the prevalence of the Metabolic Syndrome in the US.: a cross-sectional analysis of data from the Third National Health and Nutrition Examination Survey|journal=Diabetes Care|volume=27|issue=12|pages=2954–2959|date=2004|pmid=15562213 |url=http://care.diabetesjournals.org/cgi/content/full/27/12/2954|doi=10.2337/diacare.27.12.2954}} Similarly, a national survey conducted in Korea reported a J-curve association between alcohol intake and metabolic syndrome: "The results of the present study suggest that the metabolic syndrome is negatively associated with light alcohol consumption (1–15 g alcohol/d) in Korean adults," but risk increased at higher alcohol consumption.{{cite journal|vauthors=Yoon YS, Oh SW, Baik HW, Park HS, Kim WY |title=Alcohol consumption and the metabolic syndrome in Korean adults: the 1998 Korean National Health and Nutrition Examination Survey|journal=Am J Clin Nutr |volume=80 |issue=1|pages=217–224|date=2004 |pmid=15213051 |doi=10.1093/ajcn/80.1.217|doi-access=free }}

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."{{cite journal|vauthors=La Vecchia C, Decarli A, Ferraroni M, Negri E |title=Alcohol drinking and prevalence of self-reported gallstone disease in the 1983 Italian National Health Survey|journal=Epidemiology|volume=5|issue=5|pages=533–6|date=September 1994|pmid=7986868|jstor=3702209 |url=http://journals.lww.com/epidem/Abstract/1994/09000/Alcohol_Drinking_and_Prevalence_of_Self_Reported.11.aspx}} 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."{{cite journal|doi=10.1111/j.1530-0277.1999.tb04191.x |vauthors=Leitzmann MF, Giovannucci EL, Stampfer MJ, etal |title=Prospective study of alcohol consumption patterns in relation to symptomatic gallstone disease in men|journal=Alcohol Clin Exp Res|volume=23|issue=5|pages=835–41|date=May 1999|pmid=10371403}}

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.{{cite journal|vauthors=Sahi T, Paffenbarger RS, Hsieh CC, Lee IM |title=Body mass index, cigarette smoking, and other characteristics as predictors of self-reported, physician-diagnosed gallbladder disease in male college alumni|journal=Am J Epidemiol|volume=147|issue=7|pages=644–51|date=1 April 1998|pmid=9554603|doi=10.1093/oxfordjournals.aje.a009505|doi-access=free}} 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.{{cite journal|vauthors=Simon JA, Grady D, Snabes MC, Fong J, Hunninghake DB |title=Ascorbic acid supplement use and the prevalence of gallbladder disease. Heart & Estrogen-Progestin Replacement Study (HERS) Research Group|journal=J Clin Epidemiol|volume=51|issue=3|pages=257–65|date=March 1998|pmid=9495691|doi=10.1016/S0895-4356(97)80280-6}}

{{Main|Alcoholic liver disease|Cirrhosis|Hepatotoxin|Alcoholic hepatitis|Fatty liver disease}}

During the metabolism of alcohol via the respective dehydrogenases, nicotinamide adenine dinucleotide (NAD) is converted into reduced NAD. Normally, NAD is used to metabolize fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in alcohol use disorder) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called cirrhosis.

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 anti-TNFs. Certain complementary medications, e.g., milk thistle and silymarin, appear to offer some benefit.{{cite journal|vauthors=Barve A, Khan R, Marsano L, Ravindra KV, McClain C |title=Treatment of alcoholic liver disease|journal=Ann Hepatol|volume=7|issue=1|pages=5–15|year=2008|pmid=18376362|url=http://www.stopdrinkingexpert.com/pdf/ijms.pdf|doi=10.1016/S1665-2681(19)31883-6}}{{cite journal|vauthors=Fehér J, Lengyel G |title=Silymarin in the treatment of chronic liver diseases: past and future|language=hu|journal=Orv Hetil|volume=149|issue=51|pages=2413–8|date=December 2008|pmid=19073452|doi=10.1556/OH.2008.28519}} 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.{{cite journal|author=Voigt MD|title=Alcohol in hepatocellular cancer|journal=Clin Liver Dis|volume=9|issue=1|pages=151–69|date=February 2005|pmid=15763234|doi=10.1016/j.cld.2004.10.003|url=http://journals.elsevierhealth.com/retrieve/pii/S1089-3261(04)00115-1}}{{cite journal|vauthors=Morgan TR, Mandayam S, Jamal MM |title=Alcohol and hepatocellular carcinoma|journal=Gastroenterology|volume=127|issue=5 Suppl 1|pages=S87–96|date=November 2004|pmid=15508108|doi=10.1053/j.gastro.2004.09.020|doi-access=free}}

Alcohol misuse is a leading cause of both acute pancreatitis and chronic pancreatitis.{{cite journal|vauthors=Frossard JL, Steer ML, Pastor CM |title=Acute pancreatitis|journal=Lancet|volume=371|issue=9607|pages=143–52|date=January 2008|pmid=18191686|doi=10.1016/S0140-6736(08)60107-5}}{{cite journal|vauthors=Bachmann K, Mann O, Izbicki JR, Strate T |title=Chronic pancreatitis--a surgeons' view|journal=Med. Sci. Monit.|volume=14|issue=11|pages=RA198–205|date=November 2008|pmid=18971885}} Alcoholic pancreatitis can result in severe abdominal pain and may progress to pancreatic cancer.{{cite journal|vauthors=Nair RJ, Lawler L, Miller MR |title=Chronic pancreatitis|journal=Am Fam Physician|volume=76|issue=11|pages=1679–88|date=December 2007|pmid=18092710}}

Chronic pancreatitis often results in intestinal malabsorption, and can result in diabetes.{{cite journal|vauthors=Tattersall SJ, Apte MV, Wilson JS |title=A fire inside: current concepts in chronic pancreatitis|journal=Intern Med J|volume=38|issue=7|pages=592–8|date=July 2008|pmid=18715303|doi=10.1111/j.1445-5994.2008.01715.x|s2cid=205502466|doi-access=free}}

{{See also|Drunkorexia}}

Alcohol affects the nutritional state of chronic drinkers. It can decrease food consumption and lead to malabsorption. It can also create imbalances in skeletal muscle mass and cause muscle wasting. Chronic consumption of alcohol can also increase the breakdown of important proteins in the body which can affect gene expression.{{cite journal |vauthors=Molina PE, Gardner JD, Souza-Smith FM, Whitaker AM |title=Alcohol abuse: critical pathophysiological processes and contribution to disease burden |journal=Physiology |volume=29 |issue=3 |pages=203–215 |date=2014 |pmid=24789985 |pmc=4046814 |doi=10.1152/physiol.00055.2013 }}

The consumption of alcohol alone is not associated with an increased risk of oral squamous cell carcinoma (OSCC); however, the synergistic consumption of alcohol and tobacco is positively associated with the occurrence of (OSCC), and significantly increases an individual's risk. Studies confirm that alcohol dissolves the lipid component of epithelium and increases the permeability, amplifying the toxicity of carcinogenic components of tobacco. Limiting the overall consumption of the two has shown to reduce the risk of OSCC by three-fourth. The knowledge provided is useful for better understanding the differences in the effect of the combined consumption of alcohol and tobacco, in the development of OSCC.{{Cite journal |last1=Mello |first1=Fernanda Weber |last2=Melo |first2=Gilberto |last3=Pasetto |first3=Júlia Jacoby |last4=Silva |first4=Carolina Amália Barcellos |last5=Warnakulasuriya |first5=Saman |last6=Rivero |first6=Elena Riet Correa |date=July 2019 |title=The synergistic effect of tobacco and alcohol consumption on oral squamous cell carcinoma: a systematic review and meta-analysis |url=http://link.springer.com/10.1007/s00784-019-02958-1 |journal=Clinical Oral Investigations |language=en |volume=23 |issue=7 |pages=2849–2859 |doi=10.1007/s00784-019-02958-1 |pmid=31111280 |s2cid=159040972 |issn=1432-6981}}

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.{{Cite journal |last1=Singhavi |first1=Hitesh Rajendra |last2=Singh |first2=Arjun |last3=Bhattacharjee |first3=Atanu |last4=Talole |first4=Sanjay |last5=Dikshit |first5=Rajesh |last6=Chaturvedi |first6=Pankaj |date=April 2020 |title=Alcohol and cancer risk: A systematic review and meta-analysis of prospective Indian studies |journal=Indian Journal of Public Health |volume=64 |issue=2 |pages=186–190 |doi=10.4103/ijph.IJPH_529_19 |issn=0019-557X |pmid=32584303 |doi-access=free }}

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.{{Cite journal |last1=Ustrell-Borràs |first1=M. |last2=Traboulsi-Garet |first2=B. |last3=Gay-Escoda |first3=C. |date=2020-01-01 |title=Alcohol-based mouthwash as a risk factor of oral cancer: A systematic review |journal=Medicina Oral, Patologia Oral y Cirugia Bucal |volume=25 |issue=1 |pages=e1–e12 |doi=10.4317/medoral.23085 |issn=1698-6946 |pmc=6982979 |pmid=31655832}}

{{main|Periodontitis}}

File:Periodontal_Disease.png

Alcohol consumption is associated with a higher risk of periodontitis, an inflammatory disease of the gums around the teeth. There was also found to be a dose-response relationship in which the risk of periodontitis increased by 0.4% for each additional gram of daily alcohol consumption. Mechanisms explaining the relationship between the two are still unclear; however, several explanations have been suggested. One explanation is the weakening of neutrophil activity by alcohol consumption which potentially leads to bacterial overgrowth and increases bacterial penetration subsequently leading to periodontal inflammation and periodontal disease. Characteristics of the disease include shrinkage of gingival height and increased mobility of teeth which may exfoliate if the disease continues to progress. A patient's consumption of alcohol needs to be monitored to estimate the risk of periodontitis, but further well-designed cohort studies are needed to reaffirm theses results.{{Cite journal |last1=Wang |first1=Jiantao |last2=Lv |first2=Jian |last3=Wang |first3=Wanchun |last4=Jiang |first4=Xiubo |date=July 2016 |title=Alcohol consumption and risk of periodontitis: a meta-analysis |url=https://pubmed.ncbi.nlm.nih.gov/27029013 |journal=Journal of Clinical Periodontology |volume=43 |issue=7 |pages=572–583 |doi=10.1111/jcpe.12556 |issn=1600-051X |pmid=27029013}}

Chronic alcohol ingestion can impair multiple critical cellular functions in the lungs.{{Cite journal|last1=Traphagen|first1=Nicole|last2=Tian|first2=Zhi|last3=Allen-Gipson|first3=Diane|date=2015-10-20|title=Chronic Ethanol Exposure: Pathogenesis of Pulmonary Disease and Dysfunction|journal=Biomolecules|language=en|volume=5|issue=4|pages=2840–2853|doi=10.3390/biom5042840|pmid=26492278|issn=2218-273X|pmc=4693259|doi-access=free}} These cellular impairments can lead to increased susceptibility to serious complications from lung disease. Recent research cites alcoholic lung disease as comparable to liver disease in alcohol-related mortality.{{Cite journal|last=Kershaw, Guidot|first=Corey D., David M.|date=2008|title=Alcoholic lung disease|url=https://go.gale.com/ps/anonymous?id=GALE%7CA181716898&sid=googleScholar&v=2.1&it=r&linkaccess=abs&issn=15357414&p=AONE&sw=w|journal=Alcohol Research & Health|volume=31|issue=1|pages=66–75|pmid=23584753|pmc=3860447|via=U.S. Government Printing Office}} Alcoholics have a higher risk of developing acute respiratory distress syndrome (ARDS) and experience higher rates of mortality from ARDS when compared to non-alcoholics.{{Cite web|last=Gregg|first=Valerie|date=2008|title=The Hidden Truth about Alcohol|url=https://www.whsc.emory.edu/|access-date=October 22, 2020|website=Emory University School of Medicine|archive-date=October 31, 2008|archive-url=https://web.archive.org/web/20081031044426/http://www.whsc.emory.edu/|url-status=dead}} In contrast to these findings, a large prospective study has shown a protective effect of moderate alcohol consumption on respiratory mortality.{{cite journal|vauthors=Doll R, Peto R, Boreham J, Sutherland I |title=Mortality in relation to alcohol consumption: a prospective study among male British doctors|journal=Int J Epidemiol|volume=34|issue=1|pages=199–204|date=February 2005|pmid=15647313|doi=10.1093/ije/dyh369|doi-access=free}}

Research indicates that drinking beer or wine is associated with a lower risk of developing kidney stones.{{cite journal|vauthors=Hirvonen T, Pietinen P, Virtanen M, Albanes D, Virtamo J |title=Nutrient intake and use of beverages and the risk of kidney stones among male smokers|journal=Am J Epidemiol|volume=150|issue=2|pages=187–194 |date=1999|pmid=10412964 |doi=10.1093/oxfordjournals.aje.a009979|s2cid=10690400|doi-access=free}}{{cite journal|vauthors=Soucie JM, Coates RJ, McClellan W, Austin H, Thun M |title=Relation between geographic variability in kidney stones prevalence and risk factors for stones|journal=Am J Epidemiol|volume=143|issue=5|pages=487–495|date=1996 |pmid=8610664 |doi=10.1093/oxfordjournals.aje.a008769|doi-access=free}}{{cite journal|vauthors=Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ |title=Prospective study of beverage use and the risk of kidney stones|journal=Am J Epidemiol|volume=143 |issue=3|pages=240–247|date=1996|pmid=8561157 |doi=10.1093/oxfordjournals.aje.a008734|doi-access=free}}{{cite journal|vauthors=Curhan GC, Willett WC, Speizer FE, Stampfer MJ |title=Beverage use and risk for kidney stones in women |journal=Annals of Internal Medicine |volume=128|issue=7|pages=534–540|date=1998|pmid=9518397 |doi=10.7326/0003-4819-128-7-199804010-00003 |s2cid=43163872 }}

{{Main|Alcohol and sex}}

Low to moderate alcohol consumption is shown to have protective effect for men's erectile function. Several reviews and meta-analyses of existing literature show that low to moderate alcohol consumption significantly decrease erectile dysfunction risk.{{cite journal

|first1=Mark S |last1=Allen

|first2=Emma E |last2=Walter

|year=2018

|title=Health-Related Lifestyle Factors and Sexual Dysfunction: A Meta-Analysis of Population-Based Research

|journal=The Journal of Sexual Medicine

|volume=15 |issue=4

|pages=458–475

|url=https://www.jsm.jsexmed.org/article/S1743-6095(18)30124-3/fulltext

|doi=10.1016/j.jsxm.2018.02.008

|pmid=29523476

}}{{cite journal

|first1=J Y W |last1=Cheng

|first2=E M L |last2=Ng

|first3=R Y L |last3=Chen

|first4=J S N |last4=Ko

|year=2007

|title=Alcohol consumption and erectile dysfunction: meta-analysis of population-based studies

|journal=International Journal of Impotence Research

|volume=19 |issue=4

|pages=343–352

|doi=10.1038/sj.ijir.3901556

|pmid=17538641

|doi-access=free

}}{{cite journal

|first1=Xiao-Ming |last1=Wang

|first2=Yun-Jin |last2=Bai

|first3=Yu-Bo |last3=Yang

|first4=Jin-Hong |last4=Li

|first5=Yin |last5=Tang

|first6=Ping |last6=Han

|year=2018

|title=Alcohol intake and risk of erectile dysfunction: a dose-response meta-analysis of observational studies

|journal=International Journal of Impotence Research

|volume=30 |issue=6

|pages=342–351

|url=https://www.nature.com/articles/s41443-018-0022-x

|doi=10.1038/s41443-018-0022-x

|pmid=30232467

|s2cid=52300588

}}{{cite journal

|first1=Bang-Ping |last1=Jiann

|year=2010

|title=Effect of Alcohol Consumption on the Risk of Erectile Dysfunction

|journal=Urol Sci

|volume=21 |issue=4

|pages=163–168

|doi=10.1016/S1879-5226(10)60037-1

|url=https://core.ac.uk/download/pdf/82131458.pdf

|doi-access=free

}}

Men's sexual behaviors can be affected dramatically by high alcohol consumption. Both chronic and acute alcohol consumption have been shown in most studies

{{cite journal

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|last2=Torres |first2=JM

|last3=Miranda |first3=MT

|last4=Ruiz |first4=E

|last5=Ortega |first5=E

|year=2002

|title=Effects of acute alcohol intoxication on pituitary-gonadal axis hormones, pituitary-adrenal axis hormones, beta-endorphin and prolactin in human adults of both sexes

|journal=Alcohol and Alcoholism

|volume=37 |issue=2 |pages=169–73

|doi=10.1093/alcalc/37.2.169

|pmid=11912073

|doi-access=free

}}

{{cite journal

|last1=Mendelson |first1=JH

|last2=Ellingboe |first2=J

|last3=Mello |first3=NK

|last4=Kuehnle |first4=John

|year=1978

|title=Effects of Alcohol on Plasma Testosterone and Luteinizing Hormone Levels

|journal=Alcoholism: Clinical and Experimental Research

|volume=2 |issue=3 |pages=255–8

|doi=10.1111/j.1530-0277.1978.tb05808.x

|pmid=356646

}}

{{cite journal

|last1=Mendelson |first1=JH

|last2=Mello |first2=NK

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|year=1977

|title=Effects of acute alcohol intake on pituitary-gonadal hormones in normal human males

|journal=Journal of Pharmacology and Experimental Therapeutics

|volume=202 |issue=3 |pages=676–82

|pmid=894528

}} (but not all

{{cite journal

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|journal=Alcoholism: Clinical and Experimental Research

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|doi=10.1111/j.1530-0277.2003.tb04405.x

|pmid=12711931

}}) 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.

{{cite book

|last1=Emanuele |first1=MA

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|chapter=The effects of alcohol on the neuroendocrine control of reproduction

|editor1-last=Zakhari |editor1-first=S

|title=Alcohol and the Endocrine System

|pages=89–116

|publisher=National Institute of Health Publications

|id=NIH Pub 93-3533

}}

{{cite journal

|last1=Ellingboe |first1=J

|last2=Varanelli |first2=CC

|year=1979

|title=Ethanol inhibits testosterone biosynthesis by direct action on Leydig cells

|journal=Research Communications in Chemical Pathology and Pharmacology

|volume=24|issue=1|pages=87–102

|pmid=219455

}}

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.{{cite journal|vauthors=Taniguchi N, Kaneko S |title=Alcoholic effect on male sexual function|language=ja|journal=Nippon Rinsho|volume=55|issue=11|pages=3040–4|date=November 1997|pmid=9396310}} 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.{{cite journal|vauthors=Yoshitsugu M, Ihori M |title=Endocrine disturbances in liver cirrhosis—focused on sex hormones|language=ja|journal=Nippon Rinsho|volume=55|issue=11|pages=3002–6|date=November 1997|pmid=9396303}}

Excessive alcohol intake can result in hyperoestrogenisation.{{Cite journal|last1=Fentiman|first1=IS.|last2=Fourquet|first2=A.|last3=Hortobagyi|first3=GN.|title=Male breast cancer|journal=Lancet|volume=367|issue=9510|pages=595–604|date=Feb 2006|doi=10.1016/S0140-6736(06)68226-3|pmid=16488803|s2cid=21618414}} It has been speculated that alcoholic beverages may contain estrogen-like compounds. In men, high levels of estrogen can lead to testicular failure and the development of feminine traits including development of male breasts, called gynecomastia.{{Cite journal|last1=Gavaler|first1=JS.|title=Alcoholic beverages as a source of estrogens.|journal=Alcohol Health Res World|volume=22|issue=3|pages=220–7|year=1998|pmid=15706799|pmc=6761902}}{{Cite journal|last1=Weiss|first1=JR.|last2=Moysich|first2=KB.|last3=Swede|first3=H.|title=Epidemiology of male breast cancer|journal=Cancer Epidemiol Biomarkers Prev|volume=14|issue=1|pages=20–6|date=Jan 2005|doi=10.1158/1055-9965.20.14.1 |pmid=15668471|s2cid=9667914 |doi-access=free}} In women, increased levels of estrogen due to excessive alcohol intake have been related to an increased risk of breast cancer.{{Cite journal|last1=Boffetta|first1=P.|last2=Hashibe|first2=M.|title=Alcohol and cancer|journal=Lancet Oncol|volume=7|issue=2|pages=149–56|date=Feb 2006|doi=10.1016/S1470-2045(06)70577-0|pmid=16455479}}

{{Main|Alcohol and cortisol}}

Alcohol and cortisol have a complex relationship. While cortisol is a stress hormone, alcoholism can lead to increased cortisol levels in the body over time. This can be problematic because cortisol can temporarily shut down other bodily functions, potentially causing physical damage.

A meta-analysis determined the dose-response relationships by sex and end point using lifetime abstainers as the reference group. A U-shaped relationship was found for both sexes. Compared with lifetime abstainers, the relative risk (RR) for type 2 diabetes among men was most protective when consuming 22 g/day alcohol and became deleterious at just over 60 g/day alcohol. Among women, consumption of 24 g/day alcohol was most protective, and became deleterious at about 50 g/day alcohol.{{citation needed|date=April 2019}} A systematic review on intervention studies in women also supported this finding. It reported that alcohol consumption in moderation improved insulin sensitivity among women.{{cite journal |vauthors=Schrieks IC, Heil AL, Hendriks HF, Mukamal KJ, Beulens JW |title=The effect of alcohol consumption on insulin sensitivity and glycemic status: a systematic review and meta-analysis of intervention studies |journal=Diabetes Care |volume=38 |issue=4 |pages=723–732 |date=2015 |pmid=25805864 |doi=10.2337/dc14-1556 |s2cid=32005728 |doi-access=free }}

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.{{cite journal|title=Alcohol as a Risk Factor for Type 2 Diabetes |pmc=2768203 | pmid=19875607 |doi=10.2337/dc09-0227 |volume=32 |issue=11 |year=2009 |journal=Diabetes Care |pages=2123–2132 |vauthors=Baliunas DO, Taylor BJ, Irving H, Roerecke M, Patra J, Mohapatra S, Rehm J}} In the United Kingdom "advice on weekly consumption is avoided".{{citation needed|date=April 2019}} 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.{{cite journal|vauthors=Carlsson S, Hammar N, Grill V, Kaprio J |title=Alcohol consumption and the incidence of type 2 diabetes: a 20-year follow-up of the Finnish twin cohort study|journal=Diabetes Care|volume=26|issue=10|pages=2785–2790|date=2003 |pmid=14514580 |url=http://care.diabetesjournals.org/cgi/content/full/26/10/2785|doi=10.2337/diacare.26.10.2785|doi-access=free}}

Regular consumption of alcohol is associated with an increased risk of gouty arthritis{{cite journal|vauthors=Star VL, Hochberg MC |title=Prevention and management of gout|journal=Drugs|volume=45|issue=2|pages=212–22|date=February 1993|pmid=7681372|doi=10.2165/00003495-199345020-00004|s2cid=36034581}}{{cite journal|author=Eggebeen AT|title=Gout: an update|journal=Am Fam Physician|volume=76|issue=6|pages=801–8|date=September 2007|pmid=17910294}} and a decreased risk of rheumatoid arthritis.{{cite web |url=http://arc.org.uk/arthinfo/patpubs/6033/6033.asp |title=Rheumatoid Arthritis |access-date=2008-06-18 |url-status=dead |archive-url=https://web.archive.org/web/20080613202734/http://www.arc.org.uk/arthinfo/patpubs/6033/6033.asp |archive-date=2008-06-13 }}{{cite journal|vauthors=Myllykangas-Luosujärvi R, Aho K, Kautiainen H, Hakala M |title=Reduced incidence of alcohol related deaths in subjects with rheumatoid arthritis|journal=Ann. Rheum. Dis.|volume=59|issue=1|pages=75–6|date=January 2000|pmid=10627433|pmc=1752983|doi=10.1136/ard.59.1.75}}{{cite journal |vauthors=Nagata C, Fujita S, Iwata H, etal |title=Systemic lupus erythematosus: a case-control epidemiologic study in Japan|journal=Int J Dermatol|volume=34|issue=5|pages=333–7|date=May 1995|pmid=7607794|doi=10.1111/j.1365-4362.1995.tb03614.x|s2cid=24940881}}{{cite journal|vauthors=Aho K, Heliövaara M |title=Alcohol, androgens and arthritis|journal=Ann. Rheum. Dis.|volume=52|issue=12|page=897|date=December 1993|pmid=8311545|pmc=1005228|doi=10.1136/ard.52.12.897-b}}{{cite journal|vauthors=Hardy CJ, Palmer BP, Muir KR, Sutton AJ, Powell RJ |title=Smoking history, alcohol consumption, and systemic lupus erythematosus: a case-control study|journal=Ann. Rheum. Dis.|volume=57|issue=8|pages=451–5|date=August 1998|pmid=9797548|pmc=1752721|url=|doi=10.1136/ard.57.8.451}} 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.{{cite journal |vauthors=Källberg H, Jacobsen S, Bengtsson C, etal |title=Alcohol consumption is associated with decreased risk of rheumatoid arthritis; Results from two Scandinavian case-control studies|journal=Ann. Rheum. Dis.|date=July 2008|pmid=18535114|pmc=2937278|doi=10.1136/ard.2007.086314|volume=68|pages=222–7|issue=2}}

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.{{cite journal |vauthors=Jonsson IM, Verdrengh M, Brisslert M, etal |title=Ethanol prevents development of destructive arthritis|journal=Proc Natl Acad Sci USA|volume=104|issue=1|pages=258–63|date=January 2007|pmid=17185416|pmc=1765445|doi=10.1073/pnas.0608620104|doi-access=free}}

A study concluded, "Alcohol either protects from RA or, subjects with RA curtail their drinking after the manifestation of RA".{{cite journal|vauthors=Myllykangas-Luosujärvi R, Aho K, Kautiainen H, Hakala M |title=Reduced incidence of alcohol related deaths in subjects with rheumatoid arthritis|journal=Ann. Rheum. Dis.|volume=59|issue=1|pages=75–6|date=January 2000|pmid=10627433|pmc=1752983|url=|doi=10.1136/ard.59.1.75}} Another study found, "Postmenopausal women who averaged more than 14 alcoholic drinks per week had a reduced risk of rheumatoid arthritis..."{{cite journal|vauthors=Voigt LF, Koepsell TD, Nelson JL, Dugowson CE, Daling JR |title=Smoking, obesity, alcohol consumption, and the risk of rheumatoid arthritis|journal=Epidemiology|volume=5|issue=5|pages=525–32|date=September 1994|pmid=7986867}}

Moderate alcohol consumption is associated with higher bone mineral density in postmenopausal women. "...Alcohol consumption significantly decreased the likelihood [of osteoporosis]."{{cite journal |vauthors=Siris ES, Miller PD, Barrett-Connor E, etal |title=Identification and fracture outcomes of undiagnosed low bone mineral density in postmenopausal women: results from the National Osteoporosis Risk Assessment|journal=JAMA|volume=286|issue=22|pages=2815–22|date=December 2001|pmid=11735756|doi=10.1001/jama.286.22.2815}} "Moderate alcohol intake was associated with higher BMD in postmenopausal elderly women."{{cite journal|vauthors=Rapuri PB, Gallagher JC, Balhorn KE, Ryschon KL|title=Alcohol intake and bone metabolism in elderly women|journal=Am. J. Clin. Nutr.|volume=72|issue=5|pages=1206–13|date=1 November 2000|pmid=11063451|url=http://intl.ajcn.org/cgi/content/abstract/72/5/1206|url-status=dead|archive-url=https://archive.today/20120527081459/http://intl.ajcn.org/cgi/content/abstract/72/5/1206|archive-date=27 May 2012|doi=10.1093/ajcn/72.5.1206|doi-access=free}} "Social drinking is associated with higher bone mineral density in men and women [over 45]."{{cite journal|vauthors=Holbrook TL, Barrett-Connor E |title=A prospective study of alcohol consumption and bone mineral density|journal=BMJ|volume=306|issue=6891|pages=1506–9|date=June 1993|pmid=8518677|pmc=1677960|doi=10.1136/bmj.306.6891.1506}} However, heavy alcohol use is associated with bone loss.{{Cite journal|last1=Ronis|first1=MJ.|last2=Wands|first2=JR.|last3=Badger|first3=TM.|last4=de la Monte|first4=SM.|last5=Lang|first5=CH.|last6=Calissendorff|first6=J.|title=Alcohol-induced disruption of endocrine signaling.|journal=Alcohol Clin Exp Res|volume=31|issue=8|pages=1269–85|date=Aug 2007|doi=10.1111/j.1530-0277.2007.00436.x|pmid=17559547}}{{Cite journal|last1=Peer|first1=KS.|last2=Newsham|first2=KR.|title=A case study on osteoporosis in a male athlete: looking beyond the usual suspects.|journal=Orthop Nurs|volume=24|issue=3|pages=193–9; quiz 200–1|year=2005|pmid=15928528|doi=10.1097/00006416-200505000-00007 |s2cid=23377405}}

Chronic excessive alcohol use is associated with a wide range of skin disorders including urticaria, porphyria cutanea tarda, flushing, cutaneous stigmata of cirrhosis, psoriasis, pruritus, seborrheic dermatitis, and rosacea.{{cite journal|vauthors=Kostović K, Lipozencić J |title=Skin diseases in alcoholics|journal=Acta Dermatovenerol Croat|volume=12|issue=3|pages=181–90|year=2004|pmid=15369644}}

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."{{cite journal |author=Qureshi Abrar A. |author2=Dominguez Patrick L. |author3=Choi Hyon K. |author4=Han Jiali |author5=Curhan Gary | year = 2010| title = Alcohol Intake and Risk of Incident Psoriasis in US Women: A Prospective Study | journal = Arch Dermatol | volume = 146 | issue = 12| pages = 1364–1369| doi = 10.1001/archdermatol.2010.204 | pmid = 20713772| pmc = 3017376 }}

Excessive alcohol consumption seen in people with an alcohol use disorder is a known risk factor for developing pneumonia.{{citation needed|date=November 2021}}

A study on the common cold found that "Greater numbers of alcoholic drinks (up to three or four per day) were associated with decreased risk for developing colds because drinking was associated with decreased illness following infection. However, the benefits of drinking occurred only among nonsmokers. ... Although alcohol consumption did not influence risk of clinical illness for smokers, moderate alcohol consumption was associated with decreased risk for nonsmokers."{{cite journal|vauthors=Cohen S, Tyrrell DA, Russell MA, Jarvis MJ, Smith AP |title=Smoking, alcohol consumption, and susceptibility to the common cold|journal=Am J Public Health|volume=83|issue=9|pages=1277–83|date=September 1993|pmid=8363004|pmc=1694990|doi=10.2105/AJPH.83.9.1277}}

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."{{cite journal|vauthors=Takkouche B, Regueira-Méndez C, García-Closas R, Figueiras A, Gestal-Otero JJ, Hernán MA |title=Intake of wine, beer, and spirits and the risk of clinical common cold|journal=Am J Epidemiol|volume=155|issue=9|pages=853–8|date=May 2002|pmid=11978590|doi=10.1093/aje/155.9.853|doi-access=free}}

{{Main|Alcohol and cancer}}

In 1988, the International Agency for Research on Cancer (Centre International de Recherche sur le Cancer) of the World Health Organization classified alcohol as a Group 1 carcinogen, stating "There is sufficient evidence for the carcinogenicity of alcoholic beverages in humans.... Alcoholic beverages are carcinogenic to humans (Group 1)."IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Volume 44 [http://monographs.iarc.fr/ENG/Monographs/vol44/volume44.pdf Alcohol Drinking: Summary of Data Reported and Evaluation] {{webarchive|url=https://web.archive.org/web/20120617090521/http://monographs.iarc.fr/ENG/Monographs/vol44/volume44.pdf |date=2012-06-17 }} The U.S. Department of Health & Human Services' National Toxicology Program in 2000 listed alcohol as a known carcinogen.National Toxicology Program [https://ntp.niehs.nih.gov/ntp/roc/content/profiles/alcoholicbeverageconsumption.pdf Alcoholic Beverage Consumption: Known to be a human carcinogen] {{webarchive|url=https://web.archive.org/web/20100605122604/http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s007alco.pdf |date=2010-06-05 }} First listed in the Ninth Report on Carcinogens (2000)(PDF)

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."{{Cite journal|vauthors=Boffetta P, Hashibe M, La Vecchia C, Zatonski W, Rehm J |title=The burden of cancer attributable to alcohol drinking |journal=International Journal of Cancer |volume=119 |issue=4 |pages=884–7 |date=August 2006 |pmid=16557583 |doi=10.1002/ijc.21903|hdl=2434/22728 |s2cid=14938863 |hdl-access=free }} 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 [https://www.bbc.co.uk/news/health-12999000 Drinking over recommended limit 'raises cancer risk'] 8 April 2011{{cite journal | author = Schütze Madlen|display-authors=etal| year = 2011 | title = Alcohol attributable burden of incidence of cancer in eight European countries based on results from prospective cohort study | url= | journal = BMJ | volume = 342 | page = d1584 | doi = 10.1136/bmj.d1584 | pmid = 21474525 | pmc=3072472}} 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 [http://eprints.ucl.ac.uk/4841/1/4841.pdf 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] {{webarchive|url=https://web.archive.org/web/20130523121425/http://eprints.ucl.ac.uk/4841/1/4841.pdf |date=2013-05-23 }}

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.{{cite journal |vauthors=LoConte NK, Brewster AM, Kaur JS, Merrill JK, Alberg AJ |title=Alcohol and Cancer: A Statement of the American Society of Clinical Oncology |journal=J. Clin. Oncol. |volume=36 |issue=1 |pages=83–93 |date=2018 |pmid=29112463 |doi=10.1200/JCO.2017.76.1155|s2cid=25271140 |quote=Clearly, the greatest cancer risks are concentrated in the heavy and moderate drinker categories. Nevertheless, some cancer risk persists even at low levels of consumption. A meta-analysis that focused solely on cancer risks associated with drinking one drink or fewer per day observed that this level of alcohol consumption was still associated with some elevated risk for squamous cell carcinoma of the esophagus (sRR, 1.30; 95% CI, 1.09 to 1.56), oropharyngeal cancer (sRR, 1.17; 95% CI, 1.06 to 1.29), and breast cancer (sRR, 1.05; 95% CI, 1.02 to 1.08), but no discernable associations were seen for cancers of the colorectum, larynx, and liver.}}

Acetaldehyde is the major metabolite when one drinks alcohol, produced in the liver, and it is known to be carcinogenic.[http://monographs.iarc.fr/ENG/Classification/ClassificationsGroupOrder.pdf Agents Classified by the IARC Monographs, Volumes 1–111] {{Webarchive|url=https://web.archive.org/web/20111025122327/http://monographs.iarc.fr/ENG/Classification/ClassificationsGroupOrder.pdf |date=25 October 2011 }}. monographs.iarc.fr It is suspected that this metabolite is the main reason alcohol promotes cancer.{{Cite journal|last1=Garaycoechea|first1=Juan I.|last2=Crossan|first2=Gerry P.|last3=Langevin|first3=Frédéric|last4=Mulderrig|first4=Lee|last5=Louzada|first5=Sandra|last6=Yang|first6=Fentang|last7=Guilbaud|first7=Guillaume|last8=Park|first8=Naomi|last9=Roerink|first9=Sophie|date=2018-01-03|title=Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells|journal=Nature|language=En|doi=10.1038/nature25154|pmid=29323295|pmc=6047743|issn=1476-4687|volume=553|issue=7687|pages=171–177|bibcode=2018Natur.553..171G}} 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.{{cite journal | doi = 10.1002/ijc.21583 |vauthors=Homann N, Stickel F, König IR, etal | year = 2006| title = Alcohol dehydrogenase 1C*1 allele is a genetic marker for alcohol-associated cancer in heavy drinkers | journal = International Journal of Cancer | volume = 118 | issue = 8| pages = 1998–2002 | pmid=16287084|s2cid=11716548 | doi-access = free }} 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."{{cite journal | vauthors = Seitz HK, Stickel F | date = Aug 2007 | title = Molecular mechanisms of alcohol-mediated carcinogenesis | url = http://www.josorge.com/publications/Citations/JGH/001.pdf | journal = Nat Rev Cancer | volume = 7 | issue = 8 | pages = 599–612 | doi = 10.1038/nrc2191 | pmid = 17646865 | s2cid = 3231314 | access-date = 2013-01-19 | archive-url = https://web.archive.org/web/20170810204931/http://josorge.com/publications/Citations/JGH/001.pdf | archive-date = 2017-08-10 | url-status = dead }} 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."{{cite book |vauthors=Brooks P, Theruvathu J |veditors=Cho CH, Purohit V | chapter = Acetaldehyde-DNA Adducts: Implications for the Molecular Mechanism of Alcohol-Related Carcinogenesis | title = Alcohol, Tobacco and Cancer | volume = 2006 | pages = 78–94 | chapter-url = https://books.google.com/books?id=LraqfTRnMhQC&pg=RA1-PA78 | year=2006| isbn = 978-3-8055-8107-3 |place=Basel |publisher=Karger}}

{{main|Fetal alcohol spectrum disorder}}

Fetal alcohol syndrome or FAS is a birth defect that occurs in the offspring of women who drink alcohol during pregnancy. More risks than benefits according to a survey of current knowledge.{{cite journal |last1=Andréasson |first1=S |last2=Allebeck |first2=P |title=Alcohol as medication is no good. More risks than benefits according to a survey of current knowledge. |journal=Läkartidningen |volume=102 |issue=9 |pages=632–7 |pmid=15804034|year=2005 }} Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damaged neurons and brain structures, and cause other physical, mental, or behavioural problems.{{cite journal|author=Ulleland CN|title=The offspring of alcoholic mothers|journal=Annals of the New York Academy of Sciences|volume=197|issue=1|pages=167–9|date=May 1972|pmid=4504588|doi=10.1111/j.1749-6632.1972.tb28142.x|bibcode=1972NYASA.197..167U|s2cid=84514766}} Fetal alcohol exposure is the leading known cause of intellectual disability in the Western world.{{cite journal|vauthors=Abel EL, Sokol RJ |title=Incidence of foetal alcohol syndrome and economic impact of FAS-related anomalies|journal=Drug Alcohol Depend|volume=19|issue=1|pages=51–70|date=January 1987|pmid=3545731|doi=10.1016/0376-8716(87)90087-1}} Alcohol consumption during pregnancy is associated with brain insulin and insulin-like growth factor resistance.

Children raised in alcoholic families have the potential to suffer emotional distress as they move into their own committed relationships. These children are at a higher risk for divorce and separation, unstable marital conditions and fractured families.{{cite journal|last1=Kearns-Bodkin|first1=Jill N.|last2=Leonard|first2=Kenneth E.|title=Relationship Functioning Among Adult Children of Alcoholics|journal=Journal of Studies on Alcohol and Drugs|pages=941–950|date=November 2008|pmc=2583382|pmid=18925353|volume=69|issue=6|doi=10.15288/jsad.2008.69.941}} Feelings of depression and antisocial behaviors experienced in early childhood frequently contribute to marital conflict and domestic violence. Women are more likely than men to be victims of alcohol-related domestic violence.{{cite journal |last1=Finger |first1=Brent |last2=Kachadourian |first2=Lorig K. |last3=Molnar |first3=Danielle S. |last4=Eiden |first4=Rina D. |last5=Edwards |first5=Ellen P. |last6=Leonard |first6=Kenneth E. |title=Alcoholism, associated risk factors, and harsh parenting among fathers: Examining the role of marital aggression |journal=Addictive Behaviors |date=June 2010 |volume=35 |issue=6 |pages=541–548 |doi=10.1016/j.addbeh.2009.12.029|pmid=20153586 |pmc=3824378 }}{{Cite journal|last=Sher|first=K|title=Characteristics of Children of Alcoholics: Putative Risk Factors, Substance Use and Abuse, and Psychopathology|journal=Journal of Abnormal Psychology|volume=100 | issue = 4 |pages=427–448|doi=10.1037/0021-843x.100.4.427|year=1991|pmid=1757657}}{{Cite journal|last=Gerhant|first=A.|title=Personality Traits in Alcohol-Dependent Individuals in the Context of Childhood Abuse|journal= Psychiatria Polska|volume=50 | issue = 5 |pages=973–987|doi=10.12740/pp/60346|pmid=27992890|year=2016|doi-access=free}}{{Cite journal |doi = 10.15288/jsad.2013.74.674|pmid = 23948526|pmc = 3749310|title = Impact of Fathers' Alcohol Problems on the Development of Effortful Control in Early Adolescence|journal = Journal of Studies on Alcohol and Drugs|volume = 74|issue = 5|pages = 674–683|year = 2013|last1 = Adkison|first1 = Sarah E.|last2 = Grohman|first2 = Kerry|last3 = Colder|first3 = Craig R.|last4 = Leonard|first4 = Kenneth|last5 = Orrange-Torchia|first5 = Toni|last6 = Peterson|first6 = Ellen|last7 = Eiden|first7 = Rina D.}}

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.

There is currently no consistent approach to measuring the economic impact of alcohol consumption.{{Cite journal|last1=Verhaeghe|first1=Nick|last2=Lievens|first2=Delfine|last3=Annemans|first3=Lieven|last4=Vander Laenen|first4=Freya|last5=Putman|first5=Koen|date=2017-01-18|title=Methodological Considerations in Social Cost Studies of Addictive Substances: A Systematic Literature Review|journal=Frontiers in Public Health|volume=4|pages=295|doi=10.3389/fpubh.2016.00295|issn=2296-2565|pmc=5241275|pmid=28149834|doi-access=free}} The economic burden such as direct, indirect, and intangible cost of diseases can be estimated through cost-of-illness studies.{{Cite journal|last=Rice|first=Dorothy P.|date=2000-09-01|title=Cost of illness studies: what is good about them?|url= |journal=Injury Prevention|language=en|volume=6|issue=3|pages=177–179|doi=10.1136/ip.6.3.177|issn=1353-8047|pmid=11003181|pmc=1730654}} Direct costs are estimated through prevalence and incidence studies, while indirect costs are estimated through the human capital method, the demographic method, and the friction cost method. However, it is difficult to accurately measure the economic impact due to differences in methodologies, cost items related to alcohol consumption, and measurement techniques.

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.{{Cite journal|last1=Manthey|first1=Jakob|last2=Laramée|first2=Philippe|last3=Parrott|first3=Steve|last4=Rehm|first4=Jürgen|date=2016-08-31|title=Economic burden associated with alcohol dependence in a German primary care sample: a bottom-up study|journal=BMC Public Health|volume=16|issue=1 |pages=906|doi=10.1186/s12889-016-3578-8|pmid=27576562|pmc=5006576|issn=1471-2458 |doi-access=free }} 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,{{Cite journal|last1=Odlaug|first1=B.L.|last2=Gual|first2=A.|last3=DeCourcy|first3=J.|last4=Perry|first4=R.|last5=Pike|first5=J.|last6=Heron|first6=L.|last7=Rehm|first7=J.|date=2016-03-01|title=Alcohol Dependence, Co-occurring Conditions and Attributable Burden|journal=Alcohol and Alcoholism|language=en|volume=51|issue=2|pages=201–209|doi=10.1093/alcalc/agv088|pmid=26246514|issn=0735-0414|pmc=4755551}} 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.{{Cite journal|last=Rehm|first=Jürgen|date=2011|title=The Risks Associated With Alcohol Use and Alcoholism|journal=Alcohol Research & Health|volume=34|issue=2|pages=135–143|issn=1535-7414|pmc=3307043|pmid=22330211}}

Indirect costs due to alcohol dependence are significant. The biggest indirect cost comes from lost productivity, followed by premature mortality.{{Cite journal|last1=Bouchery|first1=Ellen E.|last2=Harwood|first2=Henrick J.|last3=Sacks|first3=Jeffrey J.|last4=Simon|first4=Carol J.|last5=Brewer|first5=Robert D.|date=2011-11-01|title=Economic Costs of Excessive Alcohol Consumption in the U.S., 2006|url=http://www.ajpmonline.org/article/S0749-3797(11)00538-1/fulltext|journal=American Journal of Preventive Medicine|language=en|volume=41|issue=5|pages=516–524|doi=10.1016/j.amepre.2011.06.045|pmid=22011424|issn=0749-3797|citeseerx=10.1.1.460.5582}} 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.{{Cite journal|last1=Rehm|first1=Jürgen|last2=Mathers|first2=Colin|last3=Popova|first3=Svetlana|last4=Thavorncharoensap|first4=Montarat|last5=Teerawattananon|first5=Yot|last6=Patra|first6=Jayadeep|date=2009-06-27|title=Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders|journal=Lancet|volume=373|issue=9682|pages=2223–2233|doi=10.1016/S0140-6736(09)60746-7|issn=1474-547X|pmid=19560604|s2cid=27947246}} 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.{{Cite journal|last1=Thavorncharoensap|first1=Montarat|last2=Teerawattananon|first2=Yot|last3=Yothasamut|first3=Jomkwan|last4=Lertpitakpong|first4=Chanida|last5=Thitiboonsuwan|first5=Khannika|last6=Neramitpitagkul|first6=Prapag|last7=Chaikledkaew|first7=Usa|date=2010-06-09|title=The economic costs of alcohol consumption in Thailand, 2006|journal=BMC Public Health|volume=10|pages=323|doi=10.1186/1471-2458-10-323|pmid=20534112|pmc=2896941|issn=1471-2458 |doi-access=free }} 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).{{Cite journal|last1=Thavorncharoensap|first1=Montarat|last2=Teerawattananon|first2=Yot|last3=Yothasamut|first3=Jomkwan|last4=Lertpitakpong|first4=Chanida|last5=Chaikledkaew|first5=Usa|date=2009-11-25|title=The economic impact of alcohol consumption: a systematic review|journal=Substance Abuse Treatment, Prevention, and Policy|volume=4|pages=20|doi=10.1186/1747-597X-4-20|pmid=19939238|pmc=2791094|issn=1747-597X |doi-access=free }} 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.{{Cite journal|last1=Jarl|first1=Johan|last2=Johansson|first2=Pia|last3=Eriksson|first3=Antonina|last4=Eriksson|first4=Mimmi|last5=Gerdtham|first5=Ulf-G.|last6=Hemström|first6=Orjan|last7=Selin|first7=Klara Hradilova|last8=Lenke|first8=Leif|last9=Ramstedt|first9=Mats|date=November 2008|title=The societal cost of alcohol consumption: an estimation of the economic and human cost including health effects in Sweden, 2002|journal=The European Journal of Health Economics|volume=9|issue=4|pages=351–360|doi=10.1007/s10198-007-0082-1|issn=1618-7598|pmid=18043953|s2cid=20912577}}{{Cite web|url=https://www.researchgate.net/publication/252250147|title=The Social Costs of Drug Abuse in Australia in 1988 and 1992 (PDF Download Available)|website=ResearchGate|language=en|access-date=2017-09-17}}

• Short-term effects of alcohol consumption
• Alcohol and suicide
• Self-medication on CNS depressants (alcohol)
• Self-medicated effectiveness on alcohol

{{Notelist}}

{{Reflist}}

{{Medical resources

| ICD10 = {{ICD10|F|10||f|10}}.1

}}

• [https://www.bu.edu/aodhealth/ Alcohol, Other Drugs, and Health: Current Evidence. Boston University/National Institute on Alcohol Abuse and Alcoholism Journal]
• [http://www.drinking.nhs.uk/index.html Alcohol is linked to high blood pressure, cancers and heart attack] {{Webarchive|url=https://web.archive.org/web/20101201180308/http://www.drinking.nhs.uk/index.html |date=2010-12-01 }} (NHS)

{{alcohealth}}

{{Psychoactive substance use}}

{{DEFAULTSORT:Long-Term Effects Of Alcohol}}

Long

Alc