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Long-term effects of alcohol

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The long term effects of alcohol range from possible health benefits for low levels of alcohol (ethanol) consumption to severe detrimental effects in cases of chronic alcohol abuse. There is a strong correlation between 'high levels' of alcohol consumption and an increased risk of developing alcoholism, cardiovascular disease, malabsorption, chronic pancreatitis, alcoholic liver disease, and cancer. Damage to the central nervous system and peripheral nervous system can occur from chronic alcohol abuse.[2][3] Long-term use of alcohol in excessive quantities is capable of damaging nearly every organ and system in the body.[4] The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol, as is the developing brain of the unborn, possibly resulting in the fetal alcohol syndrome (FAS).[5]

Historically doctors have promoted alcohol for its perceived health benefits and most recently for protection against coronary heart disease. This is known as the French paradox. There is evidence of cardiovascular benefits from drinking 1 - 2 drinks per day; however, the health benefits from moderate intake of alcohol are controversial. Alcohol should be regarded as a recreational drug with potentially serious adverse effects on health and it is not recommended for cardio-protection in the place of safer and proven traditional methods such as exercise and proper nutrition.[6][7]

Some experts argue that the benefits of moderate alcohol consumption may be outweighed by other increased risks, including those of injuries, violence, fetal damage, certain forms of cancer, liver disease and hypertension.[8] As the apparent health benefits of moderate alcohol consumption are limited for populations at low risk of heart disease, other experts urge caution because of the possibility that recommending moderate alcohol consumption may lead to an increased risk of alcohol abuse.[9]

Scientific StudiesEdit

BackgroundEdit

The adverse effects of long-term excessive use of alcohol are close to those seen with other sedative-hypnotics (apart from organ toxicity which is much more problematic with alcohol). Withdrawal effects and dependence are also almost identical.[10] Alcohol at moderate levels has some positive and negative effects on health. The negative effects include increased risk of liver diseases, oropharyngeal cancer, esophageal cancer and pancreatitis. Conversely moderate intake of alcohol may have some beneficial effects on gastritis and cholelithiasis.[11] Chronic alcohol misuse and abuse has serious effects on physical and mental health. Chronic excess alcohol intake, or alcohol dependence, can lead to a wide range of neuropsychiatric or neurological impairment, cardiovascular disease, liver disease, and malignant neoplasms. The psychiatric disorders which are associated with alcoholism include major depression, dysthymia, mania, hypomania, panic disorder, phobias, generalized anxiety disorder, personality disorders, schizophrenia, suicide, neurologic deficits (e.g. impairments of working memory, emotions, executive functions, visuospatial abilities and gait and balance) and brain damage. Alcohol dependence is associated with hypertension, coronary heart disease, and ischemic stroke, cancer of the respiratory system, and also cancers of the digestive system, liver, breast and ovaries. Heavy drinking is associated with liver disease, such as cirrhosis.[12] Studies have focused on both men and women, various age groups, and people of many ethnic groups. Published papers now total in the many hundreds, with studies having shown correlation between moderate alcohol use and health that may instead have been due to the beneficial effects of socialization that is often accompanied by alcohol consumption. Some of the specific ways alcohol affects cardiovascular health have been studied.[13] The impact of alcohol on aging is negative when excessive amounts of alcohol are consumed.[14]

Maximum quantity recommendedEdit

Further information: Recommended maximum intake of alcoholic beverages

Different countries recommend different maximum quantities. For most countries, the maximum quantity for men is 140 g–210 g per week. For women, the range is 84 g–140 g per week. Most countries recommend total abstinence whilst pregnant or breastfeeding.

Alcohol psychology
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Alcohol use
Alcohol abuse
Alcohol consumption and health
Treatment of alcohol problems

Alcohol-related deathsEdit

Over-consumption of alcohol is one of the leading preventable causes of death worldwide.[15] One study links alcohol to 1 in every 25 deaths worldwide and that 5% of years lived with disability are attributable to alcohol consumption.[16][17]

Countries collect statistics on alcohol-related deaths. While some categories relate to short-term effects, such as accidents, many relate to long-term effects of alcohol.

Russia Edit

Main article: Alcoholism in Russia

One study claims 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."[18] However, there are some difficulties with this study. For instance the same study also found a protective effect of heavy drinking on breast cancer mortality. This contradicts the well established scientific view that alcohol increases breast cancer risk.[19] On this account in further correspondence it was advised that "careful interpretation of mortality statistics in relation to alcohol use is needed, taking into account other relevant risk factors, incidence, and survival."[20]

The authors replied that "whether or not the apparent shortfall in breast cancer mortality among heavy drinkers is real, it accounts for only about 0·1% of adult deaths in Russia. Careful interpretation of it is therefore of little relevance to the findings for alcohol and overall mortality".

United KingdomEdit

Alcohol-related deaths in the United Kingdom are coded using the Tenth Revision of the International Classification of Diseases (ICD-10).[21] ICD-10 comprises:

  • Mental and behavioural disorders due to use of alcohol – ICD-10 F10
  • Degeneration of nervous system due to alcohol – ICD-10 G31.2
  • Alcoholic polyneuropathy – ICD-10 G62.1
  • Alcoholic cardiomyopathy – ICD-10 I42.6
  • Alcoholic gastritis – ICD-10 K29.2
  • Alcoholic liver disease – ICD-10 K70
  • Chronic hepatitis, not elsewhere classified – ICD-10 K73
  • Fibrosis and cirrhosis of liver – ICD-10 K74 (Excluding K74.3-K74.5 – Biliary cirrhosis)
  • Alcohol induced chronic pancreatitis – ICD-10 K86.0
  • Accidental poisoning by and exposure to alcohol – ICD-10 X45
  • Intentional self-poisoning by and exposure to alcohol – ICD-10 X65
  • Poisoning by and exposure to alcohol, undetermined intent – ICD-10 Y15

UK statistical bodies report 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."[22]

In Scotland, the NHS estimate that in 2003 one in every 20 deaths could be attributed to alcohol.[23]

A 2009 study found that 9,000 people are dying from alcohol-related diseases every year, three times the number 25 years previously.[24]

United StatesEdit

The Centers for Disease Control and Prevention report, "From 2001–2005, there were approximately 79,000 deaths annually attributable to excessive alcohol use. In fact, excessive alcohol use is the 3rd leading lifestyle-related cause of death for people in the United States each year."[25] A 1993 study estimated US deaths through alcohol at 100,000.[26]

Overall mortality Edit

A 23-year prospective study of 12,000 male British physicians aged 48–78, found that overall mortality was significantly lower in the group consuming less than 2 "units" (British unit = 8 g) per day than in the non-alcohol-drinking group. Greater than 2 units per day was associated with an increased risk of mortality.[27]

This is consistent with other research that found a J-curve dependency between alcohol consumption and total mortality among middle aged and older men. While the mortality rates of ex-drinkers and those drinking beyond moderation are significantly elevated, the all-cause mortality rates may be 15-18% lower among moderate drinkers (1–2 drinks per day) than among abstainers - a meta-analysis found.[28] This claim was challenged by another study[29][30] that found that in certain low quality studies occasional drinkers or ex-drinkers were included as abstainers, resulting in the increased mortality in that group. However, the J-curve for total and CHD mortality was reconfirmed by studies that took the mentioned confounders into account.[31][32][33][34]

The observed decrease in mortality of light-to-moderate drinkers comparing to abstainers can be partially explained by superior health and social status of the drinking group;[35] however, the protective effect of alcohol in light to moderate drinkers remains significant even after adjusting for these confounders.[32][34] Additionally, confounders such as underreporting of alcohol intake might lead to the underestimation of how much mortality is reduced in light-to-moderate drinkers.[31][36]

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. [37]. In fact Asian Indians who consume alcohol had a 60% higher risk of heart attack which was greater with local spirits (80%) than branded spirits (50%). [38] The harm was observed in alcohol users classified as occasional as well as regular light, moderate, and heavy consumers.[38]

Another large study of 4465 subjects in India also confirmed the possible harm of alcohol consumption on 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 HDL-C levels (2 mg/dl) and significantly higher tobacco use (63% vs. 21%).[38]

Heavy drinking leads to increased mortality. For example a US study found that men who consumed 5 or more drinks on drinking days had a 30% higher mortality rate than those consuming only 1 drink.[34] According to another study, drinkers with heavy drinking occasions (six or more drinks at a time) have a 57% higher all-cause mortality than drinkers without heavy drinking occasions.[39]

Cardiovascular systemEdit

Main article: Alcohol and cardiovascular disease

A meta-analysis of 34 studies found a reduced risk of mortality from coronary heart disease in men who drank 2 - 4 drinks per day and women who drank 1 - 2 drinks per day.[28] A meta-analysis of randomized trials found that alcohol consumption in moderation decreases serum levels of fibrinogen, a protein that promotes clot formation and increases levels of tissue type plasminogen activator, an enzyme that helps dissolve clots.[40] The serum levels of C-reactive protein (CRP), a marker of inflammation and predictor of CHD (coronary heart disease) risk, are lower in people who drink moderately than those who abstain from alcohol suggesting that alcohol consumption in moderation might have anti-inflammatory effects.[41][42][43] In addition to its psychotropic properties, alcohol has anticoagulation properties similar to warfarin.[44][45] Additionally, thrombosis is lower among moderate drinkers than teetotalers.[46]

Despite epidemiological evidence, some criticize the idea of recommending alcohol for health benefits. A doctor at the World Health Organisation stated that recommending moderate alcohol consumption for health benefits is "ridiculous and dangerous".[47][48] There have been no randomised controlled trials that have demonstrated cardiac benefits of alcohol. Due to the risks of abuse, dependence, and adverse effects, alcohol should never be recommended for cardiac benefits as a substitute to well-proven measures, such as a good diet, exercise or pharmaceutical drugs.[49] It has been argued[attribution needed] that the health benefits from alcohol are at best debatable and may have been exaggerated by the alcohol industry. Alcohol should be regarded as a recreational drug with potentially serious adverse effects on health and should not be promoted for cardio-protection.[6]

Peripheral arterial diseaseEdit

"Moderate alcohol consumption appears to decrease the risk of PAD in apparently healthy men."[50] "In this large population-based study, moderatable alcohol consumption was inversely associated with peripheral arterial disease in women but not in men. Residual confounding by smoking may have influenced the results. Among nonsmokers an inverse association was found between alcohol consumption and peripheral arterial disease in both men and women."[51][52]

Intermittent claudication (IC)Edit

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.[53]

Heart attack and strokeEdit

Drinking in moderation has been found to help those who have suffered a heart attack survive it.[54][55] However, excessive alcohol consumption leads to an increased risk of heart failure.[56] A review of the literature found that half a drink of alcohol offered the best level of protection. However, they noted that 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.[57] However, moderate alcohol consumption is associated with hypertension.[8] There is an increased risk of hypertriglyceridemia, cardiomyopathy, hypertension, and stroke if 3 or more standard drinks of alcohol are taken per day.[58]

CardiomyopathyEdit

Large amount 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.[59]

Hematologic diseasesEdit

Alcoholics may have anemia from several causes;[60] they may also develop thrombocytopenia from direct toxic effect on megakaryocytes, or from hypersplenism.

Nervous systemEdit

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Chronic heavy alcohol consumption impairs brain development, causes brain shrinkage, dementia, physical dependence, increases neuropsychiatric and cognitive disorders and causes distortion of the brain chemistry. Some studies however have shown that moderate alcohol consumption may decrease risk of dementia, including Alzheimer disease, although there are studies which find the opposite. At present, due to poor study design and methodology, the literature is inconclusive on whether moderate alcohol consumptions increases the risk of dementia or decreases it.[61] 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.[62] Some evidence suggests that low to moderate alcohol consumption may speed up brain volume loss.[63] Chronic consumption of alcohol may result in increased plasma levels of the toxic amino acid homocysteine;[64][65] which may explain alcohol withdrawal seizures,[66] alcohol-induced brain atrophy[67] and alcohol-related cognitive disturbances.[68] 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.

StrokesEdit

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.[69][70][71][72]

"The consistency in the vascular benefit associated with moderate drinking (compared with non-drinking) observed across different studies, together with the existence of credible biological pathways, strongly suggests that at least some of this benefit is real. However, because of biases introduced by: choice of reference categories; reverse causality bias; variations in alcohol intake over time; and confounding, some of it is likely to be an artefact."[73]

Drinking lots of alcohol has been negatively linked to stroke. According to the National Stroke Association, more than 2 drinks per day (one drink is ~5 ounces of wine) may increase stroke risk by 50% and lead to other medical problems.[74] Because of this and other known harmful effects of heavy drinking, care should be taken when considering safe amounts of alcohol intake.

BrainEdit

Alcohol abuse is associated with wide spread 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.[75] The long-term effects of alcohol on brain chemistry is an important cause of chronic fatigue.[76]

Adolescent brain developmentEdit

Consuming large amounts of alcohol over a period of time can impair normal brain development in humans.[77][78] Deficits in retrieval of verbal and nonverbal information and in visuospatial functioning were evident in youths with histories of heavy drinking during early and middle adolescence.[79][80]

During adolescence critical stages of neurodevelopment occur, including remodeling and functional changes in synaptic plasticity and neuronal connectivity in different brain regions. These changes may make adolescents especially susceptible to the harmful effects of alcohol. Compared to adults, adolescents exposed to alcohol are more likely to exhibit cognitive deficits (including learning and memory dysfunction). Some of these cognitive effects, such as learning impairments, may persist into adulthood.[81]

Mechanisms of actionEdit

NeuroinflammationEdit

Ethanol can trigger the activation of astroglial cells which can produce a proinflammatory response in the brain. Ethanol interacts with the TLR4 and IL-1RI receptors on these cells to activate intracellular signal transduction pathways. Specifically, ethanol induces the phosphorylation of IL-1R-associated kinase (IRAK), ERK1/2, stress-activated protein kinase (SAPK)/JNK, and p38 mitogen-activated protein kinase (p38 MAPK). Activation of the IRAK/MAPK pathway leads to the stimulation of the transcription factors NF-kappaB and AP-1. These transcription factors cause the upregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression.[82] The upregulation of these inflammatory mediators by ethanol is also associated with an increase in caspase 3 activity and a corresponding increase in cell apoptosis.[83][84] The exact mechanism by which various concentrations of ethanol either activates or inhibits TLR4/IL-1RI signaling is not currently known, though it may involve alterations in lipid raft clustering [85] or cell adhesion complexes and actin cytoskeleton organization.[86]

Changes in dopaminegric and glutamatergic signaling pathwaysEdit

Intermittent ethanol treatment causes a decrease in expression of the dopamine receptor type 2 (D2R) and a decrease in phosphorylation of 2B subunit of the NMDA receptor (NMDAR2B) in the prefrontal cortex, hippocampus, nucleus accumbens, and for only D2R the striatum. It also causes changes in the acetylation of histones H3 and H4 in the prefrontal cortex, nucleus accumbens, and striatum, suggesting chromatin remodeling changes which may mediate long-term alterations. Additionally, adolescent rats pre-exposed to ethanol have higher basal levels of dopamine in the nucleus accumbens, along with a prolonged dopamine response in this area in response to a challenge dose of ethanol. Together, these results suggest that alcohol exposure during adolescence can sensitize the mesolimbic and mesocortical dopamine pathways to cause changes in dopaminegric and glutamatergic signaling, which may affect the remodeling and functions of the adolescent brain.[87] These changes are significant as alcohol’s effect on NMDARs could contribute to learning and memory dysfunction (see Effects of alcohol on memory).

Inhibition of hippocampal neurogenesisEdit

Excessive alcohol intake (binge drinking) causes a decrease in hippocampal neurogenesis, via decreases in neural stem cell proliferation and newborn cell survival.[88][89] Alcohol decreases the number of cells in S-phase of the cell cycle, and may arrest cells in the G1 phase, thus inhibiting their proliferation.[90] Ethanol has different effects on different types of actively dividing hippocampal progenitors during their initial phases of neuronal development. Chronic alcohol exposure decreases the number of proliferating cells that are radial glia-like, preneuronal, and intermediate types, while not affecting early neuronal type cells; suggesting ethanol treatment alters the precursor cell pool. Furthermore, there is a greater decrease in differentiation and immature neurons than there is in proliferating progenitors, suggesting that the abnormal decrease in the percentage of actively dividing preneuronal progenitors results in a greater reduction in the maturation and survival of postmitotic cells.[91]

Additionally, alcohol exposure increased several markers of cell death. In these studies neural degeneration seems to be mediated by non-apoptotic pathways.[92][93] One of the proposed mechanisms for alcohol’s neurotoxicity is the production of nitric oxide (NO), yet other studies have found alcohol-induced NO production to lead to apoptosis (see Neuroinflammation section).

Cognition and dementiaEdit

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.[94] One of the organs most sensitive to the toxic effects of chronic alcohol consumption is the brain. In France 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.[95] 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.[96] However, a study concluded, "Our findings suggest that, despite previous suggestions, moderate alcohol consumption does not protect older people from cognitive decline."[97]

Acetaldehyde is produced by the liver during breakdown of ethanol. People who have a genetic deficiency for the subsequent conversion of acetaldehyde into acetic acid (a trait more prevalent in those of East Asian descent[citation needed]) may have a greater risk of Alzheimer's disease. "These results indicate that the ALDH2 deficiency is a risk factor for LOAD [late-onset Alzheimer's disease] …"[98]

Wernicke-Korsakoff syndrome is a manifestation of thiamine deficiency, usually as a secondary effect of alcohol abuse.[99] The syndrome is a combined manifestation of two eponymous disorders, Korsakoff's Psychosis and Wernicke's encephalopathy, named after Drs. Sergei Korsakoff and Carl Wernicke. 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.[100]

Essential tremorEdit

Essential tremors can be temporarily relieved in up to two-thirds of patients by drinking small amounts of alcohol.[101]

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 [102] and could underlie the ameliorative effects [103] [104]. Additionally, the effects of ethanol have been studied in different animal essential tremor models.

For more details on this topic, see Essential tremor

SleepEdit

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 abuse can also lead to profound disturbances of sleep with vivid dreams. Chronic alcohol abuse 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.[105]

Mental health effectsEdit

High rates of major depressive disorder occur in heavy drinkers and those who abuse alcohol. Whether it is more true that major depressive disorder causes self-medicating alcohol abuse, or the increased incidence of the disorder in alcohol abusers is caused by the drinking, is not known though some evidence suggests drinking causes the disorder.[106] Alcohol misuse is associated with a number of mental health disorders and alcoholics have a very high suicide rate.[107] A study of people hospitalised 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 attempters.[108] 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. Abuse of other drugs is also associated with an increased risk of suicide. About 33 percent of suicides in the under 35s are due to alcohol or other substance misuse.[109]

Social skills are significantly impaired in people suffering from 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 abuse include impairments in perceiving facial emotions, prosody perception problems and theory of mind deficits; the ability to understand humour is also impaired in alcohol abusers.[110]

Studies have shown that alcohol dependence relates directly to cravings and irritability.[111] Another study has shown that alcohol use is a significant predisposing factor towards antisocial behavior in children.[112] 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).[113] 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.[114][115][116] Psychosis is secondary to several alcohol-related conditions including acute intoxication and withdrawal after significant exposure.[117] Chronic alcohol misuse can cause psychotic type symptoms to develop, more so than with other drugs of abuse. Alcohol abuse 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 abuse a very significant cause of psychotic disorders.[118] Prominent hallucinations and/or delusions are usually present when a patient is intoxicated or recently withdrawn from alcohol.[117]

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 tranquillisers to people with alcohol problems.[119] Approximately half of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia suffer from 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 suffer very ill health and that even moderate drinking can cause rebound anxiety syndromes and sleep disorders. A person who is suffering the toxic effects of alcohol will not benefit from other therapies or medications as they do not address the root cause of the symptoms.[120]

Digestive system and weight gainEdit

The impact of alcohol on weight-gain is contentious: some studies find no effect,[121] others find decreased[122] or increased effect on weight gain.

Alcohol use increases the risk of chronic gastritis (stomach inflammation);[123][124] it is one cause of cirrhosis, hepatitis, and pancreatitis in both its chronic and acute forms.

Metabolic syndromeEdit

A study 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."[125] This is also true for Asians. A J-curve association between alcohol intake and metabolic syndrome was found: "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". However, "odds ratios for the metabolic syndrome and its components tended to increase with increasing alcohol consumption."[126]

Gallbladder effectsEdit

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."[127] 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."[128]

Consumption of alcohol is unrelated to gallbladder disease.[129] However one study suggested that drinkers who take vitamin C (ascorbic acid) might reduce their risk of gallbladder disease.[130]

Liver diseaseEdit

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 alcohol abuse 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 in alcohol abstinent patients. Research is being conducted into the effectiveness of anti-TNFs. Certain complementary medications, e.g., milk thistle and silymarin, appear to offer some benefit.[131][132] 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.[133][134] Moderate alcohol consumption also increases the risk of liver disease.[8]

PancreatitisEdit

Alcohol misuse is a leading cause of both acute pancreatitis and chronic pancreatitis.[135][136] Chronic excessive intake of alcohol can cause destruction of the pancreas resulting in severe chronic pain, which may progress to pancreatic cancer.[137] Chronic pancreatitis often results in malabsorption problems and diabetes.[138]

Other systemsEdit

Alcoholic lung diseaseEdit

Chronic alcohol ingestion impairs multiple critical cellular functions in the lung. These cellular impairments 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. 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.

Kidney stonesEdit

Research indicates that drinking alcohol is associated with a lower risk of developing kidney stones. One study concludes, "Since beer seemed to be protective against kidney stones, the physiologic effects of other substances besides ethanol, especially those of hops, should also be examined."[139] "...consumption of coffee, alcohol, and vitamin C supplements were negatively associated with stones."[140] "After mutually adjusting for the intake of other beverages, the risk of stone formation decreased by the following amount for each 240-ml (8-oz) serving consumed daily: caffeinated coffee, 10%; decaffeinated coffee, 10%; tea, 14%; beer, 21%; and wine, 39%."[141] "...stone formation decreased by the following amount for each 240-mL (8-oz) serving consumed daily: 10% for caffeinated coffee, 9% for decaffeinated coffee, 8% for tea, and 59% for wine." (CI data excised from last two quotes.).[142]

Sexual dysfunctionEdit

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. [143] This can result due to a 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.[144]

Hormonal ImbalanceEdit

Excessive alcohol intake can result in hyperoestrogenisation.[145] It has been speculated that alcohol 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.[146][147] In women, increased levels of estrogen due to excessive alcohol intake have been related to an increased risk of breast cancer.[147][148]

Diabetes mellitusEdit

Moderate drinkers may have a lower risk of diabetes than non-drinkers. On the other hand, binge drinking and high alcohol consumption may increase the risk of type 2 diabetes in women."[149] Alcohol consumption promotes insulin sensitivity.[150]

Rheumatoid arthritisEdit

Regular consumption of alcohol is associated with an increased risk of gouty arthritis[151][152] and a decreased risk of rheumatoid arthritis.[153][154][155][156][157] 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.[158]

The researchers noted that moderate alcohol consumption also reduces the risk of other inflammatory processes such as cardiovascualar disease. Some of the biological mechanisms by which ethanol reduces the risk of destructive arthritis and prevents the loss of bone mineral density (BMD), which is part of the disease process.[159]

A study concluded, "Alcohol either protects from RA or, subjects with RA curtail their drinking after the manifestation of RA".[160] Another study found, "Postmenopausal women who averaged more than 14 alcoholic drinks per week had a reduced risk of rheumatoid arthritis..."[161]

OsteoporosisEdit

Moderate alcohol consumption is associated with higher bone mineral density in postmenopausal women. "...Alcohol consumption significantly decreased the likelihood [of osteoporosis]."[162] "Moderate alcohol intake was associated with higher BMD in postmenopausal elderly women."[163] "Social drinking is associated with higher bone mineral density in men and women [over 45]."[164] However, alcohol abuse is associated with bone loss.[165][166]

SkinEdit

Chronic excessive alcohol abuse 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.[167]

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."[168]

Immune system, bacterial contamination, viral infections, and cancerEdit

Bacterial infectionEdit

There is a protective effect of alcohol consumption against active infection with H. pylori[169] In contrast, alcohol intake (comparing those who drink > 30g of alcohol per day to non-drinkers) is not associated with higher risk of duodenal ulcer.[170] Excessive alcohol consumption seen in alcoholics is a known risk factor for pneumonia.

Common coldEdit

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."[171]

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."[172]

CancerEdit

Main article: Alcohol and cancer

The International Agency for Research on Cancer (Centre International de Recherche sur le Cancer) of the World Health Organization has classified alcohol as a Group 1 carcinogen. Its evaluation states, "There is sufficient evidence for the carcinogenicity of alcoholic beverages in humans.... Alcoholic beverages are carcinogenic to humans (Group 1)."[173]

The U.S. Department of Health & Human Services’ National Toxicology Program listed alcohol as a known carcinogen in 2000.[174]

One study determined that "3.6% of all cancer cases worldwide are related to alcohol drinking, resulting in 3.5% of all cancer deaths."[175] A 2011 study found that one in 10 of all cancers in men and one in 33 in women were caused by past or current alcohol intake.[176][177]

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).[178]

High concentrations of acetaldehyde, which is produced as the body breaks down ethanol, may damage DNA in healthy cells. The National Institute on Alcohol Abuse and Alcoholism have shown that acetaldehyde reacts with polyamines which are naturally occurring compounds essential for cell growth—to create a particularly dangerous type of mutagenic DNA base called a Cr-Pdg adduct.[179] Even moderate levels of alcohol consumption are associated with an increased risk of certain forms of cancer.[8]

Alcohol's effect on the fetusEdit

Main article: Fetal alcohol syndrome

Fetal alcohol syndrome or FAS is a disorder of permanent birth defects that occurs in the offspring of women who drink alcohol during pregnancy. Drinking heavily or during the early stages of prenatal development has been conclusively linked to FAS; moderate consumption is associated with fetal damage.[8] 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.[180] Fetal alcohol exposure is the leading known cause of mental retardation in the Western world.[181] Alcohol consumption during pregnancy is associated with brain insulin and insulin-like growth factor resistance.[165]

See alsoEdit

ReferencesEdit

  1. Global Status Report on Alcohol 2004
  2. Müller D, Koch RD, von Specht H, Völker W, Münch EM (March 1985). [Neurophysiologic findings in chronic alcohol abuse]. Psychiatr Neurol Med Psychol (Leipz) 37 (3): 129–32.
  3. Testino G (2008). Alcoholic diseases in hepato-gastroenterology: a point of view. Hepatogastroenterology 55 (82-83): 371–7.
  4. (11 April 2002) Drink, Drugs and Dependence: From Science to Clinical Practice, 1st, 19–20, Routledge.
  5. (Mar 2007). Use of anesthetic agents in neonates and young children.. Anesth Analg 104 (3): 509–20.
  6. 6.0 6.1 (2009). Alcohol cardio-protection has been talked up.. N Z Med J 122 (1303): 97–101.
  7. (2009). [Alcohol and wine and cardiovascular diseases in epidemiologic studies]. Przegl Lek 66 (5): 233–8.
  8. 8.0 8.1 8.2 8.3 8.4 (28 February - 6 March 2005) [Alcohol as medication is no good. More risks than benefits according to a survey of current knowledge]. Lakartidningen 102 (9): 632–7.
  9. http://pubs.niaaa.nih.gov/publications/arh24-1/05-11.pdf
  10. (1 October 2006) Substance Use Disorders: A Practical Guide, 2nd, 101–103, USA: Lippincott Williams and Wilkins.
  11. Taylor B, Rehm J, Gmel G (2005). Moderate alcohol consumption and the gastrointestinal tract. Dig Dis 23 (3-4): 170–6.
  12. Cargiulo T (March 2007). Understanding the health impact of alcohol dependence. Am J Health Syst Pharm 64 (5 Suppl 3): S5–11.
  13. Vliegenthart R, Oei HH, van den Elzen AP, et al. (November 2004). Alcohol consumption and coronary calcification in a general population. Arch. Intern. Med. 164 (21): 2355–60.
    Koppes LL, Twisk JW, Snel J, Van Mechelen W, Kemper HC (May 2000). Blood cholesterol levels of 32-year-old alcohol consumers are better than of nonconsumers. Pharmacol Biochem Behav. 66 (1): 163–7.
    Albert MA, Glynn RJ, Ridker PM (January 2003). Alcohol consumption and plasma concentration of C-reactive protein. Circulation 107 (3): 443–7.
    Baer DJ, Judd JT, Clevidence BA, et al. (1 March 2002). Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet. Am J Clin Nutr. 75 (3): 593–9.
    Catena C, Novello M, Dotto L, De Marchi S, Sechi LA (February 2003). Serum lipoprotein(a) concentrations and alcohol consumption in hypertension: possible relevance for cardiovascular damage. J. Hypertens. 21 (2): 281–8.
  14. Stevenson JS (2005). Alcohol use, misuse, abuse, and dependence in later adulthood. Annu Rev Nurs Res 23: 245–80.
  15. Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJ (May 2006). Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet 367 (9524): 1747–57.
  16. BBC Alcohol link to one in 25 deaths
  17. Jürgen Rehm, Colin Mathers, Svetlana Popova, Montarat Thavorncharoensap, Yot Teerawattananon, Jayadeep Patra Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders The Lancet, Volume 373, Issue 9682, Pages 2223 - 2233, 27 June 2009 DOI:10.1016/S0140-6736(09)60746-7
  18. IARC Alcohol causes more than half of all the premature deaths in Russian adults
  19. (May 2007). Alcohol intake and breast cancer risk: the European Prospective Investigation into Cancer and Nutrition (EPIC).. Cancer Causes Control 18 (4): 361–73.
  20. (Sep 2009). Did alcohol protect against death from breast cancer in Russia?. Lancet 374 (9694): 975; author reply 975–6.
  21. Alcohol-related deaths in the United Kingdom and links therefrom
  22. Alcohol Deaths: Rates stabilise in the UK
  23. BBC Alcohol 'kills one in 20 Scots' 30 June 2009
  24. Sam Lister The price of alcohol: an extra 6,000 early deaths a year The Times 19 October 2009
  25. Centers for Disease Control and Prevention Alcohol and Public Health
  26. (1993). Actual Causes of Death in the United States. JAMA 270 (18): 2207–2212.
  27. Doll R, Peto R, Boreham J, Sutherland I (February 2005). Mortality in relation to alcohol consumption: a prospective study among male British doctors. Int J Epidemiol 34 (1): 199–204.
  28. 28.0 28.1 Alcohol dosing and total mortality in men and women: an updated meta-analysis of 34 prospective studies.. Arch Intern Med 166 (22): 2437–45.
  29. (May 2007). Moderate alcohol use and reduced mortality risk: systematic error in prospective studies and new hypotheses.. Ann Epidemiol 17 (5 Suppl): S16-23.
  30. (Jul 2009). A healthy dose of scepticism: four good reasons to think again about protective effects of alcohol on coronary heart disease.. Drug Alcohol Rev 28 (4): 441–4.
  31. 31.0 31.1 Ann Epidemiol. 2007. Volume 17, Issue 5. Alcohol Drinking and Total Mortality Risk Arthur L. Klatsky, MD, Natalia Udaltsova, PhD
  32. 32.0 32.1 (Jun 2009). Functional limitations, socioeconomic status, and all-cause mortality in moderate alcohol drinkers.. J Am Geriatr Soc 57 (6): 955–62.
  33. (Jan 2010). Alcohol intake and the risk of coronary heart disease in the Spanish EPIC cohort study.. Heart 96 (2): 124–30.
  34. 34.0 34.1 34.2 (Nov 2010). Late-life alcohol consumption and 20-year mortality.. Alcohol Clin Exp Res 34 (11): 1961–71.
  35. (Jun 2010). Relationship between alcohol intake, health and social status and cardiovascular risk factors in the urban Paris-Ile-De-France Cohort: is the cardioprotective action of alcohol a myth?. Eur J Clin Nutr 64 (6): 561–8.
  36. (Oct 2008). Invited commentary: never, or hardly ever? It could make a difference.. Am J Epidemiol 168 (8): 872–5; discussion 876–7.
  37. , Joshi, Prashant; Islam, Shofiqul; Pais, Prem; Reddy, Srinath; Dorairaj, Prabhakaran; Kazmi, Khawar; Pandey, Mrigendra Raj; Haque, Sirajul; Mendis, Shanthi; Rangarajan, Sumathy; Yusuf, Salim (17). Risk Factors for Early Myocardial Infarction in South Asians Compared With Individuals in Other Countries. JAMA 297 (3): 286–294.
  38. 38.0 38.1 38.2 , Roy A, Prabhakaran D, Jeemon P, Thankappan KR, Mohan V, Ramakrishnan L, Joshi P, Ahmed F, Mohan BV, Saran RK, Sinha N, Reddy KS; (26). Impact of alcohol on coronary heart disease in Indian men.. Atherosclerosis 210 (2): 531–535.
  39. (May 2003). Increased mortality related to heavy alcohol intake pattern.. J Epidemiol Community Health 57 (5): 379–84.
  40. (Dec 1999). Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors.. BMJ 319 (7224): 1523–8.
  41. (Jan 2003). Alcohol consumption and plasma concentration of C-reactive protein.. Circulation 107 (3): 443–7.
  42. (2002). Relation between alcohol consumption and C-reactive protein levels in the adult US population.. J Am Board Fam Pract 15 (6): 437–42.
  43. (Mar 2001). Effect of alcohol consumption on systemic markers of inflammation.. Lancet 357 (9258): 763–7.
  44. Mennen LI, Balkau B, Vol S, Cacès E, Eschwège E (1 April 1999). Fibrinogen: a possible link between alcohol consumption and cardiovascular disease? DESIR Study Group. Arterioscler Thromb Vasc Biol. 19 (4): 887–92.
  45. Paassilta M, Kervinen K, Rantala AO, et al. (14 February 1998). Social alcohol consumption and low Lp(a) lipoprotein concentrations in middle aged Finnish men: population based study. BMJ 316 (7131): 594–5.
  46. Lacoste L, Hung J, Lam JY (January 2001). Acute and delayed antithrombotic effects of alcohol in humans. Am J Cardiol. 87 (1): 82–5.
    Pahor M, Guralnik JM, Havlik RJ, et al. (September 1996). Alcohol consumption and risk of deep venous thrombosis and pulmonary embolism in older persons. J Am Geriatr Soc 44 (9): 1030–7.
    Ridker, P., et al. Moderate alcohol intake may reduce risk of thrombosis. American Medical Association press release, September 22, 1994
    Ridker, P. (1996). "The Pathogenesis of Atherosclerosis and Acute Thrombosis" Manson, JoAnn E. Prevention of myocardial infarction, Oxford [Oxfordshire]: Oxford University Press.
  47. Abdulla S (December 1997). Is alcohol really good for you?. J R Soc Med 90 (12): 651.
  48. Naimi TS, Brown DW, Brewer RD, et al. (May 2005). Cardiovascular risk factors and confounders among nondrinking and moderate-drinking U.S. adults. Am J Prev Med 28 (4): 369–73.
  49. (2002). Alcohol, heart disease, and mortality: a review.. Rev Cardiovasc Med 3 (1): 7–13.
  50. Camargo CA, Stampfer MJ, Glynn RJ, et al. (4 February 1997). Prospective study of moderate alcohol consumption and risk of peripheral arterial disease in US male physicians. Circulation 95 (3): 577–80.
  51. Vliegenthart R, Geleijnse JM, Hofman A, et al. (February 2002). Alcohol consumption and risk of peripheral arterial disease: the Rotterdam study. Am J Epidemiol. 155 (4): 332–8.
  52. Mingardi R, Avogaro A, Noventa F, et al. (1997). Alcohol intake is associated with a lower prevalence of peripheral vascular disease in non-insulin dependent diabetic women. Nutrition Metabolism and Cardiovascular Disease 7 (4): 301–8.
  53. Djoussé L, Levy D, Murabito JM, Cupples LA, Ellison RC (19 December 2000). Alcohol consumption and risk of intermittent claudication in the Framingham Heart Study. Circulation 102 (25): 3092–7.
  54. Muntwyler J, Hennekens CH, Buring JE, Gaziano JM (December 1998). Mortality and light to moderate alcohol consumption after myocardial infarction. Lancet 352 (9144): 1882–5.
    Mukamal KJ, Maclure M, Muller JE, Sherwood JB, Mittleman MA (April 2001). Prior alcohol consumption and mortality following acute myocardial infarction. JAMA 285 (15): 1965–70.
  55. Alcohol helps reduce damage after heart attacks
  56. Djoussé L, Gaziano JM (April 2008). Alcohol consumption and heart failure: a systematic review. Curr Atheroscler Rep 10 (2): 117–20.
  57. Kloner RA, Rezkalla SH (September 2007). To drink or not to drink? That is the question. Circulation 116 (11): 1306–17.
  58. Saremi A, Arora R (2008). The cardiovascular implications of alcohol and red wine. Am J Ther 15 (3): 265–77.
  59. (2010). Alcoholic and cocaine-associated cardiomyopathies.. Prog Cardiovasc Dis 52 (4): 289–99.
  60. Savage D, Lindenbaum J (1986). Anemia in alcoholics. Medicine (Baltimore) 65 (5): 322–38.
  61. Panza F, Capurso C, D'Introno A, et al. (2008). Vascular risk factors, alcohol intake, and cognitive decline. J Nutr Health Aging 12 (6): 376–81.
  62. (May 2009). Alcohol drinking, cognitive functions in older age, predementia, and dementia syndromes.. J Alzheimers Dis 17 (1): 7–31.
  63. (Apr 2009). Chronic effects of low to moderate alcohol consumption on structural and functional properties of the brain: beneficial or not?. Hum Psychopharmacol 24 (3): 199–205.
  64. Bleich S, Bleich K, Kropp S, et al. (2001). Moderate alcohol consumption in social drinkers raises plasma homocysteine levels: a contradiction to the 'French Paradox'?. Alcohol Alcohol. 36 (3): 189–92.
  65. Bleich S, Carl M, Bayerlein K, et al. (March 2005). Evidence of increased homocysteine levels in alcoholism: the Franconian alcoholism research studies (FARS). Alcohol. Clin. Exp. Res. 29 (3): 334–6.
  66. Bleich S, Degner D, Bandelow B, von Ahsen N, Rüther E, Kornhuber J (August 2000). Plasma homocysteine is a predictor of alcohol withdrawal seizures. NeuroReport 11 (12): 2749–52.
  67. Bleich S, Bandelow B, Javaheripour K, et al. (January 2003). Hyperhomocysteinemia as a new risk factor for brain shrinkage in patients with alcoholism. Neurosci. Lett. 335 (3): 179–82.
  68. Wilhelm J, Bayerlein K, Hillemacher T, et al. (March 2006). Short-term cognition deficits during early alcohol withdrawal are associated with elevated plasma homocysteine levels in patients with alcoholism. J Neural Transm 113 (3): 357–63.
  69. (Sep 2009). Alcohol consumption and cardiovascular risk: mechanisms of action and epidemiologic perspectives.. Future Cardiol 5 (5): 467–77.
  70. (May 2009). Alcohol and cardiovascular diseases.. Expert Rev Cardiovasc Ther 7 (5): 499–506.
  71. (Feb 2009). Lifestyle and stroke risk: a review.. Curr Opin Neurol 22 (1): 60–8.
  72. (Sep 2007). Alcohol and cardiovascular health: the razor-sharp double-edged sword.. J Am Coll Cardiol 50 (11): 1009–14.
  73. (2006). Effect of alcohol on risk of coronary heart disease and stroke: causality, bias, or a bit of both?. Vasc Health Risk Manag 2 (3): 239–49.
  74. http://www.stroke.org/site/PageServer?pagename=Alcohol
  75. (Oct 1998). Alcohol as a risk factor for brain damage: neurologic aspects.. Alcohol Clin Exp Res 22 (7 Suppl): 346S–351S.
  76. (2009). Chronic fatigue syndrome: aetiology, diagnosis and treatment.. BMC Psychiatry 9 Suppl 1: S1.
  77. White AM, Bae JG, Truesdale MC, Ahmad S, Wilson WA, Swartzwelder HS (July 2002). Chronic-intermittent ethanol exposure during adolescence prevents normal developmental changes in sensitivity to ethanol-induced motor impairments. Alcohol. Clin. Exp. Res. 26 (7): 960–8.
  78. Tapert SF, Brown GG, Kindermann SS, Cheung EH, Frank LR, Brown SA (February 2001). fMRI measurement of brain dysfunction in alcohol-dependent young women. Alcohol. Clin. Exp. Res. 25 (2): 236–45.
  79. Squeglia LM, Jacobus J, Tapert SF (January 2009). The influence of substance use on adolescent brain development. Clin EEG Neurosci 40 (1): 31–8.
  80. Brown SA, Tapert SF, Granholm E, Delis DC (February 2000). Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcohol Clin Exp Res. 24 (2): 164–71.
  81. PMID 20113871 (PMID 20113871)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  82. PMID 16272348 (PMID 16272348)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  83. PMID 16272348 (PMID 16272348)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  84. PMID 17284196 (PMID 17284196)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  85. PMID 18061674 (PMID 18061674)
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  86. PMID 12704810 (PMID 12704810)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  87. PMID 19077056 (PMID 19077056)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  88. PMID 19554644 (PMID 19554644)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  89. PMID 20534463 (PMID 20534463)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  90. PMID 19554644 (PMID 19554644)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  91. PMID 20534463 (PMID 20534463)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  92. PMID 19554644 (PMID 19554644)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  93. PMID 20534463 (PMID 20534463)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  94. (Jan 2008). The impact of excessive alcohol use on prospective memory: a brief review.. Curr Drug Abuse Rev 1 (1): 36–41.
  95. Pierucci-Lagha A, Derouesné C (December 2003). [Alcoholism and aging. 2. Alcoholic dementia or alcoholic cognitive impairment?]. Psychol Neuropsychiatr Vieil 1 (4): 237–49.
  96. Peters R, Peters J, Warner J, Beckett N, Bulpitt C (September 2008). Alcohol, dementia and cognitive decline in the elderly: a systematic review. Age Ageing 37 (5): 505–12.
  97. Claudia Cooper, Paul Bebbington, Howard Meltzer, Rachel Jenkins, Traolach Brugha, James Lindesay and Gill Livingston Alcohol in moderation, premorbid intelligence and cognition In Older Adults: results from the Psychiatric Morbidity Survey J Neurol Neurosurg Psychiatry DOI:10.1136/jnnp.2008.163964
  98. , S, Ohsawa I, Kamino K, Ando F, Shimokata H. (April 2004)Mitochondrial ALDH2 Deficiency as an Oxidative Stress. Annals of the New York Academy of Sciences 1011: 36–44.
  99. Martin PR, Singleton CK, Hiller-Sturmhöfel S (2003). The role of thiamine deficiency in alcoholic brain disease. Alcohol Res Health 27 (2): 134–42.
  100. Butters N (1981). The Wernicke-Korsakoff syndrome: a review of psychological, neuropathological and etiological factors. Curr Alcohol 8: 205–32.
  101. Bain PG, Findley LJ, Thompson PD, et al. (August 1994). A study of hereditary essential tremor. Brain 117 ((Pt 4)): 805–24.
    Lou JS, Jankovic J (February 1991). Essential tremor: clinical correlates in 350 patients. Neurology 41 (2 (Pt 1)): 234–8.
    Wasielewski PG, Burns JM, Koller WC (1998). Pharmacologic treatment of tremor. Mov Disord. 13 (Suppl 3): 90–100.
    Boecker H, Wills AJ, Ceballos-Baumann A, et al. (May 1996). The effect of ethanol on alcohol-responsive essential tremor: a positron emission tomography study. Ann. Neurol. 39 (5): 650–8.
    (December 1999) Setting a steady course for benign essential tremor. Johns Hopkins Med Lett Health After 50 11 (10): 3.
  102. PMID 20721919 (PMID 20721919&query_hl=14&itool=pubmed_docsum 20721919)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  103. PMID 21640732 (PMID 21640732 &query_hl=14&itool=pubmed_docsum 21640732 )
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  104. PMID 17366267 (PMID 17366267 &query_hl=14&itool=pubmed_docsum 17366267 )
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  105. (24 April 2008) Sleep Medicine: Essentials and Review, Oxford University Press, USA.
  106. Fergusson DM, Boden JM, Horwood LJ (March 2009). Tests of causal links between alcohol abuse or dependence and major depression. Arch. Gen. Psychiatry 66 (3): 260–6.
  107. Chignon JM, Cortes MJ, Martin P, Chabannes JP (1998). [Attempted suicide and alcohol dependence: results of an epidemiologic survey]. Encephale 24 (4): 347–54.
  108. (31 May 2000) Lexicon of psychiatry, neurology, and the neurosciences, Philadelphia: Lippincott-Williams Wilkins.
  109. (25 Aug 2004) New Approaches to Preventing Suicide: A Manual For Practitioners, 31–32, Jessica Kingsley Publishers.
  110. Uekermann J, Daum I (May 2008). Social cognition in alcoholism: a link to prefrontal cortex dysfunction?. Addiction 103 (5): 726–35.
  111. Jasova D, Bob P, Fedor-Freybergh P (December 2007). Alcohol craving, limbic irritability, and stress. Med Sci Monit. 13 (12): CR543–7.
  112. Young R, Sweeting H, West P (2008). A longitudinal study of alcohol use and antisocial behaviour in young people. Alcohol Alcohol. 43 (2): 204–14.
  113. Marinkovic K, Oscar-Berman M, Urban T, O'Reilly CE, Howard JA, Sawyer K, Harris GJ (November 2009). Alcoholism and dampened temporal limbic activation to emotional faces. Alcohol Clin Exp Res 33 (11): 1880–92.
  114. Wetterling T, Junghanns K (December 2000). Psychopathology of alcoholics during withdrawal and early abstinence. Eur Psychiatry 15 (8): 483–8.
  115. Cowley DS (24). Alcohol abuse, substance abuse, and panic disorder. Am J Med 92 (1A): 41S–8S.
  116. Cosci F, Schruers KR, Abrams K, Griez EJ (June 2007). Alcohol use disorders and panic disorder: a review of the evidence of a direct relationship. J Clin Psychiatry 68 (6): 874–80.
  117. 117.0 117.1 eMedicine med/3113
  118. Tien AY, Anthony JC (August 1990). Epidemiological analysis of alcohol and drug use as risk factors for psychotic experiences. J. Nerv. Ment. Dis. 178 (8): 473–80.
  119. Terra MB, Figueira I, Barros HM (August 2004). Impact of alcohol intoxication and withdrawal syndrome on social phobia and panic disorder in alcoholic inpatients. Rev Hosp Clin Fac Med Sao Paulo 59 (4): 187–92.
  120. Cohen SI (February 1995). Alcohol and benzodiazepines generate anxiety, panic and phobias. J R Soc Med 88 (2): 73–7.
  121. Cordain L, Bryan ED, Melby CL, Smith MJ (1 April 1997). Influence of moderate daily wine consumption on body weight regulation and metabolism in healthy free-living males. J Am Coll Nutr 16 (2): 134–9.
  122. Arif AA, Rohrer JE (2005). Patterns of alcohol drinking and its association with obesity: data from the Third National Health and Nutrition Examination Survey, 1988-1994. BMC Public Health 5: 126.
  123. National Institute on Alcohol Abuse and Alcoholism (NIAAA) (2000). Health risks and benefits of alcohol consumption. Alcohol Res Health 24 (1): 5–11.
  124. Bode C, Bode JC (1997). Alcohol's role in gastrointestinal tract disorders. Alcohol Health Res World 21 (1): 76–83.
  125. Freiberg MS, Cabral HJ, Heeren TC, Vasan RS, Curtis Ellison R (December 2004). 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. Diabetes Care 27 (12): 2954–9.
  126. Yoon YS, Oh SW, Baik HW, Park HS, Kim WY (1 July 2004). Alcohol consumption and the metabolic syndrome in Korean adults: the 1998 Korean National Health and Nutrition Examination Survey. Am J Clin Nutr. 80 (1): 217–24.
  127. La Vecchia C, Decarli A, Ferraroni M, Negri E (September 1994). Alcohol drinking and prevalence of self-reported gallstone disease in the 1983 Italian National Health Survey. Epidemiology 5 (5): 533–6.
  128. Leitzmann MF, Giovannucci EL, Stampfer MJ, et al. (May 1999). Prospective study of alcohol consumption patterns in relation to symptomatic gallstone disease in men. Alcohol Clin Exp Res. 23 (5): 835–41.
  129. Sahi T, Paffenbarger RS, Hsieh CC, Lee IM (1 April 1998). Body mass index, cigarette smoking, and other characteristics as predictors of self-reported, physician-diagnosed gallbladder disease in male college alumni. Am J Epidemiol. 147 (7): 644–51.
  130. Simon JA, Grady D, Snabes MC, Fong J, Hunninghake DB (March 1998). Ascorbic acid supplement use and the prevalence of gallbladder disease. Heart & Estrogen-Progestin Replacement Study (HERS) Research Group. J Clin Epidemiol 51 (3): 257–65.
  131. Barve A, Khan R, Marsano L, Ravindra KV, McClain C (2008). Treatment of alcoholic liver disease. Ann Hepatol 7 (1): 5–15.
  132. Fehér J, Lengyel G (December 2008). [Silymarin in the treatment of chronic liver diseases: past and future]. Orv Hetil 149 (51): 2413–8.
  133. Voigt MD (February 2005). Alcohol in hepatocellular cancer. Clin Liver Dis 9 (1): 151–69.
  134. Morgan TR, Mandayam S, Jamal MM (November 2004). Alcohol and hepatocellular carcinoma. Gastroenterology 127 (5 Suppl 1): S87–96.
  135. Frossard JL, Steer ML, Pastor CM (January 2008). Acute pancreatitis. Lancet 371 (9607): 143–52.
  136. Bachmann K, Mann O, Izbicki JR, Strate T (November 2008). Chronic pancreatitis--a surgeons' view. Med. Sci. Monit. 14 (11): RA198–205.
  137. Nair RJ, Lawler L, Miller MR (December 2007). Chronic pancreatitis. Am Fam Physician 76 (11): 1679–88.
  138. Tattersall SJ, Apte MV, Wilson JS (July 2008). A fire inside: current concepts in chronic pancreatitis. Intern Med J 38 (7): 592–8.
  139. Hirvonen T, Pietinen P, Virtanen M, Albanes D, Virtamo J (15 July 1999). Nutrient intake and use of beverages and the risk of kidney stones among male smokers. Am J Epidemiol. 150 (2): 187–94.
  140. Soucie JM, Coates RJ, McClellan W, Austin H, Thun M (1 March 1996). Relation between geographic variability in kidney stones prevalence and risk factors for stones. Am J Epidemiol. 143 (5): 487–95.
  141. Curhan GC, Willett WC, Rimm EB, Spiegelman D, Stampfer MJ (1 February 1996). Prospective study of beverage use and the risk of kidney stones. Am J Epidemiol. 143 (3): 240–7.
  142. Curhan GC, Willett WC, Speizer FE, Stampfer MJ (1 April 1998). Beverage use and risk for kidney stones in women. Ann Intern Med. 128 (7): 534–40.
  143. Taniguchi N, Kaneko S (November 1997). [Alcoholic effect on male sexual function]. Nippon Rinsho 55 (11): 3040–4.
  144. Yoshitsugu M, Ihori M (November 1997). [Endocrine disturbances in liver cirrhosis--focused on sex hormones]. Nippon Rinsho 55 (11): 3002–6.
  145. (Feb 2006). Male breast cancer.. Lancet 367 (9510): 595–604.
  146. (1998). Alcoholic beverages as a source of estrogens.. Alcohol Health Res World 22 (3): 220–7.
  147. 147.0 147.1 (Jan 2005). Epidemiology of male breast cancer.. Cancer Epidemiol Biomarkers Prev 14 (1): 20–6.
  148. (Feb 2006). Alcohol and cancer.. Lancet Oncol 7 (2): 149–56.
  149. Carlsson S, Hammar N, Grill V, Kaprio J (October 2003). Alcohol consumption and the incidence of type 2 diabetes: a 20-year follow-up of the Finnish twin cohort study. Diabetes Care 26 (10): 2785–90.
  150. J Hong1, R R Smith, A E Harvey and N P Núñez Alcohol consumption promotes insulin sensitivity without affecting body fat levels International Journal of Obesity (2009) 33, 197–203; DOI:10.1038/ijo.2008.266
  151. Star VL, Hochberg MC (February 1993). Prevention and management of gout. Drugs 45 (2): 212–22.
  152. Eggebeen AT (September 2007). Gout: an update. Am Fam Physician 76 (6): 801–8.
  153. http://arc.org.uk/arthinfo/patpubs/6033/6033.asp
  154. Myllykangas-Luosujärvi R, Aho K, Kautiainen H, Hakala M (January 2000). Reduced incidence of alcohol related deaths in subjects with rheumatoid arthritis. Ann Rheum Dis. 59 (1): 75–6.
  155. Nagata C, Fujita S, Iwata H, et al. (May 1995). Systemic lupus erythematosus: a case-control epidemiologic study in Japan. Int J Dermatol. 34 (5): 333–7.
  156. Aho K, Heliövaara M (December 1993). Alcohol, androgens and arthritis. Ann Rheum Dis. 52 (12): 897.
  157. Hardy CJ, Palmer BP, Muir KR, Sutton AJ, Powell RJ (August 1998). Smoking history, alcohol consumption, and systemic lupus erythematosus: a case-control study. Ann Rheum Dis. 57 (8): 451–5.
  158. Källberg H, Jacobsen S, Bengtsson C, et al. (July 2008). Alcohol consumption is associated with decreased risk of rheumatoid arthritis; Results from two Scandinavian case-control studies. Ann Rheum Dis. 68 (2): 222–7.
  159. Jonsson IM, Verdrengh M, Brisslert M, et al. (January 2007). Ethanol prevents development of destructive arthritis. Proc Natl Acad Sci USA. 104 (1): 258–63.
  160. Myllykangas-Luosujärvi R, Aho K, Kautiainen H, Hakala M (January 2000). Reduced incidence of alcohol related deaths in subjects with rheumatoid arthritis. Ann Rheum Dis. 59 (1): 75–6.
  161. Voigt LF, Koepsell TD, Nelson JL, Dugowson CE, Daling JR (September 1994). Smoking, obesity, alcohol consumption, and the risk of rheumatoid arthritis. Epidemiology 5 (5): 525–32.
  162. Siris ES, Miller PD, Barrett-Connor E, et al. (December 2001). Identification and fracture outcomes of undiagnosed low bone mineral density in postmenopausal women: results from the National Osteoporosis Risk Assessment. JAMA 286 (22): 2815–22.
  163. Rapuri PB, Gallagher JC, Balhorn KE, Ryschon KL (1 November 2000). Alcohol intake and bone metabolism in elderly women. Am J Clin Nutr. 72 (5): 1206–13.
  164. Holbrook TL, Barrett-Connor E (June 1993). A prospective study of alcohol consumption and bone mineral density. BMJ 306 (6891): 1506–9.
  165. 165.0 165.1 (Aug 2007). Alcohol-induced disruption of endocrine signaling.. Alcohol Clin Exp Res 31 (8): 1269–85.
  166. (2005). A case study on osteoporosis in a male athlete: looking beyond the usual suspects.. Orthop Nurs 24 (3): 193–9; quiz 200–1.
  167. Kostović K, Lipozencić J (2004). Skin diseases in alcoholics. Acta Dermatovenerol Croat 12 (3): 181–90.
  168. Abrar A. Qureshi; Patrick L. Dominguez; Hyon K. Choi; Jiali Han; Gary Curhan Alcohol Intake and Risk of Incident Psoriasis in US Women: A Prospective Study Arch Dermatology DOI:10.1001/archdermatol.2010.204
  169. Brenner H, Rothenbacher D, Bode G, Adler G (6 December 1997). Relation of smoking and alcohol and coffee consumption to active Helicobacter pylori infection: cross sectional study. BMJ 315 (7121): 1489–92.
  170. Aldoori WH, Giovannucci EL, Stampfer MJ, Rimm EB, Wing AL, Willett WC (July 1997). A prospective study of alcohol, smoking, caffeine, and the risk of duodenal ulcer in men. Epidemiology 8 (4): 420–4.
  171. Cohen S, Tyrrell DA, Russell MA, Jarvis MJ, Smith AP (September 1993). Smoking, alcohol consumption, and susceptibility to the common cold. Am J Public Health 83 (9): 1277–83.
  172. Takkouche B, Regueira-Méndez C, García-Closas R, Figueiras A, Gestal-Otero JJ, Hernán MA (May 2002). Intake of wine, beer, and spirits and the risk of clinical common cold. Am J Epidemiol. 155 (9): 853–8.
  173. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Volume 44 Alcohol Drinking: Summary of Data Reported and Evaluation
  174. National Toxicology Program Alcoholic Beverage Consumption: Known to be a human carcinogen First listed in the Ninth Report on Carcinogens (2000)(PDF)
  175. Burden of alcohol-related cancer substantial
  176. BBC Drinking over recommended limit 'raises cancer risk' 8 April 2011
  177. Madlen Schütze et al Alcohol attributable burden of incidence of cancer in eight European countries based on results from prospective cohort study BMJ 2011; 342:d1584 DOI:10.1136/bmj.d1584
  178. WCRF Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective
  179. New Scientist article "Alcohol's link to cancer explained"
  180. Ulleland CN (May 1972). The offspring of alcoholic mothers. Ann. N. Y. Acad. Sci. 197: 167–9.
  181. Abel EL, Sokol RJ (January 1987). Incidence of foetal alcohol syndrome and economic impact of FAS-related anomalies. Drug Alcohol Depend 19 (1): 51–70.

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