From Wikipedia, the free encyclopedia

 “Alcoholic” redirects here. For alcoholic beverages, see alcoholic beverage. For the song by Starsailor, see Alcoholic (song).
King Alcohol and his Prime Minister.jpg

“King Alcohol and his Prime Minister” c. 1820
Classification and external resources
Specialty Psychiatry
ICD10 F10.2
ICD9-CM 303
OMIM 103780
MedlinePlus 000944
MeSH D000437

Alcoholism, also known as alcohol use disorder (AUD) and alcohol dependence syndrome, is a broad term for any drinking ofalcohol that results in problems.[1] It was previously divided into two types: alcohol abuse and alcohol dependence.[2][3] In a medical context alcoholism is said to exist when two or more of the following is present: a person drinks large amounts over a long time period, has difficulty cutting down, acquiring and drinking alcohol takes up a great deal of time, alcohol is strongly desired, usage results in not fulfilling responsibilities, usage results in social problems, usage results in health problems, usage results in risky situations,withdrawal occurs when stopping, and alcohol tolerance has occurred with use.[3] Alcohol use can affect all parts of the body but particularly affects the brain, heart, liver, pancreas, and immune system. This can result in mental illness, Wernicke Korsakoff syndrome, an irregular heart beat, liver failure, and an increase in the risk of cancer, among other disease.[4][5] Drinking duringpregnancy can cause damage to the baby resulting in fetal alcohol spectrum disorders.[6] Generally women are more sensitive to alcohol’s harmful physical and mental effects than men.[7]

Both environmental factors and genetics are involved in causing alcoholism with about half the risk attributed to each. A person with a parent or sibling with alcoholism are three to four times more likely to be alcoholic themselves.[4] Environmental factors include social, cultural, and behavioral influences.[8] High stress levels, anxiety, as well as inexpensive easily accessible alcohol increases risk.[4][9]People may continue to drink partly to prevent or improve symptoms of withdrawal. A low level of withdrawal may last for months following stopping.[4] Medically alcoholism is considered both a physical and mental illness.[10][11] Both questionnaires and certain blood tests may detect people with possible alcoholism. Further information is then collected to confirm the diagnosis.[4]

Prevention of alcoholism is possible by regulating and limiting the sale of alcohol, taxing alcohol to increase its cost, and providing inexpensive treatment.[12] Treatment may take several steps. Because of the medical problems that can occur during withdrawal,alcohol detoxification should be carefully controlled. One common method involves the use of benzodiazepine medications, such asdiazepam. This can be either given while admitted to a health care institution or occasionally while a person remains in the community with close supervision.[13] Other addictions or mental illness may complicate treatment.[14] After detoxification support such as group therapy or support groups are used to help keep a person from returning to drinking.[15][16] One commonly used form of support is the group Alcoholics Anonymous.[17] The medications acamprosate, disulfiram, or naltrexone may also be used to help prevent further drinking.[18]

The World Health Organization estimates that as of 2010 there were 208 million people with alcoholism worldwide (4.1% of the population over 15 years of age).[7][19] In the United States about 17 million (7%) of adults and 0.7 million (2.8%) of those age 12 to 17 years of age are affected.[20] It is more common among males and young adults, becoming less common in middle and old age.[4] It is the least common in Africa at 1.1% and has the highest rates in Eastern Europe at 11%.[4] Alcoholism directly resulted in 139,000 deaths in 2013 up from 112,000 deaths in 1990.[21] A total of 3.3 million deaths (5.9% of all deaths) are believed to be due to alcohol.[20] It often reduces a person’s life expectancy by around ten years.[22] In the United States it resulted in economic costs of $224 billion USD in 2006.[20] Many terms, some insulting and others informal, have been used to refer to people affected by alcoholism including: tippler, drunkard, dipsomaniac, and souse.[23] In 1979, the World Health Organization discouraged the use of “alcoholism” due to its inexact meaning, preferring “alcohol dependence syndrome”.[24]

Signs and symptoms

File:What Alcohol Does to Your Body.webm

Effects of alcohol on the body

Early signs

The risk of alcohol dependence begins at low levels of drinking and increases directly with both the volume of alcohol consumed and a pattern of drinking larger amounts on an occasion. Young adults are particularly at risk.

Long-term misuse

Some of the possible long-term effects of ethanol an individual may develop. Additionally, in pregnant women, alcohol can cause fetal alcohol syndrome.

Alcoholism is characterised by an increased tolerance to and physical dependence on alcohol, affecting an individual’s ability to control consumption. These characteristics play a role decreasing an alcoholic’s ability to stop drinking.[25] Alcoholism can have adverse effects on mental health, causing psychiatric disorders and increasing the risk of suicide. A depressed mood is a common symptom.[26][27]


Long-term alcohol abuse can cause a number of physical symptoms, including cirrhosis of the liver,pancreatitis, epilepsy, polyneuropathy, alcoholic dementia, heart disease, nutritional deficiencies, peptic ulcers[28] and sexual dysfunction, and can eventually be fatal. Other physical effects include an increased risk of developing cardiovascular disease, malabsorption, alcoholic liver disease, and cancer. Damage to thecentral nervous system and peripheral nervous system can occur from sustained alcohol consumption.[29][30] A wide range of immunologic defects can result and there may be a generalized skeletal fragility, in addition to a recognized tendency to accidental injury, resulting a propensity to bone fractures.[31]

Women develop long-term complications of alcohol dependence more rapidly than do men. Additionally, women have a higher mortality rate from alcoholism than men.[32] Examples of long-term complications include brain, heart, and liver damage[33] and an increased risk of breast cancer. Additionally, heavy drinking over time has been found to have a negative effect on reproductive functioning in women. This results in reproductive dysfunction such as anovulation, decreased ovarian mass, problems or irregularity of themenstrual cycle, and early menopause.[32] Alcoholic ketoacidosis can occur in individuals who chronically abuse alcohol and have a recent history of binge drinking.[34][35]

The amount of alcohol that can be biologically processed and its effects differ between sexes. Equal dosages of alcohol consumed by men and women generally result in women having higher blood alcohol concentrations (BACs), since women generally have a higher percentage of body fat and therefore a lower volume of distribution for alcohol than men, and because the stomachs of men tend to metabolize alcohol more quickly.[36]


Long-term misuse of alcohol can cause a wide range of mental health problems. Severe cognitive problems are common; approximately 10 percent of all dementia cases are related to alcohol consumption, making it the second leading cause of dementia.[37] Excessive alcohol use causes damage to brain function, and psychological health can be increasingly affected over time.[38]

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.[39]

Psychiatric disorders are common in alcoholics, with as many as 25 percent suffering severe psychiatric disturbances. The most prevalent psychiatric symptoms are anxiety anddepression disorders. Psychiatric symptoms usually initially worsen during alcohol withdrawal, but typically improve or disappear with continued abstinence.[40] Psychosis,confusion, and organic brain syndrome may be caused by alcohol misuse, which can lead to a misdiagnosis such as schizophrenia.[41] Panic disorder can develop or worsen as a direct result of long-term alcohol misuse.[42][43]

The co-occurrence of major depressive disorder and alcoholism is well documented.[44][45][46] Among those with comorbid occurrences, a distinction is commonly made between depressive episodes that remit with alcohol abstinence (“substance-induced”), and depressive episodes that are primary and do not remit with abstinence (“independent” episodes).[47][48][49] Additional use of other drugs may increase the risk of depression.[50]

Psychiatric disorders differ depending on gender. Women who have alcohol-use disorders often have a co-occurring psychiatric diagnosis such as major depression, anxiety, panic disorder, bulimia, post-traumatic stress disorder (PTSD), or borderline personality disorder. Men with alcohol-use disorders more often have a co-occurring diagnosis ofnarcissistic or antisocial personality disorder, bipolar disorder, schizophrenia, impulse disorders or attention deficit/hyperactivity disorder.[51] Women with alcoholism are more likely to have a history of physical or sexual assault, abuse and domestic violence than those in the general population,[51] which can lead to higher instances of psychiatric disorders and greater dependence on alcohol.

Social effects

The social problems arising from alcoholism are serious, caused by the pathological changes in the brain and the intoxicating effects of alcohol.[37][52] Alcohol abuse is associated with an increased risk of committing criminal offences, including child abuse, domestic violence, rape, burglary and assault.[53] Alcoholism is associated with loss of employment,[54]which can lead to financial problems. Drinking at inappropriate times, and behavior caused by reduced judgment, can lead to legal consequences, such as criminal charges fordrunk driving[55] or public disorder, or civil penalties for tortious behavior, and may lead to a criminal sentence.

An alcoholic’s behavior and mental impairment, while drunk, can profoundly affect those surrounding them and lead to isolation from family and friends. This isolation can lead tomarital conflict and divorce, or contribute to domestic violence. Alcoholism can also lead to child neglect, with subsequent lasting damage to the emotional development of the alcoholic’s children.[56] For this reason, children of alcoholic parents can develop a number of emotional problems. For example, they can become afraid of their parents, because of their unstable mood behaviors. In addition, they can develop considerable amount of shame over their inadequacy to liberate their parents from alcoholism. As a result of this failure, they develop wretched self-images, which can lead to depression.[57]

Alcohol withdrawal

As with similar substances with a sedative-hypnotic mechanism, such as barbiturates and benzodiazepines, withdrawal from alcohol dependence can be fatal if it is not properly managed.[52][58] Alcohol’s primary effect is the increase in stimulation of the GABAA receptor, promoting central nervous system depression. With repeated heavy consumption of alcohol, these receptors are desensitized and reduced in number, resulting in tolerance and physical dependence. When alcohol consumption is stopped too abruptly, the person’s nervous system suffers from uncontrolled synapse firing. This can result in symptoms that include anxiety, life-threatening seizures, delirium tremens, hallucinations, shakes and possible heart failure.[59][60] Other neurotransmitter systems are also involved, especially dopamine, NMDA and glutamate.[25][61]

Severe acute withdrawal symptoms such as delirium tremens and seizures rarely occur after 1 week post cessation of alcohol. The acute withdrawal phase can be defined as lasting between one and three weeks. In the period of 3 – 6 weeks following cessation increased anxiety, depression as well as sleep disturbance is common;[62] fatigue and tension can persist for up to 5 weeks as part of the post-acute withdrawal syndrome; about a quarter of alcoholics experience anxiety and depression for up to 2 years. These post-acute withdrawal symptoms have also been demonstrated in animal models of alcohol dependence and withdrawal.[63] A kindling effect also occurs in alcoholics whereby each subsequent withdrawal syndrome is more severe than the previous withdrawal episode; this is due to neuroadaptations which occur as a result of periods of abstinence followed by re-exposure to alcohol. Individuals who have had multiple withdrawal episodes are more likely to develop seizures and experience more severe anxiety during withdrawal from alcohol than alcohol dependent individuals without a history of past alcohol withdrawal episodes. The kindling effect leads to persistent functional changes in brain neural circuits as well as to gene expression.[64] Kindling also results in the intensification of psychological symptoms of alcohol withdrawal.[62]

There are decision tools and questionnaires which help guide physicians in evaluating alcohol withdrawal. For example, the CIWA-Ar objectifies alcohol withdrawal symptoms in order to guide therapy decisions which allows for an efficient interview while at the same time retaining clinical usefulness, validity and reliability, ensuring proper care for withdrawal patients, who can be in danger of death.[65]


A complex mixture of genetic and environmental factors influences the risk of the development of alcoholism.[66] Genes that influence the metabolism of alcohol also influence the risk of alcoholism, and may be indicated by a family history of alcoholism.[67] One paper has found that alcohol use at an early age may influence the expression of genes which increase the risk of alcohol dependence.[68] Individuals who have a genetic disposition to alcoholism are also more likely to begin drinking at an earlier age than average.[69]

Also, a younger age of onset of drinking is associated with an increased risk of the development of alcoholism,[69] and about 40 percent of alcoholics will drink excessively by their late adolescence. It is not entirely clear whether this association is causal, and some researchers have been known to disagree with this view.[70]

Severe childhood trauma is also associated with a general increase in the risk of drug dependency.[66] Lack of peer and family support is associated with an increased risk of alcoholism developing.[66] Genetics and adolescence are associated with an increased sensitivity to the neurotoxic effects of chronic alcohol abuse. Cortical degeneration due to the neurotoxic effects increases impulsive behaviour, which may contribute to the development, persistence and severity of alcohol use disorders. There is evidence that with abstinence, there is a reversal of at least some of the alcohol induced central nervous system damage.[71]

Alcohol availability

Alcohol is the most available and widely abused substance. Beer alone is the world’s most widely consumed[72] alcoholic beverage; it is the third-most popular drink overall, afterwater and tea.[73] It is thought by some to be the oldest fermented beverage.[74][75][76][77]

Gender difference

Based on combined data from SAMHSA’s 2004–2005 National Surveys on Drug Use & Health, the rate of past year alcohol dependence or abuse among persons aged 12 or older varied by level of alcohol use: 44.7% of past month heavy drinkers, 18.5% binge drinkers, 3.8% past month non-binge drinkers, and 1.3% of those who did not drink alcohol in the past month met the criteria for alcohol dependence or abuse in the past year. Males had higher rates than females for all measures of drinking in the past month: any alcohol use (57.5% vs. 45%), binge drinking (30.8% vs. 15.1%), and heavy alcohol use (10.5% vs. 3.3%), and males were twice as likely as females to have met the criteria for alcohol dependence or abuse in the past year (10.5% vs. 5.1%).[78]

Genetic variation

Genetic differences exist between different racial groups which affect the risk of developing alcohol dependence. For example, there are differences between African, East Asian and Indo-racial groups in how they metabolize alcohol. These genetic factors are believed to, in part, explain the differing rates of alcohol dependence among racial groups.[79][80]The alcohol dehydrogenase allele ADH1 B*3 causes a more rapid metabolism of alcohol. The allele ADH1 B*3 is only found in those of African descent and certain Native American tribes. African Americans and Native Americans with this allele have a reduced risk of developing alcoholism.[81] Native Americans however, have a significantly higher rate of alcoholism than average; it is unclear why this is the case.[82] Other risk factors such as cultural environmental effects e.g. trauma have been proposed to explain the higher rates of alcoholism among Native Americans compared to alcoholism levels in caucasians.[83][84]



Misuse, problem use, abuse, and heavy use refer to improper use of alcohol which may cause physical, social, or moral harm to the drinker.[85] Moderate use is defined by The Dietary Guidelines for Americans as no more than two alcoholic beverages a day for men and no more than one alcoholic beverage a day for women.[86] Some drinkers may drink more than 600 ml of alcohol per day during a heavy drinking period.[87]

The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines binge drinking as the amount of alcohol leading to a blood alcohol content (BAC) of 0.08, which, for most adults, would be reached by consuming five drinks for men or four for women over a 2-hour period. According to the NIAAA, men may be at risk for alcohol-related problems if their alcohol consumption exceeds 14 standard drinks per week or 4 drinks per day, and women may be at risk if they have more than 7 standard drinks per week or 3 drinks per day. It defines a standard drink as one 12-ounce bottle of beer, one 5-ounce glass of wine, or 1.5 ounces of distilled spirits.[88] Despite this risk, a 2014 report in the National Survey on Drug Use and Health found that only 10% of either “heavy drinkers” or “binge drinkers” defined according to the above critera also met the criteria for alcohol dependence, while only 1.3% of non-binge drinkers met this criteria. An inference drawn from this study is that evidence-based policy strategies and clinical preventive services may effectively reduce binge drinking without requiring addiction treatment in most cases.[89]

The term “alcoholism” is commonly used, but poorly defined. The WHO calls alcoholism “a term of long-standing use and variable meaning”, and use of the term was disfavored by a 1979 WHO Expert Committee. The Big Book (from Alcoholics Anonymous) states that once a person is an alcoholic, they are always an alcoholic, but does not define what is meant by the term “alcoholic” in this context. In 1960, Bill W., co-founder of Alcoholics Anonymous (AA), said:

We have never called alcoholism a disease because, technically speaking, it is not a disease entity. For example, there is no such thing as heart disease. Instead there are many separate heart ailments, or combinations of them. It is something like that with alcoholism. Therefore we did not wish to get in wrong with the medical profession by pronouncing alcoholism a disease entity. Therefore we always called it an illness, or a malady—a far safer term for us to use.[90]

In professional and research contexts, the term “alcoholism” sometimes encompasses both alcohol abuse and alcohol dependence,[91] and sometimes is considered equivalent to alcohol dependence. Talbot (1989) observes that alcoholism in the classical disease model follows a progressive course: if a person continues to drink, their condition will worsen. This will lead to harmful consequences in their life, physically, mentally, emotionally and socially.[92]

Johnson (1980) explores the emotional progression of the addict’s response to alcohol. He looks at this in four phases. The first two are considered “normal” drinking and the last two are viewed as “typical” alcoholic drinking.[93][94] Johnson’s four phases consist of:

  1. Learning the mood swing. A person is introduced to alcohol (in some cultures this can happen at a relatively young age), and the person enjoys the happy feeling it produces. At this stage there is no emotional cost.
  2. Seeking the mood swing. A person will drink to regain that feeling of euphoria experienced in phase 1; the drinking will increase as more intoxication is required to achieve the same effect. Again at this stage, there are no significant consequences.
  3. At the third stage there are physical and social consequences, i.e., hangovers, family problems, work problems, etc. A person will continue to drink excessively, disregarding the problems.
  4. The fourth stage can be detrimental, as Johnson cites it as a risk for premature death. As a person now drinks to feel normal, they block out the feelings of overwhelming guilt, remorse, anxiety, and shame they experience when sober.[95]

Other theorists such as Milam & Ketcham (1983) focus on the physical deterioration of alcohol. They describe the process in three stages:

  1. Adaptive stage – The person will not experience any negative symptoms, and believe they have capacity for alcohol. Physiological changes are happening with the increase in tolerance, but this will not be noticeable to the drinker or others.
  2. Dependent stage – At this stage, symptoms build gradually. Hangover symptoms may be confused with withdrawal symptoms. Many addicts will maintain their drinking to avoid withdrawal sickness, drinking small amounts frequently. They will try to hide their problem from others, and will avoid gross intoxication.
  3. Deterioration stage – Various organs are damaged due to long-term drinking. Medical treatment will be required; otherwise the pathological changes will cause death.

In psychology and psychiatry, the DSM is the most common global standard, while in medicine, the standard is ICD. The terms they recommend are similar but not identical.

Organization Preferred term(s) Definition
APA‘s DSM-IV alcohol abuse” and “alcohol dependence
  • alcohol abuse = repeated use despite recurrent adverse consequences.[96]
  • alcohol dependence = alcohol abuse combined with tolerance, withdrawal, and an uncontrollable drive to drink.[96] The term “alcoholism” was split into “alcohol abuse” and “alcohol dependence” in 1980’s DSM-III, and in 1987’s DSM-III-R behavioral symptoms were moved from “abuse” to “dependence”.[97] It has been suggested that DSM-V merge alcohol abuse and alcohol dependence into a single new entry,[98]named “alcohol-use disorder”.[99]
WHO‘s ICD-10 “alcohol harmful use” and “alcohol dependence syndrome” Definitions are similar to that of the DSM-IV. The World Health Organisation uses the term “alcohol dependence syndrome” rather than alcoholism.[24] The concept of “harmful use” (as opposed to “abuse”) was introduced in 1992’s ICD-10 to minimize underreporting of damage in the absence of dependence.[97] The term “alcoholism” was removed from ICD between ICD-8/ICDA-8 and ICD-9.[100]

The DSM-IV diagnosis of alcohol dependence represents one approach to the definition of alcoholism. In part this is to assist in the development of research protocols in which findings can be compared to one another. According to the DSM-IV, an alcohol dependence diagnosis is: “maladaptive alcohol use with clinically significant impairment as manifested by at least three of the following within any one-year period: tolerance; withdrawal; taken in greater amounts or over longer time course than intended; desire or unsuccessful attempts to cut down or control use; great deal of time spent obtaining, using, or recovering from use; social, occupational, or recreational activities given up or reduced; continued use despite knowledge of physical or psychological sequelae.”[101]

Despite the imprecision inherent in the term, there have been attempts to define how the word “alcoholism” should be interpreted when encountered. In 1992, it was defined by theNCADD and ASAM as “a primary, chronic disease characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking.”[102] MeSH has had an entry for “alcoholism” since 1999, and references the 1992 definition.[103]

AA describes alcoholism as an illness that involves a physical allergy[104]:28 (where “allergy” has a different meaning than that used in modern medicine.[105]) and a mental obsession.[104]:23[106] The doctor and addiction specialist Dr. William D. Silkworth M.D. writes on behalf of AA that “Alcoholics suffer from a “(physical) craving beyond mental control”.[104]:XXVI

A 1960 study by E. Morton Jellinek is considered the foundation of the modern disease theory of alcoholism.[107] Jellinek’s definition restricted the use of the word “alcoholism” to those showing a particular natural history. The modern medical definition of alcoholism has been revised numerous times since then. The American Medical Association currently uses the word alcoholism to refer to a particular chronic primary disease.[108]

Social barriers

Attitudes and social stereotypes can create barriers to the detection and treatment of alcohol abuse. This is more of a barrier for women than men. Fear of stigmatization may lead women to deny that they are suffering from a medical condition, to hide their drinking, and to drink alone. This pattern, in turn, leads family, physicians, and others to be less likely to suspect that a woman they know is an alcoholic.[32] In contrast, reduced fear of stigma may lead men to admit that they are suffering from a medical condition, to display their drinking publicly, and to drink in groups. This pattern, in turn, leads family, physicians, and others to be more likely to suspect that a man they know is an alcoholic.[51]


Several tools may be used to detect a loss of control of alcohol use. These tools are mostly self-reports in questionnaire form. Another common theme is a score or tally that sums up the general severity of alcohol use.[109]

The CAGE questionnaire, named for its four questions, is one such example that may be used to screen patients quickly in a doctor’s office.

Two “yes” responses indicate that the respondent should be investigated further.The questionnaire asks the following questions:

  1. Have you ever felt you needed to Cut down on your drinking?
  2. Have people Annoyed you by criticizing your drinking?
  3. Have you ever felt Guilty about drinking?
  4. Have you ever felt you needed a drink first thing in the morning (Eye-opener) to steady your nerves or to get rid of a hangover?[110][111]
The CAGE questionnaire has demonstrated a high effectiveness in detecting alcohol-related problems; however, it has limitations in people with less severe alcohol-related problems, white women and college students.[112]

Other tests are sometimes used for the detection of alcohol dependence, such as the Alcohol Dependence Data Questionnaire, which is a more sensitive diagnostic test than theCAGE questionnaire. It helps distinguish a diagnosis of alcohol dependence from one of heavy alcohol use.[113] The Michigan Alcohol Screening Test (MAST) is a screening tool for alcoholism widely used by courts to determine the appropriate sentencing for people convicted of alcohol-related offenses,[114] driving under the influence being the most common. The Alcohol Use Disorders Identification Test (AUDIT), a screening questionnaire developed by the World Health Organization, is unique in that it has been validated in six countries and is used internationally. Like the CAGE questionnaire, it uses a simple set of questions – a high score earning a deeper investigation.[115] The Paddington Alcohol Test (PAT) was designed to screen for alcohol-related problems amongst those attending Accident and Emergency departments. It concords well with the AUDIT questionnaire but is administered in a fifth of the time.[116] Certain blood tests may also indicate possible alcoholism.[4]

Genetic predisposition testing

Psychiatric geneticists John I. Nurnberger, Jr., and Laura Jean Bierut suggest that alcoholism does not have a single cause—including genetic—but that genes do play an important role “by affecting processes in the body and brain that interact with one another and with an individual’s life experiences to produce protection or susceptibility”. They also report that fewer than a dozen alcoholism-related genes have been identified, but that more likely await discovery.[117]

At least one genetic test exists for an allele that is correlated to alcoholism and opiate addiction.[118] Human dopamine receptor genes have a detectable variation referred to as the DRD2 TaqI polymorphism. Those who possess the A1 allele (variation) of this polymorphism have a small but significant tendency towards addiction to opiates and endorphin-releasing drugs like alcohol.[119] Although this allele is slightly more common in alcoholics and opiate addicts, it is not by itself an adequate predictor of alcoholism, and some researchers argue that evidence for DRD2 is contradictory.[117]

Urine and blood tests

There are reliable tests for the actual use of alcohol, one common test being that of blood alcohol content (BAC).[120] These tests do not differentiate alcoholics from non-alcoholics; however, long-term heavy drinking does have a few recognizable effects on the body, including:[121]

With regard to alcoholism, BAC is useful to judge alcohol tolerance, which in turn is sign of alcoholism.[4]

However, none of these blood tests for biological markers is as sensitive as screening questionnaires.


The World Health Organization, the European Union and other regional bodies, national governments and parliaments have formed alcohol policies in order to reduce the harm of alcoholism.[122][123] Targeting adolescents and young adults is regarded as an important step to reduce the harm of alcohol abuse. Increasing the age at which licit drugs of abuse such as alcohol can be purchased, the banning or restricting advertising of alcohol has been recommended as additional ways of reducing the harm of alcohol dependence and abuse. Credible, evidence based educational campaigns in the mass media about the consequences of alcohol abuse have been recommended. Guidelines for parents to prevent alcohol abuse amongst adolescents, and for helping young people with mental health problems have also been suggested.[124]


Treatments are varied because there are multiple perspectives of alcoholism. Those who approach alcoholism as a medical condition or disease recommend differing treatments from, for instance, those who approach the condition as one of social choice. Most treatments focus on helping people discontinue their alcohol intake, followed up with life training and/or social support to help them resist a return to alcohol use. Since alcoholism involves multiple factors which encourage a person to continue drinking, they must all be addressed to successfully prevent a relapse. An example of this kind of treatment is detoxification followed by a combination of supportive therapy, attendance at self-help groups, and ongoing development of coping mechanisms. The treatment community for alcoholism typically supports an abstinence-based zero tolerance approach; however, some prefer a harm-reduction approach.[125]


Alcohol detoxification or ‘detox’ for alcoholics is an abrupt stop of alcohol drinking coupled with the substitution of drugs, such as benzodiazepines, that have similar effects to prevent alcohol withdrawal. Individuals who are only at risk of mild to moderate withdrawal symptoms can be detoxified as outpatients. Individuals at risk of a severe withdrawal syndrome as well as those who have significant or acute comorbid conditions are generally treated as inpatients. Detoxification does not actually treat alcoholism, and it is necessary to follow-up detoxification with an appropriate treatment program for alcohol dependence or abuse to reduce the risk of relapse.[13] Some symptoms of alcohol withdrawal such as depressed mood and anxiety typically take weeks or months to abate while other symptoms persist longer due to persisting neuroadaptations.[62] Alcoholism has serious adverse effects on brain function; on average it takes one year of abstinence to recover from the cognitive deficits incurred by chronic alcohol abuse.[126]


A regional service center forAlcoholics Anonymous.

Various forms of group therapy or psychotherapy can be used to deal with underlying psychological issues that are related to alcohol addiction, as well as provide relapse prevention skills. The mutual-help group-counseling approach is one of the most common ways of helping alcoholics maintain sobriety.[15] Alcoholics Anonymous was one of the first organizations formed to provide mutual, nonprofessional counseling, and it is still the largest. Others include LifeRing Secular Recovery, SMART Recovery, Women For Sobriety, and Secular Organizations for Sobriety.

Rationing and moderation programs such as Moderation Management and DrinkWise do not mandate complete abstinence. While most alcoholics are unable to limit their drinking in this way, some return to moderate drinking. A 2002 US study by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) showed that 17.7 percent of individuals diagnosed as alcohol dependent more than one year prior returned to low-risk drinking. This group, however, showed fewer initial symptoms of dependency.[127] A follow-up study, using the same subjects that were judged to be in remission in 2001–2002, examined the rates of return to problem drinking in 2004–2005. The study found abstinence from alcohol was the most stable form of remission for recovering alcoholics.[128] A long-term (60 year) follow-up of two groups of alcoholic men concluded that “return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence.”[129]


In the United States there are four currently approved medications for alcoholism: disulfiram, two forms of naltrexone, and acamprosate.[130] Several other drugs are also used and many are under investigation.

  • Acamprosate (Campral) may stabilise the brain chemistry that is altered due to alcohol dependence via antagonising the actions of glutamate, a neurotransmitter which is hyperactive in the post-withdrawal phase.[131] By reducing excessive NMDA activity which occurs at the onset of alcohol withdrawal, acamprosate can reduce or prevent alcohol withdrawal related neurotoxicity.[132] Acamprosate reduces the risk of relapse amongst alcohol dependent persons.[133][134]
  • Benzodiazepines, while useful in the management of acute alcohol withdrawal, if used long-term can cause a worse outcome in alcoholism. Alcoholics on chronic benzodiazepines have a lower rate of achieving abstinence from alcohol than those not taking benzodiazepines. This class of drugs is commonly prescribed to alcoholics for insomnia or anxiety management.[135] Initiating prescriptions of benzodiazepines or sedative-hypnotics in individuals in recovery has a high rate of relapse with one author reporting more than a quarter of people relapsed after being prescribed sedative-hypnotics. Those who are long-term users of benzodiazepines should not be withdrawn rapidly, as severe anxiety and panic may develop, which are known risk factors for relapse into alcohol abuse. Taper regimes of 6–12 months have been found to be the most successful, with reduced intensity of withdrawal.[136][137]
  • Calcium carbimide (Temposil) works in the same way as disulfiram; it has an advantage in that the occasional adverse effects of disulfiram, hepatotoxicity and drowsiness, do not occur with calcium carbimide.[138]
  • Disulfiram (Antabuse) prevents the elimination of acetaldehyde, a chemical the body produces when breaking down ethanol. Acetaldehyde itself is the cause of many hangoversymptoms from alcohol use. The overall effect is severe discomfort when alcohol is ingested: an extremely fast-acting and long-lasting uncomfortable hangover. This discourages an alcoholic from drinking in significant amounts while they take the medicine.
  • Naltrexone is a competitive antagonist for opioid receptors, effectively blocking the effects of endorphins and opiates. Naltrexone is used to decrease cravings for alcohol and encourage abstinence. Alcohol causes the body to release endorphins, which in turn release dopamine and activate the reward pathways; hence when naltrexone is in the body there is a reduction in the pleasurable effects from consuming alcohol.[139] Evidence supports a reduced risk of relapse among alcohol dependent persons and a decrease in excessive drinking.[134] Nalmefene also appears effective and works by a similar manner.[134]

Evidence does not support the use of selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), antipsychotics, or gabapentin.[134]

Dual addictions and dependences

Alcoholics may also require treatment for other psychotropic drug addictions and drug dependences. The most common dual dependence syndrome with alcohol dependence isbenzodiazepine dependence, with studies showing 10–20 percent of alcohol-dependent individuals had problems of dependence and/or misuse problems of benzodiazepines. Benzodiazepines increase cravings for alcohol and the volume of alcohol consumed by problem drinkers.[140] Benzodiazepine dependency requires careful reduction in dosage to avoid benzodiazepine withdrawal syndrome and other health consequences.

Dependence on other sedative hypnotics such as zolpidem and zopiclone as well as opiates and illegal drugs is common in alcoholics.

Alcohol itself is a sedative-hypnotic and is cross-tolerant with other sedative-hypnotics such as barbiturates, benzodiazepines and nonbenzodiazepines. Dependence upon and withdrawal from sedative hypnotics can be medically severe and, as with alcohol withdrawal, there is a risk of psychosis or seizures if not managed properly.[141]


Disability-adjusted life year for alcohol use disorders per 100,000 inhabitants in 2004.

  no data

Total recorded yearly alcohol per capita consumption (15+), in litres of pure alcohol[142]

The World Health Organization estimates that as of 2010 there are 208 million people with alcoholism worldwide (4.1% of the population over 15 years of age).[7][19]

Substance use disorders are a major public health problem facing many countries. “The most common substance of abuse/dependence in patients presenting for treatment is alcohol.”[125] In the United Kingdom, the number of ‘dependent drinkers’ was calculated as over 2.8 million in 2001.[143] About 12% of American adults have had an alcohol dependence problem at some time in their life.[144] In the United States and Western Europe, 10 to 20 percent of men and 5 to 10 percent of women at some point in their lives will meet criteria for alcoholism.[145]

Within the medical and scientific communities, there is broad consensus regarding alcoholism as a disease state. For example, the American Medical Association considers alcohol a drug and states that “drug addiction is a chronic, relapsing brain disease characterized by compulsive drug seeking and use despite often devastating consequences. It results from a complex interplay of biological vulnerability, environmental exposure, and developmental factors (e.g., stage of brain maturity).”[108]

Alcoholism has a higher prevalence among men, though in recent decades, the proportion of female alcoholics has increased.[33] Current evidence indicates that in both men and women, alcoholism is 50–60 percent genetically determined, leaving 40–50 percent for environmental influences.[146] Most alcoholics develop alcoholism during adolescence or young adulthood.[66] 31 percent of college students show signs of alcohol abuse, while six percent are dependent on alcohol. Under the DSM‘s new definition of alcoholics, that means about 37 percent of college students may meet the criteria.[147]


Alcoholism often reduces a person’s life expectancy by around ten years.[22] The most common cause of death in alcoholics is from cardiovascular complications.[148]

There is a high rate of suicide in chronic alcoholics, which increases the longer a person drinks. Approximately 3–15 percent of alcoholics commit suicide,[149] and research has found that over 50 percent of all suicides are associated with alcohol or drug dependence. This is believed to be due to alcohol causing physiological distortion of brain chemistry, as well as social isolation. Suicide is also very common in adolescent alcohol abusers, with 25 percent of suicides in adolescents being related to alcohol abuse.[150]

Among those with alcohol dependence after one year, some met the criteria for low-risk drinking, even though only 25.5 percent of the group received any treatment, with the breakdown as follows: 25 percent were found to be still dependent, 27.3 percent were in partial remission (some symptoms persist), 11.8 percent asymptomatic drinkers (consumption increases chances of relapse) and 35.9 percent were fully recovered — made up of 17.7 percent low-risk drinkers plus 18.2 percent abstainers.[151]

In contrast, however, the results of a long-term (60-year) follow-up of two groups of alcoholic men indicated that “return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence.”[152] There was also “return-to-controlled drinking, as reported in short-term studies, is often a mirage.”


Adriaen Brouwer, Inn with Drunken Peasants, 1620s

1904 advertisement describing alcoholism as a disease.

Historically the name “dipsomania” was coined by German physician Dr. C. W. Hufeland in 1819 before it was superseded by “alcoholism”.[153][154] That term now has a more specific meaning.[155] The term “alcoholism” was first used in 1849 by the Swedish physician Magnus Huss to describe the systematic adverse effects of alcohol.[156]

Alcohol has a long history of use and misuse throughout recorded history. Biblical, Egyptian and Babylonian sources record the history of abuse and dependence on alcohol. In some ancient cultures alcohol was worshiped and in others its abuse was condemned. Excessive alcohol misuse and drunkenness were recognised as causing social problems even thousands of years ago. However, the defining of habitual drunkenness as it was then known as and its adverse consequences were not well established medically until the 18th century. In 1647 a Greek monk named Agapios was the first to document that chronic alcohol misuse was associated with toxicity to the nervous system and body which resulted in a range of medical disorders such as seizures, paralysis and internal bleeding. In 1920 the effects of alcohol abuse and chronic drunkenness led to the failed prohibition of alcohol being considered and eventually enforced briefly in America. In 2005 the cost of alcohol dependence and abuse was estimated to cost the US economy approximately 220 billion dollars per year, more than cancer and obesity.[157]

Society and culture

The various health problems associated with long-term alcohol consumption are generally perceived as detrimental to society, for example, money due to lost labor-hours, medical costs, and secondary treatment costs. Alcohol use is a major contributing factor for head injuries, motor vehicle accidents, violence, and assaults. Beyond money, there are also significant social costs to both the alcoholic and their family and friends.[52] For instance, alcohol consumption by a pregnant woman can lead to fetal alcohol syndrome,[158] an incurable and damaging condition.[159]

Estimates of the economic costs of alcohol abuse, collected by the World Health Organization, vary from one to six percent of a country’s GDP.[160]One Australian estimate pegged alcohol’s social costs at 24% of all drug abuse costs; a similar Canadian study concluded alcohol’s share was 41%.[161] One study quantified the cost to the UK of all forms of alcohol misuse in 2001 as £18.5–20 billion.[143][162] All economic costs in the United States in 2006 have been estimated at $223.5 billion.[163]

Stereotypes of alcoholics are often found in fiction and popular culture. The “town drunk” is a stock character in Western popular culture. Stereotypes of drunkenness may be based on racism or xenophobia, as in the depiction of the Irish as heavy drinkers.[164] Studies by social psychologists Stivers and Greeley attempt to document the perceived prevalence of high alcohol consumption amongst the Irish in America.[165]

Alcohol consumption is relatively similar between many European cultures, the United States, and Australia. In Asian countries that have a high gross domestic product, there is heightened drinking compared to other Asian countries, but it is nowhere near as high as it is in other countries like the United States. It is also inversely seen, with countries that have very low gross domestic product showing high alcohol consumption.[166]

In a study done on Korean immigrants in Canada, they reported alcohol was even an integral part of their meal, and is the only time solo drinking should occur. They also believe alcohol is necessary at any social event as it helps conversations start.[167]

Caucasians have a much lower abstinence rate (11.8%) and much higher tolerance to symptoms (3.4±2.45 drinks) of alcohol than Chinese (33.4% and 2.2±1.78 drinks respectively). Also, the more acculturation there is between cultures, the more influenced the culture is to adopt Caucasians drinking practices.[168]

Peyote, a psychoactive agent, has even shown promise in treating alcoholism. Alcohol had actually replaced peyote as Native Americans’ psychoactive agent of choice in rituals when peyote was outlawed.[169]


Topiramate, a derivative of the naturally occurring sugar monosaccharide D-fructose, has been found effective in helping alcoholics quit or cut back on the amount they drink. Evidence suggests that topiramate antagonizes excitatory glutamate receptors, inhibits dopamine release, and enhances inhibitory gamma-aminobutyric acid function. A 2008 review of the effectiveness of topiramate concluded that the results of published trials are promising, however as of 2008, data was insufficient to support using topiramate in conjunction with brief weekly compliance counseling as a first-line agent for alcohol dependence.[170] A 2010 review found that topiramate may be superior to existing alcohol pharmacotherapeutic options. Topiramate effectively reduces craving and alcohol withdrawal severity as well as improving quality-of-life-ratings.[171]

Baclofen, a GABAB receptor agonist, is under study for the treatment of alcoholism.[172] A 2015 systematic review concluded that there is insufficient evidence for the use of baclofen for withdrawal symptoms in alcoholism.[173] There is tentative data supporting baclofen in alcohol dependence however further trials are needed as of 2013.[174]

Ondansetron, a 5HT3 antagonist, appears promising.[175]

See also


  1. Jump up^ Jill Littrell (2014). Understanding and Treating Alcoholism Volume I: An Empirically Based Clinician’s Handbook for the Treatment of Alcoholism:volume Ii: Biological, Psychological, and Social Aspects of Alcohol Consumption and Abuse. Hoboken: Taylor and Francis. p. 55. ISBN 9781317783145. The World Health Organization defines alcoholism as any drinking which results in problems
  2. Jump up^ Hasin, Deborah (December 2003). “Classification of Alcohol Use Disorders”. Retrieved 28 February 2015.
  3. ^ Jump up to:a b “Alcohol Use Disorder: A Comparison Between DSM–IV and DSM–5”. November 2013. Retrieved9 May 2015.
  4. ^ Jump up to:a b c d e f g h i Association, American Psychiatric (2013). Diagnostic and statistical manual of mental disorders : DSM-5. (5 ed.). Washington, D.C.: American Psychiatric Association. pp. 490–497.ISBN 9780890425541.
  5. Jump up^ “Alcohol’s Effects on the Body”. Retrieved 9 May2015.
  6. Jump up^ “Fetal Alcohol Exposure”. Retrieved 9 May 2015.
  7. ^ Jump up to:a b c Global status report on alcohol and health 2014 (PDF). World Health Organization. 2014. p. s8,51. ISBN 9789240692763.
  8. Jump up^ Agarwal-Kozlowski K, Agarwal DP (April 2000). “[Genetic predisposition for alcoholism]”. Ther Umsch 57(4): 179–84. doi:10.1024/0040-5930.57.4.179.PMID 10804873.
  9. Jump up^ Moonat, S; Pandey, SC (2012). “Stress, epigenetics, and alcoholism.”. Alcohol research : current reviews 34(4): 495–505. PMID 23584115.
  10. Jump up^ Mersy, DJ (1 April 2003). “Recognition of alcohol and substance abuse.”. American family physician 67 (7): 1529–32. PMID 12722853.
  11. Jump up^ “HEALTH AND ETHICS POLICIES OF THE AMA HOUSE OF DELEGATES” (PDF). June 2008. p. 33. Retrieved 10 May 2015. H-30.997 Dual Disease Classification of Alcoholism: The AMA reaffirms its policy endorsing the dual classification of alcoholism under both the psychiatric and medical sections of the International Classification of Diseases. (Res. 22, I-79; Reaffirmed: CLRPD Rep. B, I-89; Reaffirmed: CLRPD Rep. B, I-90; Reaffirmed by CSA Rep. 14, A-97; Reaffirmed: CSAPH Rep. 3, A-07)
  12. Jump up^ World Health Organization (January 2015).“Alcohol”. Retrieved 10 May 2015.
  13. ^ Jump up to:a b Blondell RD (February 2005). “Ambulatory detoxification of patients with alcohol dependence”. Am Fam Physician 71 (3): 495–502. PMID 15712624.
  14. Jump up^ DeVido, JJ; Weiss, RD (December 2012). “Treatment of the depressed alcoholic patient.”. Current psychiatry reports 14 (6): 610–8. PMID 22907336.
  15. ^ Jump up to:a b Morgan-Lopez AA, Fals-Stewart W (May 2006). “Analytic complexities associated with group therapy in substance abuse treatment research: problems, recommendations, and future directions”. Exp Clin Psychopharmacol 14 (2): 265–73. doi:10.1037/1064-1297.14.2.265. PMID 16756430.
  16. Jump up^ Albanese, AP (November 2012). “Management of alcohol abuse.”. Clinics in liver disease 16 (4): 737–62.PMID 23101980.
  17. Jump up^ Tusa, AL; Burgholzer, JA (2013). “Came to believe: spirituality as a mechanism of change in alcoholics anonymous: a review of the literature from 1992 to 2012.”. Journal of addictions nursing 24 (4): 237–46.PMID 24335771.
  18. Jump up^ Testino, G; Leone, S; Borro, P (December 2014). “Treatment of alcohol dependence: recent progress and reduction of consumption.”. Minerva medica 105 (6): 447–66. PMID 25392958.
  19. ^ Jump up to:a b “Global Population Estimates by Age, 1950–2050”. Retrieved 10 May 2015.
  20. ^ Jump up to:a b c “Alcohol Facts and Statistics”. Retrieved9 May 2015.
  21. Jump up^ GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). “Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013.”. Lancet 385 (9963): 117–71.doi:10.1016/S0140-6736(14)61682-2.PMC 4340604. PMID 25530442.
  22. ^ Jump up to:a b Schuckit, MA (27 November 2014). “Recognition and management of withdrawal delirium (delirium tremens).”. The New England journal of medicine 371(22): 2109–13. PMID 25427113.
  23. Jump up^ Chambers English Thesaurus. Allied Publishers. p. 175. ISBN 9788186062043.
  24. ^ Jump up to:a b WHO. “Lexicon of alcohol and drug terms published by the World Health Organization”. World Health Organisation.
  25. ^ Jump up to:a b Hoffman PL, Tabakoff B (July 1996). “Alcohol dependence: a commentary on mechanisms”. Alcohol Alcohol 31 (4): 333–40.doi:10.1093/oxfordjournals.alcalc.a008159.PMID 8879279.
  26. Jump up^ Dunn N, Cook CC (March 1999). “Psychiatric aspects of alcohol misuse”. Hospital medicine (London, England : 1998) 60 (3): 169–72.doi:10.12968/hosp.1999.60.3.1060. ISSN 1462-3935. PMID 10476237.
  27. Jump up^ Wilson, Richard; Kolander, Cheryl A. (2003). Drug abuse prevention: a school and community partnership. Sudbury, Mass.: Jones and Bartlett. pp. 40–45. ISBN 978-0-7637-1461-1.
  28. Jump up^ American Medical Association (2003). Leiken, Jerrold B. MD, Lipsky, Martin S. MD, ed. Complete Medical Encyclopedia (Encyclopedia) (First ed.). New York, NY: Random House Reference. p. 485. ISBN 0-8129-9100-1.
  29. Jump up^ Müller D, Koch RD, von Specht H, Völker W, Münch EM (March 1985). “[Neurophysiologic findings in chronic alcohol abuse]”. Psychiatr Neurol Med Psychol (Leipz)(in German) 37 (3): 129–32. PMID 2988001.
  30. Jump up^ Testino G (2008). “Alcoholic diseases in hepato-gastroenterology: a point of view”.Hepatogastroenterology 55 (82–83): 371–7.PMID 18613369.
  31. Jump up^ 10th Special Report to the U.S. Congress on Alcohol and Health, 2000, U.S. Department of Health and Human Services, Public Health Service National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism.
  32. ^ Jump up to:a b c Blum, Laura N.; Nielsen, Nancy H.; Riggs, Joseph A.; Council on Scientific Affairs, American Medical Association (September 1998). “Alcoholism and alcohol abuse among women: report of the council on scientific affairs”. Journal of Women’s Health (Mary Ann Liebert, Inc.) 7 (7): 861–870.doi:10.1089/jwh.1998.7.861.
  33. ^ Jump up to:a b Walter H, Gutierrez K, Ramskogler K, Hertling I, Dvorak A, Lesch OM (November 2003). “Gender-specific differences in alcoholism: implications for treatment”.Archives of Women’s Mental Health 6 (4): 253–8.doi:10.1007/s00737-003-0014-8. PMID 14628177.
  34. Jump up^ Mihai B, Lăcătuşu C, Graur M (April–June 2008). “[Alcoholic ketoacidosis]”. Rev Med Chir Soc Med Nat Iasi 112 (2): 321–6. PMID 19294998.
  35. Jump up^ Sibaï K, Eggimann P (September 2005). “[Alcoholic ketoacidosis: not rare cause of metabolic acidosis]”.Rev Med Suisse 1 (32): 2106, 2108–10, 2112–5.PMID 16238232.
  36. Jump up^ Cederbaum AI (2012). “Alcohol metabolism”. Clin Liver Dis 16 (4): 667–85.doi:10.1016/j.cld.2012.08.002. PMC 3484320.PMID 23101976.
  37. ^ Jump up to:a b Professor Georgy Bakalkin (8 July 2008).“Alcoholism-associated molecular adaptations in brain neurocognitive circuits”. Retrieved11 January 2012.
  38. Jump up^ Oscar-Berman M, Marinkovic K (2003). “Alcoholism and the brain: an overview”. Alcohol Res Health 27 (2): 125–33. PMID 15303622.
  39. Jump up^ Uekermann J, Daum I (May 2008). “Social cognition in alcoholism: a link to prefrontal cortex dysfunction?”.Addiction 103 (5): 726–35. doi:10.1111/j.1360-0443.2008.02157.x. PMID 18412750.
  40. Jump up^ Wetterling T, Junghanns K; Junghanns, K (September 2000). “Psychopathology of alcoholics during withdrawal and early abstinence”. Eur Psychiatry 15 (8): 483–8.doi:10.1016/S0924-9338(00)00519-8. ISSN 0924-9338. PMID 11175926.
  41. Jump up^ Schuckit MA (November 1983). “Alcoholism and other psychiatric disorders”. Hosp Community Psychiatry 34(11): 1022–7. doi:10.1176/ps.34.11.1022. ISSN 0022-1597. PMID 6642446.
  42. Jump up^ Cowley DS (24 January 1992). “Alcohol abuse, substance abuse, and panic disorder”. Am J Med 92(1A): 41S–48S. doi:10.1016/0002-9343(92)90136-Y.ISSN 0002-9343. PMID 1346485.
  43. Jump up^ Cosci F, Schruers KR, Abrams K, Griez EJ; Schruers, KR; Abrams, K (June 2007). “Alcohol use disorders and panic disorder: a review of the evidence of a direct relationship”. J Clin Psychiatry 68 (6): 874–80.doi:10.4088/JCP.v68n0608. ISSN 0160-6689.PMID 17592911.
  44. Jump up^ Grant BF, Harford TC (October 1995). “Comorbidity between DSM-IV alcohol use disorders and major depression: results of a national survey”. Drug Alcohol Depend 39 (3): 197–206. doi:10.1016/0376-8716(95)01160-4. ISSN 0376-8716.PMID 8556968.
  45. Jump up^ Kandel DB, Huang FY, Davies M (October 2001). “Comorbidity between patterns of substance use dependence and psychiatric syndromes”. Drug Alcohol Depend 64 (2): 233–41. doi:10.1016/S0376-8716(01)00126-0. ISSN 0376-8716.PMID 11543993.
  46. Jump up^ Cornelius JR, Bukstein O, Salloum I, Clark D (2003). “Alcohol and psychiatric comorbidity”. Recent Dev Alcohol. Recent Developments in Alcoholism 16: 361–74. doi:10.1007/0-306-47939-7_24. ISBN 0-306-47258-9. ISSN 0738-422X. PMID 12638646.
  47. Jump up^ Schuckit MA, Tipp JE, Bergman M, Reich W, Hesselbrock VM, Smith TL (July 1997). “Comparison of induced and independent major depressive disorders in 2,945 alcoholics”. Am J Psychiatry 154 (7): 948–57.doi:10.1176/ajp.154.7.948. ISSN 0002-953X.PMID 9210745.
  48. Jump up^ Schuckit MA, Tipp JE, Bucholz KK, Nurnberger JI, Hesselbrock VM, Crowe RR, Kramer J (October 1997). “The life-time rates of three major mood disorders and four major anxiety disorders in alcoholics and controls”.Addiction 92 (10): 1289–304. doi:10.1111/j.1360-0443.1997.tb02848.x. ISSN 0965-2140.PMID 9489046.
  49. Jump up^ Schuckit MA, Smith TL, Danko GP, Pierson J, Trim R, Nurnberger JI, Kramer J, Kuperman S, Bierut LJ, Hesselbrock V (November 2007). “A comparison of factors associated with substance-induced versus independent depressions”. J Stud Alcohol Drugs 68 (6): 805–12. doi:10.15288/jsad.2007.68.805. ISSN 1937-1888. PMID 17960298.
  50. Jump up^ Schuckit M (June 1983). “Alcoholic patients with secondary depression”. Am J Psychiatry 140 (6): 711–4. doi:10.1176/ajp.140.6.711. ISSN 0002-953X.PMID 6846629.
  51. ^ Jump up to:a b c Karrol Brad R. (2002). “Women and alcohol use disorders: a review of important knowledge and its implications for social work practitioners”. Journal of social work 2 (3): 337–356.doi:10.1177/146801730200200305.
  52. ^ Jump up to:a b c McCully, Chris (2004). Goodbye Mr. Wonderful. Alcohol, Addition and Early Recovery. London: Jessica Kingsley Publishers. ISBN 978-1-84310-265-6.
  53. Jump up^ Isralowitz, Richard (2004). Drug use: a reference handbook. Santa Barbara, Calif.: ABC-CLIO. pp. 122–123. ISBN 978-1-57607-708-5.
  54. Jump up^ Langdana, Farrokh K. (27 March 2009).Macroeconomic Policy: Demystifying Monetary and Fiscal Policy (2nd ed.). Springer. p. 81. ISBN 978-0-387-77665-1.
  55. Jump up^ Gifford, Maria (22 October 2009). Alcoholism (Biographies of Disease). Greenwood Press. pp. 89–91. ISBN 978-0-313-35908-8.
  56. Jump up^ Schadé, Johannes Petrus (October 2006). The Complete Encyclopedia of Medicine and Health. Foreign Media Books. pp. 132–133. ISBN 978-1-60136-001-4.
  57. Jump up^ Gold, Mark. “Children of Alcoholics”. Psych Central. Retrieved 27 November 2011.
  58. Jump up^ Galanter, Marc; Kleber, Herbert D. (1 July 2008). The American Psychiatric Publishing Textbook of Substance Abuse Treatment (4th ed.). United States of America: American Psychiatric Publishing Inc. p. 58.ISBN 978-1-58562-276-4.
  59. Jump up^ Dart, Richard C. (1 December 2003). Medical Toxicology (3rd ed.). USA: Lippincott Williams & Wilkins. pp. 139–140. ISBN 978-0-7817-2845-4.
  60. Jump up^ Idemudia SO, Bhadra S, Lal H (June 1989). “The pentylenetetrazol-like interoceptive stimulus produced by ethanol withdrawal is potentiated by bicuculline and picrotoxinin”. Neuropsychopharmacology 2 (2): 115–22.doi:10.1016/0893-133X(89)90014-6. ISSN 0893-133X. PMID 2742726.
  61. Jump up^ Chastain G (October 2006). “Alcohol, neurotransmitter systems, and behavior”. The Journal of general psychology 133 (4): 329–35.doi:10.3200/GENP.133.4.329-335. ISSN 0022-1309.PMID 17128954.
  62. ^ Jump up to:a b c Heilig M, Egli M, Crabbe JC, Becker HC (April 2010). “Acute withdrawal, protracted abstinence and negative affect in alcoholism: are they linked?”. Addict Biol 15 (2): 169–84. doi:10.1111/j.1369-1600.2009.00194.x. PMC 3268458.PMID 20148778.
  63. Jump up^ Johnson, Bankole A. (2011). Addiction medicine : science and practice. New York: Springer. pp. 301–303. ISBN 978-1-4419-0337-2.
  64. Jump up^ Breese GR, Sinha R, Heilig M (February 2011).“Chronic alcohol neuroadaptation and stress contribute to susceptibility for alcohol craving and relapse.”.Pharmacol Ther 129 (2): 149–71.doi:10.1016/j.pharmthera.2010.09.007.PMC 3026093. PMID 20951730.
  65. Jump up^ Sullivan JT, Sykora K, Schneiderman J, Naranjo CA, Sellers EM. (November 1989). “Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar).”. Br J Addict.84 (11): 1353–7. doi:10.1111/j.1360-0443.1989.tb00737.x. PMID 2597811.
  66. ^ Jump up to:a b c d Enoch MA (December 2006). “Genetic and environmental influences on the development of alcoholism: resilience vs. risk”. Annals of the New York Academy of Sciences 1094 (1): 193–201.doi:10.1196/annals.1376.019. PMID 17347351.
  67. Jump up^ Bierut LJ, Schuckit MA, Hesselbrock V, Reich T (2000). “Co-occurring risk factors for alcohol dependence and habitual smoking”. Alcohol Res Health24 (4): 233–41. PMID 15986718.
  68. Jump up^ Agrawal A, Sartor CE, Lynskey MT, Grant JD, Pergadia ML, Grucza R, Bucholz KK, Nelson EC, Madden PA, Martin NG, Heath AC (2009). “Evidence for an Interaction Between Age at 1st Drink and Genetic Influences on DSM-IV Alcohol Dependence Symptoms”. Alcoholism: Clinical and Experimental Research 33 (12): 2047–56. doi:10.1111/j.1530-0277.2009.01044.x. PMC 2883563.PMID 19764935.
  69. ^ Jump up to:a b “Early Age At First Drink May Modify Tween/Teen Risk For Alcohol Dependence”. Medical News Today. 21 September 2009.
  70. Jump up^ Schwandt ML, Lindell SG, Chen S, Higley JD, Suomi SJ, Heilig M, Barr CS (February 2010). “Alcohol Response and Consumption in Adolescent Rhesus Macaques: Life History and Genetic Influences”.Alcohol 44 (1): 67–80.doi:10.1016/j.alcohol.2009.09.034. PMC 2818103.PMID 20113875.
  71. Jump up^ Crews FT, Boettiger CA (September 2009).“Impulsivity, Frontal Lobes and Risk for Addiction”.Pharmacol Biochem Behav 93 (3): 237–47.doi:10.1016/j.pbb.2009.04.018. PMC 2730661.PMID 19410598.
  72. Jump up^ “Volume of World Beer Production”. European Beer Guide. Archived from the original on 28 October 2006. Retrieved 17 October 2006.
  73. Jump up^ Nelson, Max (2005). The Barbarian’s Beverage: A History of Beer in Ancient Europe. Abingdon, Oxon: Routledge. p. 1. ISBN 0-415-31121-7. Retrieved21 September 2010.
  74. Jump up^ Rudgley, Richard (1993). The Alchemy of Culture: Intoxicants in Society. London: British Museum Press. p. 411. ISBN 978-0-7141-1736-2. Retrieved13 January 2012.
  75. Jump up^ Arnold, John P (2005). Origin and History of Beer and Brewing: From Prehistoric Times to the Beginning of Brewing Science and Technology. Cleveland, Ohio: Reprint Edition by BeerBooks. p. 411. ISBN 0-9662084-1-2. Retrieved 13 January 2012.
  76. Jump up^ Joshua J. Mark (2011). Beer. Ancient History Encyclopedia.
  77. Jump up^ World’s Best Beers: One Thousand. Google Books. 6 October 2009. ISBN 978-1-4027-6694-7. Retrieved7 August 2010.
  78. Jump up^ “Gender differences in alcohol use and alcohol dependence or abuse: 2004 or 2005.” The NSDUH Report.Accessed 22 June 2012.
  79. Jump up^ Moore S, Montane-Jaime LK, Carr LG, Ehlers CL (2007). “Variations in alcohol-metabolizing enzymes in people of East Indian and African descent from Trinidad and Tobago”. Alcohol Res Health 30 (1): 28–30.PMID 17718398.
  80. Jump up^ Eng MY, Luczak SE, Wall TL (2007). “ALDH2, ADH1B, and ADH1C genotypes in Asians: a literature review”. Alcohol Res Health 30 (1): 22–7.PMID 17718397.
  81. Jump up^ Scott DM, Taylor RE (2007). “Health-related effects of genetic variations of alcohol-metabolizing enzymes in African Americans”. Alcohol Res Health 30 (1): 18–21.PMID 17718396.
  82. Jump up^ Ehlers CL (2007). “Variations in ADH and ALDH in Southwest California Indians”. Alcohol Res Health 30(1): 14–7. PMID 17718395.
  83. Jump up^ Szlemko WJ, Wood JW, Thurman PJ (October 2006). “Native Americans and alcohol: past, present, and future”. J Gen Psychol 133 (4): 435–51.doi:10.3200/GENP.133.4.435-451. PMID 17128961.
  84. Jump up^ Spillane NS, Smith GT (May 2007). “A theory of reservation-dwelling American Indian alcohol use risk”.Psychol Bull 133 (3): 395–418. doi:10.1037/0033-2909.133.3.395. PMID 17469984.
  85. Jump up^ American Heritage Dictionaries (12 April 2006). The American Heritage dictionary of the English language(4 ed.). Boston: Houghton Mifflin. ISBN 978-0-618-70172-8. To use wrongly or improperly; misuse: abuse alcohol
  86. Jump up^ “Dietary Guidelines for Americans 2005”. USA: 2005. Dietary Guidelines
  87. Jump up^ See question 16 of the Severity of Alcohol Dependence Questionnaire.
  88. Jump up^
  89. Jump up^ Esser, Marissa B.; Hedden, Sarra L.; Kanny, Dafna; Brewer, Robert D.; Gfroerer, Joseph C.; Naimi, Timothy S. (20 November 2014). “Prevalence of Alcohol Dependence Among US Adult Drinkers, 2009–2011”.Preventing Chronic Disease 11.doi:10.5888/pcd11.140329.
  90. Jump up^ Thomas F. McGovern; William L. White (20 May 2003). Alcohol Problems in the United States: Twenty Years of Treatment Perspective. Routledge. pp. 7–.ISBN 978-0-7890-2049-9. Retrieved 17 April 2010.
  91. Jump up^ alcoholism” at Dorland’s Medical Dictionary
  92. Jump up^ Thombs, Dennis L (1999). Introductive To Addictive Behaviors 2ed. London: The Guildford Press. p. 64.
  93. Jump up^ Thombs, Dennis L (1999). Introduction to Addictive Behaviours 2ed. London: The Guildford Press. p. 64.
  94. Jump up^ Thombs, Dennis (1999). Introduction to Addictive Behaviors. London: The Guildford Press. p. 64.
  95. Jump up^ Thombs, Dennis L (1999). Introduction to Addictive Behaviors 2ed. London: The Guildford Press. p. 65.
  96. ^ Jump up to:a b VandenBos, Gary R. (15 July 2006). APA dictionary of psychology. Washington, DC: American Psychological Association. ISBN 978-1-59147-380-0.
  97. ^ Jump up to:a b “Diagnostic Criteria for Alcohol Abuse and Dependence – Alcohol Alert No. 30-1995”. Archivedfrom the original on 27 March 2010. Retrieved 17 April2010.
  98. Jump up^ Martin CS, Chung T, Langenbucher JW (August 2008). “How Should We Revise Diagnostic Criteria for Substance Use Disorders in the DSM—V?”. J Abnorm Psychol 117 (3): 561–75. doi:10.1037/0021-843X.117.3.561. PMC 2701140. PMID 18729609.
  99. Jump up^ “Proposed Revision | APA DSM-5”. Archived from the original on 25 March 2010. Retrieved 17 April 2010.
  100. Jump up^ “A System to Convert ICD Diagnostic Codes for Alcohol Research”. Retrieved 17 April 2010.
  101. Jump up^ Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association. 31 July 1994. ISBN 978-0-89042-025-6.
  102. Jump up^ Morse RM, Flavin DK (August 1992). “The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism”. JAMA: the Journal of the American Medical Association 268 (8): 1012–4. doi:10.1001/jama.1992.03490080086030.ISSN 0098-7484. PMID 1501306.
  103. Jump up^ Alcoholism at the US National Library of MedicineMedical Subject Headings (MeSH)
  104. ^ Jump up to:a b c The first 100 members of AA (2001) [1939].Alcoholics Anonymous: the story of how many thousands of men and women have recovered from alcoholism. New York City: Alcoholics Anonymous World Services. xxxii, 575 p. ISBN 1-893007-16-2.
  105. Jump up^ Kay AB (2000). “Overview of ‘allergy and allergic diseases: with a view to the future'”. Br. Med. Bull. 56(4): 843–64. doi:10.1258/0007142001903481.ISSN 0007-1420. PMID 11359624.
  106. Jump up^ “The Big Book Self Test:”. Retrieved19 February 2008.
  107. Jump up^ “OCTOBER 22 DEATHS”. from the original on 7 February 2008. Retrieved 18 February 2008.
  108. ^ Jump up to:a b Nora Volkow. “Science of Addiction” (PDF). American Medical Association.
  109. Jump up^ Kahan M (April 1996). “Identifying and managing problem drinkers”. Can Fam Physician 42: 661–71.PMC 2146411. PMID 8653034.
  110. Jump up^ Ewing JA (October 1984). “Detecting alcoholism. The CAGE questionnaire”. JAMA: the Journal of the American Medical Association 252 (14): 1905–7.doi:10.1001/jama.252.14.1905. ISSN 0098-7484.PMID 6471323.
  111. Jump up^ “CAGE questionnaire – screen for alcohol misuse”(PDF).
  112. Jump up^ Dhalla S, Kopec JA (2007). “The CAGE questionnaire for alcohol misuse: a review of reliability and validity studies”. Clin Invest Med 30 (1): 33–41.PMID 17716538.
  113. Jump up^ Raistrick, D.; Dunbar, G.; Davidson, R. (1983).“Alcohol Dependence Data Questionnaire (SADD)”. European Monitoring Centre for Drugs and Drug Addiction.
  114. Jump up^ “Michigan Alcohol Screening Test”. The National Council on Alcoholism and Drug Dependence.
  115. Jump up^ Thomas F. Babor; John C. Higgins-Biddle; John B. Saunders; Maristela G. Monteiro (2001). “The Alcohol Use Disorders Identification Test, Guidelines for Use in Primary Care” (PDF). World Health Organization.
  116. Jump up^ Smith SG, Touquet R, Wright S, Das Gupta N; Touquet, R; Wright, S (September 1996). “Detection of alcohol misusing patients in accident and emergency departments: the Paddington alcohol test (PAT)”.Journal of Accident and Emergency Medicine (British Association for Accident and Emergency Medicine) 13(5): 308–312. doi:10.1136/emj.13.5.308. ISSN 1351-0622. PMC 1342761. PMID 8894853.
  117. ^ Jump up to:a b Nurnberger, Jr., John I., and Bierut, Laura Jean.“Seeking the Connections: Alcoholism and our Genes.” Scientific American, April 2007, Vol. 296, Issue 4.
  118. Jump up^ New York Daily News (William Sherman) Test targets addiction gene 11 February 2006
  119. Jump up^ Berggren U, Fahlke C, Aronsson E, Karanti A, Eriksson M, Blennow K, Thelle D, Zetterberg H, Balldin J (September 2006). “The taqI DRD2 A1 allele is associated with alcohol-dependence although its effect size is small” (Free full text). Alcohol and alcoholism (Oxford, Oxfordshire) 41 (5): 479–85.doi:10.1093/alcalc/agl043. ISSN 0735-0414.PMID 16751215.
  120. Jump up^ Jones AW (2006). “Urine as a biological specimen for forensic analysis of alcohol and variability in the urine-to-blood relationship”. Toxicol Rev 25 (1): 15–35.doi:10.2165/00139709-200625010-00002.PMID 16856767.
  121. Jump up^ Das SK, Dhanya L, Vasudevan DM (2008). “Biomarkers of alcoholism: an updated review”. Scand J Clin Lab Invest 68 (2): 81–92.doi:10.1080/00365510701532662. PMID 17852805.
  122. Jump up^ World Health Organisation (2010). “Alcohol”.
  123. Jump up^ “Alcohol policy in the WHO European Region: current status and the way forward” (PDF). World Health Organisation. 12 September 2005.
  124. Jump up^ Crews F, He J, Hodge C (February 2007). “Adolescent cortical development: a critical period of vulnerability for addiction”. Pharmacol Biochem Behav 86 (2): 189–99.doi:10.1016/j.pbb.2006.12.001. PMID 17222895.
  125. ^ Jump up to:a b Gabbard, Glen O. (2001). Treatments of psychiatric disorders (3 ed.). Washington, DC: American Psychiatric Press. ISBN 978-0-88048-910-2.
  126. Jump up^ Stavro K, Pelletier J, Potvin S (January 2012). “Widespread and sustained cognitive deficits in alcoholism: a meta-analysis.”. Addict Biol 18 (2): 203–13. doi:10.1111/j.1369-1600.2011.00418.x.PMID 22264351.
  127. Jump up^ Dawson DA, Grant BF, Stinson FS, Chou PS, Huang B, Ruan WJ (2005). “Recovery from DSM-IV alcohol dependence: United States, 2001–2002”. Addiction100 (3): 281–92. doi:10.1111/j.1360-0443.2004.00964.x. PMID 15733237.
  128. Jump up^ Dawson DA, Goldstein RB, Grant BF (2007). “Rates and correlates of relapse among individuals in remission from DSM-IV alcohol dependence: a 3-year follow-up”.Alcoholism: Clinical and Experimental Research 31 (12): 2036–45. doi:10.1111/j.1530-0277.2007.00536.x.PMID 18034696.
  129. Jump up^ Vaillant GE (2003). “A 60-year follow-up of alcoholic men”. Addiction (Abingdon, England) 98 (8): 1043–51.doi:10.1046/j.1360-0443.2003.00422.x.PMID 12873238.
  130. Jump up^ National Institute on Alcohol Abuse and Alcoholism.
  131. Jump up^ Mason BJ, Heyser CJ (January 2010). “The neurobiology, clinical efficacy and safety of acamprosate in the treatment of alcohol dependence”. Expert Opin Drug Saf 9 (1): 177–88.doi:10.1517/14740330903512943. PMID 20021295.
  132. Jump up^ Mason BJ, Heyser CJ (March 2010). “Acamprosate: A prototypic neuromodulator in the treatment of alcohol dependence”. CNS Neurol Disord Drug Targets 9 (1): 23–32. doi:10.2174/187152710790966641.PMC 2853976. PMID 20201812.
  133. Jump up^ Rösner S, Hackl-Herrwerth A, Leucht S, Lehert P, Vecchi S, Soyka M (2010). Rösner, Susanne, ed. “Acamprosate for alcohol dependence”. Cochrane Database of Systematic Reviews (9): CD004332.doi:10.1002/14651858.CD004332.pub2.PMID 20824837.
  134. ^ Jump up to:a b c d Jonas DE, Amick HR, Feltner C, Bobashev G, Thomas K, Wines R, Kim MM, Shanahan E, Gass CE, Rowe CJ, Garbutt JC (14 May 2014). “Pharmacotherapy for Adults With Alcohol Use Disorders in Outpatient Settings”. JAMA 311 (18): 1889–900.doi:10.1001/jama.2014.3628. PMID 24825644.
  135. Jump up^ Lindsay, S.J.E.; Powell, Graham E., eds. (28 July 1998). The Handbook of Clinical Adult Psychology(2nd ed.). Routledge. p. 402. ISBN 978-0-415-07215-1.
  136. Jump up^ Gitlow, Stuart (1 October 2006). Substance Use Disorders: A Practical Guide (2nd ed.). USA: Lippincott Williams and Wilkins. pp. 52 and 103–121.ISBN 978-0-7817-6998-3.
  137. Jump up^ Kushner MG, Abrams K, Borchardt C (March 2000). “The relationship between anxiety disorders and alcohol use disorders: a review of major perspectives and findings”. Clin Psychol Rev 20 (2): 149–71.doi:10.1016/S0272-7358(99)00027-6.PMID 10721495.
  138. Jump up^ Ogborne AC (June 2000). “Identifying and treating patients with alcohol-related problems”. CMAJ 162(12): 1705–8. PMC 1232509. PMID 10870503.
  139. Jump up^ Soyka M, Rösner S (November 2008). “Opioid antagonists for pharmacological treatment of alcohol dependence – a critical review”. Curr Drug Abuse Rev 1(3): 280–91. doi:10.2174/1874473710801030280.PMID 19630726.
  140. Jump up^ Poulos CX, Zack M (November 2004). “Low-dose diazepam primes motivation for alcohol and alcohol-related semantic networks in problem drinkers”. Behav Pharmacol 15 (7): 503–12. doi:10.1097/00008877-200411000-00006. ISSN 0955-8810.PMID 15472572.
  141. Jump up^ Johansson BA, Berglund M, Hanson M, Pöhlén C, Persson I (November 2003). “Dependence on legal psychotropic drugs among alcoholics” (PDF). Alcohol Alcohol. 38 (6): 613–8. doi:10.1093/alcalc/agg123.ISSN 0735-0414. PMID 14633651.
  142. Jump up^ Catherine Le Galès-Camus (2004). Global Status Report on Alcohol 2004 (PDF). World Health Organization. ISBN 92-4-156272-2.
  143. ^ Jump up to:a b “Alcohol misuse: How much does it cost?”(PDF). Cabinet Office Strategy Unit. September 2003.
  144. Jump up^ Hasin DS, Stinson FS, Ogburn E, Grant BF (2007). “Prevalence, Correlates, Disability, and Comorbidity of DSM-IV Alcohol Abuse and Dependence in the United States”. Archives of General Psychiatry 64 (7): 830–42.doi:10.1001/archpsyc.64.7.830. PMID 17606817.
  145. Jump up^ “alcoholism”. Encyclopædia Britannica. 2010.
  146. Jump up^ Dick DM, Bierut LJ (April 2006). “The genetics of alcohol dependence”. Current psychiatry reports 8 (2): 151–7. doi:10.1007/s11920-006-0015-1. ISSN 1523-3812. PMID 16539893.
  147. Jump up^ “About 37 percent of college students could now be considered alcoholics”. Emerald Media.
  148. Jump up^ Zuskin E, Jukić V, Lipozencić J, Matosić A, Mustajbegović J, Turcić N, Poplasen-Orlovac D, Bubas M, Prohić A (December 2006). “[Alcoholism—how it affects health and working capacity]”. Arh Hig Rada Toksikol 57 (4): 413–26. PMID 17265681.
  149. Jump up^ American Psychiatric Association practice guidelines for the treatment of psychiatric disorders. Arlington, Virg.: American Psychiatric Association. 2006. p. 1346.ISBN 9780890423851.
  150. Jump up^ O’Connor, Rory; Sheehy, Noel (29 January 2000).Understanding suicidal behaviour. Leicester: BPS Books. pp. 33–37. ISBN 978-1-85433-290-5.
  151. Jump up^ The National Institute on Alcohol Abuse and Alcoholism; U.S. Department of Health and Human Services, NIH News (18 January 2005). “2001–2002 Survey Finds That Many Recover From Alcoholism”. National Institutes of Health.
  152. Jump up^ Vaillant GE (August 2003). “A 60-year follow-up of alcoholic men”. Addiction. 98 (8): 1043–51.doi:10.1046/j.1360-0443.2003.00422.x. ISSN 0965-2140. PMID 12873238.
  153. Jump up^ Peters, Uwe Henrik (30 April 2007). Lexikon Psychiatrie, Psychotherapie, Medizinische Psychologie. Urban Fischer bei Elsev. ISBN 978-3-437-15061-6.
  154. Jump up^ Valverde, Mariana (1998). Diseases of the Will. Cambridge: Cambridge University Press. p. 48.ISBN 978-0-521-64469-3.
  155. Jump up^ Tracy, Sarah J. (25 May 2005). Alcoholism in America: from reconstruction to prohibition. Baltimore: Johns Hopkins University Press. pp. 31–52.ISBN 978-0-8018-8119-0.
  156. Jump up^ Alcoholismus chronicus, eller Chronisk alkoholssjukdom:. Stockholm und Leipzig. 1852. Retrieved 19 February 2008.
  157. Jump up^ Potter, James V. (14 January 2008). Substances of Abuse 2. AFS Publishing Co. pp. 1–13. ISBN 978-1-930327-46-7.
  158. Jump up^ Julie Louise Gerberding; José Cordero; R. Louise Floyd (May 2005). “Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis” (PDF). USA: Centers for Disease Control and Prevention.
  159. Jump up^ Streissguth, Ann Pytkowicz (1 September 1997).Fetal alcohol syndrome: a guide for families and communities. Baltimore, MD, USA: Paul H Brookes Pub. ISBN 978-1-55766-283-5.
  160. Jump up^ “Global Status Report on Alcohol 2004” (PDF). World Health Organization. Archived (PDF) from the original on 30 December 2006. Retrieved 3 January2007.
  161. Jump up^ “Economic cost of alcohol consumption”. World Health Organization Global Alcohol Database. Retrieved3 January 2007.
  162. Jump up^ “Q&A: The costs of alcohol”. BBC. 19 September 2003.
  163. Jump up^ Bouchery EE, Harwood HJ, Sacks JJ, Simon CJ, Brewer RD (2011). “Economic Costs of Excessive Alcohol Consumption in the U.S., 2006”. American Journal of Preventive Medicine 41 (5): 516–524.doi:10.1016/j.amepre.2011.06.045. PMID 22011424.
  164. Jump up^ “World/Global Alcohol/Drink Consumption”. Finfacts Ireland. 2009.
  165. Jump up^ Stivers, Richard (May 2000). Hair of the dog: Irish drinking and its American stereotype. New York: Continuum. ISBN 978-0-8264-1218-8.
  166. Jump up^ Chen CC, Yin SJ (2008). “Alcohol abuse and related factors in Asia”. International Review of Psychiatry 20(5): 425–433. doi:10.1080/09540260802344075.PMID 19012127.
  167. Jump up^ Wooksoo, K. (2009). Drinking Culture of Elderly Korean Immigrants in Canada: A Focus Group Study. Journal of Cross-Cultural Gerontology, 24(4), 339–353.
  168. Jump up^ Li, H. Z., & Rosenblood, L. (1994). Exploring factors influencing alcohol consumption patterns among Chinese and Caucasians. Journal of Studies on Alcohol, 55(4), 427. Retrieved from EBSCOhost.
  169. Jump up^ French, L. (2008). Psychoactive agents and Native American spirituality: Past and present. Contemporary Justice Review, 11(2), 155–163.
  170. Jump up^ Olmsted CL, Kockler DR (October 2008). “Topiramate for alcohol dependence”. Ann Pharmacother 42 (10): 1475–80. doi:10.1345/aph.1L157. ISSN 1060-0280.PMID 18698008.
  171. Jump up^ Kenna GA, Lomastro TL, Schiesl A, Leggio L, Swift RM (May 2009). “Review of topiramate: an antiepileptic for the treatment of alcohol dependence”. Curr Drug Abuse Rev 2 (2): 135–42.doi:10.2174/1874473710902020135.PMID 19630744.
  172. Jump up^ Leggio L, Garbutt JC, Addolorato G (March 2010). “Effectiveness and safety of baclofen in the treatment of alcohol dependent patients.”. CNS & neurological disorders drug targets 9 (1): 33–44.doi:10.2174/187152710790966614.PMID 20201813.
  173. Jump up^ Liu, J; Wang, LN (3 April 2015). “Baclofen for alcohol withdrawal.”. The Cochrane database of systematic reviews 4: CD008502. PMID 25836263.
  174. Jump up^ “Baclofen and severe alcohol dependence: an uncertain harm-benefit balance as of early 2013.”.Prescrire Int 22 (141): 214–7. September 2013.PMID 24171218.
  175. Jump up^ Kenna GA (2010). “Medications acting on the serotonergic system for the treatment of alcohol dependent patients.”. Current pharmaceutical design 16(19): 2126–35. doi:10.2174/138161210791516396.PMID 20482508.

Further reading

  • Cannon, Eoin F. (2013). The Saloon and the Mission: Addiction, Conversion, and the Politics of Redemption in American Culture. Amherst, MA: University of Massachusetts Press.
  • Galanter, Marc (2005). Alcohol Problems in Adolescents and Young Adults: Epidemiology, Neurobiology, Prevention, Treatment. New York, NY: Kluwer Academic/Plenum.ISBN 0-306-48625-3. OCLC 133155628 56653179 57724687 71290784.
  • Hedblom, Jack H. (2007). Last Call: Alcoholism and Recovery. Baltimore, MD: Johns Hopkins University Press. ISBN 978-0-8018-8677-5. OCLC 237901552 77708730.
  • National Institute on Alcohol Abuse and Alcoholism. “Etiology and Natural History of Alcoholism“.
  • The Online Resource for Addiction Recovery, Addiction Treatment & Addiction help. “Addiction Recovery“.
  • O’Farrell, Timothy J. and William Fals-Stewart (2006). Behavioral Couples Therapy for Alcoholism and Drug Abuse. New York, NY: Guilford Press. ISBN 1-59385-324-6.OCLC 64336035.
  • Osborn, Matthew Warner (2014). Rum Maniacs: Alcoholic Insanity in the Early American Republic. Chicago: University of Chicago Press.
  • Pence, Gregory, “Kant on Whether Alcoholism is a Disease,” Ch. 2, The Elements of Bioethics, McGraw-Hill Books, 2007.
  • Plant, Martin A. and Moira Plant (2006). Binge Britain: Alcohol and the National Response. Oxford, UK; New York, NY: Oxford University Press. ISBN 0-19-929940-4.OCLC 238809013 64554668.
  • Smart, Lesley (2007). Alcohol and Human Health. Oxford, UK: Oxford University Press. ISBN 978-0-19-923735-7. OCLC 163616466.
  • Sutton, Philip M. (2007). “Alcoholism and Drug Abuse”. In Michael L. Coulter, Stephen M. Krason, Richard S. Myers, and Joseph A. Varacalli. Encyclopedia of Catholic Social Thought, Social Science, and Social Policy. Lanham, MD; Toronto, Canada; Plymouth, UK: Scarecrow Press. pp. 22–24. ISBN 978-0-8108-5906-7.
  • Thompson, Warren, MD, FACP. “Alcoholism.”, 6 June 2007. Retrieved 2007-09-02.
  • Erdozain AM, Callado LF (2014). “Neurobiological alterations in alcohol addiction: a review”. Adicciones 26 (4): 360–370. PMID 25578004.

External links

Categories: Addiction

Leave a Reply