出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/23 15:01:59」(JST)
| Alcoholism | |
|---|---|
|
"King Alcohol and his Prime Minister" c. 1820
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| Classification and external resources | |
| ICD-10 | F10.2 |
| ICD-9 | 303 |
| MedlinePlus | 000944 |
| MeSH | D000437 |
Alcoholism, also known as alcohol use disorder (AUD) and alcohol dependence syndrome, is a broad term for any drinking of alcohol that results in problems.[1] It was previously divided into two main 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 problem, usage results in risky situations, withdrawal occurs when stopping, and alcohol tolerance has occurred to 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 the risk of cancer, among other disease.[4][5] Drinking during pregnancy can cause damage to the baby resulting in fetal alcohol syndrome.[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.[citation needed] 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 as diazepam. This can be either given well 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 expectacy 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 it inexact meaning, preferring "alcohol dependence syndrome".[24]
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.
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 the central 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 the menstrual 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 and depression 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 of narcissistic 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.
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 for drunk 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 to marital 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]
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 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, after water and tea.[73] It is thought by some to be the oldest fermented beverage.[74][75][76][77]
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 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]
Alcohol's rewarding and reinforcing (i.e., addictive) properties are mediated through its effects on dopamine neurons in the mesolimbic reward pathway, which connects the ventral tegmental area to the nucleus accumbens (NAcc).[85][86] One of alcohol's primary effects is the allosteric inhibition of NMDA receptors and facilitation of GABAA receptors (e.g., enhanced GABAA receptor-mediated chloride flux through allosteric regulation of the receptor).[87] At high doses, ethanol inhibits most ligand gated ion channels and voltage gated ion channels in neurons as well.[87]
With acute alcohol consumption, dopamine is released in the synapses of the mesolimbic pathway, in turn heightening activation of postsynaptic D1 receptors.[85][86] The activation of these receptors triggers postsynaptic internal signaling events through protein kinase A which ultimately phosphorylate cAMP response element binding protein (CREB), inducing CREB-mediated changes in gene expression.[85][86]
With chronic alcohol intake, consumption of ethanol similarly induces CREB phosphorylation through the D1 receptor pathway, but it also alters NMDA receptor function through phosphorylation mechanisms;[85][86] an adaptive downregulation of the D1 receptor pathway and CREB function occurs as well.[85][86] Chronic consumption is also associated with an effect on CREB phosphorylation and function via postsynaptic NMDA receptor signaling cascades through a MAPK/ERK pathway and CAMK-mediated pathway.[86] These modifications to CREB function in the mesolimbic pathway induce expression (i.e., increase gene expression) of ΔFosB in the NAcc,[86] where ΔFosB is the "master control protein" that, when overexpressed in the NAcc, is necessary and sufficient for the development and maintenance of an addictive state (i.e., its overexpression in the nucleus accumbens produces and then directly modulates compulsive alcohol consumption).[86][88][89][90]
| This section requires expansion. (May 2015) |
Misuse, problem use, abuse, and heavy use refer to improper use of alcohol which may cause physical, social, or moral harm to the drinker.[91] 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.[92] Some drinkers may drink more than 600 ml of alcohol per day during a heavy drinking period.[93]
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.[94] 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.[95]
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:
In professional and research contexts, the term "alcoholism" sometimes encompasses both alcohol abuse and alcohol dependence,[97] 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.[98]
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.[99][100] Johnson's four phases consist of:
Other theorists such as Milam & Ketcham (1983) focus on the physical deterioration of alcohol. They describe the process in three stages:
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" |
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".[103] It has been suggested that DSM-V merge alcohol abuse and alcohol dependence into a single new entry,[104] named "alcohol-use disorder".[105] |
| 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.[103] The term "alcoholism" was removed from ICD between ICD-8/ICDA-8 and ICD-9.[106] |
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."[107]
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 the NCADD 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."[108] MeSH has had an entry for "alcoholism" since 1999, and references the 1992 definition.[109]
AA describes alcoholism as an illness that involves a physical allergy[110]:28 (where "allergy" has a different meaning than that used in modern medicine.[111]) and a mental obsession.[110]:23[112] 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".[110]:XXVI
A 1960 study by E. Morton Jellinek is considered the foundation of the modern disease theory of alcoholism.[113] 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.[114]
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.[115]
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:
- Have you ever felt you needed to Cut down on your drinking?
- Have people Annoyed you by criticizing your drinking?
- Have you ever felt Guilty about drinking?
- 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?[116][117]
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 the CAGE questionnaire. It helps distinguish a diagnosis of alcohol dependence from one of heavy alcohol use.[119] 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,[120] 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.[121] 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.[122]
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.[123]
At least one genetic test exists for an allele that is correlated to alcoholism and opiate addiction.[124] 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.[125] 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.[123]
There are reliable tests for the actual use of alcohol, one common test being that of blood alcohol content (BAC).[126] These tests do not differentiate alcoholics from non-alcoholics; however, long-term heavy drinking does have a few recognizable effects on the body, including:[127]
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.[128][129] 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.[130]
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.[131]
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.[132]
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.[133] 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.[134] 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."[135]
In the United States there are four currently approved medications for alcoholism: disulfiram, two forms of naltrexone, and acamprosate.[136] Several other drugs are also used and many are under investigation.
Evidence does not support the use of selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), antipsychotics, or gabapentin.[140]
Alcoholics may also require treatment for other psychotropic drug addictions and drug dependences. The most common dual dependence syndrome with alcohol dependence is benzodiazepine 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.[146] 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.[147]
Disability-adjusted life year for alcohol use disorders per 100,000 inhabitants in 2004.
|
no data
<50
50-170
170-290
290-410
410-530
530-650
|
650-770
770-890
890-1010
1010-1130
1130–1250
>1250
|
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."[131] In the United Kingdom, the number of 'dependent drinkers' was calculated as over 2.8 million in 2001.[149] About 12% of American adults have had an alcohol dependence problem at some time in their life.[150] 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.[151]
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)."[114]
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.[152] 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.[153]
Alcoholism often reduces a person's life expectacy by around ten years.[22] The most common cause of death in alcoholics is from cardiovascular complications.[154] There is a high rate of suicide in chronic alcoholics, which increases the longer a person drinks. 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.[155] Approximately 3–15 percent of alcoholics commit suicide,[156] and research has found that over 50 percent of all suicides are associated with alcohol or drug dependence. The figure is higher for adolescents, with alcohol or drug misuse playing a role in up to 70 percent of suicides.[157]
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.[158]
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."[159] There was also "return-to-controlled drinking, as reported in short-term studies, is often a mirage."
Historically the name "dipsomania" was coined by German physician Dr. C. W. Hufeland in 1819 before it was superseded by "alcoholism".[160][161] That term now has a more specific meaning.[162] The term "alcoholism" was first used in 1849 by the Swedish physician Magnus Huss to describe the systematic adverse effects of alcohol.[163]
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.[164]
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,[165] an incurable and damaging condition.[166]
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.[167] 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%.[168] One study quantified the cost to the UK of all forms of alcohol misuse in 2001 as £18.5–20 billion.[149][169] All economic costs in the United States in 2006 have been estimated at $223.5 billion.[170]
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.[171] Studies by social psychologists Stivers and Greeley attempt to document the perceived prevalence of high alcohol consumption amongst the Irish in America.[172]
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.[173]
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.[174]
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.[175]
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.[176]
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.[177] 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.[178]
Baclofen, a GABAB receptor agonist, is under study for the treatment of alcoholism.[179] A systematic review concluded that there is insufficient evidence for the use of baclofen for withdrawal symptoms in alcoholism.[180] There is tentative data supporting baclofen in alcohol dependence however further trials are needed as of 2013.[181]
Ondansetron, a 5HT3 antagonist, appears promising.[182]
The World Health Organization defines alcoholism as any drinking which results in problems
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)
As one of the primary mediators of the rewarding effects of alcohol, dopaminergic ventral tegmental area (VTA) projections to the nucleus accumbens (NAc) have been identified. Acute exposure to alcohol stimulates dopamine release into the NAc, which activates D1 receptors, stimulating PKA signaling and subsequent CREB-mediated gene expression, whereas chronic alcohol exposure leads to an adaptive downregulation of this pathway, in particular of CREB function. The decreased CREB function in the NAc may promote the intake of drugs of abuse to achieve an increase in reward and thus may be involved in the regulation of positive affective states of addiction. PKA signaling also affects NMDA receptor activity and may play an important role in neuroadaptation in response to chronic alcohol exposure.
Despite the high concentrations required for its psychoactive effects, ethanol exerts specific actions on the brain. The initial effects of ethanol result primarily from facilitation of GABAA receptors and inhibition of NMDA glutamate receptors. At higher doses, ethanol also inhibits the functioning of most ligand- and voltage-gated ion channels. It is not known whether ethanol selectively affects these channels via direct low affinity binding or via nonspecific disruption of plasma membranes which then selectively influences these highly complex, multimeric, transmembrane proteins. Ethanol allosterically regulates the GABAA receptor to enhance GABA-activated Cl− flux. The anxiolytic and sedative effects of ethanol, as well as those of barbiturates and benzodiazepines, result from enhancement of GABAergic function. Facilitation of GABAA receptor function is also believed to contribute to the reinforcing effects of these drugs. Not all GABAA receptors are ethanol sensitive. ... Ethanol also acts as an NMDA antagonist by allosterically inhibiting the passage of glutamate-activated Na+ and Ca2+ currents through the NMDA receptor. ... The reinforcing effects of ethanol are partly explained by its ability to activate mesolimbic dopamine circuitry, although it is not known whether this effect is mediated at the level of the VTA or NAc. It also is not known whether this activation of dopamine systems is caused primarily by facilitation of GABAA receptors or inhibition of NMDA receptors, or both. Ethanol reinforcement also is mediated in part by ethanol-induced release of endogenous opioid peptides within the mesolimbic dopamine system, although whether the VTA or NAc is the predominant site of such action is not yet known. Accordingly, the opioid receptor antagonist naltrexone reduces ethanol self-administration in animals and is used with modest effect to treat alcoholism in humans.
ΔFosB as a therapeutic biomarker
The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. If ΔFosB detection is indicative of chronic drug exposure (and is at least partly responsible for dependence of the substance), then its monitoring for therapeutic efficacy in interventional studies is a suitable biomarker (Figure 2). Examples of therapeutic avenues are discussed herein. ...
Conclusions
ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.
DESPITE THE IMPORTANCE OF NUMEROUS PSYCHOSOCIAL FACTORS, AT ITS CORE, DRUG ADDICTION INVOLVES A BIOLOGICAL PROCESS: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement
ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states. ... ΔFosB serves as one of the master control proteins governing this structural plasticity.
To use wrongly or improperly; misuse: abuse alcohol
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| リンク元 | 「アルコール中毒」「alcoholic intoxication」「alcohol poisoning」「アルコール嗜癖」 |
| 関連記事 | 「addiction」「alcohol」 |