Alcohol use disorder refers the inability to stop or control alcohol use despite harmful consequences-health, job, or relationships; alternative terms include alcoholism, alcohol abuse, alcohol dependence, or alcohol addiction and alcohol use is the third leading cause of early death in the United States.
Alcohol, like other addictive drugs, stimulates regions of the brain associated with reward by releasing the neurotransmitter dopamine, which reinforces behavior and increases the likelihood that a behavior will be repeated.
Characterized by craving of alcohol, inability to stop intake of alcohol, development of withdrawal symptoms after stopping drinking and tolerance.
Additionally characterized by loss of control over alcohol consumption and is accompanied by changes in the brain regions responsible for execution of motivated behaviors, i.e. the midbrain and limbic and prefrontal cortex.
The reward pathway for alcohol facilitates early of alcohol use is mediated by dopamine release and opioid peptide neuron activity in the ventral tegmental area and the nucleus accumbens, resulting in a euphoric state.
Evidence exists to support alcohol induced Gamma-aminobutyric acid (GABA) release and glutamate suppression in the central nucleus of the amygdala producing a calming sensation.
These systems create positive reinforcement of use.
Prolonged exposure to alcohol causes neurochemical changes resulting in sensitization, tolerance, withdrawal, and dependence which can cause subsequent additional negative reinforcement of use.
Prolonged alcohol exposure is associated with decrease volume in the prefrontal cortex and orbitofrontal cortex which have central roles in impulsivity and decision making.
Excessive alcohol use accounted for an estimated 80,000 deaths and 2.3 million years of potential life lost in the US during each year from 2001-2005.
About 7% of the US population is addicted to alcohol.
Low risk alcohol consumption is defined as four or a fewer drinks per day or 14 or fewer drinks per week for men and three or fewer drinks per day or seven or fewer drinks per week for women (National Institute on AlcoholAbuse and Alcoholism).
The nociceptin/nociceptin opioid receptor system is involved in the reinforcing or conditioning effects of alcohol.
Alcohol use disorder is approximately 50% heritable and 50% secondary to environmental factors.
Unhealthy alcohol use was estimated to be the third leading preventable cause of mortality in the US in 2000, with 9.8% of deaths attributed it to alcohol consumption from 2006 to 2010.
Globally excess use of alcohol is responsible for about 33 deaths per 100,000 people
and 85 million disability adjusted life years annually.
Risky use of alcohol as defined by the National Institute on Alcohol Abuse and Alcoholism exceeds the recommended limits for drinks per day or 14 drinks per week for healthy adult men age 21-64 or three drinks per day or seven drinks per week for all adult women of any age in men 65 years or older.
Hazardous use of alcohol increases the risk of future negative consequences.
Alcohol use during pregnancy is one of the major preventable causes of birth defects and developmental disabilities.
Between 2006-2010 the annual number of alcohol associated deaths in the US was approximately 88,000, or 9.8% of US deaths.
Estimated alcohol is responsible for 3.8% of global deaths and 4.6% of global disability-adjusted life years worldwide (Rehm J et al).
In 2010 the estimated alcohol related costs in the US were $249 billion, 77% of which were attributable to binge drinking.
In 2016 it is estimated 6.6% of the US adult population reported heavy alcohol use
and 26.2% reported at least 2 episode of binge drinking during the preceding month.
In a 2016 study 4.9% of adolescents and 6.6% reported heavy alcohol use episodes of five or more drinks on the same occasion on one day or more in the previous month.
Alcohol use disorders result in 3 fold increased rates of early mortality.
Alcohol use disorders experienced in about 36% of male and 22.7% of female adults some time in their lives.
Alcohol use disorders rise from combined personal, social, and biological factors.
Associated with positive and negative reinforcement mechanisms that play a role in the maladaptive pattern of alcohol consumption.
As alcoholism severity worsens, negative reinforcement mechanisms predominate whereby negative affective state is relieved by alcohol consumption, leading to relapse.
Prevalence of alcohol use disorders increases in cultures encouraging adults to drink to intoxication.
The early initiation of alcohol use and hazardous consumption in adolescence predicts for a higher risk of development of alcohol use disorders in adulthood.
About 17.6% of men and 10.4% of women have had an alcohol use disorder in the past year.
Alcohol excess >21 standard drinks/week for men and >14 for women in the USA.
Alcohol use disorders most prevalent in young adulthood.
Alcohol consumption linked to approximately 60 illnesses.
Alcohol use can exacerbate or cause a wide range of medical conditions commonly encountered including gastrointestinal, cardio pulmonary, dermatologic, reproductive, and neurologic conditions.
Alcohol can interact dangerously with many prescriptions and over-the-counter medications.
Differences in the diagnosis of alcohol use disorder among the sexes has narrowed because women’s drinking patterns have become similar to men’s in recent years.
Patients with alcohol use disorders receive poorer quality care than patients with other common chronic conditions.
Alcohol abuse accounts for the third leading preventable cause of death and the second most common cause of cirrhosis following hepatitis C in the US.
Associated with long term and sort term liver damage, cancers of multiple types, unintentional injuries, violence, impaired social and family relationships.
A family history of early onset alcohol use associated with a high risk of alcohol use disorders.
Alcohol abuse refers to a pattern of drinking leading to physical or psychological harm within a 12 month period.
Alcoholism is associated with dampened activation in brain networks responsible for emotional processing (amygdala).
Alcohol use disorders risk factors include family history of dependence, low parental monitoring, poor family support, history of childhood conduct and mood disorders, low-self-control, impulsivity and positive alcohol expectations.
Twin studies estimate 50-70% of risk of alcohol use disorders related to genetic factors.
Alcohol dehydrogenase and mitochondrial form of aldehyde dehydrogenase (ALDH2) are liver enzymes that metabolize alcohol and ALDH2 genotype is expressed by 2 alleles ALDH2*1 and ALDH2*2.
Carriers of ALDH@*2 have impaired alcohol metabolism, and with exposure to alcohol suffer with flushing, sweating, headache tachycardia, nausea and vomiting and headache.
Having ALDH2*2 polymorphism is protective against alcohol use disorders and is carried by about 23% of Asians, but is rare in Westerners.
Less than 1% of alcohol use disorders are associated with alleles that affect neurotransmitter response to alcohol in the dopaminergic, opioidergic, GABA, serotonergic, cholinergic,and glutametergic systems.
Rates on a medical/surgical unit determined by screening test reveals about a 7% of patients have alcoholism.
Excessive alcohol accounts for one in 10 deaths among working age adults in the US.
Peer use is a strong predictor of adolescent alcohol abuse.
Alcoholism Is the fourth leading cause of death in the US.
About 4% of U.S. residents are alcohol dependent are given care, and less than less than one quarter of such patients ever receive treatment (Hasin).
Community hospitals treated nearly 210,000 patients in 2003.
In 2003 more than 1 million hospital admissions for reasons other than alcoholism had the diagnosis of alcohol abuse and about 3% of hospitalized patients had some mention of the problem.
Problem drinking cost the US $249 billion in 2010, or $2.05 per drink.
Binge drinking is responsible for about 77% of problem drinking costs, followed by underage drinking at 10% and drinking among pregnant women of 2%.
Costs of problem drinking are due to reduced productivity at 72% and treating health related problems at 11%.
Remission from the dependence on alcohol is based on consequences and does not require the patient to abstain from alcohol.
Remission is considered early after three months and sustained after 12 months.
Of adults with prior alcohol dependence data shows, 52% continued to drink with consequences, 18% abstain completely, 12% remain heavy drinkers without consequences, and only 18% drink within lower risk limits (Dawson DA et al).
Long-term studies revealed always 11% of men with alcohol dependence maintain nonindependent drinking over 50 years (Vaillant GE).
History of alcohol abuse common in 10% of patients hospitalized in intensive care units, with an associated doubling of hospital mortality.
Associated mortality disproportionately higher among young persons.
Approximately 30 years of life lost per alcohol associated death.
In 2001 2.3 million years of potential life lost (MMWR 2004) in the U.S.
Overall 65% of alcoholism admissions also involved a substance abuse disorder, 34% have mood disorders, and 11% have alcohol related liver disease and more than 8% have anxiety related disorders.
Approximately 25% of patients with an alcohol abuse process present to a hospital with metabolic acidosis.
Alcoholic acidosis and lactic acidosis related to alcohol ingestion.
Alcoholic ketoacidosis associated with nausea, vomiting, abdominal pain, abdominal distension, tachypnea, tachycardia and of a high anion gap acidosis.
Alcoholic acidosis related to starvation, glycogen depletion, increased NADH:NAD ratio related to alcohol metabolism by alcohol dehydrogenase and volume depletion resulting in ketogenesis.
Treatment of alcoholic acidosis includes intravenous fluids and glucose infusions to prevent ketosis, stimulate insulin production and secretion, increase glycogen stores and promote NADH oxidation.
Lactic acidosis can occur with alcohol abuse by a direct effect of alcohol and may follow as a result of seizures.
American College of Surgeons Committee on Trauma mandates routine screening for alcohol abuse for level one and two trauma centers.
Laboratory evaluation of critical ill patients with alcohol abuse or dependence include, complete blood count, renal and electrolyte studies, liver function tests, amylase, lipase, CPK, urinalysis, coagulation studies, urine toxicology screen and blood alcohol level.
Most common cause of thiamine deficiency in western world.
Binge drinking which is defined as five or more drinks for men or greater than 4 drinks for women, on one occasion, is the most common form of excessive alcohol consumption.
Binge drinking is responsible for half of deaths and three quarters of economic costs of excessive drinking.
Among 29.5 million people reported to have alcohol use disorder in 2021 only an estimated 0.9% receipt received for pharmacotherapy for alcohol use disorder.
FDA presently has approved three drugs for treatment of alcohol dependence: disulfiram, acamprosate topiramate, and naltrexone.
These drugs are intended to affect the desire to drink: by directly reducing cravings as with acamprosate and topiramate, or by producing unpleasant effects when alcohol is consumed, as with disulfiram.
Gabapentin use prevents heavy drinking and promotes alcohol abstinence among patients with alcohol use disorder and the history of alcohol withdrawal symptoms.
Naltrexone, an opioid receptor antagonist has been demonstrated to be effective in about 30 clinical trials.
Naltrexone responders often have strong family history, earlier onset of dependence, and strong craving for alcohol.
Patients with dependence who carry the mu-opioid receptor gene (OPRMI) are more likely to response to treatment with naltrexone (Anton).
Naltrexone works as a non-selective antagonist of the mu,kappa , and delta opioid receptors.
Endogenous opioids are released following alcohol consumption, contributing to positive reinforcement effects that promote continue drinking in the alcohol dependent individually, and by blocking this activity naltrexone reduces the rewarding effects of alcohol and result in reduction in alcohol consumption.
Naltrexone efficacy may favor males in reducing alcohol cravings and reduces relapse to heavy drinking compared to placebo.
The prevalence of alcohol use disorders was greater in the second year postoperative, and was associated with male sex, younger age, numerous preoperative variables in patients undergoing a Roux-en-Y gastric bypass procedure (King WC et al).
Fewer than one third of patients with alcohol use disorders receive treatment and about 10% receive medications to assist in reducing alcohol consumption.
Patients with mild AUD should receive a brief intervention, consisting of feedback on alcohol use and its associated harm.
Psychosocial interventions, including brief interventions, motivational enhancement therapy, cognitive behavioral therapy, family therapies and the 12 step facilitation have shown been shown to be er fective components of alcohol use disorder treatment and may reduce alcohol consumption and improve abstinence rates.
Treating comorbid psychiatric conditions searches attention deficit hyper reactive disorder and depression, with medication decreases heavy drinking and prolong time to relapse.
Patients with moderate to severe AUD may benefit from evaluation by an addiction specialist.
The long-term prognosis of Alcohol liver disease is determined primarily by alcohol relapse, which occurs within one year and 30 to 50% of patients with severe alcohol hepatitis.
Acamprosate and oral naltrexone are associated with a reduction in return to drinking in patients with alcohol use disorders.When directly compared to each other acamprosate and naltrexone, there is no significant differences in controlling alcohol consumption ( Jonas DE et al).
Acamprosate and oral naltrexone are the strongest options for reducing alcohol consumption or in maintaining sobriety.
Acamprosate in a comparison study was found to be more useful in promoting abstinence, while oral naltrexone was found to help reduce heavy drinking.
Disulfiram has modest efficacy in relapse prevention of alcohol abuse.
Disulfiram works by blocking aldehyde dehydrogenase2 in the liver and brain.
Odansetron may be used in patients with alcohol use disorder before age 25 years decreasing heavy, drinking and increasing abstinence.
Aldehyde dehydrogenase 2 catalyzes the oxidation of the alcohol metabolite acetaldehyde into acetic acid and its elevation increases acetaldehyde levels after alcohol consumption.
Elevated acetaldehyde causes nausea, vomiting, headache, and flushing, all unpleasant effects following alcohol consumption leading to negative reinforcement.
The American psychiatric association guidelines recommend: naltrexone, or acamprosate to first line patients with moderate to severe alcohol use disorder.
It recommends disulfiram, topiramate, and gabapentin as second line options for patients, who have different preferences, or who are intolerant to the previous drugs.