see ((Alcoholism))
Criteria used to diagnose alcohol use disorder (AUD) are based on neurobiological changes due to excessive alcohol use that contributes to predictable patterns of drinking and other behaviors.
AUD is a chronic relapsing and remitting syndrome with excessive drinking of alcohol persisting, despite causing health and social problems.
Symptoms are related to drinking behavior and its consequences and not directly to the amount of alcohol consumed.
Moderate drinking is defined as up to one drink per day for women and two for men when each standard drink containing 14 g of alcohol.
A history of alcohol withdrawal or intoxication should be sought for diagnosis.
Common associated physical findings include overweight, hypertension, and stigmata of liver disease.
Liver enzyme concentrations have limited sensitivity and specificity for detection of alcohol use disorder.
GGT is the most useful liver function bio marker for chronic alcohol intake, but levels of this enzyme anre elevated and only half of men with the alcohol use disorder, and even if few women or younger people.
AUD is a leading contributor to illness and death and frequently not diagnosed but is creates a burden of disease that is high, estimated between 29 million people being affected by this disorder.
The most common physical conditions associated with AUD includes: obesity, hypertension, and liver disease.
AUD is associated with difficulty maintaining adequate nutrition related to the empty calories of alcohol, deficiency of micro nutrients, particularly thiamine and zinc, and the presence of electrolyte disorders, protein deficiency, and cognitive impairment.
Alcohol related liver disease is now the most common underlying indication for liver transplantation.
Cognitive impairment may be related to head trauma, drug abuse, Wernicke Korsakoff syndrome, and subdural hematoma.
Osteopenia is commonly associated with aUD, particularly in women.
AUD led to approximately 178,000 deaths in 2021, a health burden that is approximately two times that associated with the use of opioids.
Alcohol use contributes to injuries and many diseases, including malignancies of the oropharynx, esophagus, liver, colon, rectum, and breast, and also liver disease such as hepatitis and cirrhosis.
People at risk of harm from alcohol use include: young people who are vulnerable to injuries and accidents, older people who are at increased risk of complications of the interaction of alcohol and medications, such as opioids, benzodiazepines, anti-depressants, and antihistamines and alcohol attributable falls.
Alcohol use in pregnancy creates a risk of fetal alcohol syndrome.
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.
In patients with AUD, dopamine increases in brain regions associated with reward in anticipation of alcohol use results in strong physiological cravings.
Such adaptations can lead to reduced enjoyment from every day experiences, resulting in low mood and the prioritization of alcohol use above other daily activities.
Chronic alcohol use increases reactivity to stress, further contributing to motivations to drink.
Excessive alcohol use affects the prefrontal brain areas associated with self regulation, decreasing one’s ability to resist cravings or impulses to use alcohol.
Alcohol use disorder has mythically been believed to result from a moral failure, and has influenced public and professional views of the process.
An estimated 50% of the risk of alcohol use disorder is thought to be inherited.
The presence of coexisting conditions with AUD is the rule rather than the exception: substance use disorders, mental health disorders, or physical health disorders.
The most common coexisting condition is smoking, coexistent mental health disorders is seen in most patients with AUD and is more common in women than men.
Anxiety and depression and externalizing disorder is of antisocial personality , attention deficit disorder, and hyperactivity, are particularly common and patient with AUD.
The risk of suicide is increased, particularly the first five years after diagnosis of AUD.
Mental health disorders are associated with a double risk of alcohol use disorders.
Adverse early life experiences an adult traumas reportedly increase risk for AUD.
Social problems commonly associated with AUD or lack of employment, occupational, safety, risks, problems with housing and personal relationship, relationships, and legal issues.
Alcohol use is associated with approximately 3 million deaths per year globally.
However, chronic heavy alcohol use results in reductions in dopamine release and decreased density of dopamine receptors, as well as physiological tolerance to alcohols effects.
Repeated exposure to alcohol the neurotransmitter responses are blunted: this results in increasing doses of alcohol needed to produce the same effect, and alcohol withdrawal syndrome emerges when high levels of consumption are reduced or ceased.
Alcohol consumption activates the reward regions of the brain, increases the release of dopamine and the additional involvement of endogenous opioids, gamma aminobutyric acid, endocannbinoids and other neurotransmitters.
The reward system projects to the orbital terminal contacts and provides a pathway for alcohol to influence decision-making, including, impaired inhibitory control.
US deaths attributed to alcohol exceed 140,000 annually and account for one and five deaths among US adults age 20 to 49.
Phosphatidylethanol is a conjugate of phosphatidyl choline and ethanol and is present in red cells for several weeks after drinking.
It has a half-life of approximately 10 days yielding a detection window for alcohol use of 3 to 5 weeks.
Ethyl glucuronide is a conjugated ethanol metabolite detectable in urine for approximately 48 hours after consumption of alcohol.
Carbohydrate deficient transferrin has a sensitivity and specificity to detect alcohol use, less than previous discussed alcohol metabolites.
Long-term alcohol use is assessed by Gamma-gluttony peptidase levels, carbohydrate deficient, transferrin percentage or Phosphatidylethanol levels.
Hair testing for alcohol metabolites can provide a measure of alcohol use of a period of several months.
Management:
Treatment of AUD is generally effective, but affected individuals often do not receive treatment related to stigmatization, including by clinicians, and self-reproach.
Management of alcohol use disorder (AUD) involves a combination of behavioral therapies, medications, and support systems.
Behavioral Treatments
Cognitive-Behavioral Therapy (CBT)
Motivational Enhancement Therapy:
Family and Couples Counseling: Involves loved ones to improve relationships and support recovery.
Medications
Naltrexone: Reduces the pleasurable effects of alcohol and helps prevent heavy drinking.
Acamprosate: Alleviates cravings after stopping alcohol use.
Disulfiram: Causes unpleasant reactions when alcohol is consumed, discouraging drinking.
Support Systems:Mutual-Support Groups: Alcoholics Anonymous provide peer support for sustained recovery.
Residential Treatment: Intensive programs with therapy, education, and medical care for severe cases.
Acute Management of AUD:
For withdrawal symptoms, benzodiazepines are the standard treatment to prevent complications like seizures or delirium tremens.
Recovery is an ongoing process that often combines these methods with lifestyle changes and continued support.
The management of alcohol use disorder (AUD) involves a combination of pharmacotherapy and psychosocial interventions.
Pharmacotherapy:
Naltrexone, available in both oral (50 mg/day) and injectable forms, has been shown to reduce the likelihood of returning to heavy drinking..
Acamprosate is another first-line option, particularly effective in maintaining abstinence, with a typical dosage of 666 mg three times daily.
Disulfiram, can be effective in highly motivated patients.
Gabapentin and baclofen are used off-label, particularly in patients with contraindications to first-line medications.
Psychosocial Interventions:
Behavioral treatments are essential regardless of medication use.
Cognitive-behavioral therapy (CBT), motivational enhancement therapy (MET), and 12-step facilitation are recommended.
See alcohol withdrawal syndrome
Withdrawal is best managed with the benzodiazepines, in the hospital setting with intravenous fluid to maintain hydration and nutritional support.
Long acting benzodiazepines, and active metabolite such as diazepam are effective, but are subject to misuse and shorter acting agents, oxazepam, and lorazepam, which also lack active metabolites are preferred for patients with liver disease.
In severe cases of withdrawal, intravenous midazolam, phenobarbital, or dexmedetomidine are effective for amelioration of symptoms.
Prophylactic thiamine 100 mg day orally for three days is recommended.