Alcohol and Alcohol Use Disorder _ _____________________________________________________________
Alcohol and the Brain Alcohol affects most neurochemical systems including NMDA, GABA, serotonin, dopamine (DA), and opioid systems. Alcohol inhibits NMDA systems, which may contribute to feeling intoxicated. NMDA receptors change as tolerance develops. These receptor systems are overactive during withdrawal. Alcohol also enhances the action of the GABA system, producing some of the symptoms of acute intoxication. GABA receptors are especially sensitive to alcohol. The GABA system is underactive during withdrawal, and the genes that control these receptors may have an impact on the risk of alcohol use disorder [169; 170]. Alcohol causes the release of 5-HT, or serotonin. Lower 5-HT levels in the brain are associated with increased alcohol intake in animals and humans, while higher 5-HT levels are associated with slightly reduced alcohol intake. Several 5-HT genes may be related to the genetic risk of alcohol use disorder [11; 46]. Alcohol activates DA in the reward system in the ventral tegmental area of the brain. Alcohol also causes the release of DA. Several DA receptors may be related to the genetic risk of alcohol use disorder [11; 46]. Finally, alcohol causes the release of endogenous opioids. Opioid receptors change with tolerance and withdrawal. Some receptors may affect genetic predisposition for alcohol use disorder, and opioid antagonists can decrease voluntary alcohol consumption. Alcohol may also affect acetylcholine, norepinephrine, and steroids. Most people who drink do not develop brain damage. However, studies do indicate that impaired cognition and motor abilities occur in some individuals who are heavy drinkers. Older persons with alcohol use disorder exhibit more brain tissue loss than both older and younger persons without alcohol use disorder. These results suggest that aging may render a person more susceptible to the effects of chronic excessive alcohol. Most studies suggest that, following long-term abstinence, most brain changes resolve. Magnetic resonance imaging has been used to measure changes in the brain structure and volume in persons with alcohol use disorder at three weeks after abstinence from alcohol [171]. The results indicated that the brain volume in men and women with alcohol use disorder was significantly reduced as compared with healthy men and women. The differences, however, were much more significant in women than in men [172]. These results indicate that alcohol inflicts greater neurotoxic effects in women with alcohol use disorder than men, but again, these brain changes may resolve with long-term abstinence. Results from a 2021 study found significant impacts of age, but not sex, on white matter microstructure in individuals with alcohol use disorder [173].
The consumption of alcohol alters T-lymphocyte functions, immunoglobulin production by B cells, NK cell function, and neutrophil and macrophage activities making patients with alcohol use disorder more susceptible to septic infection [151; 152; 153]. Studies have shown that animals given ethanol are unable to suppress infections that can ultimately result in progressive organ damage and death [154; 155; 156]. SLEEP DISORDERS Although some people believe that alcohol helps them sleep, chronic excessive drinking can induce sleep disorders by disrupting the sequence and duration of sleep states and by altering total sleep time, as well as the time required to fall asleep [157; 158]. Specifically, drinking within an hour of bedtime appears to disrupt the second half of the sleep period [159]. The person may sleep poorly during the second half of sleep, awakening from dreams and returning to sleep with difficulty, resulting in daytime fatigue and sleepiness [157; 160]. Individuals with alcohol use disorder may be at increased risk for sleep apnea, a disorder in which the upper air passage narrows or closes during sleep [161; 162; 163; 164]. The combination of alcohol, obstructive sleep apnea, and snoring increases a person’s risk for heart attack, arrhythmia, stroke, and sudden death [165]. Obstructive sleep apnea significantly increases the risk of stroke or death from any cause, independent of other risk factors, including hypertension [166; 167]. NERVOUS SYSTEM DYSFUNCTION The most common neurologic abnormality among patients with alcohol use disorder is dementia syndrome, which manifests primarily as impairment in recent memory, and more subtle fluctuations in abstractions, calculations, and other aspects of cognitive functions. As previously stated, one specific neurologic complication resulting from thiamine deficiency is Wernicke-Korsakoff syndrome, which involves delirium, clouded sensorium, confusion, ophthalmoplegia, nystagmus, and ataxia [168]. Immediate administration of thiamine is usually successful in treating the symptoms, but in some cases permanent memory loss occurs [168]. Once delirium and confusion resolve, there is sometimes a profound loss in recent memory (out of proportion to the other cognitive deficits) and alcoholic peripheral neuropathy, which results in diminished sensitivity to touch, pinprick, and vibration (objectively, and paraesthesias subjectively). The acute effects of alcohol on the nervous system are signs people commonly think of when they envision an intoxicated person, such as slurred speech, loss of coordination, unsteady gait, impairment of attention or memory, nystagmus, stupor, or coma. The degree to which the central nervous system is impaired is directly proportional to the BAC and degree of tolerance.
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MDMI1826
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