______________________________________________________________ Alcohol and Alcohol Use Disorder
and rejection by more mainstream peers at school may make it more likely for these children to join peer groups where drinking and other risky behaviors are encouraged. Parents with alcohol use disorders will likely not monitor their children closely and will lose control over them at an early age. These children will begin drinking early, often before 15 years of age [69]. If such a child is genetically predisposed to alcohol use disorders, these environmental factors may further increase the tendency [70]. Stress and Distress Another model of risk factors leading to alcohol use disorder focuses on drinking to regulate inner distress [71]. Some children have temperaments that make them highly reactive to stress and disruption. This type of child may be born into a family with history of alcohol use disorder, where the stressors may be intense, or a nonalcoholic family, with everyday types of low-level stressors. Regardless of the child’s family environment, he or she maintains higher levels of inner distress (anxious and depressed feelings) than other children. When they take their first drink, the inner distress dissipates for a while. This leads to more drinking and may lead to alcohol use disorder. However, for some individuals, at certain doses, alcohol may induce rather than reduce the stress response. Research demonstrates that alcohol actually induces the stress response by stimulating hormone release by the hypothalamus, pituitary, and adrenal glands [72]. Research also demonstrates a bidirectional relationship between alcohol and stress [73]. More research is required before the role of stress as a risk factor in alcohol use disorders is understood. Sensitivity to Alcohol’s Effects A third risk factor model focuses on sensitivity to the effects of alcohol, both to its sedative properties and its stimulating qualities [74]. The stimulant-like (increased heart rate and blood pressure) and sedative properties (impaired vigilance and psychomotor performance) depend on the quantity of alcohol consumed, the time elapsed since consumption, and individual differences in response [75; 76]. Researchers believe that this subjective response to alcohol may be an important endophenotype in understanding genetic influences on drinking behavior and alcohol use disorders. While subjective response predicts alcohol use and problems, the exact pattern of association remains unclear [77; 78; 79]. Two prominent models of subjective response have been discussed in the literature. The low level of response model suggests that high- risk individuals experience decreased sensitivity to the full range of the effects of alcohol. The differentiator model suggests that high risk for alcohol problems is associated with increased sensitivity to alcohol’s positive effects but decreased sensitivity to its negative effects [77; 78]. A literature review of studies that employed challenge paradigms to assess a range of the effects of alcohol (i.e., impairment, stimulation, sedation) found some support for both models [77]. Results of a quantitative review and meta-analysis suggest that the two models may describe two distinct sets of phenotypic risk with different etiologies and predictions for development of alcohol use disorder [78].
A total of 32 independent samples were combined to produce estimates of the effects of risk-group status (i.e., positive family history of alcohol use disorder or heavy alcohol consumption). Groups with positive family history for alcohol experienced reduced overall subjective response relative to groups with negative family history, as predicted by the low level of response model. In contrast, consistent with the differentiator model, heavy drinkers of both genders responded less on measures of sedation than did lighter drinkers, but more on measures of stimulation [78]. The effects of alcohol on the electroencephalogram (EEG) of subjects at risk for developing alcoholism are well known [80; 81; 82]. Researchers found that low EEG response to small amounts of alcohol may be associated with future development of alcohol use disorder. Additionally, differences in EEG response to alcohol may have ethnic variations [82]. Other studies have shown that heavy drinkers had less sedation and cortisol response after alcohol consumption than light drinkers. In addition, heavy drinkers were more sensitive to the positive stimulant-like properties as blood alcohol levels increased [74; 83]. KNOWN RISK FACTORS FOR ALCOHOL USE DISORDER With these three models in mind, a review of some of the research findings on genetic and psychosocial risk factors may provide a better understanding of the factors leading to alcohol use disorders [11; 84]: • Temperament: Moodiness, negativity, and provocative behavior may lead to a child being criticized by teachers and parents. These strained adult-child interactions may increase the chances that a child will drink. • Hyperactivity: Hyperactivity in childhood is a risk factor for the development of adult alcohol use disorders. Children with attention deficit hyperactivity disorder (ADHD) and conduct disorders have increased risk of developing an alcohol use disorder. Childhood aggression also may predict adult alcohol abuse. • Parents: The most compelling and largest body of research shows parents’ use and attitudes toward use to be the most important factor in an adolescent’s decision to drink. • Gender: Among adults, heavy alcohol use is almost three times more common among men than women and also more common among boys in middle or high school than among girls. Men with ADHD and/or conduct disorders are more likely to use alcohol than men without these disorders, while women who experience more depression, anxiety, and social avoidance as children are more likely to begin using alcohol as teens than women who do not experience these negative states.
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