Stress, Hormones, Adolescence, and Alcohol Abuse

by National Institute of Health

(Page 5 of 5)

Ontogeny of Initial Tolerance and Sensitivity to Alcohol

Adolescent rats consume higher absolute levels of alcohol than do older animals as a result of multiple factors. One is that adolescents are less sensitive than adult animals to the aversive effects of acute intoxication. Another is their greater sensitivity to alcohol-induced social facilitation and stimulation of alcohol intake by social experiences. The neural basis for the developmental differences in initial response to alcohol remains speculative. Recent evidence suggests, however, that the relative resistance of adolescents to the sedative effects of alcohol is related in part to both accelerated development of acute tolerance and developmental immaturity of the GABA and/or NMDA receptor systems. The available data on the consequences of longer-term adaptations (rapid and chronic tolerance) to alcohol's effects in adolescents are inconsistent, with studies indicating more tolerance in adolescents than adults, similar levels of tolerance, or the appearance of sensitization rather than tolerance after repeated adolescent exposures.

Late childhood and adolescence are periods marked by dramatic sexual and psychosocial development. Between the ages of 5 and 9, adrenarche occurs, resulting in increased secretion of many adrenal steroids (cortisol, androstenedione, dehydroepiandosterone). Adrenal androgens in humans are associated with auxiliary and pubic hair growth and a slight increase in bone and skeletal growth. This is followed by maturation of the reproductive system, also referred to as "gonadarche," which is characterized by increased activity of gonadotropins and the sex steroids (estradiol in females and testosterone in males). The hypothalamic-pituitary- adrenal axis response to stress also undergoes development during the pubertal period. Increased life stressors associated with sexual and social maturation, together with hormonally induced mood and behavior changes, could contribute to increased consumption of alcohol during the adolescent period.

In adult humans and animals, the relationships among stress, drinking, and underlying neuroendocrine or neurochemical mechanisms are complex. However, basic animal research suggests that stress-induced changes in glucocorticoids (corticosterone) may interact with neurotransmitters in the mesolimbic reward system to facilitate drinking. In adolescents, the interaction between stress and drinking is even more complicated because the neural systems involved in modulating alcohol reward and/or stress are undergoing development.

In a few studies of adolescent nonhuman primates, it has been shown that under conditions of social separation stress, subjects double their rates of alcohol consumption. In these studies, individual differences in stress-induced drinking are attributed to anxietylike behaviors mediated by ontogenetic changes in cortisol and corticotropin levels or to poor impulse control and impaired social competence associated with reduced serotonin functioning.

In rats, findings indicate that adolescent animals exhibit an attenuated corticosterone response to alcohol challenge compared with adults, and that gender differences in this response begin to emerge at adolescence. If elevations in corticosterone contribute to the rewarding effects of alcohol, as indicated in adult animals, then adolescents may need to increase their levels of alcohol to attain the reinforcing value reached by more mature animals at lower levels. At this point, however, any hypothesized interactions between stress-induced changes in hormones and reward-related neurotransmitters, and their impact on adolescent drinking, remain tentative.

Gonadal hormones influence many aspects of brain development and behavior outside the realm of reproductive functions via their actions on receptors located throughout the brain. Alcohol's disruptive effects on pubertal hormone secretion may interfere with hormonally mediated developmental processes and result in negative behavioral outcomes. For example, alcohol-induced increases in testosterone are related to augmented aggression in male hamsters following chronic alcohol exposure during adolescence. Evidence from adult female nonhuman primates indicates that sensitivity to the subjective effects of ethanol changes during different phases of the menstrual cycle as a result of alterations in endogenous levels of ovarian-derived hormones. However, virtually nothing is known about adolescent females' sensitivity to the subjective or aggressive effects of alcohol or the correlation of these effects with cyclical hormonal changes. Given that adolescence is a time when hormonal and brain systems are still developing in humans and animals, research on the relationships among life stressors, affective states, and hormonal/neurotransmitter interactions may be critical to understanding the onset, maintenance, and consequences of adolescent drinking.

About the Author

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