Norman E Spear1, Juan C Molina. 1. Department of Psychology, Center for Developmental Psychobiology, Binghamton University, Binghamton, NY 13902, USA. nspear@binghamton.edu
Abstract
BACKGROUND: Despite good evidence that ethanol abuse in adulthood is more likely the earlier human adolescents begin drinking, it is unclear why the early onset of drinking occurs in the first place. A review of experimental studies with animals complemented by clinical, epidemiologic and experimental studies with humans supports the idea that precipitating conditions for ethanol abuse occur well before adolescence, in terms of very early exposure to ethanol as a fetus or infant. Experimental studies with animals indicate, accordingly, that ethanol intake during adolescence or adulthood is potentiated by much earlier exposure to ethanol as a fetus or infant. METHODS: Two broad theoretical frameworks are suggested to explain the increase in affinity for ethanol that follows very early exposure to ethanol, one based on effects of mere exposure and the other on associative conditioning. Studied for 50 years or more in several areas of psychology, "effects of mere exposure" refers to enhanced preference expressed for flavors, or just about any stimuli, that are relatively familiar. An alternative framework, in terms of associative conditioning, is guided by this working hypothesis: During ethanol exposure the fetus or infant acquires an association between ethanol's orosensory (odor/taste) and pharmacological consequences, causing the animal subsequently to seek out ethanol's odor and taste. RESULTS AND CONCLUSIONS: The implication that ethanol has rewarding consequences for the fetus or young infant is supported by recent evidence with perinatal rats. Paradoxically, several studies have shown that such early exposure to ethanol may in some circumstances make the infant treat ethanol-related events as aversive, and yet enhanced intake of ethanol in adolescence is nevertheless a consequence. Alternative interpretations of this paradox are considered among the varied circumstances of early ethanol exposure that lead subsequently to increased affinity for ethanol.
BACKGROUND: Despite good evidence that ethanol abuse in adulthood is more likely the earlier human adolescents begin drinking, it is unclear why the early onset of drinking occurs in the first place. A review of experimental studies with animals complemented by clinical, epidemiologic and experimental studies with humans supports the idea that precipitating conditions for ethanol abuse occur well before adolescence, in terms of very early exposure to ethanol as a fetus or infant. Experimental studies with animals indicate, accordingly, that ethanol intake during adolescence or adulthood is potentiated by much earlier exposure to ethanol as a fetus or infant. METHODS: Two broad theoretical frameworks are suggested to explain the increase in affinity for ethanol that follows very early exposure to ethanol, one based on effects of mere exposure and the other on associative conditioning. Studied for 50 years or more in several areas of psychology, "effects of mere exposure" refers to enhanced preference expressed for flavors, or just about any stimuli, that are relatively familiar. An alternative framework, in terms of associative conditioning, is guided by this working hypothesis: During ethanol exposure the fetus or infant acquires an association between ethanol's orosensory (odor/taste) and pharmacological consequences, causing the animal subsequently to seek out ethanol's odor and taste. RESULTS AND CONCLUSIONS: The implication that ethanol has rewarding consequences for the fetus or young infant is supported by recent evidence with perinatal rats. Paradoxically, several studies have shown that such early exposure to ethanol may in some circumstances make the infant treat ethanol-related events as aversive, and yet enhanced intake of ethanol in adolescence is nevertheless a consequence. Alternative interpretations of this paradox are considered among the varied circumstances of early ethanol exposure that lead subsequently to increased affinity for ethanol.
Authors: Lidush Goldschmidt; Gale A Richardson; Natacha M De Genna; Marie D Cornelius; Nancy L Day Journal: Neurotoxicol Teratol Date: 2018-11-03 Impact factor: 3.763
Authors: Roberto Sebastián Miranda-Morales; Juan Carlos Molina; Norman E Spear; Paula Abate Journal: Psychopharmacology (Berl) Date: 2011-07-13 Impact factor: 4.530
Authors: Roberto Sebastián Miranda-Morales; Michael E Nizhnikov; Dustin H Waters; Norman E Spear Journal: Alcohol Date: 2014-04-08 Impact factor: 2.405
Authors: Amber M Eade; Paul R Sheehe; Juan C Molina; Norman E Spear; Lisa M Youngentob; Steven L Youngentob Journal: Behav Brain Funct Date: 2009-01-15 Impact factor: 3.759