Fetal or infantile exposure to ethanol promotes ethanol ingestion in adolescence and adulthood: a theoretical review.
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.


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.
Department of Psychology, Center for Developmental Psychobiology, Binghamton University, Binghamton, NY 13902, USA. nspear@binghamton.edu
Norman E
NE
Spear
Juan C
JC
Molina
D000293:Adolescent; D000428:Alcohol Drinking / Q000009:adverse effects / Q000453:epidemiology*; D000437:Alcoholism / Q000453:epidemiology* / Q000523:psychology; D000818:Animals; D001245:Association Learning / Q000502:physiology; D002657:Child Development / Q000187:drug effects* / Q000502:physiology; D003213:Conditioning, Psychological / Q000502:physiology; D004781:Environmental Exposure / Q000009:adverse effects*; D000431:Ethanol / Q000009:adverse effects* / Q000506:poisoning; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000453:epidemiology / Q000523:psychology; D006801:Humans; D007223:Infant; D009812:Odorants; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D012201:Reward; D012903:Smell / Q000502:physiology; D013649:Taste / Q000502:physiology
D000431:Ethanol