The history of cocaine use is reviewed. Cocaine teratogenesis has only
recently been studied, and initial human studies had serious methodol
ogical flaws. These flaws included ascertainment bias, publication bia
s (studies finding cocaine effects have been more likely to be present
ed or published), and overemphasis on the perinatal period. Comparison
with alcohol teratogenesis shows that alcohol is a more potent terato
gen, which, however, produces major and specific effects (fetal alcoho
l syndrome) in less than 10% of offspring with heavy alcohol exposure
during pregnancy. Nonspecific minor congenital anomalies or fetal alco
hol effects are seen in a larger number. Personal experience with two,
groups of children exposed to cocaine in utero is reviewed. Insurance
patients gained weight, took vitamins, and generally, their children
did well in spite of cocaine use. Indigent patients were usually unmar
ried and often ''street people,'' probably used more cocaine, generall
y used other drugs as well, often did not gain weight during pregnancy
, and were much more likely to have children with problems. Surveys sh
ow that most cocaine users also use alcohol, often simultaneously. Tho
se who use both agents are more likely to have troubled backgrounds an
d antisocial behavior and to drop out of treatment programs than those
who use only alcohol. Cocaethylene or ethylbenzoylecgonine is formed
in the liver when cocaine and alcohol are simultaneously ingested. It
is a potent stimulant and dopamine uptake blocker that is more toxic t
o myocardial cells than is cocaine. Good nutrition is now known to be
very important in preventing congenital anomalies and fetal death. A m
ultihit model of neurologic handicap, which stresses the importance of
a good postnatal environment, is briefly outlined. This model explain
s why cocaine use during pregnancy is more dangerous to the street per
son who uses multiple drugs than to the middle class mother who takes
prenatal vitamins.