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Home > Publications > NIDA Notes > Vol. 19, No. 4 > Director's Column

Drug-Related Damage That Begins Before Birth
Director's Column
Vol. 19, No. 4 (December 2004)

By NIDA Director Nora D. Volkow, M.D.

NIDA Director, Dr. Nora D. Volkow

NIDA has long been concerned about the damaging effects of maternal drug abuse on unborn children. Our investigations began more than three decades ago, and the continued research commitment is providing an increasingly detailed picture of the scope and sequence of damage done by prenatal exposure to drugs of abuse. The effects are seen in reduced weight in newborns, behavioral disorders in toddlers, cognitive deficits in young schoolchildren, and increased vulnerability to drugs in adolescents.

Recently, NIDA, along with the National Institute of Child Health and Human Development and the National Institute of Health's Office of Research on Women's Health, sponsored a conference ("Long-Term Follow-Up of Prenatal Drug Exposure: Advances, Challenges, and Opportunities," held March 23 and 24 in Bethesda, Maryland) where more than 100 researchers gathered to discuss the findings and future direction of more than 20 NIDA-supported investigations into the consequences of maternal drug abuse on child development. The largest of these research studies evaluates cocaine's impact on more than 1,300 children now entering adolescence. The longest ongoing study is investigating the effects of nicotine exposure from birth into early adulthood. The newest study will investigate possible effects of MDMA ("Ecstasy"). Research presented at the conference shows that prenatal exposure produces developmental damage that can be measured in day-old infants, school-age children, and young adults. The studies also establish that some of the damage can be overcome.

NIDA's long-term research on tobacco use provides convincing documentation of the harm done by maternal smoking during pregnancy. It is seen in 1- to 2-day-old infants, who scored higher than unexposed newborns on measures of stress and excitability. These symptoms are dose dependent: Children whose mothers were heavier smokers exhibit more pronounced effects (see "The Neurobehavioral Legacy of Prenatal Tobacco Exposure"). Nicotine's effects persist. Teenagers whose mothers smoked during pregnancy perform more poorly on tasks requiring auditory memory than do teens who were not exposed. On tests of general intelligence, on which "normal" scores range from 99 to 109, children of nonsmoking mothers scored an average of 113.4, children of light smokers 109.8, and children of heavy smokers 105.2 (see "Cognitive Deficits Persist Into Early Adolescence for Children of Smoking Mothers"). In some measures of cognitive function, however, the gap between exposed and unexposed children narrows with age, and the pattern of improvement suggests that environment helps. Exposed children show improved achievement as they grow older, and their better performance is associated most strongly with the educational level of the parents: Home and family factors that support learning appear to help overcome the damage of exposure.

NIDA's research shows that maternal cocaine use has multiple effects on mental development. Though small, these effects are measurable and have the potential to influence experience, ability, and achievement in childhood and later in life. Cocaine-exposed children, compared with children whose mothers did not use the drug, are more likely to score nearer the lower end of a normal range in tests of alertness and attention. Exposed children have also a downward shift averaging 3.26 points in scores on IQ tests where 100 is average. As is the case with nicotine, some of cocaine's damage can be overcome. Recently, NIDA-supported scientists at Case Western Reserve University in Cleveland, Ohio, reported that exposed children raised in stimulating and enriching environments had IQ scores similar to those of unexposed children when tested at age 4.

Human studies that span decades allow us to monitor the long-term developmental effects of prenatal drug exposure. Animal studies can more quickly provide important clues to the effects of drugs on fetal development. For example, our research on possible developmental effects of MDMA shows that in rats, prenatal exposure to the drug alters brain development and appears to cause damage that remains after the rats mature. Animals exposed to MDMA during a crucial prenatal developmental period late in pregnancy take significantly longer than unexposed animals to learn and remember, when fully grown, the strategies for escaping a maze (see "Prenatal Exposure to Ecstasy May Impair Memory and Cognition"). Other research reveals damage done by MDMA exposure in the earliest period of brain development. When tested 3 weeks after birth, rats with early prenatal exposure took significantly longer than did unexposed animals to become accustomed to a new environment (see "Animal Study Finds Effects on Behavior, Brain Chemistry of Prenatal MDMA Exposure").

The results of our animal studies of MDMA will help guide research, now under way, on the effects of prenatal exposure of humans to MDMA. NIDA has initiated similar studies to assess the effects of methamphetamine. This research is in its earliest stages, but, like our investigations of nicotine and cocaine, will track the progress of prenatally exposed children as they grow through adolescence into adulthood. Through short-term animal research and decades-long longitudinal studies, NIDA is committed to providing the scientific foundation necessary for the development of social and clinical programs to prevent and treat the life-shaping prenatal damage associated with drug abuse.


Volume 19, Number 4 (December 2004)

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