Goal: Research neurodevelopment of children exposed to cocaine in the uterus.
Subjects: Two groups were observed. Group A: were children exposed to cocaine while in the womb and adopted after birth. Group B: The control group were children not exposed to cocaine while in the womb, and who had mothers with the same socioeconomical status, maternal IQ, and had children of the same gestational age.
Hypothesis: Children will have problems with neurodevelopment because of the cocaine and not the environment.
Variables: The physical dependent variables in this experiment were birth weight, gestational age, age at the time of the study, weight, height, and head circumference. The mother’s dependent variables were maternal IQ, socioeconomical status, and age. Other variables in this experiment included cognitive development of the children, language abilities, temperament (which was judged on a 6 point scale), and parent’s stress.
Testing: 26 families with adopted children that were referred by the Motherisk Program were asked for a follow up interview when their adopted children were 30 months of age. All of these subjects were identified as having mothers who took cocaine while pregnant. A variety of tests were conducted that evaluated both mother and child’s ability levels. Using average scores per age ground, the test subjects scores were converted to z scores.
Data: Data was analyze first with univariate and then with multivariate analysis. The multivariate analysis was used to examine the many different relationships between the criterion variables in the group as well as with many different suspected outcomes in the test group.
Results: The results of this experiment supported the hypothesis in that subjects with in utero exposure to cocaine had lower birth weights, and at the time of the test had smaller head circumferences and were shorter than the children in the control group. Their scores in language tests and on the global cognitive index (GCI) were considerably lower than the control group. Hyperactivity seemed to be the only behavioral difference between the control group and the test group. The control group was observed as being more outgoing and easier to adapt to new situations.
Confounds: While this particular experiment was well developed and organized with little room for bias, there were variables that were not accounted for that may have effected the results. Biological mothers who take cocaine are statistically more likely to abuse other substances like tobacco, alcohol, and other drugs that have documented effects on the observed biodata like head circumference, size, weight, and developmental patterns. (Greenbaum et al., 2001)
Biology Behind the Study
It is known that cocaine stimulates the central nervous system. In cases of chronic abuse toxic psychotic symptoms that encompass visual, auditory, and tactual perceptions create hallucinations that mirror those in acute schizophrenia. The stimulation focuses on the cortex of the brain. At first the symptoms are pleasurable and accentuate sexual feelings and excitement, however prolonged use creates a numbing and inability to attain pleasure leading to deep depressions in users. (Carson, Butcher, Mineka , 2000, pp.403-405)
Cocaine blocks the reabsorption of norepionephrine, dopamine, and other neurotransmitters which in turn creates a pleasurable rush. The molecules accumulate in the synaptic clefts, and continuously stimulate postsynaptic cells. As a result heart rate, blood pressure, and sexual appetite increase. After a period of time these molecules dissipate. Neurons aren’t capable of synthesizing replacement molecules rapidly enough to balance the ones that are being lost. Hypersensitive postsynaptic cells increase their demands and the initial sense of pleasure vanishes. After extensive abuse, pleasure is no longer attainable. The side effects to this deprivation include weight loss, insomnia, weakened immune system, and the development of heart abnormalities. (Starr & Taggart, 2001, pp. 586-587, & 600-601)
These symptoms are detrimental to the development of a fetus that relies on its mother for nourishment and biological support. Cocaine causes the maternal blood vessels to contract and result in a deprivation of oxygen and nutrients to the developing fetus. The use of cocaine while pregnant can lead to placental abruption, lower infant weights, prematurity, microcephaly, congenital urologic abnormalities and neurobehavioral dysfunction in the baby. (Warner, 1993, pp. 226-235)
While the Toronto test presented results that supported its hypothesis that neurodevelopment would be impacted by in utero exposure to cocaine, it did fail to take into account other possible influences on the development and cognitive ability levels in the test subjects. A mother who is addicted to cocaine is more likely to use alcohol, tobacco, and other drugs that are known to have effects on the development of a fetus.
Other research presented indicates that cocaine’s effects depend on contextual factors such as the child’s history of prematurity, age at the time of assessment, and the effects of prenatal exposure to other substances. A study presented in the March 28, 2001 issue of JAMA indicated that 6-month old infants whose mothers used cocaine, alcohol, and marijuana attained mean scores lower than infants in the control group. But their scores were identical to those of infants whose mothers had used alcohol and marijuana without cocaine. This suggests that cocaine is not the substance causing the negative scores, but in fact is attributable to the presence of other toxic substances like alcohol and marijuana whose developmental and cognitive impacts are documented as being damaging to a developing fetus. (Frank, Augustyn, Knight, Pell, & Zuckerman 2001, pp. 1613-1625)
At the moment, the effects of cocaine on the developing fetus are inconclusive. The Toronto study provided supporting evidence of its detrimental effect on behavior, cognitive development, and physical development. This particular study on cocaine’s effects on development was unique in that it made provisions to rule out the possible effects of the environment that the child was raised in. However it did not make provisions for the maternal use of other toxic substances that could effect the developing fetus in the areas of study: physical, cognitive, and behavior. Other studies on the same subject have concluded that cocaine in combination with other substances like alcohol and marijuana have the same results on the developing fetus as alcohol and marijuana alone. This indicates that cocaine alone is not the cause of the developmental, cognitive, and behavioral problems observed in the test subjects.
It is clear that further study is needed in this area. One possible experiment would to be to examine the developmental effects on children whose mother is known to only have used cocaine while pregnant. This would provide more conclusive evidence of cocaine’s effect on the fetus.
Carson, Butcher, Mineka. (2000). Abnormal Psychology and Modern Life. 11th ed. Boston, MA: Allyn & Bacon.
Frank, D., Augustyn, M., Knight, W., Pell, I., and Zuckerman, B. (2001 March 28). Growth, Development, and Behavior in Early Childhood Following Prenatal Cocaine Exposure: A Systematic Review. JAMA, 12, 1613-1625. (Vol. 285).
Greenbaum, R., Koren, G., Loebstein, M., Nulman, I., Pace-Aesciak, P., Rovet, J., & Wolpin, J. (2001). Neurodevelopment of adopted children exposed in utero to cocaine: the Toronto Adoption Study. Clin Invest Med, 24, 129.
Starr and Taggart. (2001). Biology: The Unity and Divesity of Life. 9th ed. Pacific Grove, CA: Brooks/Cole: Thomas Learning.
Warner, E. (1993, August 1). Review: Cocaine Abuse. Medline, 3, 226-235.