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- Criminalizing substance abuse during pregnancy discourages
substance-using or abusing women from seeking prenatal care, drug treatment,
and other social services, and sometimes leads to unnecessary
abortions.
Sources: Cole, H.M., "Legal Interventions during Pregnancy:
Court-Ordered Medical Treatment and Legal Penalties for Potentially Harmful
Behavior by Pregnant Women," Journal of the American Medical
Association, 264: 2663-2670 (1990); Polan, M.L., Dombrowski, M.P., Ager,
J.W., & Sokol, R.J., "Punishing Pregnant Drug Users: Enhancing the Flight
from Care," Drug and Alcohol Dependence, 31: 199-203 (1993); Koren, G.,
Gladstone, D. Robeson, C. & Robieux, I., "The Perception of Teratogenic
Risk of Cocaine," Teratology, 46: 567-571 (1992).
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"Our study found significant cognitive deficits with cocaine-exposed
children twice as likely to have significant delay throughout
the first 2 years of life. The 13.7% rate of mental retardation
is 4.89 times higher than that expected in the population at large,
and the percentage of children with mild or greater delays
requiring intenvetion was 38%, almost double the rate of the
high-risk noncocaine- but polydrug-exposed comparison group. Because
2-year Mental Development Index scores are predictive of later
cognitive outcomes, it is possible that these children will continue
to have learning difficulties at school age.
"Cognitive delays could not be attributed to exposure to other drugs
or to a large numbe of potentially confounding variables. Further,
poorer cognitive outcomes were related to higher amounts of cocaine
metabolites in infant meconium as well as to maternal self-reported
measures of amount and frequency of cocaine use during pregnancy,
providing further support for a teratologic model."
. . .
"Some limitations to this study should be considered. Although
examiners were masked to infant drug status, it may have been possible
to identify drug exposure through maternal or caregiver characteristics,
since all children were assessed with the caregiver present. The
sample was also recruited according to hospital screening measures
and reflects outcomes only of more heavily exposed infants. Also, the
drug assessments were made retrospectively, making reliability
of maternal report problematic."
Source: Singer, Lynn T., PhD, Robert Arendt, PhD, Sonia Minnes, PhD,
Kathleen Farkas, PhD, Ann Salvator, MS, H. Lester Kirchner, PhD,
Robert Kliegman, MD, "Cognitive and Motor Outcomes of Cocaine-
Exposed Infants," Journal of the American Medical Association,
April 17, 2002, Vol. 287, No. 15, pp. 1957-1959.
- Research paid for by the National Institute on Drug Abuse (NIDA) and the
Albert Einstein Medical Center in Philadelphia states, "Although numerous
animal experiments and some human data show potent effects of cocaine on the
central nervous system, we were unable to detect any difference in Performance,
Verbal or Full Scale IQ scores between cocaine-exposed and control children at
age 4 years."
Source: Hallam Hurt, MD; Elsa Malmud, PhD; Laura Betancourt; Leonard E.
Braitman, PhD; Nancy L. Brodsky, Phd; Joan Giannetta, "Children with In Utero
Cocaine Exposure Do Not Differ from Control Subjects on Intelligence Testing,
"Archives of Pediatrics & Adolescent Medicine, Vol. 151: 1237-1241
(1997), American Medical Association.
- Well-controlled studies
find minimal or no increased risk of Sudden
Infant Death Syndrome (SIDS) among cocaine-exposed infants.
Sources: Bauchner, H., Zuckerman, B., McClain, M., Frank, D., Fried,
L.E., & Kayne, H., "Risk of Sudden Infant Death Syndrome among Infants with
In Utero Exposure to Cocaine," Journal of Pediatrics, 113: 831-834
(1988), (Note: Early studies reporting increased risk of SIDS did
not control for socioeconomic characteristics and other unhealthy behaviors.
See, e.g., Chasnoff, I.J., Hunt, C., & Kletter, R., et al.,
"Increased
Risk of SIDS and Respiratory Pattern Abnormalities in Cocaine-Exposed Infants,
"Pediatric Research, 20: 425A (1986); Riley, J.G., Brodsky, N.L. &
Porat, R., "Risk for SIDS in Infants with In Utero Cocaine Exposure: a
Prospective Study," Pediatric Research, 23: 454A (1988)).
- Among the general population there has been no detectable increase in
birth defects which may be associated with cocaine use during
pregnancy.
Source: Martin, M.L., Khoury, M.J., Cordero, J.F. & Waters, G.D.,
"Trends in Rates of Multiple Vascular Disruption Defects, Atlanta, 1968-1989:
Is There Evidence of a Cocaine Teratogenic Epidemic?"
Teratology, 45:647-653 (1992).
- The lack of quality prenatal care is associated with undesirable effects
often attributed to cocaine exposure: prematurity, low birth weight, and fetal
or infant death.
Sources: Klein, L., & Goldenberg, R.L., "Prenatal Care and its
Effect on Pre-Term Birth and Low Birth Weight," in Merkatz, I.R. &
Thompson, J.E. (eds.), New Perspectives on Prenatal Care (New York,
NY:
Elsevier, 1990), pp. 511-513; MacGregor, S.N., Keith, L.G., Bachicha,
J.A.
& Chasnoff, I.J., "Cocaine Abuse during Pregnancy: Correlation between
Prenatal Care and Perinatal Outcome," Obstetrics and
Gynecology, 74:882-885 (1989).
- Provision of quality prenatal care to heavy cocaine users (with or
without drug treatment) has been shown to significantly improve fetal health
and development.
Source: Chazotte, C., Youchah, J., & Freda, M.C., "Cocaine Use
during Pregnancy and Low Birth Weight: The Impact of Prenatal Care and Drug
Treatment," Seminars in Perinatology, 19: 293-300 (1995).
- Presented with children randomly labeled "prenatally cocaine-exposed" and
"normal," childcare professionals ranked the performance of the "prenatally
cocaine-exposed" children below that of "normal," despite
actual performance.
Source: Thurman, S.K., Brobeil, R.A., Duccette, J.P., & Hurt, H.,
"Prenatally Exposed to Cocaine: Does the Label Matter?" Journal of Early
Intervention, 18: 119-130 (1994).
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According to a study published by the Journal of the American
Medical Association in 2002, "Consistent with previous studies,
we found that maternal cigarette smoking was associated with
reduced birth weight and an increased risk of LBW, shortened
gestation and an increased risk of preterm birth, and intrauterine
growth restriction. Our data indicate that maternal cigarette
smoking likely affects infant birth weight via both reduced fetal
growth and shortened gestation."
Source: Wang, Xiaobin, MD, MPH, ScD, Barry Zuckerman, MD, et al.,
"Maternal Cigarette Smoking, Metabolic Gene Polymorphism, and
Infant Birth Weight," Journal of the American Medical Association
(Chicago, IL: American Medical Association, January 9, 2002),
Vol. 287, No. 2, p. 200.
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According to a study published by the Journal of the American
Medical Association in 2002, "For the ever smokers, the mean birth
weight was 280 g lower (95% confidence interval [CI], -413 to -147)
and the odds ratio (OR) for LBW was higher (OR, 1.8; 95% CI, 1.3-2.7)
compared with the never smokers. The mean gestational age for ever
smokers was 0.8 weeks shorter (95% CI, -1.3 to -0.2) and the OR
of preterm birth was higher (OR, 1.8; 95% CI, 1.3-2.7)."
Source: Wang, Xiaobin, MD, MPH, ScD, Barry Zuckerman, MD, et al.,
"Maternal Cigarette Smoking, Metabolic Gene Polymorphism, and Infant
Birth Weight," Journal of the American Medical Association
(Chicago, IL: American Medical Association, January 9, 2002),
Vol. 287, No. 2, p. 198.
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According to a study published by the Journal of the American
Medical Association in 2002, "As shown in Table 2, without
consideration of genotype, continuous maternal smoking during
pregnancy was associated with an OR of 2.1 (95% CI, 1.2-3.7) for
LBW and a mean reduction of 377 g (SE, 89 g) in birth weight
compared with the never smokers."
Source: Wang, Xiaobin, MD, MPH, ScD, Barry Zuckerman, MD, et al.,
"Maternal Cigarette Smoking, Metabolic Gene Polymorphism, and Infant
Birth Weight," Journal of the American Medical Association
(Chicago, IL: American Medical Association, January 9, 2002),
Vol. 287, No. 2, p. 198.
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According to a study published by the British Medical Journal
in 2002, "In utero exposures due to smoking during pregnancy may
increase the risk of both diabetes and obesity through programming,
resulting in lifelong metabolic dysregulation, possibly due to
fetal malnutrition or toxicity. The odds ratios for obesity without
type 2 diabetes are more modest than those for diabetes and the
scope for confounding may be greater. Smoking during pregnancy
may represent another important determinant of metabolic
dysregulation and type 2 diabetes in offspring. Smoking during
pregnancy should always be strongly discouraged."
Source: Montgomery, Scott M., and Anders Ekborn, "Smoking During
Pregnancy and Diabetes Mellitus In a British Longitudinal Birth
Cohort," British Medical Journal (London, England: British Medical
Association, January 5, 2002), Vol. 321, p. 27.
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