期刊
NEUROTOXICOLOGY AND TERATOLOGY
卷 33, 期 2, 页码 188-197出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.ntt.2010.11.002
关键词
Prenatal cocaine exposure; Prenatal alcohol exposure; Childhood obesity; Growth; Fetal origins
资金
- National Institute on Drug Abuse (NIDA)
- National Institute of Child Health and Human Development (NICHD)
- National Institute of Mental Health (NIMH)
- Warren Alpert Medical School of Brown University [U10-DA-024119, U10-HD-27904, N01-2-3159]
- Wayne State University [U10-DA-024117, U10-HD-21385]
- University of Tennessee [U10-DA-024118, U10-HD-21415]
- University of Miami [U10-DA-024118, U10-HD-21397]
- RTI International [U01-HD-36790]
- National Institute on Drug Abuse
- National Institute of Child Health and Human Development
Little is known about the association between prenatal cocaine exposure and obesity. We tested whether prenatal cocaine exposure increases the likelihood of obesity in 561 9-year-old term children from the Maternal Lifestyle Study (MLS). Overall, 21.6% of children met criterion for obesity (body mass index [BMI]>= 95th percentile, age and sex-specific). While there was no overall cocaine effect on obesity, multivariate logistic analysis revealed that children exposed to cocaine but not alcohol were 4 times more likely to be obese (OR 4.11, CI 2.04-9.76) than children not exposed to either drug. No increase in obesity prevalence was found in children exposed to alcohol but not cocaine (OR 1.08, Cl .59-1.93) or both (OR 1.21, CI 0.66-2.22). Alcohol exposure may attenuate the effect of cocaine exposure on obesity. Increased obesity associated with cocaine but not alcohol exposure was first observed at 7 years. BMI was also elevated from 3 to 9 years in children exposed to cocaine but not alcohol, due to increasing weight but normal height. Prenatal exposure to cocaine may alter the neuroendocrine system and metabolic processes resulting in increased weight gain and childhood obesity. (C) 2010 Elsevier Inc. All rights reserved.
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