4.2 Article

Effects of Heavy Prenatal Alcohol Exposure and Iron Deficiency Anemia on Child Growth and Body Composition through Age 9 Years

期刊

ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
卷 36, 期 11, 页码 1973-1982

出版社

WILEY
DOI: 10.1111/j.1530-0277.2012.01810.x

关键词

Fetal Alcohol Syndrome; Intrauterine Growth Retardation; Postnatal Growth; Body Composition; Bioelectric Impedance Analysis; Prenatal Alcohol Exposure; Iron Deficiency; Food Security

资金

  1. 2 administrative supplements [R01 AA09524]
  2. NIH Office of Research on Minority Health
  3. Foundation for Alcohol Related Research, Cape Town, South Africa
  4. NIAAA Collaborative Initiative on Fetal Alcohol Spectrum Disorder (CIFASD)
  5. CIFASD [U01 AA014790, U24 AA014815, U01 AA014809]
  6. NICHD [K24 HD058795]
  7. NIH [KL2 RR025757]
  8. NIAAA [K23 AA020516]
  9. State of Michigan
  10. [R01 AA016781]

向作者/读者索取更多资源

Background Prenatal alcohol exposure has been associated with pre- and postnatal growth restriction, but little is known about the natural history of this restriction throughout childhood or the effects of prenatal alcohol on body composition. The objective of this study was to examine the effects of heavy prenatal alcohol exposure on longitudinal growth and body composition. Methods Eighty-five heavy drinking pregnant women (=2 drinks/d or =4 drinks/occasion) and 63 abstaining and light-drinking controls (<1 drink/d, no binging) were recruited at initiation of prenatal care in an urban obstetrical clinic in Cape Town, South Africa and prospectively interviewed during pregnancy about alcohol, smoking, drug use, and demographics. Among their children, length/height, weight, and head circumference were measured at 6.5 and 12 months and at 5 and 9 years. Percent body fat (BF) was estimated at age 9 years using bioelectric impedance analysis. Results In multiple regression models with repeated measures (adjusted for confounders), heavy alcohol exposure was associated with reductions in weight (0.6 SD), length/height (0.5 SD), and head circumference (0.9 cm) from 6.5 months to 9 years that were largely determined at birth. These effects were exacerbated by iron deficiency in infancy but were not modified by iron deficiency or measures of food security at 5 years. An alcohol-related postnatal delay in weight gain was seen at 12 months. Effects on head circumference were greater at age 9 than at other age points. Although heavy alcohol exposure was not associated with changes in body composition, children with fetal alcohol syndrome (FAS) and partial fetal alcohol syndrome (PFAS) had lower percent BF than heavy exposed nonsyndromal and control children. Conclusions Heavy prenatal alcohol exposure is related to prenatal growth restriction that persists through age 9 years and an additional delay in weight gain during infancy. FAS and PFAS diagnoses are associated with leaner body composition in later childhood.

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