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Several large-scale cohort studies suggest that obese mothers are at increased risk of having infants with neural tube defects and, possibly, other central nervous system (CNS) birth defects. Because obesity and diabetes share similar metabolic abnormalities, a study was planned to determine whether gestational diabetes influences the association between maternal obesity and CNS birth defects. In this population-based case-control study, covering the years 1997 to mid-2000, structured telephone interviews were conducted with mothers of offspring having anencephaly (n ϭ 120), spina bifida (n ϭ 184), holoprosencephaly (n ϭ 49), or isolated hydrocephaly (n ϭ 124). Control women whose infants were neurologically normal were randomly chosen from the same hospitals. Approximately 60% of both cases and control subjects responded. Maternal obesity was defined as a body mass index of 30 kg/m 2 or higher.Pregestational diabetes, both type 1 and type 2, correlated closely with holoprosencephaly (adjusted odds ratio [OR], 47; 95% confidence interval [CI],, and isolated hydrocephaly (OR, 12; 95% CI, 2.9-47). There was no increase in the risk of anencephaly or spina bifida.Gestational diabetes increased only the risk of holoprosencephaly (OR, 2.9; 95% CI, 1.0-8.4). Mothers of infants with anencephaly were less likely than control mothers to have gestational diabetes. Obese mothers were likelier than control subjects to have infants with any of the 4 CNS birth defects. Underweight women were less likely to have an infant with spina bifida. The association between maternal obesity and an increased risk of neural tube defects and isolated hydrocephaly held for all ethnic groups. Associations between maternal obesity and anencephaly (OR, 2.3; 95% CI, 1.2-4.3), spina bifida (OR, 2.8; 95% CI, 1.7-4.5), and isolated hydrocephaly (OR, 2.7; 95% CI, 1.5-5.0) persisted after adjusting for maternal age, ethnicity, education, smoking, alcohol use, and periconceptional vitamin use. For both spina bifida and holoprosencephaly, the joint effects of maternal obesity and gestational diabetes appeared to be interactive.These findings suggest that gestational diabetes and maternal obesity may increase the risk of CNS birth defects through common mechanisms, and they strongly support the need for ways of preventing these conditions. EDITORIAL COMMENT(The epidemic of obesity is worldwide. The prevalence of a body mass index (BMI) Ն30 kg/m 2 in women 18 years of age and older increased from 12% to 18% from 1991 to 1998 (Mokdad AH, et al. JAMA 1999;282:1519). The relationship between obesity and diabetes is well known. Does the combination increase the risk of congenital malformations? To investigate the risk of neural tube defect (NTD)-affected pregnancies among obese women (BMI Ն29 kg/m 2 ) compared with women of average prepregnancy weight, Shaw performed a population-based case-controlled study of all hospitals in 55 of 58 counties in California. Compared OBSTETRICS Volume 60, Number 6 OBSTETRICAL AND GYNECOLOGICAL SURVEY 341 with women whose BMI...

Younger maternal age, poverty, lower education, and lack of social support were all significantly associated with increased maternal depression in multivariate regression models. Younger age, black race, unemployment, single status, lack of social support, and poor general health were all risk factors for increased prevalence of maternal depression.

Background Approximately 85% of primary congenital hypothyroidism (CH) is sporadic and due to malformations of the thyroid gland. Past studies have reported an increased birth weight among infants with CH. We have attempted to replicate and expand these observations, examining the association between different birth weight categories and CH stratified by infant's sex. We have also examined the prevalence of CH by mother's age and infant's ethnicity, gender, and year of birth. Methods A cross‐sectional study was conducted on 5,049,185 infants screened by the statewide California Newborn Screening Program between 1990 and 1998, an estimated 98.6% of all newborns in the state. Dried blood spots from a heel stick were assayed for thyroxine (T4), and presumptive positives had follow‐up assays of thyroid‐stimulating hormone (TSH) to determine definite positives. Results A total of 1,806 cases of CH were identified. The following findings are unlikely to be due to chance. Compared with infants with birth weights of 3,000–3,499 g, infants weighing <2,000 g and those weighing ≥4,500 g had a twofold or greater increase in the prevalence of CH. This was not explained as a result of confounding by the infant's ethnicity or gender. Compared with whites, elevated prevalence rates were found in most ethnic groups, which include the following: Hispanics, Chinese, Vietnamese, Asian Indians, Filipinos, Middle Easterners, and Hawaiians. As reported previously, black infants had about one‐third the prevalence rate of whites. We also observed the frequently described female preponderance of CH. The female excess was maintained at all birth weights, however it varied by infant's ethnicity. Trends in the prevalence of CH were not associated with mother's age or with the time interval between 1990 and 1998. Conclusions We observed an increased risk of CH in both low‐birth‐weight (<2,000‐g) and macrosomic (≥4,500‐g) infants. This U‐shaped association has not been described in past studies. We have also expanded the previously described ethnic differences in CH risk to include ethnic groups not previously studied. The unique pattern of CH occurrence suggests that further studies to define modifiable risk factors may be useful. Teratology 62:36–41, 2000. © 2000 Wiley‐Liss, Inc.

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