Maternal and fetal genetic contribution to gestational weight gain.

BACKGROUND: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. PARTICIPANTS AND METHODS: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight). RESULTS: Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG. CONCLUSIONS: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

Smoking and pregnancy-related pelvic pain.

OBJECTIVE: To investigate possible associations between smoking and pregnancy-related pelvic pain. DESIGN: Nested case-control study. SETTING: Denmark 2000-2001. POPULATION: The Danish National Birth Cohort. METHODS: The women were interviewed twice in pregnancy and twice after childbirth. The first pregnancy interview provided information on smoking and possible confounding factors,whereas the first interview after birth addressed case identification.Cases (n = 2302) were defined on the basis of self-reported pelvic pain, and controls were selected among women who did not report pelvic pain (n = 2692). Logistic regression analysis was used to estimate associations between smoking and pelvic pain. MAIN OUTCOME MEASURE: Pregnancy-related pelvic pain. RESULTS: Compared with non-smokers, women who smoked during pregnancy had an adjusted odds ratio of 1.2 (1.0-1.4) for overall pelvic pain, similar to women who stopped smoking in early pregnancy 1.3 (1.1-1.7). The equivalent adjusted odds ratio for severe pelvic pain was 1.2 (1.0-1.5) for smokers, and 1.5 (1.2-1.9)for women who stopped smoking. Smoking intensity, measured as number of cigarettes smoked per day, was associated with pelvic pain in a dose-response pattern. Information about smoking was collected prospectively, which makes it unlikely that differential recall alone explains the results. CONCLUSIONS: Smoking was associated with pregnancy-related pelvic pain, with a dose-response pattern between reported smoking intensity and pelvic pain. These findings suggest a possible new risk factor for a common ailment during pregnancy