Obesity among pregnant women is becoming one of the most important women's health issues. Obesity is associated with increased risk of almost all pregnancy complications: gestational hypertension, preeclampsia, gestational diabetes mellitus, delivery of large-for-GA infants, and higher incidence of congenital defects all occur more frequently than in women with a normal BMI. Evidence shows that a child of an obese mother may suffer from exposure to a suboptimal in utero environment and that early life adversities may extend into adulthood.
It is evident that obese pregnant women are at increased risk of maternal death and complications during pregnancy and labor. Obesity is associated with increased risk of almost all pregnancy complications such as gestational hypertension, preeclampsia, gestational diabetes mellitus (GDM), delivery of a large for gestational age (LGA) infant, and a higher incidence of congenital defects all occur more frequently than in women with a normal BMI. Cesarean section rates are also much higher, and anesthesia may be problematic.
Desired gestational weight gain is as follows: In underweight (BMI <18.5; recommended weight gain 12.5–18 kg), normal weight (BMI, 18.5–24.9; 11.5–16 kg), overweight (BMI, 25.0–29.9; 7–11.5 kg), and obese (BMI ≥30; 5–9 kg) pregnant women.
The “Developmental Origins of Disease” hypothesis suggests that elements of heritability can be transmitted in a non-Mendelian way from generation to generation. Several cohort studies report an association between maternal early or prepregnancy BMI and offspring BMI assessed at birth, in infancy, childhood, and early adulthood. Although such associations are not very clear, they urgently need to be addressed in cohorts with an incidence of maternal obesity that reflects contemporary populations.
Maternal prepregnancy obesity is strongly associated with risk of GDM, and all risks associated with GDM are directly related to maternal obesity. so, we also considered the association of GDM with offspring health, including LGA babies, fetal hypoglycemia, hypocalcemia and neonatal hypoglycemia.
Several metabolic pathways are likely to influence fetal development and neonatal outcomes and contribute to adverse maternal outcomes. Placental nutrient transport could also be influenced by maternal obesity.m Maternal blood glucose is subtly increased among obese mothers, along with raised inflammatory markers in the mother. Animal models have provided strong evidence for persistent and adverse effects of maternal obesity on the offspring. The precise mechanisms remain unclear; for effects to be persistent, “programming” must include permanent changes in cellular structure or function in the offspring in response to the metabolic consequences of maternal obesity. Fetal increase in leptin, glucocorticoids, insulin and triglycerides all increase the fetal neuroprogramming. It is recommended that Dietary interventions in future RCTs in obese pregnant women should be better tailored to current theory, e.g. to reduce the maternal glycemic load and prevent insulin resistance, reduce maternal dietary n-6:n-3 ratio, and lower neonatal leptin.
Obesity among pregnant women is becoming one of the most important women's health issues for this decade. The evidence available on both the short-term and long-term health impact for mother and child currently favors actions directed at controlling prepregnancy weight and preventing obesity in women of reproductive ages. This recommendation is driven by the paucity of good research evidence from either RCTs or through basic scientific mechanisms, which would underpin putative benefit from GWG recommendations for health outcomes in mother and child. This applies to all pregnant women and subgroups. RCTs are urgently needed to evaluate the effect of nutritional and behavioral interventions in pregnancy on short-term and long-term outcomes in mother and child, with a sound scientific basis. The suggestion that maternal obesity may transfer risk of obesity to the child through nongenomic mechanisms, although supported by studies in animals, requires further detailed investigation in human RCTs with provision for long-term follow-up of the children.