The Epidemiology and Mechanisms of Lifetime Cardiopulmonary Morbidities Associated With Pre-Pregnancy Obesity and Excessive Gestational Weight Gain

Abstract

Obesity has reached pandemic proportions in the last few decades. The global increase in obesity has contributed to an increase in the number of pregnant women with pre-pregnancy obesity or with excessive gestational weight gain. Obesity during pregnancy is associated with higher incidence of maternal co-morbidities such as gestational diabetes and hypertension. Both obesity during pregnancy and its associated complications are not only associated with immediate adverse outcomes for the mother and their newborns during the perinatal period but, more importantly, are linked with long-term morbidities in the offsprings. Neonates born to women with obesity are at higher risk for cardiac complications including cardiac malformations, and non-structural cardiac issues such as changes in the microvasculature, e.g., elevated systolic blood pressure, and overt systemic hypertension. Pulmonary diseases associated with maternal obesity include respiratory distress syndrome, asthma during childhood and adolescence, and adulthood diseases, such as chronic obstructive pulmonary disease. Sequelae of short-term complications compound long-term outcomes such as long-term obesity, hypertension later in life, and metabolic complications including insulin resistance and dyslipidemia. Multiple mechanisms have been proposed to explain these adverse outcomes and are related to the emerging knowledge of pathophysiology of obesity in adults. The best investigated ones include the role of obesity-mediated metabolic alterations and systemic inflammation. There is emerging evidence linking metabolic and immune derangements to altered biome, and alteration in epigenetics as one of the intermediary mechanisms underlying the adverse outcomes. These are initiated as part of fetal adaptation to obesity during pregnancy which are compounded by rapid weight gain during infancy and early childhood, a known complication of obesity during pregnancy. This newer evidence points toward the role of specific nutrients and changes in biome that may potentially modify the adverse outcomes observed in the offsprings of women with obesity.

Recent Insights and Recommendations for Preventing Excessive Gestational Weight Gain

“…EGWG is an increasingly observed phenomenon and is estimated to affect up to 43% of pregnant women. Pre-pregnancy BMI > 25 is one of the most significant risk factors of EGWG, and the BMI before conception is the most important predictor of GWG in general [ 7 , 8 , 9 , 10 , 11 ]. According to Restall et al [ 9 ], women who were overweight and obese at 14–16 weeks of gestation were, respectively, 3 and 2.5 times more likely to gain more gestational weight than recommended.…”

“…According to Restall et al [ 9 ], women who were overweight and obese at 14–16 weeks of gestation were, respectively, 3 and 2.5 times more likely to gain more gestational weight than recommended. Pre-pregnancy obesity, resulting from a high-calorie diet or genetic predisposition, alters lipid/energy metabolism during pregnancy [ 11 ]. During pregnancy, maternal weight influences levels of insulin, leptin, triglycerides (TGs), and c-reactive protein (CRP) [ 12 ].…”

“…Their action may contribute to the occurrence of insulin resistance in pregnancy [ 13 ]. Women affected by obesity have higher concentrations of glucose transporter 1 (GLUT1) receptors and sodium-coupled neutral amino acid transporters (SNAT), and their maternal adipose tissue is involved in increasing insulin resistance [ 11 ]. Perichart-Perera et al [ 12 ] observed elevated insulin levels in pregnant patients with EGWG.…”

The Role of Helicobacter pylori and Metabolic Syndrome-Related Mast Cell Activation Pathologies and Their Potential Impact on Pregnancy and Neonatal Outcomes

“…Specifically, MetS-related parameters, IR, dyslipidemia, and AH are contributors to systemic pathologies [18], including negative pregnancy and neonatal outcomes like heightened preeclampsia risk, altered fetal growth, and premature birth [20][21][22]. MAFLD, as the hepatic component of MetS, is associated with a high risk of adverse outcomes for both the mother and the fetus [23,24].…”