ObjectiveWe evaluated long-term impact of sustained weight loss versus weight regain on cardiovascular risk factors in real-world clinical practice.MethodsWe evaluated 129 obese patients with diabetes enrolled in Weight Achievement and Intensive Treatment (Why WAIT) program, a 12-week clinical model of intensive lifestyle intervention. After 1 year, we divided participants into group A, who maintained <7% weight loss (47.3%) and group B (52.7%), who maintained ≥7% weight loss. We continued to follow them for a total of 5 years.ResultsThe total cohort lost 23.8 lbs (−9.7%) at 12 weeks and maintained −16.2 lbs (−6.4%) at 5 years (p<0.001). Group A maintained −8.4 lbs (−3.5%) and group B maintained −23.1 lbs (−9.0%) at 5 years. In group A, A1C decreased from 7.5±1.3% to 6.7±0.9% at 12 weeks but increased to 7.7±1.4% at 1 year and 8.0±1.9% at 5 years. In group B, A1C decreased from 7.4±1.2% to 6.4±0.9% at 12 weeks and rose to 6.8±1.2% at 1 year and 7.3±1.5% at 5 years. Despite weight regain, group A maintained improvement in low-density lipoprotein-cholesterol and high-density lipoprotein-cholesterol with worsening of serum triglycerides and no change in blood pressure (BP). Group B maintained improvement in lipid profile for 5 years and had significantly lower BP for 18 months.ConclusionsWeight reduction in patients with diabetes can be maintained for 5 years and is predicted by patients’ ability to maintain ≥7% weight loss at 1 year. A1C and triglycerides deteriorate with weight regain, while other lipid improvements are maintained. Sustained weight loss is associated with significantly lower A1C for 5 years and lowers BP for 18 months.Trial registration numberNCT01937845.

Glucocorticoids (GCs), cortisol in humans, influence multiple essential maturational events during gestation. In the human fetus, fetal hypothalamic-pituitary-adrenal (HPA) axis function, fetal adrenal steroidogenesis, placental 11β- hydroxysteroid dehydrogenase type 2 activity, maternal cortisol concentrations, and environmental factors impact fetal cortisol exposure. The beneficial effects of synthetic glucocorticoids (sGCs), such as dexamethasone and betamethasone, on fetal lung maturation have significantly shifted the management of preterm labor and threatened preterm birth. Accumulating evidence suggests that exposure to sGCs in utero at critical developmental stages can alter the function of organ systems and that these effects may have sequelae that extend into adult life. Maternal stress and environmental influences may also impact fetal GC exposure. This article explores the vulnerability of the fetal HPA axis to endogenous GCs and exogenous sGCs.

No abstract