A longitudinal investigation of breastfeeding planning, initiation, and duration among individuals with pre-pregnancy overweight or obesity.

Individuals with a body mass index (BMI)≥25 kg/m2 are less likely to initiate and continue breastfeeding than are those with BMIs<25. Given the intergenerational health benefits of breastfeeding, it is important to understand breastfeeding behaviors and their correlates among individuals with BMIs≥25. Thus, in an observational cohort with BMI≥25 (N = 237), we aimed to characterize longitudinal relationships among breastfeeding planning, initiation, and duration and their sociodemographic/clinical correlates and determine if pre-pregnancy BMI predicts breastfeeding planning, initiation, and duration. Breastfeeding behaviors, weight/BMI, and sociodemographic/clinical characteristics were assessed in early, mid, and late pregnancy, and at six-months postpartum. Most participants planned to (84%) and initiated (81%) breastfeeding, of which 37% breastfed for ≥6 months. Participants who were married, first-time parents, higher in education/income, and had never smoked tobacco were more likely to plan, initiate, and achieve ≥6 months of breastfeeding. Higher pre-pregnancy BMI was not associated with breastfeeding planning or initiation but was associated with lower adjusted odds of breastfeeding for ≥6 months relative to <6 months. Findings suggest that support aimed at extending breastfeeding among those with elevated pre-pregnancy BMI may be warranted. Future interventions should also address sociodemographic and clinical inequities in breastfeeding.

Associations between prenatal loss of control eating and cardiovascular health during pregnancy.

OBJECTIVE: Loss of control (LOC) eating (feeling unable to control food type/amount eaten) during pregnancy is common and linked to risk for poor cardiovascular health (CVH), but it is unclear whether prenatal LOC eating directly relates to CVH during pregnancy. The current study tested associations between prenatal LOC eating and CVH during pregnancy in a sample with prepregnancy body mass index (BMI) ≥ 25. METHOD: At 12-20 weeks' gestation, participants (N = 124) self-reported: prenatal LOC eating, diet, physical activity, nicotine use, sleep; height/weight were measured. Data were collected during 2015-2017. We dichotomized LOC eating (0 = absent; 1 = present) and scored CVH metrics using Life's Essential 8 to create a composite CVH score (range = 0-100; higher = better). Linear and binary logistic regression models tested if LOC eating is related to composite CVH score and odds of scoring low (0)/moderate-high (1) on each CVH metric, respectively. All models employed propensity score adjustment, since those with/without LOC eating may differ in ways affecting CVH, and covaried for: age, gestational age, prepregnancy BMI, ethnicity, race, education, and income. RESULTS: Compared to those without, participants with LOC eating had significantly poorer composite CVH scores (b = -9.27, t(111) = -2.70, p < .01) and lower odds of scoring moderate-high on nicotine use (OR = 0.20, 95% CI [0.04, 0.85], p = .03) and sleep duration (OR = 0.19, 95% CI [0.04, 0.83], p = .03) CVH metrics. CONCLUSIONS: Prenatal LOC eating was associated with poorer CVH during pregnancy in this sample with prepregnancy BMI ≥ 25, even after controlling for propensity of experiencing LOC eating and known risk factors for poor CVH. Thus, prenatal LOC may represent a modifiable factor related to prenatal health risk. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Lipase regulation of cellular fatty acid homeostasis as a Parkinson's disease therapeutic strategy.

Synucleinopathy (Parkinson's disease (PD); Lewy body dementia) disease-modifying treatments represent a huge unmet medical need. Although the PD-causing protein α-synuclein (αS) interacts with lipids and fatty acids (FA) physiologically and pathologically, targeting FA homeostasis for therapeutics is in its infancy. We identified the PD-relevant target stearoyl-coA desaturase: inhibiting monounsaturated FA synthesis reversed PD phenotypes. However, lipid degradation also generates FA pools. Here, we identify the rate-limiting lipase enzyme, LIPE, as a candidate target. Decreasing LIPE in human neural cells reduced αS inclusions. Patient αS triplication vs. corrected neurons had increased pSer129 and insoluble αS and decreased αS tetramer:monomer ratios. LIPE inhibition rescued all these and the abnormal unfolded protein response. LIPE inhibitors decreased pSer129 and restored tetramer:monomer equilibrium in αS E46K-expressing human neurons. LIPE reduction in vivo alleviated αS-induced dopaminergic neurodegeneration in Caenorhabditis elegans. Co-regulating FA synthesis and degradation proved additive in rescuing PD phenotypes, signifying co-targeting as a therapeutic strategy.