INTRODUCTION: Excessive gestational weight gain (GWG) is associated with adverse maternal and neonatal outcomes. Current guidelines established by the United States' Institute of Medicine (IOM) in 2009 recommend GWG of 11–20 lb for all obese patients. In 2019, a JAMA meta-analysis proposed recommending less weight gain in obesity (0–13 lb), not accounting for pre-existing maternal co-morbidities. We aim to ascertain whether, in obese diabetic pregnancies, GWG within the updated JAMA guidelines is associated with better outcomes. METHODS: IRB approval was obtained. Using a large urban hospital's de-identified obstetric database, obese diabetic patients from 2011 to 2020 were categorized into two groups: IOM and JAMA, depending on their GWG. Diagnosis codes were used to assess outcomes. Chi-square test, independent samples T-test, and Wilcoxon rank-sum test were used. RESULTS: Of 240 patients with obesity and diabetes, 135 fell within IOM weight gain guidelines and 65 within JAMA. The groups were not significantly different in age, BMI, A1C, or proportion with prior cesarean delivery. For maternal outcomes, chronic hypertension was independently associated with weight gain within the JAMA guidelines versus IOM (55% vs. 36%, P =.0082). There were no significant differences in rates of cesarean delivery ( P =.73) or pre-eclampsia ( P =.92). For neonatal outcomes, no differences were noted in NICU admission ( P =.73), macrosomia ( P =.72), or preterm delivery ( P =.21) rates. CONCLUSION: For women with obesity and diabetes, chronic hypertension was associated with marginally less weight gain. Further research may be needed before clinicians advise the stricter GWG recommendations in the new JAMA guidelines rather than the current standard of IOM guidelines.
Objective Obesity is a major public health problem that increases the risk for a broad spectrum of co-morbid conditions. Despite evidence for a strong genetic contribution to susceptibility to obesity, previous efforts to discover the relevant genes using positional cloning have failed to account for most of the apparent genetic risk variance. Design and Methods Deploying a strategy combining analysis of exome sequencing data in extremely obese members of four consanguineous families with segregation analysis, we screened for causal genetic variants. Filter-based analysis and homozygosity mapping were used to identify and prioritize putative functional variants. Results Two novel frameshift mutations in the leptin receptor in two of the families were identified. Conclusions These results provide proof-of-principle that whole-exome sequencing of families segregating for extreme obesity can identify causal pathogenic mutations. The methods described here can be extended to additional families segregating for extreme obesity and should enable the identification of mutations in novel genes that predispose to obesity.
Dissociative identity disorder (DID) is a complex and controversial psychiatric condition in which one person maintains at least two separate and distinct personalities. Patients with DID often report a history of childhood abuse and may have other comorbid psychiatric conditions. Psychosocial stressors may be triggers for DID inception or recurrence. While anesthetic agents, in particular ketamine, may induce a temporary dissociative state, it has not yet been reported that anesthesia can precipitate a dissociative identity.We report a case of a woman with a history of childhood sexual abuse and past suicide attempt who experienced an episode of dissociative identity on emergence from anesthesia. The episode resolved within 90 minutes and the patient was discharged home safely on hospital day two.This case adds to the literature of potentially precipitating factors of DID and we provide a unifying mechanistic hypothesis linking anesthesia to functional brain connectivity.
Brain-derived neurotrophic factor (BDNF) haploinsufficiency is associated with hyperphagia and obesity in both animals and humans. BDNF appears to function downstream of the leptin-melanocortin signaling pathway to control energy balance. The potential role of BDNF in the etiology of the severe hyperphagia associated with PWS has not been previously explored.The aim was to compare BDNF concentrations in subjects with PWS and obese controls (OC) and lean controls (LC).We conducted a cross-sectional study at an outpatient clinical research center.We studied 13 subjects with PWS [five females and eight males; mean + or - sd: age, 11.0 + or - 4.1 yr; body mass index (BMI)-Z, 2.05 + or - 0.78], 13 OC (eight females, five males; age, 12.3 + or - 2.7 yr; BMI-Z, 2.18 + or - 0.61), and 13 LC (six females, seven males; age, 12.4 + or - 2.6 yr; BMI-Z, -0.57 + or - 0.73).BDNF was measured in serum and plasma by ELISA. Analysis of covariance adjusted for age, sex, and BMI-Z.All groups were comparable for age (P = 0.50) and sex distribution (P = 0.49). BMI-Z was comparable between PWS and OC (P = 0.89) and lower in LC (P < 0.001). Adjusted serum BDNF was comparable (P = 0.35) in OC (mean + or - sem: 13.5 + or - 1.2 ng/ml) and LC (19.2 + or - 1.3 ng/ml), but lower in PWS (8.3 + or - 1.2 ng/ml; P = 0.01 vs. OC; P = 0.03 vs. LC). Adjusted plasma BDNF in PWS (217 + or - 130 pg/ml) was lower than OC (422 + or - 126 pg/ml; P = 0.02), but statistically comparable with LC (540 + or - 143 pg/ml; P = 0.10).Lower BDNF in PWS suggests insufficient central BDNF production because BDNF in peripheral circulation is believed to reflect cerebral BDNF output. Decreased BDNF may be a potential cause for the disordered satiety and morbid obesity associated with PWS. Further studies are needed to confirm this preliminary pilot study in a larger cohort of patients with PWS.
