Effects of Oral Contraception and Lifestyle Modification on Incretins and TGF-ß Superfamily Hormones in PCOS.

OBJECTIVE: To examine the effects of common treatments for polycystic ovary syndrome (PCOS) on a panel of hormones (reproductive/metabolic). DESIGN: Secondary analysis of blood from a randomized controlled trial of three 16-week preconception interventions designed to improve PCOS-related abnormalities: continuous oral contraceptive pills (OCPs, N = 34 subjects), intensive lifestyle modification (Lifestyle, N = 31), or a combination of both (Combined, N = 29). MATERIALS AND METHODS: Post-treatment levels of activin A and B, inhibin B, and follistatin (FST), as well as Insulin-like growth factor 1 (IGF-1), insulin-like growth factor binding protein 2 (IGFBP-2), glucagon, glucagon-like peptide 1 (GLP-1) and 2, and oxyntomodulin were compared to baseline, and the change from baseline in these parameters were correlated with outcomes. RESULTS: Oral contraceptive pill use was associated with a significant suppression in activin A, inhibin A, and anti-mullerian hormone (AMH), but a significant increase in FST. IGF-1, IGFBP-2, glucagon, and GLP-2 levels were significantly decreased. Oxyntomodulin was profoundly suppressed by OCPs (ratio of geometric means: 0.09, 95% confidence interval [CI]: 0.05, 0.18, P < 0.001). None of the analytes were significantly affected by Lifestyle, whereas the effects of Combined were similar to OCPs alone, although attenuated. Oxyntomodulin was significantly positively associated with the change in total ovarian volume (rs = 0.27; 95% CI: 0.03, 0.48; P = 0.03) and insulin sensitivity index (rs = 0.48; 95% CI: 0.27, 0.64; P < 0.001), and it was inversely correlated with change in area under the curve (AUC) glucose [rs = -0.38; 95% CI: -0.57, -0.16; P = 0.001]. None of the hormonal changes were associated with live birth, only Activin A was associated with ovulation (risk ratio per 1 ng/mL increase in change in Activin A: 6.0 [2.2, 16.2]; P < 0.001). CONCLUSIONS: In women with PCOS, OCPs (and not Lifestyle) affect a wide variety of reproductive/metabolic hormones, but their treatment response does not correlate with live birth.

Associations between causal attributions for obesity and long-term weight loss.

Obesity is a complex disease caused by a wide array of behavioral, biological, and environmental factors. However, obesity is often attributed to oversimplified and stigmatizing causal factors such as laziness, lack of willpower, and failure to take personal responsibility for one's health. Understanding of the causal factors that contribute to obesity among people with obesity may affect their weight management efforts. The current study explored associations between causal attributions for obesity and long-term weight loss, as well as examined potential changes in attributions with weight reduction. The 16-item Causal Attributions for Obesity scale (rated 1-7) was administered to 178 patients seeking behavioral/pharmacological weight-loss treatment. Causal attributions and weight were assessed at baseline, after 14 weeks of a low-calorie diet, and again at weeks 24 and 52 of a subsequent randomized trial (i.e., 66 weeks total). Logistic and linear regression examined effects of baseline causal attribution ratings on weight loss. Higher baseline ratings of personal responsibility attributions predicted 38% reduced odds of achieving ≥10% weight loss at week 52 (p = 0.02). Causal attribution ratings did not change over time or correlate continuously with weight change. Thus, attributing obesity to a failure of personal responsibility may impair long-term weight management efforts for individuals seeking ≥10% weight loss. Targeted techniques are needed to reduce patients' stigmatizing beliefs about the causes of obesity.

Hallazgos neuroendocrinos en el síndrome de ingesta nocturna / Neuroendocrine levels, circadian profiles, and sleep in night eating syndrome: integration of findings

El síndrome de ingesta nocturna (SIN) se caracteriza porhiperfagia vespertina y despertares acompañados deingesta nocturna de alimentos. Dilucidar el trastorno enla fisiología del sueño y la fisiología neuroendocrina subyacenteal síndrome clínico es fundamental y ayudará acentrar los tratamientos. Llevamos a cabo un estudio con15 mujeres internadas con sobrepeso y SIN y 14 participantescontroles similares para comparar las concentracionesen 25 horas y los patrones circadianos de los perfilesneuroendocrinos y de ingesta calórica y las característicaspolisomnográficas...

Night eating syndrome (NES) is characterized by eveninghyperphagia and awakenings with nocturnal foodingestions. Elucidation of the disturbance in sleep and neuroendocrine physiology that underlies the clinical syndrome is crucial and helps to target treatments. We conducted an inpatient study of 15 overweight women with NES and 14 similar control participants to compare the 25 h levels and circadian patterns of neuroendocrine and caloric intake profiles and polysomnographic features...