These findings add relevance to the usefulness of metformin and flutamide in the treatment of dieting overweight-obese PCOS women and provide a rationale for targeting different therapeutic options according to the required outcomes in the long term.
Chronic exposure to environmental stress may play a role in the development of obesity, through hyperactivation of the hypothalamic–pituitary–adrenocortical (HPA) axis. This study investigated the dynamics of weight gain and the activity of the HPA axis in women who developed weight gain after a stressful event. This is a case–control retrospective study. Two groups of age‐matched premenopausal women were selected. One (n = 14) included women characterized by a rapid weight gain following a stressful event, defined as the “stress‐related obesity” (SRO) group, and the other (n = 21) women with nonstress‐related development of obesity, defined as the “nonstress‐related obesity” (NSRO) group. Twenty‐one healthy premenopausal women served as normal‐weight controls. Baseline hormonal and metabolic parameters, and 24‐h urinary free cortisol (UFC/24 h) excretion rate (as a measure of HPA‐axis activity) were measured in all women. Anthropometry, diet, and physical activity were similar in both obese groups. Both obese groups showed similar metabolic and hormonal profiles, but the SRO group had UFC/24 h values (41.1 ± 14.3 µg) significantly higher (P < 0.001) with respect to the NSRO (26.6 ± 17.6 µg) or the normal‐weight control groups (21.1 ± 9.8 µg). Moreover, time (years) to achieve maximum Δweight gain (kg) and the Δweight gain/time ratio were significantly shorter (P < 0.001) and higher (P < 0.001) in the SRO group with respect to the NSRO group, respectively. In the SRO group, there was a tendency to a significant correlation between UFC/24 h and the Δweight gain/time ratio. These findings support the concept that SRO has distinct pathophysiological mechanisms, including hyperactivity of the HPA axis.
This study did not find major differences in dietary habits between PCOS and normoandrogenic control women. Our findings support the hypothesis that specific foods may influence metabolic and hormonal pattern and that this relationship may be differently regulated in PCOS and normoandrogenic women; however, they give little support to the hypothesis of a strong dependence of PCOS status on nutritional factors.
Background: Treatment of obesity improves all features of the polycystic ovary syndrome (PCOS). There is, however, a heterogeneous response to weight loss, and predictive factors are unknown.Objective: This follow-up study aimed to investigate obese women with PCOS treated with a long-term lifestyle program to evaluate responsiveness and predictability. Methods: One hundred PCOS women meeting the criteria for selection were invited to participate and 65 of them agreed. Lifestyle intervention had consisted of a 1200-1400 kcal/day diet for 6 months, followed by mild calorie restriction and physical activity. The protocol, which was similar at baseline and follow-up, included anthropometry, clinical evaluation, pelvic ultrasound, and laboratory investigations. The mean follow-up period was 20.4G12.5 months. Results: After the follow-up period, women were reclassified into three groups according to the persistence (group 1, 15.4%), partial (group 2, 47.7%), or complete (group 3, 36.9%) disappearance of the categorical features of PCOS (hyperandrogenism, menses, and ovulatory dysfunctions). Duration of the follow-up and extent of weight loss were similar among the three groups, as were fasting and glucose-stimulated insulin and indices of insulin resistance. Baseline waist circumference, waist to hip ratio (WHR), and androstenedione blood levels were negatively correlated with a better outcome in the univariate analysis. However, only basal androstenedione values persisted to a highly significant extent (P!0.001) in the multivariate analysis. Conclusions: Responsiveness to weight loss in overweight/obese PCOS women varies considerably and more than one third of women may achieve full recovery. These findings add new perspectives to the impact of obesity on the pathophysiology of PCOS.
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