BACKGROUND: Modifying diet, exercise, sunlight exposure and sleep patterns may be useful in the treatment of depression. METHOD: Eighty nonseasonal depressive outpatients on anti-depressant treatment were randomly assigned either to the active or control group. Four hygienic-dietary recommendations were prescribed together. Outcome measures were blinded assessed before and after the six month intervention period. RESULTS: A better evolution of depressive symptoms, a higher rate of responder and remitters and a lesser psychopharmacological prescription was found in the active group. LIMITATIONS: Small sample size. Lacked homogeneity concerning affective disorders (major depression, dysthimia, bipolar depression). CONCLUSIONS: This study suggests lifestyle recommendations can be used as an effective antidepressant complementary strategy in daily practice.

BACKGROUND: The aim of the present study was to determine the mechanisms underlying Type 2 diabetes remission after gastric bypass (GBP) surgery by characterizing the short- and long-term changes in hormonal determinants of blood glucose. METHODS: Eleven morbidly obese women with diabetes were studied before and 1, 6, and 12 months after GBP; eight non-diabetic morbidly obese women were used as controls. The incretin effect was measured as the difference in insulin levels in response to oral glucose and to an isoglycemic intravenous challenge. Outcome measures were glucose, insulin, C-peptide, proinsulin, amylin, glucagon, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1) levels and the incretin effect on insulin secretion. RESULTS: The decrease in fasting glucose (r = 0.724) and insulin (r = 0.576) was associated with weight loss up to 12 months after GBP. In contrast, the blunted incretin effect (calculated at 22%) that improved at 1 month remained unchanged with further weight loss at 6 (52%) and 12 (52%) months. The blunted incretin (GLP-1 and GIP) levels, early phase insulin secretion, and other parameters of beta-cell function (amylin, proinsulin/insulin) followed the same pattern, with rapid improvement at 1 month that remained unchanged at 1 year. CONCLUSIONS: The data suggest that weight loss and incretins may contribute independently to improved glucose levels in the first year after GBP surgery.

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The goal of this study was to understand the mechanisms of greater weight loss by gastric bypass (GBP) compared to gastric banding (GB) surgery. Obese weight- and age-matched subjects were studied before (T0), after a 12 kg weight loss (T1) by GBP (n = 11) or GB (n = 9), and at 1 year after surgery (T2). peptide YY(3-36)(PYY(3-36)), ghrelin, glucagon-like peptide-1 (GLP-1), leptin, and amylin were measured after an oral glucose challenge. At T1, glucose-stimulated GLP-1 and PYY levels increased significantly after GBP but not GB. Ghrelin levels did not change significantly after either surgery. In spite of equivalent weight loss, leptin and amylin decreased after GBP, but not after GB. At T2, weight loss was greater after GBP than GB (P = 0.003). GLP-1, PYY, and amylin levels did not significantly change from T1 to T2; leptin levels continued to decrease after GBP, but not after GB at T2. Surprisingly, ghrelin area under the curve (AUC) increased 1 year after GBP (P = 0.03). These data show that, at equivalent weight loss, favorable GLP-1 and PYY changes occur after GBP, but not GB, and could explain the difference in weight loss at 1 year. Mechanisms other than weight loss may explain changes of leptin and amylin after GBP.

PURPOSE OF REVIEW: Chronic stress, combined with positive energy balance, may be a contributor to the increased risk for obesity, especially upper body obesity, and other metabolic diseases. This association may be mediated by alterations in the hypothalamic-pituitary-adrenal (HPA) axis. In this review, we summarize the major research that has been conducted on the role of the HPA axis in obesity and metabolic disease. RECENT FINDINGS: Dysregulation in the HPA axis has been associated with upper body obesity, but data are inconsistent, possibly due to methodological differences across studies. In addition to systemic effects, changes in local cortisol metabolism in adipose tissue may also influence the risk for obesity. HPA axis dysregulation may be the causal link between conditions such as maternal malnutrition and sleep deprivation with metabolic disease. SUMMARY: The present review provides evidence for the relationship between chronic stress, alterations in HPA activity, and obesity. Understanding these associations and its interactions with other factors will be important in developing effective treatments for obesity and related metabolic diseases.

OBJECTIVE:: To examine the effect of an equivalent weight loss, by gastric bypass surgery (GBP) or by diet, on peptide YY3-36 (PYY3-36), ghrelin, and leptin levels and to determine the effect of diabetes status on PYY3-36 levels. SUMMARY BACKGROUND DATA:: The increased PYY3-36 levels after GBP may be involved in the magnitude and the sustainability of weight loss after surgery. METHODS:: Of the 30 morbidly obese women who participated in the study, 21 had type 2 diabetes mellitus, and were studied before and after equivalent weight loss of 10 kg by either GBP (n = 11) or by diet (n = 10). RESULTS:: PYY3-36 levels were higher in obese diabetic as compared with nondiabetic individuals (64.1 +/- 34.4 pg/mL vs. 39.9 +/- 21.1 pg/mL; P < 0.05). PYY3-36 levels increased markedly in response to oral glucose after GBP (peak: 72.3 +/- 20.5 pg/mL-132.7 +/- 49.7 pg/mL; P < 0.001; AUC0-180: 51.5 +/- 23.3 pg/mL.min-91.1 +/- 32.2 pg/mL.min P < 0.001), but not after diet (peak: 85.5 +/- 51.9 pg/mL-84.8 +/- 41.13 pg/mL; P = NS; AUC0-180: 68.3 +/- 38.5 pg/mL.min-61.1 +/- 42.2 pg/mL.min P = NS). Fasting ghrelin levels increased after diet (425 +/- 91 pg/mL-519 +/- 105 pg/mL; P < 0.05), but did not change after GBP (506 +/- 121 pg/mL-482 +/- 196 pg/mL; P = NS). CONCLUSIONS:: Diabetes status seems to be a determinant of PYY3-36 levels. GBP, but not diet-induced weight loss, resulted in markedly increased glucose-stimulated PYY3-36 levels. The increase in stimulated PYY3-36 levels after GBP is likely a result of the surgery rather than a secondary outcome of weight loss. Changes in PYY3-36 levels and ghrelin could contribute to the success of GBP in sustaining weight loss.

Gastric bypass surgery (GBP), in addition to weight loss, results in dramatic remission of type 2 diabetes (T2DM). The mechanisms by which this remission occurs are unclear. Besides weight loss and caloric restriction, the changes in gut hormones that occur after GBP are increasingly gaining recognition as key players in glucose control. Incretins are gut peptides that stimulate insulin secretion postprandially; the levels of these hormones, particularly glucagon-like peptide-1, increase after GBP in response to nutrient stimulation. Whether these changes are causal to changes in glucose homeostasis remain to be determined. The purpose of this review is to assess the evidence on incretin changes and T2DM remission after GBP, and the possible mechanisms by which these changes occur. Our goals are to provide a thorough update on this field of research so that recommendations for future research and criteria for bariatric surgery can be evaluated.

Context: Gastric bypass surgery (GBP) results in rapid weight loss, improvement of type 2 diabetes (T2DM) and increase in incretins levels. Diet-induced weight loss also improves T2DM and may increase incretin levels. Objective: To determine whether the magnitude of the change of the incretin levels and effect is greater after GBP compared to a low caloric diet, after equivalent weight loss. Design and Methods: Obese women with T2DM studied before and 1 month after GBP (n=9) or after a diet-induced equivalent weight loss (n=10). Patients from both groups were matched for age, body weight, BMI, diabetes duration and control, and amount of weight loss. Setting: Outpatient GCRC. Main Outcome Measures: Glucose, insulin, proinsulin, glucagon, GIP and GLP-1 levels were measured after 50 gr oral glucose. The incretin effect was measured as the difference in insulin levels in response to oral and to an isoglycemic iv glucose load. Results: At baseline, none of the outcome variables (fasting and stimulated values) were different between the GBP and the diet group. Total GLP-1 levels after oral glucose markedly increased 6 times (peak:17+/-6 to 112+/-54 pmol/L, p<0.001) and the incretin effect increased 5 times (9.4+/-27.5% to 44.8+/-12.7%, p<0.001) after GBP but not after diet. Post-prandial glucose levels (p=0.001) decreased more after GBP. Conclusions: These data suggest that early after GBP, the greater GLP-1 and GIP release and improvement of incretin effect are related not to weight loss but rather to the surgical procedure. This could be responsible for better diabetes outcome after GBP.

OBJECTIVE: The aim of this paper is to assess personality disorder (PD) comorbidity in somatization disorder (SD) patients compared with psychiatric controls in a Spanish sample. METHODS: This is a case-control study. Selection of 70 consecutive SD patients was made, and an age-, sex-, and ethnic-group-matched control group of 70 mood and/or anxiety disorder patients recruited in psychiatric outpatient clinics was selected. PDs were measured using the International Personality Disorder Examination, and Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Axis I morbidity was measured by means of the Standardized Polyvalent Psychiatric Interview. RESULTS: PD comorbidity in SD patients was 62.9%, compared to 28.2% in controls [odds ratio (OR)=3.7; 95% confidence interval (95% CI)=1.8-7.6]. The highest ORs of PD in SD patients, compared with controls, were for paranoid (OR=9.2; 95% CI=1.9-43), obsessive-compulsive (OR=6.2; 95% CI=1.2-53.6), and histrionic (OR=3.6; 95% CI=0.9-13.9) PDs. CONCLUSIONS: This is a controlled study with the largest sample of SD patients. The prevalence of PD comorbidity is similar to that of a previously published controlled study but is different from those of the most frequent PD subtypes.