Feasibility of a novel wearable thermal device for management of bothersome hot flashes in patients with prostate cancer.

Background: This single-arm prospective study evaluated the feasibility of a novel wrist-worn thermal device that applies cooling to the inside of the wrist for management of bothersome hot flashes in prostate cancer survivors.

Methods: 57 individuals were enrolled and instructed to use the thermal device as needed for management of hot flashes for 4 weeks. The primary outcome was thermal device usage (hours and sessions per day).

Stress-associated weight gain, fibromyalgia symptoms, cardiometabolic markers, and human growth hormone suppression respond to an amino acid supplement blend: Results of a prospective, cohort study.

Introduction: An orally administered amino acid-based test supplement was recently shown to increase human growth hormone (hGH) in healthy adults. This prospective, observational, single-center, single-arm cohort study investigated the effects of 24 weeks of daily oral administration of the test supplement in individuals with stress-related weight gain, fibromyalgia (FM) and stress-related low-normal hGH production (15-30 percentile for age-appropriate levels) on insulin-like growth factor 1 (IGF-1), an indicator of hGH levels caused by stress related stimulation of somatostatin.

Methods: Participants continued to receive standard care.

Effect of time restricted eating on body weight and fasting glucose in participants with obesity: results of a randomized, controlled, virtual clinical trial.

Background: Time restricted eating (TRE) is an emerging dietary intervention for weight loss that is hypothesized to reinforce the metabolic benefits of nightly fasting/ketosis. This pilot study investigated the effectiveness of a daily 14-h metabolic fast (14:10 TRE beginning after dinner, a "fasting snack" at hour 12, and ending with breakfast 14 h later) combined with a commercial weight management program on body weight and fasting blood glucose (FBG) in individuals with obesity. We also investigated the effect of the low-calorie, high-fat, low-carbohydrate, and low-protein "fasting snack" on blood glucose.

Naltrexone/bupropion for obesity: an investigational combination pharmacotherapy for weight loss.

The mechanism of action of the combination therapy, naltrexone/bupropion (NB), for obesity has not been fully described to date. Weight loss attempts rarely result in long-term success. This is likely a result of complex interactions among multiple peripheral and CNS systems that defend against weight loss, and may explain the overwhelming lack of effective obesity treatments.

Leptin reduces food intake via a dopamine D2 receptor-dependent mechanism.

Food intake is generally accepted to be regulated by the melanocortin system, however recent data suggests that mesolimbic dopaminergic neurons also influence food intake. Whether dopamine signaling is crucial for the acute effect of leptin on feeding is unknown. Using pharmacological and genetic strategies, we tested the hypothesis that the acute inhibitory effect of leptin on food intake is partially mediated by dopamine.

Combination therapy with naltrexone and bupropion for obesity.

Introduction: Although pharmacological treatments for obesity represent only one option in managing obesity, they are a useful tool in an otherwise extremely limited armamentarium. Naltrexone/bupropion combination therapy was developed by using technological advances that have improved our understanding of how the brain regulates body weight.

Areas Covered: This review covers the development of naltrexone/bupropion combination therapy for obesity, as well as the published clinical trials on the safety and efficacy of the combination in overweight and obese humans.

An open-label study of naltrexone and bupropion combination therapy for smoking cessation in overweight and obese subjects.

A combination of sustained release (SR) naltrexone (32 mg/day) and bupropion SR (360 mg/day) plus behavioral counseling was evaluated for the treatment of smoking cessation and mitigation of nicotine withdrawal and weight gain. Thirty overweight or obese nicotine-dependent subjects were enrolled in a 24-week, open-label study; 85% and 63% completed 12 and 2 4weeks, respectively. The target quit date was Week 4.

Catecholamine reuptake inhibition causes weight loss by increasing locomotor activity and thermogenesis.

Bupropion (BUP) is a dopamine (DA) and norepinephrine (NE) reuptake inhibitor that causes mild weight loss in obese adults. Subchronic (7 day) coadministration of selective DA and NE reuptake inhibitors also causes weight loss in mice. Because weight loss was not associated with decreased caloric intake, subchronic BUP might cause weight loss through increased energy expenditure.

Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons.

Despite high leptin levels, most obese humans and rodents lack responsiveness to its appetite-suppressing effects. We demonstrate that leptin modulates NPY/AgRP and alpha-MSH secretion from the ARH of lean mice. High-fat diet-induced obese (DIO) mice have normal ObRb levels and increased SOCS-3 levels, but leptin fails to modulate peptide secretion and any element of the leptin signaling cascade.

Inhibition of dopamine and norepinephrine reuptake produces additive effects on energy balance in lean and obese mice.

Although originally developed as an antidepressant, long-term bupropion (BUP) treatment was recently shown to cause 5-8% weight loss over placebo in clinical trials with obese adults. BUP's antidepressant properties probably stem from its ability to increase extracellular brain dopamine (DA) and norepinephrine (NE) levels by inhibiting their reuptake, although the mechanism of BUP-induced weight loss is unknown. Consequently, the acute effects of DA and NE reuptake inhibition on energy homeostasis were determined by measuring food intake and body weight in mice following peripheral (intraperitoneal (i.

Peptide YY(3-36) inhibits morning, but not evening, food intake and decreases body weight in rhesus macaques.

Peptide YY(3-36) [PYY(3-36)] is a hormone that is released after meal ingestion that is currently being investigated for the treatment of obesity; however, there are conflicting reports of the effects of PYY(3-36) on energy balance in rodent models. To shed light on this controversy, we studied the effect of PYY(3-36) on food intake and body weight in a nonhuman primate. Intravenous PYY(3-36) infusions before a morning meal transiently suppressed the rate of food intake but did not suppress the evening meal or 24-h intake.