Effects of bariatric surgery on night eating and depressive symptoms: a prospective study.

BACKGROUND: Night eating syndrome (NES) is characterized by a delayed pattern of food intake and is clinically defined by the presence of evening hyperphagia, nocturnal ingestion, morning anorexia, and sleep problems. Although most studies report an association of obesity, depressive mood, and NES, very little is known about the impact of bariatric surgery in the course of this syndrome, particularly in patients with depressive symptoms. OBJECTIVES: To assess the effects of bariatric surgery on night eating and depressive symptoms. SETTING: Tertiary hospital, Brazil. METHODS: Sixty patients consecutively submitted to bariatric surgery were included in the study. Baseline depressive symptoms were assessed by the Beck Depression Inventory-Short Form (BDI-SF) and night eating by the Night Eating Questionnaire. Measurements were repeated postoperatively for comparison. RESULTS: Participants were predominantly female (M/F = 9/51). Mean (±SD) age was 34.7±9.2 years and body mass index was 46.04±7.52 kg/m². On average, BDI-SF scores improved after bariatric surgery (9.77±7.01 versus 4.70±4.60; P = .001). Patients with baseline depressive symptoms (BDI-SF>4), in contrast to those without, showed a significant improvement in Night Eating Questionnaire scores (16.03±7.73 versus 12.80±7.76; P = .01), despite a similar postoperative reduction in weight. CONCLUSION: Bariatric surgery is associated with a reduction in depressive symptoms. After the surgical intervention, improvement of night eating can be observed predominantly in patients with preoperative depressive symptoms. These findings are consistent with the hypothesis of an important role of mood problems in NES.

Effect of exogenous melatonin on sleep and motor dysfunction in Parkinson's disease. A randomized, double blind, placebo-controlled study.

Insomnia, sleep fragmentation and excessive daytime sleepiness are common in Parkinson's disease (PD) and may contribute to the reduction of cognition and alertness in those patients. Melatonin has been shown to improve sleep in several conditions. In experimental models of PD, melatonin can ameliorate motor symptoms. To evaluate the effect of melatonin on sleep and motor dysfuntion in PD, we studied 18 patients (Hoehn & Yahr I to III) from a PD clinic. Prior to treatment, motor dysfunction was assessed by UPDRS II, III and IV. Subjective sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI) and daytime somnolence by the Epworth Sleepiness Scale (ESS). Full polysomnography (PSG) was performed in all subjects. Patients were then randomized to receive melatonin (3mg) or placebo one hour before bedtime for four weeks. All measures were repeated at the end of treatment. On initial assessment, 14 patients (70%) showed poor quality sleep (PSQI > 6) and eight (40%) excessive daytime sleepiness (ESS > 10). Increased sleep latency (50%), REM sleep without atonia (66%), and reduced sleep efficiency (72%) were found on PSG. Eight patients had an apnea/ hipopnea index greater than 15 but no severe oxygen desaturation was observed. Sleep fragmentation tended to be more severe in patients on lower doses of levodopa (p = 0.07). Although melatonin significantly improved subjective quality of sleep (p = 0.03) as evaluated by the PSQI index, PSG abnormalities were not changed. Motor dysfunction was not improved by the use of melatonin. Undetected differences in motor scores and PSG findings may have been due to a small sample size and a type II error.