Night eating syndrome is associated with depression, low self-esteem, reduced daytime hunger, and less weight loss in obese outpatients.

OBJECTIVE: The objective of this study was to assess the relationship between the night eating syndrome (NES), measures of depression and self-esteem, test meal intake, and weight loss in obese participants. RESEARCH METHODS AND PROCEDURES: The study included 76 overweight (body mass index = 36.7 +/- 6.5 SD) outpatients (53 women and 23 men; aged 43.5 +/- 9.5 years) entering a weight loss program. They completed a Night Eating Questionnaire, the Zung Depression Inventory, and the Rosenberg Self-Esteem SCALE: Based on criteria by Stunkard et al. (Stunkard A, Berkowitz R, Wadden T, Tanrikut C, Reiss E, Young L. Binge eating disorder and the night eating syndrome. Int J Obes Relat Metab DISORD: 1996;20:1-6), participants had NES if they reported: (1) skipping breakfast > or =4 d/wk, interpreted as morning anorexia; (2) consuming more than 50% of total daily calories after 7 PM; and (3) difficulty falling asleep or staying asleep > or =4 d/wk. Eleven (14%) participants met the criteria for NES. After an 8-hour fast, all participants ingested a nutritionally complete liquid meal through a straw from a large opaque cooler until extremely full. They also completed ratings of hunger and fullness before and after this meal. RESULTS: Night eaters had higher depression (p = 0.04), lower self-esteem (p = 0.003), and less hunger (p = 0.005), and a trend for more fullness (p = 0.06) before the daytime test meal than the others. However, there were no significant differences in test-meal intake between groups. Nevertheless, test-meal intake was greater later in the day only for the night eaters (p = 0.01). Over a 1-month period, the night eaters lost less weight (4.4 +/- 3.2 kg) than the others (7.3 +/- 3.2 kg; p = 0.04), after controlling for body mass index. DISCUSSION: NES is a syndrome with distinct psychopathology and increased food intake later in the day, both of which may contribute to poorer weight loss outcome. NES criteria need to be better quantified and NES deserves consideration as a diagnostic eating disorder.

Weight Loss-associated changes in acute effects of nateglinide on insulin secretion after glucose loading: results of glucose loading on 2 consecutive days.

AIM: The aim of this study was to investigate the influence of changes in insulin resistance and early insulin secretion on the insulin secretagogic effects of nateglinide. METHODS: Oral glucose tolerance testing (OGTT, 75 g) was performed in obese patients before and after weight loss on 2 consecutive days (first day OGTT without nateglinide, second day OGTT with nateglinide), to compare any weight loss associated changes in the nateglinide-induced insulin response to glucose loading. RESULTS: Reductions in visceral fat, liver fat, skeletal muscle fat and homeostasis model assessment (HOMA)-R due to weight loss were associated with increased Delta insulin 30 min/Delta glucose 30 min (DeltaI30/DeltaG30), and reduced area under the curve (AUC) for plasma glucose as seen in OGTT results. Results from OGTT showed that nateglinide administration was associated with reductions in plasma glucose AUC, both before and after weight loss. Before weight loss, although there was a significant elevation of DeltaI30/DeltaG30 associated with nateglinide treatment, no major change in the insulin-secreting dynamics after glucose loading was observed. After weight loss, nateglinide administration produced a significant increase in DeltaI30/DeltaG30, with insulin secretion peaking more quickly. CONCLUSION: Insulin response to nateglinide after glucose loading varied greatly in conjunction with weight loss. This may be accounted for not only by the enhancement of early insulin response to nateglinide associated with the improvement of early insulin response with weight loss but also by the reduced visceral fat, which in turn led to reduced levels of free fatty acids in portal blood and hepatic triglycerides, as well as increased hepatic insulin clearance.

Leptin levels are associated with fat oxidation and dietary-induced weight loss in obesity.

OBJECTIVE: To examine the relationship between fasting plasma leptin and 24-hour energy expenditure (EE), substrate oxidation, and spontaneous physical activity (SPA) in obese subjects before and after a major weight reduction compared with normal weight controls. To test fasting plasma leptin, substrate oxidations, and SPA as predictive markers of success during a standardized weight loss intervention. RESEARCH METHODS AND PROCEDURES: Twenty-one nondiabetic obese (body mass index: 33.9 to 43.8 kg/m(2)) and 13 lean (body mass index: 20.4 to 24.7 kg/m(2)) men matched for age and height were included in the study. All obese subjects were reexamined after a mean weight loss of 19.2 kg (95% confidence interval: 15.1-23.4 kg) achieved by 16 weeks of dietary intervention followed by 8 weeks of weight stability. Twenty-four-hour EE and substrate oxidations were measured by whole-body indirect calorimetry. SPA was assessed by microwave radar. RESULTS: In lean subjects, leptin adjusted for fat mass (FM) was correlated to 24-hour EE before (r = -0.56, p < 0.05) but not after adjustment for fat free mass. In obese subjects, leptin correlated inversely with 24-hour and resting nonprotein respiratory quotient (r = -0.47, p < 0.05 and r = -0.50, p < 0.05) both before and after adjustments for energy balance. Baseline plasma leptin concentration, adjusted for differences in FM, was inversely related to the size of weight loss after 8 weeks (r = -0.41, p = 0.07), 16 weeks (r = -0.51, p < 0.05), and 24 weeks (r = -0.50, p < 0.05). DISCUSSION: The present study suggests that leptin may have a stimulating effect on fat oxidation in obese subjects. A low leptin level for a given FM was associated with a greater weight loss, suggesting that obese subjects with greater leptin sensitivities are more successful in reducing weight.

Are meal replacements an effective strategy for treating obesity in adults with features of metabolic syndrome?

Background - Meal replacements as a weight loss strategy are widely used, however their effectiveness outside controlled clinical trial environments is unknown. Objective - To compare meal replacements with a structured weight reduction diet in overweight/obese Australians with raised triglycerides. Design - In a randomised parallel design, 2 groups [Meal Replacement (MR) and Control (C)] of 66 matched subjects underwent a 6000kj intervention for 3 months (stage 1) and a further 3 months (stage 2). Groups were provided oral and written information. C was supplied shopping vouchers and followed a low fat/energy diet. MR was supplied Slimfast(tm) product for two meals (1800kj) and consumed a low fat evening meal. Clients were weighed every 2-wk, received structured supervision without professional dietary input, with compliance assessed by 3d-weighed food records. Blood biomarkers assessed fruit/vegetable intake and questionnaire assessed attitudes to treatment. Outcomes - Fifty-five subjects completed stage 1 and 42 stage 2. Mean weight loss was comparable in both groups at 3 months (6.0+/-4.2 kg +/- sem MR, 6.6+/-3.4 kg C) and at 6 months (9.0+/-6.9 kg MR, 9.2+/-5.1 kg C). Serum folate and plasma beta-carotene were higher in MR, and plasma homocysteine fell in both groups. Diets were nutritionally adequate in both groups, but some nutrient intakes were higher in MR than C. The MR program was viewed by subjects remaining in the study as acceptable and convenient, thereby aiding compliance. Conclusions - A meal replacement program is equally effective for losing weight compared to a conventional but structured weight loss diet. Meal replacements offer a convenient and potentially nutritionally beneficial weight loss alternative than conventionally structured weight loss diets.

Performance status of male and female advanced cancer patients is independently predicted by mid-upper arm circumference measurement.

In the advanced cancer patient, performance status has considerable prognostic power. Karnofsky performance status, together with variables reported to influence its score, was measured in advanced gastrointestinal cancer patients (n = 148). For male and female patients, age, body mass index, weight loss, triceps skinfold thickness, mid-upper arm circumference, albumin, C-reactive protein, and tumor type and stage were regressed against Karnofsky performance status. On multiple regression analysis, only mid-upper arm circumference and log10 C-reactive protein in men (r2 = 0.462, P < 0.0001) and only mid-upper arm circumference and weight loss in women (r2 = 0.485, P < 0.01) were independent predictors of Karnofsky performance status. There was a significant partial correlation, with gender as a covariable, between log10 C-reactive protein and albumin (r = -0.530, P < 0.0001) and mid-upper arm circumference (r = -0.269, P = 0.035) and weight loss (r = 0.286, P = 0.024). The results of the present study indicate that mid-upper arm circumference is a major factor that influences performance status in male and female patients with advanced gastrointestinal cancer.

The enigma of increased non-cancer mortality after weight loss in healthy men who are overweight or obese.

OBJECTIVE: To study effects on non-cancer mortality of observational weight loss in middle-aged men stratified for body mass index (BMI), taking a wide range of possible confounders into account. DESIGN: Prospective, population based study. SETTING: Male population of Malmo, Sweden. PARTICIPANTS: In all 5722 men were screened twice with a mean time interval of 6 years in Malmo, southern Sweden. They were classified according to BMI category at baseline (<21, 22-25, overweight: 26-30, and obesity: 30+ kg m(-2)) and weight change category until second screening (weight stable men defined as having a baseline BMI +/- 0.1 kg m(-2) year-1 at follow-up re-screening). MAIN OUTCOME MEASURES: Non-cancer mortality calculated from national registers during 16 years of follow-up after the second screening. Data from the first year of follow-up were excluded to avoid bias by mortality caused by subclinical disease at re-screening. RESULTS: The relative risk (RR; 95% CI) for non-cancer mortality during follow-up was higher in men with decreasing BMI in all subgroups: RR 2.64 (1.46-4.71, baseline BMI <21 kg m(-2)), 1.39 (0.98-1.95, baseline BMI 22-25 kg m(-2)), and 1.71 (1.18-2.47, baseline BMI 26+ kg m(-2)), using BMI-stable men as reference group. Correspondingly, the non-cancer mortality was also higher in men with increasing BMI, but only in the obese group (baseline BMI 26+ kg m(-2)) with RR 1.86 (1.31-2.65). In a subanalysis, nonsmoking obese (30+ kg m(-2)) men with decreased BMI had an increased non-cancer mortality compared with BMI-stable obese men (Fischer's test: P=0.001). The mortality risk for nonsmoking overweight men who increased their BMI compared with BMI-stable men was also significant (P=0.006), but not in corresponding obese men (P=0.094). CONCLUSIONS. weight loss in self-reported healthy but overweight middle-aged men, without serious disease, is associated with an increased non-cancer mortality, which seems even more pronounced in obese, nonsmoking men, as compared with corresponding but weight-stable men. The explanation for these observational findings is still enigmatic but could hypothetically be because of premature ageing effects causing so-called weight loss of involution.

Weight Loss in rats exposed to repeated acute restraint stress is independent of energy or leptin status.

Acute release of corticotropin-releasing factor (CRF) during repeated restraint (3-h restraint on each of 3 days) causes temporary hypophagia but chronic suppression of body weight in rats. Here we demonstrated that a second bout of repeated restraint caused additional weight loss, but continuing restraint daily for 10 days did not increase weight loss because the rats adapted to the stress. In these two studies serum leptin, which suppresses the endocrine response to stress, was reduced in restrained rats. Peripheral infusion of leptin before and during restraint did not prevent stress-induced weight loss, although stress-induced corticosterone release was suppressed. Restrained rats were hyperthermic during restraint, but there was no evidence that fever or elevated free interleukin-6 caused the sustained reduction in weight. Restraining food-restricted rats caused a small but significant weight loss. Food-restricted rats fed ad libitum after the end of restraint showed a blunted hyperphagia and slower rate of weight regain than their controls. These results indicate that repeated acute stress induces a chronic change in weight independent of stress-induced hypophagia and may represent a change in homeostasis initiated by repeated acute activation of the central CRF system.

Weight Loss and weight maintenance, ambulatory blood pressure and cardiac autonomic tone in obese persons with the metabolic syndrome.

BACKGROUND: Cardiac autonomic function may play a role in obesity-associated hypertension. Most studies on the effects of weight loss on blood pressure and autonomic function do not distinguish between acute or continuing weight loss and steady-state weight maintenance after weight loss. OBJECTIVES: We sought to clarify the changes in ambulatory blood pressure, heart rate and heart rate variability as assessed by spectral analysis during rapid weight loss and extended weight maintenance. PARTICIPANTS: Abdominally obese (body mass index 35.2 +/- 2.1 kg/m2, waist 114.3 +/- 9.0 cm) men and women (n = 41) with the metabolic syndrome. METHODS AND RESULTS: The 34 men and women completing the 1-year weight maintenance period lost 14.6 +/- 3.5 kg during the 9-week very-low-calorie diet and maintained a 12.5 +/- 7.5 kg weight loss to the end of the trial. Ambulatory 24-h blood pressure decreased dramatically during the diet (-9.0 +/- 8.0/-4.6 +/- 4.9 mmHg), but had risen to near baseline levels by the end of weight maintenance (-2.2 +/- 8.2 /-1.2 +/- 6.1 mmHg). Night-time heart rate decreased (-5.5 +/- 9.6 beats/min, P = 0.012), and heart rate variability total and low-frequency power measured during 5 min of controlled breathing increased by 46-56% (P = 0.003-0.09) during rapid weight loss. These changes gradually attenuated during weight maintenance, and only the change in night-time heart rate was still of borderline significance after 1 year of weight maintenance (-3.6 +/- 8.6 beats/min, P = 0.063). Heart rate variability high-frequency power tended to increase during weight loss and weight maintenance. CONCLUSION: Despite successful weight maintenance, the decrease in ambulatory blood pressure after rapid weight loss was largely transient. The increase in parasympathetic tone was more sustained, but also gradually attenuated during 1 year of weight maintenance.