CONTEXT: Chitosan, a deacetylated chitin, is a widely available dietary supplement purported to decrease body weight and serum lipids through gastrointestinal fat binding. Although evaluated in a number of trials, its efficacy remains in dispute. OBJECTIVE: To evaluate the efficacy of chitosan for weight loss in overweight and obese adults. Participants were randomly assigned to receive 3 g chitosan/day (n ¼ 125) or placebo (n ¼ 125). All participants received standardised dietary and lifestyle advice for weight loss. Adherence was monitored by capsule counts. MAIN OUTCOME MEASURES: The primary outcome measure was change in body weight. Secondary outcomes included changes in body mass index, waist circumference, body fat percentage, blood pressure, serum lipids, plasma glucose, fat-soluble vitamins, faecal fat, and health-related quality of life. RESULTS:In an intention-to-treat analysis with the last observation carried forward, the chitosan group lost more body weight than the placebo group (mean (s.e.), À0.4 (0.2) kg (0.4% loss) vs þ 0.2 (0.2) kg (0.2% gain), P ¼ 0.03) during the 24-week intervention, but effects were small. Similar small changes occurred in circulating total and LDL cholesterol, and glucose (Po0.01). There were no significant differences between groups for any of the other measured outcomes. CONCLUSION: In this 24-week trial, chitosan treatment did not result in a clinically significant loss of body weight compared with placebo.

The present study demonstrated a prolonged lag phase and delayed gastric emptying in obese women when compared to lean women. This delay may be as a consequence of high-fat diets, a sedentary lifestyle and increased gastric distension associated with obesity, or a contributing factor in the pathogenesis of obesity resulting from the inactivation of gastrointestinal satiety signals and in an increase in food intake.

OBJECTIVES: To investigate the in¯uences of inactivity and dietary macronutrient composition on energy and fat balance and to look for interactions between them. DESIGN: Two-day measurements of energy expenditure and substrate oxidation on ®ve occasions; ad libitum food intake from diets of 35% and 60% energy as fat, with and without imposed activity, and a ®xed overfeeding at 35% fat with free activity. SUBJECTS: Eight normal-weight male volunteers. MEASUREMENTS: Energy expenditure and substrate oxidation by indirect whole-body calorimetry, and macronutrient intakes from food consumption on ad libitum regimens. RESULTS: Subjects consumed the same energy, mean 11.6 MJad, regardless of activity level, on the 35% diet. Subjects consumed more energy on the 60% than the 35% diet, mean 14 vs 11.6 MJad. Inactivity induced a strong positive energy balance: 5.1 (60% diet), and 2.6 MJad (35% diet). Energy balance with activity was not signi®cantly different between diets, nor signi®cantly different from zero: 1.1 MJad (60% diet), and 7 0.2 MJad (35% diet). When intentionally overfed, subjects failed to compensate by raising voluntary activity. CONCLUSION: Energy intake was not regulated over a 2-day period in response to either imposition of inactivity or a high-fat diet. Activity proved essential to the avoidance of signi®cant positive energy balance.

Objective: Ghrelin and leptin play a role in control of food intake and adiposity but mechanisms regulating these hormones in man are poorly defined and evidence that dietary fats may have adverse effects is inconclusive. We investigated whether high-fat meals, which differed in saturated fatty acid (SFA) content acutely modified these hormones. Design: Randomised, double-blind, crossover trial. A high-fat (HF) test meal (5974 g fat; 71% of energy as fat) was given for breakfast on two occasions. Meals comprised either high (B70:30) or low (B55:45) saturated:unsaturated fatty acid (SFA:USFA) ratio. Fasting and postprandial measurements of serum total ghrelin (RIA), leptin (enzyme-linked immunosorbent assay (ELISA)) and insulin (RIA) were made over 6 h. Postprandial measurements were also made at 10 and 24 h following a fat-exclusion lunch, snack and dinner. Subjects: A total of 18 lean, healthy men. Results: There was no significant effect of the fatty meal (time, P40.05), nor a differential effect of SFA:USFA ratio (treatment * time, P40.05) on ghrelin over 6 h. Leptin decreased in response to both HF treatments (time, Po0.001) but increased SFA content did not further inhibit hormone secretion (treatment * time, P40.05). There was no significant correlation between ghrelin or leptin and circulating insulin (P40.05). Conclusion:We conclude that HF diets may adversely effect serum leptin, although the circadian decrease may account in part for this response. Increasing dietary SFAs had no deleterious effects on leptin or total ghrelin.