Objectives:To determine the effectiveness of a structured multidisciplinary non-surgical obesity therapy program on the basis of a temporary low-calorie-diet for 12 weeks, and additional intervention modules to enhance nutritional education, to increase physical activity and to modify eating behavior.Design:Prospective multicenter observational study in obese individuals undergoing a medically supervised outpatient-based 52-week treatment in 37 centers in Germany.Subjects:A total of 8296 participants with a body mass index (BMI) of >30 kg m−2 included within 8.5 years.Measurements:Main outcome measures were body weight loss, waist circumference (WC), blood pressure, quality of life and adverse events.Results:In females, initial body weight was reduced after the 1-year-intervention by 19.6 kg (95% confidence intervals 19.2–19.9 kg) and in males by 26.0 kg (25.2–26.8) according to per protocol analysis of 4850 individuals. Intention-to-treat (ITT) analysis revealed a weight reduction of 15.2 kg (14.9–15.6) in females and 19.4 kg (18.7–20.1) in males. Overall, the intervention resulted in mean reduction in WC of 11 cm; it reduced the prevalence of the metabolic syndrome by 50% and the frequency of hypertension from 47 to 29% of all participants (ITT, all P<0.001). The beneficial effects could be documented for up to 3 years and comprised significant improvement of health-related quality of life. The incidence of adverse effects was low; the only event repeatedly observed and possibly related to either the intervention or the underlying disease was biliary disorders.Conclusion:The present non-surgical intervention program is a highly effective treatment of obesity grades I–III and obesity-related diseases, and therefore, could be a valuable basis for future weight maintenance strategies required for sustained success.

Background/Aims: To assess the prevalence and correlates of addictive-like eating behavior in Germany. Methods: The German version of the Yale Food Addiction Scale (YFAS) 2.0 was used to investigate, for the first time, the prevalence of ‘food addiction' in a representative sample aged 18-65 years (N = 1,034). Results: The prevalence of ‘food addiction' measured by the YFAS 2.0 was 7.9%. Individuals meeting criteria for ‘food addiction' had higher BMI and were younger than individuals not meeting the threshold. Underweight (15.0%) and obese (17.2%) individuals exhibited the highest prevalence rate of ‘food addiction'. Addictive-like eating was not associated with sex, education level, or place of residence. Conclusion: YFAS 2.0 ‘food addiction' was met by nearly 8% of the population. There is a non-linear relationship between addictive-like eating and BMI, with the highest prevalence among underweight and obese persons. These findings suggest that ‘food addiction' may be a contributor to overeating but may also reflect a distinct phenotype of problematic eating behavior not synonymous with obesity. Further, the elevated prevalence of YFAS 2.0 ‘food addiction' among underweight individuals may reflect an overlap with eating disorders and warrants attention in future research.

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The concept of food addiction is currently a highly debated subject within both the general public and the scientific communities. The term food addiction suggests that individuals may experience addictive-like responses to food, similar to those seen with classic substances of abuse. An increasing number of studies have established the prevalence and correlates of food addiction. Moreover, food addiction may be associated with obesity and disordered eating. Thus, intervening on food addiction may be helpful in the prevention and therapy of obesity and eating disorders. However, controversy exists about if this phenomenon is best defined through paradigms reflective of Diagnostic and Statistical Manual of Mental Disorders (DSM-5) substance-related disorders (e.g. food addiction) or non-substance-related disorders (e.g. eating addiction) criteria. This review paper will give a brief summarisation of the current state of research on food addiction, a more precise definition of its classification, its differentiation from eating addiction and an overview on potential overlaps with eating disorders. Based on this review, there is evidence that food addiction may represent a distinct phenomenon from established eating disorders such as bulimia nervosa or binge-eating disorder. Future studies are needed to further examine and establish orthogonal diagnostic criteria specific to food addiction. Such criteria must differentiate the patterns of eating and symptoms that may be similar to those of eating disorders to further characterise food addiction and develop therapy options. To date, it is too premature to draw conclusions about the clinical significance of the concept of food addiction.

Clinical studies have shown that elevated leptin levels are an independent cardiovascular risk factor. However, little is known about the existence of platelet resistance to leptin in the setting of obesity. We examined the effects of leptin on platelet aggregation in morbidly obese subjects (n = 40; BMI, 41.6 +/- 1.1 kg/m2; leptin, 49.7 +/- 3.4 ng/ml) in comparison to normal-weight controls (n = 36; BMI, 23.3 +/- 0.4 kg/m2; leptin, 6.5 +/- 0.7 ng/ml). The aggregatory response to increasing concentrations of adenosine diphosphate (ADP) (2, 3, 4, and 5 microM) was significantly increased in platelets from obese compared to lean donors, reflecting a left shift in the dose-response curve. Plasma leptin levels, but not BMI, were significantly higher in subjects with stronger (above the median) compared to weaker (below the median) platelet aggregation at all ADP concentrations tested. In further experiments, stimulation (preincubation) with leptin (500 ng/ml) promoted ADP-induced platelet aggregation by approximately 25%, and there was no difference between platelets from obese and those from lean donors regarding the responsiveness to leptin (p = 0.99). Western blotting revealed that leptin induced phosphorylation of JAK2 and STAT3 to a similar extent in platelets from both groups. Expression of potential mediators of leptin resistance (SOCS3 and PTP1B) also did not differ in platelets from obese and control subjects. In conclusion, our data indicate that platelets from obese donors show increased aggregatory response to ADP, and that this might partly be the consequence of increased circulating leptin levels. Platelets from obese donors are not resistant to the enhancing effects of leptin on ADP-induced platelet aggregation.