Restrained Eating im Zusammenhang mit dem Leptin- und Insulinserumspiegel bei einem untergewichtigen Probandenkollektiv

The term “restrained eating” was first introduced to the literature in 1975. Restrained eating describes the cognitive control of food intake and the override of physiological sensation of hunger with the ambition to loose or maintain weight through the reduced caloric intake. Several studies exist that demonstrate a connection between restrained eating and the adipocyte derived hormone leptin. For example, von Prittwitz et al. (1997) found a significant correlation between underweight restrained eaters and their serum leptin levels. The authors were able to show that female underweight restrained eaters have lower serum leptin levels than female underweight unrestrained eaters. On the contrary, in the entire study group (i.e., female and male subjects), no significant correlation between restrained and unrestrained eaters was found. This dissertation aimed to further examine the results from the study group by von Prittwitz et al. (1997) with an independent cohort of 121 underweight subjects (n = 84 females; n = 37males; ≤ 15. BMI percentile). As a control group, 100 normal weight subjects (n = 72 females; n = 28 males; 40. - 60. BMI percentile) were recruited. This resulted in a study group of 156 women and 65 men between the ages of 20 to 30 years old. The “Fragebogen zum Essverhalten”, the German version of the “Three-Factor Eating Questionnaire” was used to screen for restrained eating. The main hypothesis of this dissertation is that underweight restrained eaters have lower serum leptin levels than underweight unrestrained eaters. Since the literature also reports on a connection between restrained eating and insulin levels, our second hypothesis is that underweight restrained eaters have lower serum insulin levels than underweight unrestrained eaters. In the entire sample of underweight subjects, no significant correlation between the cognitive control of food intake and the serum leptin levels could be found. Even when divided into gender subgroups, no significant correlation between the cognitive control of food intake and serum leptin levels could be seen for underweight female subjects (r = - 0.129, p = 0.243) or underweight male subjects (r = 0.116, p = 0.496). After adjusting for BMI, a significant correlation between the cognitive control of food intake and serum leptin levels was revealed for the female underweight subjects only (r = 0.504, p = 0.033). The analyses of the results could not demonstrate a significant correlation between the cognitive control of food intake and serum insulin levels for the underweight group; r = - 0.026, p = 0.783. The separate examination of the female and male underweight subgroups was also not able to show a significant correlation between the cognitive control of food intake and serum insulin levels (r = 0.119, p = 0.291 for females; r = 0.084, p = 0.647 for males). In summary, neither the main hypothesis about the correlation between the cognitive control of food intake and serum leptin levels nor the second hypothesis about the correlation between the cognitive control of food intake and serum insulin levels could be verified. However, like in the study by von Prittwitz et al. (1997), a significant correlation between the cognitive control of food intake and serum leptin levels was demonstrated for the female underweight subjects, although this was only apparent after adjustment for BMI. More studies are needed that examine the relationship between cognitive control of food intake and leptin and insulin serum levels. Such studies should involve a greater number of patients and take to consideration the potential confounds of BMI and % body fat.