Eating dependence and weight gain; no human evidence for a ‘sugar-addiction’ model of overweight

BACKGROUND AND AIMS: There is an increasing societal concern that consumption of specific foods such as sugar might become 'addictive' and, hence, promote weight gain. Claims about the addictiveness of sugar however are based largely on findings from few animal studies, whereas there is a lack of direct human evidence for symptoms of sugar-related substance dependence. The current study examined in a large sample of human participants whether foods mainly containing sugar in particular might cause 'addiction-like' problems that meet clinical DSM criteria for substance dependence, and, also whether in turn this relates to body weight and negative affectivity (depressed mood). METHODS: In a cross-sectional study, n = 1495 university students from a variety of faculties were assessed for DSM-related signs of food addiction for particular food categories (YFAS), and, also BMI and negative affectivity. RESULTS: Results revealed that from the total sample, 95% experienced at least one symptom of food dependence and 12.6% met the YFAS classification for 'food addiction' as related to DSM-IV criteria. The majority of respondents experienced these problems for combined high-fat savoury (30%) and high-fat sweet (25%) foods, whereas only a minority experienced such problems for low-fat/savoury (2%) and mainly sugar-containing foods (5%). Overweight correlated only with addictive-like problems for high-fat savoury and high-fat sweet foods (P < 0.0001), while this was not found for foods mainly containing sugar. CONCLUSION: The current findings indicate that sugary foods contribute minimally to 'food dependence' and increased risk of weight gain. Instead, they are consistent with the current scientific notion that food energy density, and the unique individual experience of eating, plays an important role in determining the reward value of food and promoting excessive energy intake

Donut worry: the role of 5-HTTLPR genotype and ruminative thinking in emotional eating behaviour

In times of stress people often crave fatty or sweet food that is high in calories. This emotional eating behaviour could potentially lead to excess weight or obesity. Despite many studies it is still mostly unclear why many people have this unhealthy eating pattern. This dissertation shows that a combination of biological and cognitive stress susceptibilities, such as the S-allele of the 5-HTTLPR genotype and a strong tendency to ruminate, increases the risk of developing an emotional eating pattern

The interaction between 5-HTTLPR genotype and ruminative thinking on BMI

Negative affect or stress is often found to increase energy intake for high palatable energy-rich foods and hence weight gain. Reduced brain serotonin (5-HT) function is known to increase stress vulnerability and the risk for eating-related disturbances. A short (S) allele polymorphism in the serotonin transporter gene (5-HTTLPR) is associated with a less efficient functioning brain serotonin system and therefore higher stress vulnerability. It has been suggested that this genotype may be directly linked to an increased risk for weight gain and/or obesity. However, a high amount of variability has been apparent in replicating such a direct gene on weight gain relationship. A most recent suggestion is that this gene by weight relationship might be moderated by an additional (cognitive) vulnerability factor involving repetitive negative thinking (rumination). Our objective was to investigate whether the S-allele of 5-HTTLPR contributes to weight gain particularly in high cognitive ruminating individuals. A total of 827 healthy young male and female college students (aged 21·3 (SD 3·0) years; BMI 16–41·7 kg/m2) were genotyped for the 5-HTTLPR polymorphism and assessed for rumination (Event Related Ruminative Index) and body weight. In line with the hypothesis, a hierarchical regression model showed that higher BMI scores were observed in specifically high ruminating S'-carriers (P=0·031, f² = 0·022). These results suggest that cognitive rumination may be a critical moderator of the association between 5-HTTLPR and body mass