Stress-induced laboratory eating behavior in obese women with binge eating disorder

Abstract

Aim of the study was to compare the microstructural eating behavior of obese patients with and without binge eating disorder (BED) after stress induction in laboratory. Seventy-one female subjects were investigated (mean BMI 36.9). Thirty-five fulfilled criteria for BED. A 2 × 2 factorial design with repeated measurement (stress vs. no stress) on the second factor was applied. Stress was induced by the Trier Social Stress Test (TSST) and chocolate pudding served as laboratory food. Variables of eating behavior were measured by a universal eating monitor (UEM). Only in participants with BED stress was associated with an increase in the initial eating rate and a diminished deceleration of eating at the end of the meal. Generally, BED subjects ate with larger size of spoonfuls during the laboratory meal than non BED controls. The eating behavior of obese patients with binge eating disorder seems to be significantly affected by stress. The stress-induced eating behavior of BED patients is characterized by a stronger motivation to eat (indicated by a fast initial eating rate) as well as by a lack of satiety perception (indicated by less deceleration of eating rate).

Introduction

Binge eating disorder (BED) is defined by binge eating episodes at least at two days per week for 6 months (American Psychiatric Association, 2000). Binge eating episodes are characterized by the intake of large amounts of food in a discrete time period and loss of control over eating. In addition, binge eating episodes are associated with behavioral changes in eating such as eating much more rapidly than normal, eating until feeling uncomfortably full or eating large amounts of food when not physically hungry. In contrast to bulimia nervosa, BED subjects do not practise compensatory behaviors such as vomiting or the misuse of laxatives after a binge episode.

Although in day-to-day clinical practice a generally accepted category (Dingemans, Bruna, & van Furth, 2002), BED is included in the appendix for diagnostic categories requiring further study in DSM-IV. When applying DSM-IV-TR criteria, the lifetime prevalence of BED in community samples is about 2–5% (de Zwaan, 2002, Dingemans et al., 2002, Hudson et al., 2007, Spitzer et al., 1993). In clinical samples with participants in weight control programs, up to 30% suffer from BED (Spitzer et al., 1993).

BED is associated with obesity. Although a causal link has not been established, longitudinal studies suggest that BED leads to weight gain and obesity (Devlin, 2007). However, there is evidence that individuals with BED differ from individuals who are just obese (Hilbert, 2005). Laboratory studies can give objective support to the discrimination of BED from obesity and therefore to the validity of the BED diagnosis (Wonderlich, Gordon, Mitchell, Crosby, & Engel, 2009). They can also give insight in underlying mechanisms of the eating disorder.

Many laboratory studies show that individuals with BED tend to eat more calories than weight matched individuals without BED in a variety of different paradigms (Wonderlich et al., 2009). It remains unclear from these studies, why individuals with BED consume more calories than non-BED. Biological studies found correlates in individuals with BED which are related to increased hunger, such as reduced serotonin transporter binding (Wadden, Foster, Letizia, & Wilk, 1993) and increase of the regional cerebral blood flow in the left hemisphere under food exposure (Karhunen et al., 2000). Other studies have suggested a decreased satiety response in BED. Geliebter and Hashim (2001) found a higher gastric capacity in obese binge eaters compared to non-BED individuals which may lead to a decreased satiety response. In line with that, Sysko, Devlin, Walsh, Zimmerli, and Kissileff (2007) reported that BED was associated with less fullness following food intake.

Increased hunger or a disturbance in the satiation process should be observable in characteristics of the eating style (e.g., a higher eating rate at the beginning of the meal or a less pronounced slowing down of the eating rate at the end of the meal (Kissileff, Thornton, & Becker, 1982).

Although not explicitly investigated, in a study of Yanovski et al. (1992) the rate of caloric consumption per minute (measured as total amount consumed/duration of the meal) was not higher in obese participants with BED compared to obese non-BED individuals when they were either asked to “eat normal” or to “binge eat and let themselves go and eat as much as they could”. It remains unclear if this finding can be replicated or if it is due to the specific instructions given. Also, the overall eating rate does not give insight into processes of hunger and satiety. Therefore it is necessary to investigate the microstructure of eating in more detail with variables that reflect these processes.

There is also a lack of information, which stimuli will induce an aberrant eating pattern in BED patients. The most well established antecedent for binge eating is negative mood (Hilbert, 2005). There is also evidence that experience of daily stress is followed by episodes of binge eating (Crowther, Sanftner, Bonifazi, & Shepherd, 2001). Further more, Gluck, Geliebter, Hung, and Yahav (2004) showed that after a physical stressor (cold pressure test), obese BED participants reported higher levels of hunger and stronger desire to binge eat than obese non-BED participants. Empirical evidence supporting the selfish brain theory point to a close relationship between psychosocial stress and food intake (Peters, Kubera, Hubold, & Langemann, 2011). The role of psychosocial stress and food intake in binge eating disorder is, however, unclear.

In a previous study we investigated the role of a psychosocial stressor, the Trierer Social Stress Test (TSST, Kirschbaum, Pirke, & Hellhammer, 1993), on the microstructure of eating in individuals with BED compared to non BED under the instruction “to eat as much and as long as you like” (Laessle & Schulz, 2009). From a non stress to a stress condition, individuals with BED showed a greater increase in average eating rate (p < 0.01) and a different change in acceleration/deceleration at the end of the meal (p < 0.04). Unfortunately, the sample size in the above mentioned study was relatively small.

The present study therefore aimed to further investigate the effect of a psychosocial stressor on the microstructure of eating behavior (in particular variables which indicate hunger and satiation) in obese women with and without BED with a greater sample size. Stress was hypothesized to change the microstructural characteristics of eating behavior specifically in obese women with BED.