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OBJECTIVE The present study investigates the impact of psychosocial stress on chewing and eating behavior in patients with anorexia nervosa (PAN ). METHOD The eating and chewing behavior of PAN were examined in a standardized setting by means of a chewing sensor. These procedures encompassed n = 19 PAN , age, and gender matched to n = 19 healthy controls (HC). Food intake and chewing frequency were assessed in two experimental conditions: rest versus stress (via Trier Social Stress Test). To verify stress induction, two appraisal scales were employed. In addition, chronic stress, psychological distress and eating disorder symptoms were assessed. RESULTS In terms of food intake and chewing frequency, the results of the 2x2 ANOVA demonstrated a significant effect of condition and group. During stress, all participants demonstrated a higher chewing frequency and a decreased ingestion. In general, patients ate less at a lower chewing frequency (vs. HC). However, sample specific analyses demonstrated that the eating and chewing behavior of PAN remained unchanged regardless of the condition, except for their drinking. Food choices were comparable between the groups, but appetite values significantly differed. DISCUSSION The increase in chewing frequency in all participants during stress suggests that chewing might impact affect regulation, however, not specifically in PAN . Future research should clarify to what extent the normalization of chewing behavior could ameliorate ED-symptoms (incl. food intake) in PAN . The application of a chewing sensor could support this aim and future interventions.

In order to understand the psychopathology of the social anxiety disorder (SAD) at the neuroendocrine level, standardized experimental studies on endocrine and physiological markers are necessary, especially since empirical data are still ambiguous. Hence, differences in both, the autonomic nervous system (ANS) and the endocrine stress responses (ACTH, salivary and plasma cortisol) were investigated in a particularly homogenous sample after a standardized stressor (Trier Social Stress Test). The sample consisted of n = 35 patients with SAD, age, and gender matched to n = 35 healthy controls (HC). In terms of the heart rate, the response pattern was comparable in both groups. Concerning ACTH, no significant group differences in the response pattern nor in the total output (AUCG) were exhibited. Significant differences were noticeable only in the plasma cortisol response pattern with less total output (AUCG) in patients suggesting a blunted response. The salivary cortisol response indicated comparable patterns between groups. However, the patients’ total output (AUCG) was significantly smaller relative to the controls. In sum, evidence for a hypo-responsiveness of the HPA-axis in SAD by means of blood cortisol was observed, with no differences in ACTH between the two groups. This reduced reactivity of the HPA-axis might be associated with an inability to elicit an adequate hormone release, possibly accompanied by an enhanced perception of the stress stimulus. This might be explained by an adaptation of the adrenocortical system due to prolonged repeated stress exposure such as social evaluation.