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Introduction Anecdotal reports from patients with smell loss provided the basic motivation for the present study on sexual dysfunction among patients with olfactory dysfunction. The aim of the present study was to investigate the sexual appetite and the subject’s depression in regard to olfactory function. Methods Eighty-six patients referred to our smell and taste clinic with olfactory dysfunction were investigated. Olfactory function was assessed by means of the “Sniffin’ Sticks” test battery consisting of tests for odor threshold (T), odor discrimination (D), and odor identification (I). Their results were summed up to a composite score, the so-called “TDI score.” All participants completed a questionnaire including the Beck Depression Inventory (BDI) and 11 questions for evaluation of the sexual appetite in regard to the time before the onset of olfactory dysfunction and since the olfactory dysfunction. The points received for the latter questions were summed up to the so called Sexual Appetite Index (SAI). Results Olfactory testing revealed that 38 patients were functionally anosmic, 39 patients were hyposmic, and nine patients were normosmic. The average BDI score was 11.0 ± 8.4 points. Evaluation of the SAI questionnaire revealed a significant decrease (P = 0.003) of the score from 22.7 ± 4.5 points from the time before to 21.4 ± 4.9 points since the onset of olfactory loss. No significant correlation was found between olfactory function and the SAI since the onset of olfactory dysfunction. However, the BDI score correlated negatively with the SAI since the onset of olfactory dysfunction (r85 = −0.36; P = 0.001). Conclusion The present study does not confirm the hypothesis that loss of olfactory function directly impacts on sexual appetite. It seems that depression caused by olfactory loss is the main cause for the self-reported decrease in sexual appetite as the onset of olfactory dysfunction.

There is a need of experimental studies on biomarkers in patients with anorexia nervosa (P AN), especially in the context of stress, in order to foster understanding in illness maintenance. To this end, the cortisol response to an acute stressor was investigated in n = 26 P AN (BMI: 19.3 ± 3.4 kg/m 2), age, and gender matched to n = 26 healthy controls (HC; BMI: 23.08 ± 3.3 kg/m 2). For this purpose, salivary cortisol parameters were assessed in two experimental conditions: (1) rest/ no intervention and (2) stress intervention (TSST; Trier Social Stress Test). In addition, psychological indicators of stress were assessed (Primary Appraisal Secondary Appraisal, Visual Analogue Scale, and Trier Inventory for the assessment of Chronic Stress), as well as psychological distress, depression, and eating disorder (ED) symptoms. A 2 × 2 × 8 ANOVA demonstrated elevated cortisol levels in P AN in the resting condition. In the stress intervention no significant group effect in terms of cortisol (F (1, 50) = 0.69; p = 0.410; η 2 p ¼ 0:014). A significant condition (F (1, 50) = 20.50; p = 0.000; η 2 p ¼ 0:291) and time effect (F(2.71, 135.44) = 11.27; p = 0.000; η 2 p ¼ 0:20) were revealed, as well as two significant interaction effects. First: Condition × group (F (1, 50) = 4.17, p = 0.046; η 2 p ¼ 0:077) and second: Condition × time (F (2.71, 135.44) = 16.07, p = 0.000, η 2 p ¼ 0:24:). In terms of AUC G , no significant differences between both groups were exhibited. Regardless, significant results were evinced in terms of an increase (AUC i : F(1, 50) = 20.66, p = 0.015, η 2 p ¼ 0:113), baseline to peak (+20 min post-TSST: t 5 = 16.51 (9.02), p = 0.029) and reactivity (M PAN = 0.73 vs. M HC = 4.25, p = 0.036). In addition, a significant correlation between AUC G and BMI: r (24) = −0.42, p = 0.027 was demonstrated, but not between AUC i and BMI (r (24) = −0.26, p = 0.20). Psychological indices suggested higher levels of chronic and perceived stress in P AN relative to HC. However, stress perception in the stress condition (VAS) was comparable. Additional analyses demonstrated that ED-symptoms are highly correlated with psychological distress and depression, but not with BMI. In addition, it could be demonstrated that reactivity is rather related to EDsymptoms and psychological burden than to BMI. In conclusion, P AN showed elevated basal cortisol levels at rest and exhibited a blunted cortisol reactivity to the TSST as evinced by salivary cortisol parameters. Further, it was shown that weight recovery influences reversibility of hypercortisolemia, i.e., cortisol levels normalize with weight gain. However, HPAA (hypothalamus-pituitary-adrenal axis) irregularities in terms of reactivity persist even at a BMI ≤ 19.3 (±3.4). Our data suggest that pronounced psychological burden in P AN , have a greater impact on the HPAA functionality (secondary to the ED) than BMI itself.

A Correction to this paper has been published: https://doi.org/10.1038/s41398-021-01326-6

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