Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.06.27.661259

Orthorexia is associated with a paradoxical appetitive gastric response to unhealthy foods

Abstract

Orthorexia involves an obsessive tendency towards "healthy" foods. It is a risk factor for eating disorders (anorexia nervosa and the proposed "orthorexia nervosa") and psychological distress, but its biological mechanism remains unknown. We hypothesised that this mechanism operates through the stomach: increased gastric power differentiates appetising from unappetising foods, vagal stimulation reduces food liking, and gastric proto-nausea can be evoked by disgust; all contributors to disordered eating. We used electrogastrography alongside high-density facial landmark tracking to gauge responses to minimally processed ("healthy"), highly processed ("unhealthy"), and culturally unaccepted ("disgusting") foods in a non-clinical sample (N=77). Trait orthorexia was associated with increased self-reported desire to eat healthy foods. Moreover, we found that higher orthorexia was associated with increasing disgust-related facial responses to unhealthy and disgusting foods. We then identified a relationship between food-healthiness ratings and gastric power: those who generally assigned lower healthiness ratings to foods showed higher gastric power for unhealthy than healthy foods, whereas those who expressed higher healthiness ratings showed higher gastric power for healthy over unhealthy foods. This suggests that the stomach tracks individual differences in eating preferences. Crucially, and contrary to our expectations, higher trait orthorexia was associated with a paradoxical increase in gastric power to unhealthy foods. One explanation is that higher gastric power for unhealthy foods reflects increased appetite for self-denied foods. Alternatively, orthorexia itself could be an adaptive response to exert stronger cognitive control over a pre-existing gastric appetite for unhealthy foods.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Gumussoy, M., Anisimova, E., Lee, S., Velummylum, A., Cox, S., Bagley, E., Nord, C. L., Dalmaijer, E. S.. 2025-07-03. Orthorexia is associated with a paradoxical appetitive gastric response to unhealthy foods. https://doi.org/10.1101/2025.06.27.661259

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Thoracoabdominal pressure transmission during prone and supine cardiopulmonary resuscitation in fresh-frozen human cadavers

Background: Prone cardiopulmonary resuscitation (CPR) may be necessary when turning a prone patient supine would delay chest compressions. Although prone compressions can generate arterial pressures comparable with or greater than supine CPR, the pathway of pressure transmission is uncertain. We examined synchronized intrathoracic, intra-abdominal, and central arterial pressures in both supine and prone positions. Methods: Two thawed fresh-frozen adult cadavers underwent three, 2-minute mechanical CPR trials per position in a counterbalanced crossover sequence. Solid-state catheters recorded pleural, peritoneal, and central arterial pressures simultaneously. Trial-level outcomes included peak pressure, mean pressure, pressure-time area, and the mean peritoneal-to-pleural pressure gradient. Exploratory fixed-effects models included position, cadaver, and their interaction. Results: Prone CPR increased peak intrathoracic pressure by 7.04 mmHg, peak intra-abdominal pressure by 21.69 mmHg, and peak arterial pressure by 15.40 mmHg. Mean intra-abdominal and arterial pressures increased by 16.22 and 9.90 mmHg, respectively. The mean peritoneal-to-pleural gradient reversed direction from -8.46 mmHg supine to 4.85 mmHg prone. Intrathoracic pressure-time area increased 3.4-fold, from 1.62 to 5.46 mmHg{middle dot}s, and arterial pressure-time area increased 2.2-fold, from 2.96 to 6.42 mmHg{middle dot}s. Conclusions: Compared to supine, prone mechanical CPR generated higher arterial pressures and reversed the pressure relationship across the thoracoabdominal boundary in both cadavers. Higher abdominal pressure coincided with a larger intrathoracic pressure-time area, a pattern compatible with reduced caudal pressure dissipation.

physiology↗

Hypothalamic Farnesoid X Receptor deficiency alters energy balance by modulating hepatic glucose production and adipose tissue metabolism through central insulin signaling.

Objectives: The bile acid nuclear receptor Farnesoid X Receptor (FXR, NR1H4) is a major regulator of metabolism and energy homeostasis in peripheral organs. It modulates bile acid, glucose, and lipid metabolism, as well as fat mass and body weight. However, FXR is also expressed in the brain, particularly in the hypothalamus, a key center for the regulation of energy homeostasis. Although one study has demonstrated a role for brain FXR activation in energy balance, its specific hypothalamic role is still unknown. Here, we examined the role of FXR in the mediobasal hypothalamus in the regulation of energy balance. Methods: We used a genetic approach combined with metabolic phenotyping to determine the effect of FXR invalidation in the mediobasal hypothalamus on metabolic parameters involved in the central regulation of energy homeostasis. Results: Our results demonstrate that hypothalamic FXR deficiency induces a positive energy balance, resulting in a reduction in energy expenditure due to alterations in glucose metabolism accompanied by structural changes in white adipose tissues. Conclusion: This study uncovers a previously unrecognized role for hypothalamic FXR in the central homeostatic control of energy balance, providing new insights into its contribution to peripheral glucose metabolism and adipose tissue structural remodeling.

physiology↗

Rad and Phospholamban are Key Drivers of the Ventricular Adrenergic Response and Stress-Induced Arrhythmia

The adrenergic response is a fundamental mechanism that regulates heart rate (chronotropy), cardiac contractility (inotropy) and relaxation (lusitropy). Adrenergic stress is also a recognized trigger of arrhythmia in disease. Yet, our understanding of the underlying molecular basis remains incomplete. Protein kinase A (PKA) and the calcium/calmodulin-dependent kinase II (CaMKII) phosphorylate multiple targets proposed to participate in the adrenergic response, including the GTP-binding protein Rad, phospholamban (PLB) and ryanodine receptor 2 (RyR2). Here we demonstrate that phosphorylation of both Rad and PLB is necessary for inotropy and lusitropy. We show that changes in cardiac contractility and relaxation are primarily dependent on intracellular calcium handling. Finally, we report that Rad and PLB control stress-induced arrhythmogenesis, despite the phosphorylation of other pro-arrhythmic targets. We have identified the essential molecular components of the adrenergic response, resolving a long-standing debate in cardiac excitation-contraction coupling and refining current models of sympathetic regulation in health and disease.

physiology↗