2026 ECNP Congress

EP01-1004

When control becomes reward: an integrative starvation-driven addiction-like model of anorexia nervosa

Wojciech Ziemichód — N. Kajka, K. Kister, D. Juchnowicz, A. Rymuszka, H. Karakuła-Juchnowicz · Medical University of Lublin, I Department of Psychiatry- Psychotherapy and Early Intervention, Lublin, Poland

2026 ECNP Congress

Background

Anorexia nervosa (AN) is a severe psychiatric disorder characterized by persistent food restriction, high relapse and mortality rates. Beyond metabolic disturbance, AN is increasingly conceptualized as a disorder of altered motivation, compulsion and reinforcement. Clinical features such as compulsive restriction, persistence despite adverse consequences, and relapse resemble addiction-like processes [1]. However, existing models of compulsivity do not fully account for the persistence and rigidity of behavior observed in AN particularly in relation to neurobiological mechanisms linking metabolic state and central regulation among three neuronal systems: dopaminergic, endocannabinoid and dopaminergic. This gap limits the integration of behavioral and biological findings into a coherent explanatory framework [2].

Objectives

To explain addiction-like persistence in anorexia nervosa by proposing new neurobiological model that extends existing frameworks of compulsivity through integration of metabolic, reward, and arousal systems

. Methods: We synthesized evidence from 146 studies (1998–2026) across psychiatry, neuroscience, and pharmacology. The analysis focused on behavioral and biochemical findings related to reward processing, motivation, habit formation, and compulsivity in AN and addictive disorders. Particular emphasis was placed on interactions between metabolic signals and central regulatory systems, as well as on mechanisms linking energy balance with reinforcement processes.

Results

Converging evidence indicates that AN shares key features with addictive disorders, including persistence despite harm, reinforcement-like processes, and relapse vulnerability. [1]. However, existing conceptualizations of compulsivity capture only selected aspects of AN and do not sufficiently explain the transition from goal-directed restriction to persistent, rigid behavior. Neurobiologically, dopaminergic dysregulation contributes to altered reward valuation and reinforcement learning [3], while endocannabinoid signaling modulates reward sensitivity, emotional processing, and appetite regulation [2,4]. The orexin system provides a critical interface between metabolic state and motivational processes, influencing arousal and reward-seeking behavior [5]. We propose that starvation itself may function as a primary reinforcing signal, modulating dopaminergic activity and promoting habit formation [2]. Through repeated cycles of restriction, this mechanism may induce a shift from goal-directed behavior to compulsive, addiction-like patterns. Importantly, this process reflects starvation-induced neuroadaptation rather than a primary disturbance of reward alone. Furthermore, this framework provides a mechanistic explanation for the persistence of symptoms despite clinical improvement, suggesting that normalization of metabolic signals may not be sufficient to restore central regulatory function. Existing models of compulsivity fail to account for this dissociation. Our model extends these frameworks by incorporating cross-system interactions and a progressive decoupling of metabolic and central regulatory processes, which may sustain pathological behavior over time.

Conclusions

We introduce the Starvation-Driven Model of Addiction-Like Neuroadaptation in Anorexia Nervosa, in which prolonged energy deficit induces persistent changes in reward, motivation, and arousal systems. This framework explains how self-starvation paradoxically engages reinforcement mechanisms, promoting the maintenance of restrictive behavior. By integrating metabolic and neurobiological perspectives, the model reframes AN as a disorder of maladaptive neuroadaptation with addiction-like persistence, without implying diagnostic equivalence. This approach highlights novel targets for intervention, particularly systems linking energy balance with reward processing, and may inform the development of mechanism-based therapeutic strategies [2].

References

  1. Godier, L.R., Park, R.J., 2015. A novel measure of compulsive food restriction in anorexia nervosa: validation of the Self-Starvation Scale (SS). Eat. Behav. 17, 10–13. https://doi.org/10.1016/j.eatbeh.2014.12.004.
  2. Ziemichód, W., Kajka, N., Rząd, Z., Metelska, A., Janas-Kozik, M., Biała, G., Wilczyński, K. M., Grabowska, K., & Karakuła-Juchnowicz, H. (2026). Rethinking anorexia nervosa through the lens of control, compulsion and reward: Neurobiological insights into addiction-like features via the dopaminergic, endocannabinoid, and orexinergic systems - A narrative review. Neuroscience and biobehavioral reviews, 185, 106615. https://doi.org/10.1016/j.neubiorev.2026.106615
  3. Frank, G.K.W., 2021. From desire to dread—A neurocircuitry based model for food avoidance in Anorexia nervosa. J. Clin. Med. 10 (11), 2228. https://doi.org/10.3390/jcm10112228.
  4. Monteleone, P., Matias, I., Martiadis, V., De Petrocellis, L., Maj, M., Di Marzo, V., 2005. Blood levels of the endocannabinoid anandamide are increased in anorexia nervosa and in binge eating disorder, but not in bulimia nervosa. Neuropsychopharmacol. Off. Publ. Am. Coll. Neuropsychopharmacol. 30 (6), 1216–1221. https://doi.org/10.1038/sj.npp.1300695.
  5. Borgland, S.L., Chang, S.J., Bowers, M.S., Thompson, J.L., Vittoz, N., Floresco, S.B., et al., 2009. Orexin A/hypocretin-1 selectively promotes motivation for positive reinforcers. J. Neurosci. 29 (36), 11215–11225.