Individuals with Borderline Personality Disorder (BPD) and eating disorders (EDs) often share serotonin (5-HT) gene variants that may contribute to overlapping symptoms such as impulsivity and poor emotion regulation. Research consistently shows that people with one or both disorders display anomalies in serotonergic functioning (Steiger, 2024). For example, Steiger found that Binge Eating Disorder (BED) and Bulimia Nervosa (BN) are more commonly associated with BPD, likely due to the impulsive behavioral tendencies that characterize all three disorders.

Animal studies have further demonstrated that increased 5-HT levels are associated with dietary restriction, while lower 5-HT levels may precede binge or compulsive eating behaviors (Steiger, 2024). In the context of BPD specifically, reduced serotonergic function has been widely implicated in affective instability and impulsive aggression. Ni et al. (2009), for instance, found that serotonin receptor activity tends to be diminished in individuals with BPD.

Furthermore, Ni et al. identified higher frequencies of specific serotonin-related gene variants in BPD patients, such as the 5-HT2C rs6318G allele. However, the presence of these variants does not necessarily indicate increased receptor activity; rather, it highlights a genetic predisposition toward dysregulated serotonergic function that may underlie core symptoms of BPD.

The Role of Serotonin in both BPD and EDs

Hormonal dysregulation is a significant area of research in Borderline Personality Disorder (BPD), with findings pointing to several key anomalies:

 Hypothalamic-Pituitary-Adrenal (HPA) Axis Activity: Individuals with BPD often display abnormal activity in the HPA axis (Bozzatello et al., 2021). These anomalies are thought to arise primarily from traumatic environments or experiences of maltreatment, leading to elevated cortisol levels (Bozzatello et al., 2021). While genetic predisposition was once considered a major factor, current research suggests that the strenuous climate may play a more significant role in adapting neurobiology.

Cortisol Levels:
Elevated in Trauma: Studies have revealed significantly higher cortisol levels in children with BPD who have experienced child abuse compared to those who have not. This reinforces the idea that the environment likely contributes to increased cortisol levels in individuals with BPD.

Comparison with Eating Disorders: Unlike BPD, where environmental factors are linked to higher cortisol, in eating disorders, particularly Anorexia Nervosa (AN), cortisol levels tend to decrease as individuals establish regular eating patterns gradually (Steiger, 2004). However, individuals with BPD also show frequent disruptions in cortisol levels, similar to those seen in eating disorders.

Testosterone Levels: A unique study by Dyson et al. (2023) identified that women with BPD specifically tend to have higher levels of testosterone. This finding is not commonly observed among individuals with eating disorders.

Recognizing these hormone imbalances is crucial, as these findings may help in elucidating potential medications that could enhance the daily lives of individuals with BPD.


Hormone Disruption in BPD and EDs

Neurochemical effects include different variants of serotonin, unique activity rates of serotonin, and hormone imbalances.

Serotonin (5-HT) plays a role in:
- Mood regulation
- Appetite
- Impulse control

- Low serotonin function has been linked to both binge-purge behaviors and BPD symptoms such as aggression and affective instability.

- Cortisol dysregulation (HPA axis) from chronic stress or trauma may exacerbate both conditions.

Saint Olaf College

Like many disorders, there are biological components in interplay with the environment, or past childhood experiences, that create foundations for a disorder to build from. Overlapping biological causes of BPD and EDs include the following:

- Neurochemical Effects
- Genetic Predispositions
- Neurobiological Effects

Biological Etiologies of Both BPD and EDs

Costa, J., Marôco, J., Pinto-Gouveia, J., Ferreira, C., & Castilho, P. (2016). Validation of the Psychometric Properties of the Self-Compassion Scale. Testing the Factorial Validity and Factorial Invariance of the Measure among Borderline Personality Disorder, Anxiety Disorder, Eating Disorder and General Populations. Clinical Psychology and Psychotherapy, 23(5), 460–468. https://doi.org/10.1002/cpp.1974

Bozzatello, P., Garbarini, C., Rocca, P., & Bellino, S. (2021). Borderline Personality Disorder: Risk Factors and Early Detection. Diagnostics (Basel, Switzerland), 11(11), 2142. https://doi.org/10.3390/diagnostics11112142
Khosravi, M. Eating disorders among patients with borderline personality disorder: understanding the prevalence and psychopathology. J Eat Disord 8, 38 (2020). https://doi.org/10.1186/s40337-020-00314-3

Dyson Tori, Thomas Susan J., Townsend Michelle L., Finch Adam, South Alexandra, Barkus Emma, Walter Emma, Mendonca Carley, Grenyer Brin F. S., Pickard Judy A. (2023). Salivary testosterone and cortisol levels in borderline personality disorder before and after a 12-week group dialectical behavior therapy intervention. Frontiers in Psychology, 14(14). https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2023.1195187

Federici, A. (2009). Dialectical Behaviour Therapy for the Treatment of Eating Disorders. NEDIC, NEDIC Eating Disorders Bulletin.

Lee, K. S., & Vaillancourt, T. (2024). Trajectories, comorbidity, and risk factors for adolescent disordered eating and borderline personality disorder features. Development and Psychopathology, 36(4), 1546–1557. doi:10.1017/S0954579423000792

Lee, S. S. M., Keng, S.-L., & Hong, R. Y. (2024). Validating the biosocial model of borderline personality disorder: Findings from a longitudinal study. Development and Psychopathology, 36(4), 1752–1762. doi:10.1017/S0954579423001116

Lester, R. J. (2009). Brokering Authenticity: Borderline Personality Disorder and the Ethics of Care in an American Eating Disorder Clinic. Current Anthropology, 50(3), 281–302. https://doi.org/10.1086/598782

Miller, A. E., Hotte-Meunier, A., Bain, T., Macdonald, E. P., Steiger, H., & Racine, S. E. (2025). A Qualitative Study of the Lived Treatment Experiences of Women With an Eating Disorder and Comorbid Borderline Personality Disorder. The International journal of eating disorders, 58(5), 860–867. https://doi.org/10.1002/eat.24390

Navarro-Haro, M. V., Botella, C., Guillen, V., Moliner, R., Marco, H., Jorquera, M., Baños, R., & Garcia-Palacios, A. (2018). Dialectical Behavior Therapy in the Treatment of Borderline Personality Disorder and Eating Disorders Comorbidity: A Pilot Study in a Naturalistic Setting. Cognitive Therapy and Research, 42(5), 636–649. https://doi.org/10.1007/s10608-018-9906-9

Newton, J. R. (2019). Borderline personality disorder and eating disorders: a trans-diagnostic approach to unravelling diagnostic complexity. Australasian Psychiatry : Bulletin of the Royal Australian and New Zealand College of Psychiatrists, 27(6), 556–558. https://doi.org/10.1177/1039856219852297

Ni, X., Chan, D., Chan, K., McMain, S., & Kennedy, J. L. (2009). Serotonin genes and gene–gene interactions in borderline personality disorder in a matched case-control study. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 33(1), 128–133. https://doi.org/10.1016/j.pnpbp.2008.10.022.

Ntshingila, N., Poggenpoel, M., Myburgh, C. P. H., & Temane, A. (2016). Experiences of women living with borderline personality disorder. Health SA = SA Gesondheid, 21(1), 110–119. https://doi.org/10.1016/j.hsag.2016.01.001

Sansone, R. A., & Sansone, L. A. (2007). Childhood Trauma, Borderline Personality, and Eating Disorders: A Developmental Cascade. Eating Disorders, 15(4), 333–346. https://doi.org/10.1080/10640260701454345

Sansone, R. A., & Sansone, L. A. (2010). Personality Disorders as Risk Factors for Eating Disorders: Clinical Implications. Nutrition in Clinical Practice, 25(2), 116–121. https://doi.org/10.1177/0884533609357563.

Steiger, H. (2004). Eating disorders and the serotonin connection: state, trait, and developmental effects. Journal of psychiatry & neuroscience: JPN, 29(1), 20–29.

Power, R. A., & Pluess, M. (2015). Heritability estimates of the Big Five personality traits based on common genetic variants. Translational psychiatry, 5(7), e604. https://doi.org/10.1038/tp.2015.96

Reference List: Comorbidity of Borderline Personality Disorder and Eating Disorders

Neurochemical Anomalies for Both BPD and EDs.

Both genetic and environmental factors shape personality. Twin studies suggest that approximately 40–60% of personality trait variation is heritable (Power et al., 2015). However, these findings can be influenced by shared environmental conditions in twin rearing.

Power et al. (2015) also found that neuroticism and openness are more strongly inherited within families than traits like extraversion, agreeableness, or conscientiousness. This is notable for research on Borderline Personality Disorder (BPD) and eating disorders (EDs), as neuroticism—characterized by emotional instability, anxiety, and perfectionism—is a shared trait in both.

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