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.

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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

Serotonin genes and gene–gene interactions in borderline personality disorder in a matched case-control study. Progress in Neuro-Psychopharmacology & Biological Psychiatry

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

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