The Neurobiology of Borderline Personality Disorder (BPD)

By: Dr. Fabiano de Abreu Agrela Rodrigues

The Interaction Between Genes, Trauma, and Inflammation

Borderline Personality Disorder (BPD) is often misunderstood, but modern science reveals that it resides at the complex intersection of biology and experience. It is not a behavioral “choice,” but a neurobiological inability to regulate emotions.

The Weight of Genetics and Environment

Hereditary studies indicate that between 40% and 60% of the risk of developing BPD is genetic. However, genes are not destiny in isolation. They create a vulnerability that, when combined with childhood trauma or severe environmental stress, can trigger the disorder. Trauma during brain development causes lasting alterations in the HPA axis (stress response system) and neurotransmitter synthesis.

The Biochemistry of Instability:
The neuroscience of BPD reveals clear biological markers.

Neuroinflammation: Patients exhibit elevated levels of pro-inflammatory cytokines (such as TNF-α and IL-6). This inflammatory state impairs the production of serotonin and brain-derived neurotrophic factor (BDNF), which is essential for neuronal resilience.

Genetic Pathways: Specific variants in the HTR2C, TPH2, ANKK1/DRD2, OXTR, and FKBP5 genes alter how the brain processes pleasure, social connection, and stress.

Circadian Rhythm: There is a strong correlation between dysregulation of the biological clock and impulsivity. Delayed sleep stages and insomnia are common and worsen emotional lability.

Identification and Comorbidities

Borderline Personality Disorder (BPD) is characterized by symptoms such as intense fear of abandonment, unstable relationships, impulsivity, and splitting (viewing people or situations as only “good” or “bad”). It is common for the disorder to be accompanied by anxiety, depression, bipolar disorder, or substance abuse, making accurate diagnosis and neuroscientific monitoring essential.

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