A neuroimmunological model of antisocial and borderline personality disorders

• Published in: Human psychopharmacology 1997-07, Vol.12 (4), p.291-308
• Main Authors: Holden, Robyn J., Pakula, Irwin S., Mooney, Phyllis A.
• Format: Article
• Language: English
• Subjects: antisocial personality disorder; borderline personality disorder; immunological change; neuropeptides
• ISSN: 0885-6222; 1099-1077
• DOI: 10.1002/(SICI)1099-1077(199707/08)12:4<291::AID-HUP878>3.0.CO;2-H

The neurobiology of the dramatic personality disorders (DSM‐IV—Cluster B) has remained somewhat elusive, with the consequence that pharmacological treatment of these disorders is far from satisfactory. The clinical feature that characterizes the borderline personality disorder (BPD) is repeated acts of self‐mutilation, whereas those with an antisocial personality disorder (ASPD) are disposed to repeated acts of criminality. While the antisocial group are inevitably incarcerated in penal institutions, the borderline patient, despite their acute psychological suffering, is often refused hospitalization primarily due to the absence of effective interventions. In this paper it will be hypothesized that both these disorders are due to a primary dysregulation of interferon‐gamma (IFN‐γ), neuropeptide Y (NPY), β‐endorphin and insulin. A gender bias has also been observed in relation to these two conditions with females being predisposed to developing a BPD and males an ASPD—a gender bias that can be directly attributed to β‐endorphin. Other perplexing features of these disorders are the self‐injurious behaviour (SIB) and frequent ammenorhoea of the BPD, a complete lack of morality often combined with heightened cognition and the ‘low serotonin syndrome’ (low serotonin, low LDL (low density lipoprotein) cholesterol and mild hypoglycaemia) of the ASPD. A neuroimmunological explanation of this curious constellation of symptoms will be advanced in this paper. © 1997 John Wiley & Sons, Ltd.