Systematic review, structural analysis, and new theoretical perspectives on the role of serotonin and associated genes in the etiology of psychopathy and sociopathy

• Psychopathy arises mainly out of genetic contributions to emotional hyporesponsivity.
• Sociopathy arises out of interactive gene–environment effects on emotional dysregulation.
• Enhanced versus dampened serotonergic functionality may define these profiles respectively.
• High testosterone can increase emotional dysfunctions and the risk for aggression.

Since its theoretical inception, psychopathy has been considered by philosophers, clinicians, theorists, and empirical researchers to be substantially and critically explained by genetic factors. In this systematic review and structural analysis, new hypotheses will be introduced regarding gene–gene and gene–environment interactions in the etiology of psychopathy and sociopathy. Theory and research from neurobiological and behavioral sciences will be integrated in order to place this work in a broader conceptual framework and promote synergy across fields. First, a between groups comparison between psychopathy and sociopathy is made based on their specific dysfunctions in emotional processing, behavioral profiles, etiological pathways, HPA-axis functioning, and serotonergic profiles. Next, it is examined how various polymorphisms in serotonergic genes (e.g., TPH, 5HTT, HTR1A, HTR2A, HTR2C, and HTR3) might contribute either individually or interactively to the development of these disorders and through which specific biological and behavioral endophenotypes this effect could be mediated. A short introduction is made into mediating variables such as GABAergic functioning and testosterone which could potentially alter the decisive effect of serotonergic genotypes on behavior and physiology. Finally, critical commentary is presented on how to interpret the hypotheses put forward in this review.