Genetic factors explain a non-negligible part of the vulnerability to alcohol dependence, the genetic influence in males being estimated at around 60%. The search for gene(s) potentially implicated in alcoholism is counteracted by the clinical heterogeneity of alcoholism, but also by heterogeneity of the etiologic factors involved. It is thus necessary to redefine more specific phenotypes with more simple determinism, and to focus on more specific subsets of candidate genes. In this view, the existence of co-occurrence (presence at the same time, whatever the cause) between antisocial personality and alcoholism is frequently reported. Three hypotheses have been previously proposed to explain this co-occurrence. Firstly, it could be a pure artefact or contamination, due to common items in diagnostic manuals widely used, such as the DSM or ICD. Secondly, antisocial personality and alcoholism could share common etiologic factor(s), and determine a ‘real’ co-morbidity. Finally, common genetic factors between these two disorders may exist, with the observation of a co-transmission of both disorders more often than expected by chance alone, meaning the existence of co-aggregation. Each of these three hypotheses will be reviewed and discussed.

Presence of a family history of alcoholism may predict clinical characteristics in affected subjects, such as an earlier age at onset. More frequent and severe social maladjustment and somatic complications are also regularly cited for familial alcoholism, although subject to many other confusing factors. We analysed the clinical specificities of 79 alcohol-dependent inpatients according to the absence versus presence of family history of alcoholism.

Patients were evaluated for lifetime psychiatric morbidity with the Diagnostic Interview for Genetic Studies (DIGS), for somatic complications with a systematic screening list, and first-degree relatives (N  =  428) were assessed with the Family Inventory Schedule and Criteria (FISC).

Age at onset and social complications were predicting familial versus sporadic alcoholism, even when considering censored data and/or interaction between variables. But differences became non-significant when excluding patients with antisocial personality.

If age at onset effectively appears to be the most informative characteristic for predicting familial versus sporadic alcoholism, it seems that it may be necessary in future studies to systematically take into account antisocial personality diagnosis, because of a probable contamination.

Across a significant body of research, psychopathy has often been conceptualized as a biologically based malady. In this research, genetic and neurobiological differences have been conceptualized to underlie psychopathy, while affected individuals’ life experiences only influence expressed psychopathic features and their severity. Psychopathy research has largely ignored developmental evidence demonstrating significant influences of environment on both biological and behavioral processes, resulting in several prominent criticisms (Edens & Vincent, 2008; Loeber, Byrd, & Farrington, 2015). The current review was conducted with two main aims: (a) to collect and consider etiological evidence from the extant body of research on genetic and neurobiological factors in psychopathy; and (b) to evaluate findings from genetic, neurotransmitter, brain structure, and brain function studies in the context of relevant evidence from developmental research. Examples from research on adversity and traumatic stress, a common correlate of psychopathy, were used to highlight current research gaps and future directions to aid in the integration of developmental and neurobiological research agendas. While some promising evidence exists regarding possible underlying neurobiological processes of psychopathic traits, this evidence is insufficient to suggest a largely biological etiology for the disorder. Further, information from developmental and epigenetic research may suggest complex, multidimensional trajectories for individuals experiencing psychopathy. Based on these observations, the authors make several recommendations for future research, as well as for current clinical application and practice.

Sociopaths are “outstanding” members of society in two senses: politically, they draw our attention because of the inordinate amount of crime they commit, and psychologically, they hold our fascination because most ofus cannot fathom the cold, detached way they repeatedly harm and manipulate others. Proximate explanations from behavior genetics, child development, personality theory, learning theory, and social psychology describe a complex interaction of genetic and physiological risk factors with demographic and micro environmental variables that predispose a portion of the population to chronic antisocial behavior. More recent, evolutionary and game theoretic models have tried to present an ultimate explanation of sociopathy as the expression of a frequency-dependent life strategy which is selected, in dynamic equilibrium, in response to certain varying environmental circumstances. This paper tries to integrate the proximate, developmental models with the ultimate, evolutionary ones, suggesting that two developmentally different etiologies of sociopathy emerge from two different evolutionary mechanisms. Social strategies for minimizing the incidence of sociopathic behavior in modern society should consider the two different etiologies and the factors that contribute to them.

The present study examined event-related potentials (ERPs) elicited by a visual discrimination task in a community sample of adult males with a lifetime diagnosis of alcohol dependence. Study participants were subtyped by the presence of additional comorbid disorders (antisocial personality, depression, and drug abuse or dependence). In all groups of alcohol-dependent subjects, even those without any additional comorbid disorders, P3 amplitude differed from that of a comparison group. Alcohol-dependent subjects with a diagnosis of illicit drug abuse or dependence, especially if they had antisocial personality as well, had the smallest amplitude responses. The amplitude profile of the P3 across the parietal electrodes used as active sites was flattened among alcoholic subjects, with P3 amplitude disproportionately reduced at the midline. Among alcoholic subjects with a lifetime diagnosis of depression, the flattened amplitude profile was due to elevated mean amplitude of the P3 at lateral leads, especially P4, relative to the comparison group. Alterations in ERP responses appear to be a general characteristic of alcoholism in men, although the presence of other comorbid disorders, particularly drug abuse or dependence together with antisocial personality, results in the greatest reductions in P3 amplitude.