Investigators commonly distinguish between primary and secondary psychopathy (H. Cleckley, 1976; D.T. Lykken, 1995), though there is a lack of consensus regarding the best means to achieve this distinction. To address the validity of using R. D. Hare's (2003) Psychopathy Checklist and the G. Welsh (1956) Anxiety Scale for this purpose, the authors used 2 measures of J. A. Gray's (1987) behavioral inhibition system/behavioral activation system (BIS/BAS). Following D. T. Lykken (1995) and D. C. Fowles (1980), the authors hypothesized that primary psychopathy would be associated with a weak BIS and a normal BAS, whereas secondary psychopathy would be associated with a strong BAS and a normal BIS. Results for primary psychopathy were as predicted. Results for secondary psychopathy clearly supported the strong BAS prediction but provided mixed support for the normal BIS prediction.

Posttraumatic stress disorder (PTSD) is associated with elevated risk for a variety of age-related diseases and neurodegeneration. In this paper, we review evidence relevant to the hypothesis that chronic PTSD constitutes a form of persistent life stress that potentiates oxidative stress (OXS) and accelerates cellular aging. We provide an overview of empirical studies that have examined the effects of psychological stress on OXS, discuss the stress-perpetuating characteristics of PTSD, and then identify mechanisms by which PTSD might promote OXS and accelerated aging. We review studies on OXS-related genes and the role that they may play in moderating the effects of PTSD on neural integrity and conclude with a discussion of directions for future research on antioxidant treatments and biomarkers of accelerated aging in PTSD.