Cortisol function, adversity, and subtypes of aggression in adolescent and young adult males / Melissa Peskin.

Format:

Book

Manuscript

Thesis/Dissertation

Author/Creator:

Peskin, Melissa.

Contributor:

Raine, Adrian, advisor.

Flanagan-Cato, Loretta, committee member.

Ruscio, Ayelet M., committee member.

University of Pennsylvania. Psychology.

Language:

English

Subjects (All):

Penn dissertations--Psychology.

Psychology--Penn dissertations.

Local Subjects:

Penn dissertations--Psychology.

Psychology--Penn dissertations.

Physical Description:

vi, 132 pages : illustrations ; 29 cm

Production:

2012.

Summary:

There is increasing evidence that aggressive individuals are characterized by neuroendocrine abnormalities. However, previous research investigating the relationship between cortisol function and aggression in adolescents has often yielded conflicting findings. Possible reasons for this may be failure to differentiate between subtypes of aggression or consider the effects of moderating factors. In addition, there are a lack of longitudinal studies examining cortisol function as a predictor of later aggression. Three studies were designed to address these gaps in the literature by examining relationships between cortisol function, subtypes of aggression, and possible moderators in a sample of 328 males in both cross-sectional (Studies 1 and 2) and longitudinal (Study 3) designs. Study 1 examined whether individual differences in cortisol function differentially related to total, reactive, and proactive aggression. Study 1 also examined whether psychosocial adversity moderated the relationship between cortisol function and aggression subtypes. Contrary to predictions, there were no significant relationships between cortisol function and aggression subtypes, and no significant interactions between cortisol function and psychosocial adversity in relation to aggression subtypes; however, there was a marginally significant main effect of psychosocial adversity on proactive aggression, β = .118, t(318) = 1.82, p = .070. Study 2 examined whether PTSD, a response to more extreme adversity, moderates the relationship between cortisol function and total, reactive, and proactive aggression. There was a significant interaction between PTSD and cortisol reactivity in relation to total aggression, β = -0.514, t(319) = -2.77, p = .006, and reactive aggression, β = -0.512, t(319) =-2.76, p = .006. For adolescents with PTSD, lower levels of cortisol reactivity were associated with higher total aggression, β = -0.513, t(23) = -2.80, p = .010, and reactive aggression, β = -0.585, t(23) = -3.38, p = .003, while for adolescents without PTSD, no relationship between cortisol reactivity and aggression was found. There was no significant interaction between PTSD and cortisol reactivity in relation to proactive aggression. Study 3 reexamined these relationships using a longitudinal framework to determine whether cortisol function at age 16 was associated with total violence at age 25, and whether this relationship was moderated by psychosocial adversity or PTSD. Low cortisol reactivity at age 16 significantly predicted recidivistic violence χ2(1) = 4.67, p = .031, but not infrequent violence, at age 25, compared to no violence. In analyses examining only those subjects who committed violent acts, there was an inverse relationship between cortisol reactivity and violence frequency, r = -.298, p = .016. While cross-sectional findings are mixed, longitudinal findings are broadly consistent with Moffitt's (1993) life-course persistent versus adolescence-limited theory of antisocial behavior. Implications of these findings and directions for future research are discussed.

Notes:

Adviser: Adrian Raine.

Thesis (Ph.D. in Psychology) -- University of Pennsylvania, 2012.

Includes bibliographical references.

OCLC:

829426769