Early life stress and psychopharmacology

Abstract

The concept of early life stress (ELS) has long been a central focus in clinical psychiatry and psychology, owing in no small part to the primacy of this concept in psychoanalytic theory. Perhaps in response to that legacy, both clinical and preclinical biologically oriented researchers have become increasingly invested in understanding the adult sequelae of adverse environmental factors occurring early in development. Several factors stand out in considering the drivers of this changing zeitgeist: (1) new efforts to integrate preclinical and clinical findings on the pathogenesis of major psychiatric disorders, especially by focusing on model neurobiological systems (e.g., Heim et al. 1997); (2) empirical demonstration of the relevance of the classic diathesis-stress theory using gene×environment (G×E) experimental designs (e.g., Caspi et al. 2003) and, more recently, epigenetic approaches (e.g., McGowan and Szyf 2010); (3) increased recognition of the adverse psychiatric and biomedical sequelae of ELS (e.g., Gluckman and Hanson 2004; Scott et al. 2010); (4) convincing demonstration of ELS as a major global public health challenge (e.g., Krug et al. 2002). The diversity of work covered in this Special Issue reflects the remarkable progress that has been made in this area in a relatively brief span of time. The relationship between ELS and clinical phenotypes remains a major focus of investigation. The review by Yehuda et al. (2010), published in October as a prelude to the present issue, examines how ELS interacts with adulthood stressors in the pathogenesis of post-traumatic stress disorder. The review by Enoch (2010) of the role of ELS in the development of alcohol and drug abuse underscores the pluripotentiality of early adversity. From the developmental perspective, Rudolph et al. (2010) present a study showing how individual differences in stress sensitivity shape the clinical response to peer victimization in children. This is mirrored in the preclinical arena, with findings that animals exposed to ELS are affected in their response to drugs of abuse (Rodrigues et al. 2010), cognitive function (Hedges and Woon 2010; Jones et al. 2010; Oomen et al. 2010), anxiety-related behaviors (Peleg-Raibstein and Feldon 2010), depressionand psychosis-related behaviors (Markham and Koenig 2010), stress sensitivity and hypothalamic–pituitary–adrenal (HPA) axis function (Claessens et al. 2010), and sleep (Pryce et al. 2010), as well as in the brain–gut axis (modeling aspects of irritable bowel syndrome) (O'Mahony et al. 2010). Certainly, limitations to these models do exist (Schmidt et al. 2010; Van Waes et al. 2010), reflecting a variety of individual differences (Claessens et al. 2010), including whether animals are tested during adolescence or adulthood (Peleg-Raibstein and Feldon 2010). Long-term cognitive sequelae of ELS are now well documented, and two reviews in this issue address this burgeoning literature. Hedges and Woon (2010) organize the findings with an emphasis on specific functional effects, while Pechtel and Pizzagali (2010) utilize a neurodevelopmental framework to integrate observations on cognitive and affective processes. The seminal preclinical studies of ELS and the HPA axis (Claessens et al. 2010; O'Malley et al. 2010), which L. H. Price (*) Department of Psychiatry and Human Behavior, The Warren Alpert Medical School of Brown University, Butler Hospital, 345 Blackstone Blvd., Providence, RI 02906, USA e-mail: lawrence_price_md@brown.edu