Objective: Exposure to traumatic experiences, especially those occurring in childhood, has been linked to substance use disorders (SUDs), including abuse and dependence. SUDs are also highly comorbid with Posttraumatic Stress Disorder (PTSD) and other mood-related psychopathology. Most studies examining the relationship between PTSD and SUDs have examined veteran populations or patients in substance treatment programs. The present study further examines this relationship between childhood trauma, substance use, and PTSD in a sample of urban primary care patients. Method: There were 587 participants included in this study, all recruited from medical and OB/GYN clinic waiting rooms at Grady Memorial Hospital in Atlanta, GA. Data were collected through both screening interviews as well as follow-up interviews. Results: In this highly traumatized population, high rates of lifetime dependence on various substances were found (39% alcohol, 34.1% cocaine, 6.2% heroin/opiates, and 44.8% marijuana). The level of substance use, particularly cocaine, strongly correlated with levels of childhood physical, sexual, and emotional abuse as well as current PTSD symptoms. In particular, there was a significant additive effect of number of types of childhood trauma experienced with history of cocaine dependence in predicting current PTSD symptoms, and this effect was independent of exposure to adult trauma. Conclusions: These data show strong links between childhood traumatization and SUDs, and their joint associations with PTSD outcome. They suggest that enhanced awareness of PTSD and substance abuse comorbidity in high-risk, impoverished populations is critical to understanding the mechanisms of substance addiction as well as in improving prevention and treatment. Depression and Anxiety, 2010.

Exposure to stressful events during development has consistently been shown to produce long‐lasting alterations in the hypothalamic‐pituitary‐adrenal (HPA) axis, which may increase vulnerability to disease, including posttraumatic stress disorder and other mood and anxiety disorders. Recently reported genetic association studies indicate that these effects may be mediated, in part, by gene×environment interactions involving polymorphisms within two key genes, CRHR1 and FKBP5. Data suggest that these genes regulate HPA axis function in conjunction with exposure to child maltreatment or abuse. In addition, a large and growing body of preclinical research suggests that increased activity of the amygdala‐HPA axis induced by experimental manipulation of the amygdala mimics several of the physiological and behavioral symptoms of stress‐related psychiatric illness in humans. Notably, interactions between the developing amygdala and HPA axis underlie critical periods for emotional learning, which are modulated by developmental support and maternal care. These translational findings lead to an integrated hypothesis: high levels of early life trauma lead to disease through the developmental interaction of genetic variants with neural circuits that regulate emotion, together mediating risk and resilience in adults. Depression and Anxiety Depression and Anxiety 26:984–992, 2009. Published 2009 Wiley‐Liss, Inc.

Neurobiological systems may be particularly susceptible to the deleterious impact of childhood trauma, and the impact of childhood trauma on development and subsequent functional outcomes across the life span has been well documented. The current review addresses the neurobiological impact of exposure to interpersonal trauma in childhood in the context of executive function, emotion regulation, and dissociation/interoceptive awareness. Subsequent risk for PTSD and depression is also discussed. The pathway of risk from childhood trauma to these cognitive, emotional, and psychiatric outcomes is addressed in terms of potential structural and functional alterations within the hippocampus, prefrontal cortex, and amygdala resulting from chronic or repeated activation of the hypothalamic–pituitary–adrenal (HPA) axis and its interaction with and influence on genetic and epigenetic processes during sensitive periods of development. Implications for practice are discussed.