This is a report on the research design and findings of a 23-year longitudinal study of the impact of intrafamilial sexual abuse on female development. The conceptual framework integrated concepts of psychological adjustment with theory regarding how psychobiological factors might impact development. Participants included 6- to 16-year-old females with substantiated sexual abuse and a demographically similar comparison group. A cross-sequential design was used and six assessments have taken place, with participants at median age 11 at the first assessment and median age 25 at the sixth assessment. Mothers of participants took part in the early assessments and offspring took part at the sixth assessment. Results of many analyses, both within circumscribed developmental stages and across development, indicated that sexually abused females (on average) showed deleterious sequelae across a host of biopsychosocial domains including: earlier onsets of puberty, cognitive deficits, depression, dissociative symptoms, maladaptive sexual development, hypothalamic–pituitary–adrenal attenuation, asymmetrical stress responses, high rates of obesity, more major illnesses and healthcare utilization, dropping out of high school, persistent psottraumatic stress disorder, self-mutilation, Diagnostic and Statistical Manual of Mental Disorders diagnoses, physical and sexual revictimization, premature deliveries, teen motherhood, drug and alcohol abuse, and domestic violence. Offspring born to abused mothers were at increased risk for child maltreatment and overall maldevelopment. There was also a pattern of considerable within group variability. Based on this complex network of findings, implications for optimal treatments are elucidated. Translational aspects of extending observational research into clinical practice are discussed in terms that will likely have a sustained impact on several major public health initiatives.

Inconsistencies exist in literature examining hypothalamic–pituitary–adrenal (HPA) axis activity in children and adults who have experienced childhood abuse. Hence, the extent and manner to which childhood abuse may disrupt HPA axis development is largely unknown. To address these inconsistencies, the developmental course of nonstress cortisol in a long-term longitudinal study was assessed at six time points from childhood through adolescence and into young adulthood to determine whether childhood abuse results in disrupted cortisol activity. Nonstress, morning cortisol was measured in 84 females with confirmed familial sexual abuse and 89 nonabused, comparison females. Although dynamically controlling for co-occurring depression and anxiety, hierarchical linear modeling (HLM) showed that relative to comparison females, the linear trend for abused females was significantly less steep when cortisol was examined across development from age 6 to age 30, t (1, 180)= −22.55, p < .01, indicating attenuation in cortisol activity starting in adolescence with significantly lower levels of cortisol by early adulthood, F (1, 162) =4.78, p < .01. As a more direct test of the attenuation hypothesis, supplemental HLM analyses of data arrayed by time since the disclosure of abuse indicated that cortisol activity was initially significantly higher, t (1, 425) = 2.18, p < .05, and slopes were significantly less steep t (1, 205) = −22.66, p < .01, for abused females. These findings demonstrate how the experience of childhood abuse might disrupt the neurobiology of stress, providing some support for the attenuation hypothesis that victims of abuse may experience cortisol hyposecretion subsequent to a period of heightened secretion.

Lifetime trauma histories were ascertained for females with confirmed histories of childhood sexual abuse and comparison females participating in a longitudinal, prospective study. Abused participants reported twice as many subsequent rapes or sexual assaults (p = .07), 1.6 times as many physical affronts including domestic violence (p = .01), almost four times as many incidences of self-inflicted harm (p = .002), and more than 20% more subsequent, significant lifetime traumas (p = .04) than did comparison participants. Sexual revictimization was positively correlated with posttraumatic stress disorder symptoms (PTSD), peritraumatic dissociation, and sexual preoccupation. Physical revictimization was positively correlated with PTSD symptoms, pathological dissociation, and sexually permissive attitudes. Self-harm was positively correlated with both peritraumatic and pathological dissociation. Competing theoretical explanations for revictimization and self-harm are discussed and evaluated.