In this chapter we examine the question of whether psychosocial stress during pregnancy might be one factor predisposing offspring to the development of psychopathology. We review relevant data from nonhuman primates, rodents, other mammals, and some human studies. The impetus for this chapter is derived from several sources. The first is the observation that prenatal stress effects in both humans and animals appear to share similarities with some forms of psychopathology in humans. These similarities include dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, sleep disturbances, and alterations in brain biogenic amine chemical activity – disturbances that are similar to those found in humans with psychiatric disorders.
The second impetus is the recent move in the field of developmental psychopathology from a deficit model to a risk model. From the perspective of a “deficits” model, a researcher would tend to look for cause-and-effect relationships wherein a specific event, early in life, results in altered developmental outcome (Brown, 1993). Alternately, in a risk model, early life events are not viewed as singular causes of developmental outcomes, but rather they are considered as probabilistic contributors to development along with other events within a dynamic interacting complex process. Also, in a risk model, early life events are viewed as probabilistically associated with a variety of different developmental outcomes; this construct is called multifinality. For example, from a “deficit” viewpoint, preterm delivery can be viewed as a cause of later developmental problems, such as cerebral palsy, subtle neuromotor abnormalities, learning disabilities, and behavior problems (Goldson, 1983; Hertzig, 1981; Koops & Harmon, 1980).
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