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From Neurons to Neighborhoods: The Science of Early Childhood Development
digestive system, break down fat stores making energy available to cells, and dampen activity of the immune system. Cortisol is a steroid hormone that plays a myriad of roles in stress physiology. It helps to break down protein stores, liberating energy for use by the body. It suppresses the immune system, suppresses physical growth, inhibits reproductive hormones, and affects many aspects of brain functioning, including emotions and memory.
Current understanding of how psychological stimuli, such as experiences of fear and anxiety, set in motion stress physiology is centered on an area of the brain called the amygdala (Miller and Davis, 1997; Rolls, 1992; Schulkin et al., 1994), which has close back-and-forth communication with areas of the brain involved in attention, memory, planning, and behavior control. In animals, experimentally causing a hyperstimulation of the amygdala (a process termed “kindling”) seems to create a hypersensitization of the fear-stress circuits of the brain and changes in behavior that look like an animal version of posttraumatic stress disorder (Rosen et al., 1996). It is as if the fear circuits get locked in the “on” mode and have trouble shutting off. These circuits course through the amygdala and an area called the bed nucleus of the stria terminalis. They appear to be pathways through which circumstances outside the body set in motion the cascade of events inside the body and the brain that undergird fear-stress responses. These events involve the elevation of cortisol and stimulation of the sympathetic arm of the stress response. In animals, flooding the brain with cortisol for prolonged periods of time produces changes in this process that may lower the threshold for activating the fear-stress system (Makino et al., 1994). The result is an animal that more readily experiences fear, anxiety, and stress and may have a harder time dampening or regulating these responses.
The amygdala is a fairly mature brain area at birth in humans and seems to be fully mature at least as early as a child's first birthday. All anatomical evidence suggests that by the end of the first year, young children should be capable of experiencing psychologically driven fear, anxiety, and stress. Indeed, fear reactions to strangers (Bronson, 1971; Schaffer, 1966; Waters et al., 1975) and anxiety reactions to separation from familiar caregivers (Ainsworth and Bell, 1970; Bowlby, 1973; Sroufe, 1979) are hallmarks of emotional development in late infancy. Brief periods of stress are not expected to be problematic. Indeed, survival requires the capacity to mount a stress response. However, because the stress system functions to put growth-oriented processes on hold, frequent or prolonged periods of stress may negatively affect development.
Evidence from research on rodents and primates suggests that experiences of neglect early in life constitute the kinds of stressful experiences to which young offspring are especially sensitive and may result in a more reactive stress system. In studies of rats, for example, when experimenters