triggered by stimuli associated with the original traumatic event (flashbacks) and in some people are so intrusive that normal functioning is no longer possible. Those strong traumatic memories are often expressed in the form of intrusive recollections, flashbacks, and repetitive nightmares (McGaugh et al. 1992).
Epinephrine plays a critical role in the encoding of memory for events and stimuli that are arousing, stressful, or fear provoking. In animal models, it has been implicated in memory consolidation, and the effect appears to be time-dependent (Gold and Van Buskirk 1975). As discussed earlier, the acute stress response activates the fast pathway in which the locus coeruleus releases epinephrine in response to signals from the amygdala and BNST. Most nerve projections from the locus coeruleus are excitatory in function and activate, for example, the sympathetic nervous system, amygdala, and HPA axis. However, some of the projections are inhibitory and act on the prefrontal cortex and the parasympathetic nervous system, the systems that normally keep the sympathetic nervous system in check. Inhibiting the prefrontal cortex favors instinctual responses at the expense of more complex thinking and planning (Charney 2004). Chronic stress also increases the activity of the locus coeruleus with the same effects as acute stress but over longer periods, thereby contributing to chronic anxiety, fear, and intrusive memories (Charney 2004). As previously discussed, chronic stress also goes on to increase concentrations of epinephrine outside the brain that can affect other organ systems.
During the acute stress response, epinephrine mobilizes the body’s energy for fight or flight. The energy comes from stored fats and from glycogen in the liver. When mobilized by epinephrine during the acute stress response, the liver breaks down fats into fatty acids and glycerol and breaks down glycogen into glucose and releases them into the circulation. Circulating glucose, fatty acids, and glycerol are distributed to each cell in the body, particularly muscles (during the acute stress response) where they are oxidized for energy. With the cessation of acute stress, cortisol acts to replenish energy supplies in the liver and adipose tissue. Many of the basic metabolic functions related to food intake, storage, and conversion to energy are altered by excess concentrations of cortisol and epinephrine in chronic stress (McEwen and Lasley 2002). The endocrine system can respond to chronic stress with an array of effects that are often overlapping and interactive; some of these are described below.
Chronic stress has long been associated with obesity in humans and animal models (McEwen 2002a; Rosmond et al. 1996). Cortisol enhances pathways that lead to increased deposition of fat (adipose tissue) in the abdominal area. An increase in abdominal fat, as opposed to that in the hips and buttocks, is an important risk factor associated with hypertension, diabetes, and cardiovascular diseases (Black and Garbutt 2002).
Obesity is also caused by higher food intake, which commonly occurs with chronic stress, either as a coping strategy (Dallman et al. 2003) or because of sleep deprivation. Sleep deprivation appears to increase hunger through its association with lower concentrations of an appetite-suppressing hormone (leptin) and higher concentrations of an appetite-enhancing hormone (ghrelin) (Spiegel et al. 2004). An association has been found between body-mass