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Embodying psychological thriving: physical thriving in response to stress - Thriving: Broadening the Paradigm Beyond Illness to Health
Journal of Social Issues, Summer, 1998 by Elissa S. Epel, Bruce S. McEwen, Jeannette R. Ickovics
Acute stressors, chronic stressors, and growth. It is clear that chronicity of stress is one of the most important moderators of thriving simply because chronic stress blocks opportunities to thrive physically. As with psychological coping, physical responses must be flexible to cope with different types of stressors. However, chronic stress leads to altered response profiles that reflect allostatic load and the loss of flexibility to respond to stressors efficiently, which prevents growth. For example, when chronic stress leads to elevated cortisol, overexposure to cortisol itself can damage many systems (McEwen, 1998; McEwen & Stellar, 1993; Munck et al., 1984) and impair the hypothalamic-pituitary-adrenal axis negative feedback loop's ability to suppress further cortisol secretion (Sapolsky, Kray, & McEwen, 1986). This in turn leads to a poor shutoff response and thus slower cortisol recovery. In addition to this failure to shut off the stress response, chronic stress can lead to other stereotyped aberrant response profiles, such as failure to mount an adequate stress response or being unable to adapt to familiar stressors (McEwen). These rigid responses lead to over- or underexposure to cortisol.
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Chronic stress and elevated cortisol can in turn transform effects of anabolic hormones from protective to detrimental. For example, high cortisol leads to high insulin, and together, these lead to insulin resistance and greater central fat deposition, a risk factor for disease (Kissebah & Krakower, 1994). Acutely, high cortisol leads to high growth hormone, which leads to the growth-promoting IGF- 1. Chronically, high cortisol can lead to high growth hormone but low IGF- 1, and thus growth hormone resistance (Bentham et al., 1993; Unterman & Phillips, 1985), rendering growth hormone ineffective at countering the stress response. Needless to say, these altered hormonal levels lead to a predominantly catabolic state, preventing growth and thriving.
On the other hand, acute stress, partly via cortisol reactivity, can actually enhance immunity temporarily (Dhabhar & McEwen, 1996; Dhabhar, Miller, McEwen, & Spencer, 1996). The cortisol response to acute stressors also prevents other components of the stress response from becoming too toxic and damaging organs (Munck et al., 1984). A growing body of evidence from animal studies shows that arousal from stress can have other positive effects on physiology, mainly when the stress is intermittent rather than chronic (for reviews, see Aldwin & Stokols, 1988; Dienstbier, 1989). Acute intermittent stress necessitates the opposing anabolic systems to bounce back, allowing tight allostasis, whereas chronic stress wears catabolic systems out and results in allostatic load, which facilitates disease processes.
Toughening and growth. Stress arousal can lead to enhanced health by toughening up the stress response systems and thus conditioning the body to be resistant to future stressors. A series of classic animal studies by Weiss and colleagues (Weiss & Glazer, 1975; Weiss, Glazer, Pohorecky, Brick, & Miller, 1975) demonstrated that when animals were under chronic stress, they suffered from learned helplessness and reduced central norepinephrine. However, when exposed to intermittent stressors, they showed signs of physiological toughening (Miller, 1980; e.g., resistance to catecholamine depletion, high peripheral catecholamine responsivity, increased beta receptor sensitivity, and suppression of cortisol). Toughening was in turn related to better performance and stable emotionality (Dienstbier, 1989). Having time to recover from stress appears to be a crucial moderator in determining the effects of stress on both psychological well-being and physiological functioning.
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