NTERNATIONAL R EVIEW OF I NDUSTRIAL AND O RGANIZATIONAL P SYCHOLOGY 2005 the allostatic response on target cells is prolonged, and when the mediators of

280 I NTERNATIONAL R EVIEW OF I NDUSTRIAL AND O RGANIZATIONAL P SYCHOLOGY 2005 the allostatic response on target cells is prolonged, and when the mediators of

this response, when no longer needed, remain operative, receptor desensitiza- tion andtissue damage may follow, representing allostatic load(McEwen, 1998, 1999). An initial operationalization of the notion of allostatic load comprisedassessments of ten biological parameters reflecting functioning of the HPA axis, sympathetic nervous system, cardiovascular system, and metabolic processes (Seeman, McEwen, Rowe, & Singer, 2001). Higher scores on a summary numerical measure of allostatic loadwere shown in several studies to predict four major health outcomes: incidence of CVD, decline in physical and cognitive functioning, and mortality (Seeman et al., 2001). Empirical evidence supporting this possible pathway is meager: only one study, employing a cross-sectional design, measured a variable analogous to burnout andallostatic load(Schnorpfeil et al., 2003). In this study, job demands were found to be related significantly to allostatic load. This finding is consistent with the idea that burnout, representing a cumulative measure of the effects of chronic stress on persons’ affective states, may be linkedto allostatic load. Allostatic load emphasizes the point that there are multiple pathways to morbidity and mortality (Seeman et al., 2001). Analogously, the burnout–allostatic loadlinkage may represent the idea that high scores on burnout could be regarded as an early warning system indicating that potentially deleterious physiological processes are under way.

An additional possible biological mechanism that may explain burnout’s effects on physical health is hypocortisolism, observedto occur in chronically stressed persons (Heim, Ehlert, & Hellhammer, 2000). For individuals with depleted coping resources, repeated exposures to chronic stress may result in reduced HPA axis reactivity (Mathews, Gump, & Owens, 2001; McEwen, 1998, 1999). This is probably associatedwith prolongedactivation of the hypothalamic corticotrophin releasing factor (CRF) secretion that leads to down-regulation of pituitary CRF receptors, ultimately producing cortisol levels below the normal baseline (Heim et al., 2000). Hypocortisolism may be

a relevant factor in the pathogenesis of several disorders, including inflam- matory andautoimmune disorders, andhas been reportedin healthy subjects exposed to chronic stress such as parents of terminally ill children, soldiers in Vietnam, andBosnian prisoners of war (Heim et al., 2000; Rohled er, Joksimovic, Wolf, & Kirschbaum, 2004). For example, white-collar employ- ees with high work loads have been shown to demonstrate decreased basal plasma morning cortisol levels as well as bluntedcortisol responses to increases in their work responsibilities (cf. Heim et al., 2000). The study by Pruessner, Hellhammer, and Kirschbaum (1999) provides direct evidence supporting the conjecturedpathway leading from burnout to physical health in finding lower overall cortisol secretion for teachers with high burnout levels (measuredby the MBI) while perceivedstress was foundto be corre- lated with increased cortisol levels, indicative of differential effects of stress andof burnout on HPA axis regulation. Yet another recent study (Moch,

281 Panz, Joffe, Havlik, & Moch, 2003) of 16 female patients diagnosed, by

B URNOUT AND H EALTH R EVIEW

using cut-off scores basedon the MBI, to have clinical burnout, concluded that there is functional hypocortisolism in burnout which is not restored with stress management intervention, despite clinical and psychological improvements.

The fieldof psychoneuroimmunology may provid e insights into yet another possible biological pathway linking burnout andhealth. The current paradigm guiding health research, which views brain functioning andthe end ocrine, nervous, andimmune systems as continuously inter- acting, is the prevailing paradigm in this field (for reviews see Dantzer, 2004; Maier & Watkins, 1998). Evidence accumulated in this field indicates that psychosocial stress, as well as chronic inflammation, through the mediating factors of peripheral and brain cytokines, may induce depressed mood, fatigue, andalterations in the cognitive functions, andthat the latter may compromise the individual’s immune competence and, via external andinternal pathogens, may leadto chronic inflammation (Baum & Posluszny, 1999; Dantzer, 2004; Dougall & Baum, 2001). There is evidence that mental andphysical exhaustion are relatedto inflammation biomarkers (Appels, Bar, Bar, Bruggeman, & de Baets, 2000). However, it is unclear if inflammation causes exhaustion or burnout, whether pre-existing feelings of burnout or exhaustion set the stage for the unfolding of inflammatory processes in the body, or whether they are reciprocally interrelated. Longitudinal studies in which the participants’ levels of burnout and physical health are monitoredover time may provide solidsupport to the expectation that the causal pathway is from burnout to physical health, with several possible mediating variables. To our knowledge, such studies have yet to