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EDITORIAL COMMENT |
Department of Psychiatry, University of California, San Diego, and VA San Diego Healthcare System, La Jolla, CA 92093-0680, Email: igrant@ucsd.edu
Dyck et al. (1) report an association between amount of burden and number of infectious illnesses experienced by those providing care for a person with schizophrenia and the severity and type of symptoms exhibited by the patient. More specifically, more severe "negative" symptoms of schizophrenia are associated with increased caregiver burden, whereas increased "positive" symptoms are associated with more episodes of infectious illness in caregivers. Regression models indicated that about 40% of the variation in caregiver burden was explained by a combination of negative schizophrenic symptoms, caregiver coping activity characterized by increased anger control and self-blame, and reduced tangible social support. Approximately 29% of the variation in illness episodes reported by caregivers was explained by a combination of positive symptoms of schizophrenia, reduced satisfaction with social support, and isolated illness events. Additional associations of interest were that number of infectious illnesses reported by the caregiver was inversely correlated with caregiver age and inversely related to the number of years since the patient was diagnosed with schizophrenia.
The report by Dyck et al. contributes to a growing body of literature suggesting that, from the perspective of the caregiver, caregiving may be not only burdensome but actually hazardous to the caregiver’s health (2). Much of the evidence for this association comes from research with caregivers of patients with Alzheimer’s disease, in which typically older caregivers have been found to report high burden, depression, and infectious illnesses more often than persons in comparison groups. The present study usefully extends this work in two ways. First, the caregivers studied here are middle aged and are caring for a person with a chronic mental disorder. Considering that as many as 1% of Americans are schizophrenic and that the typical age of diagnosis is early adulthood, the time horizon for caring for persons with this disorder is considerably longer than that for persons with Alzheimer’s disease. As the authors point out, caregivers of Alzheimer patients can see an end to their caregiving, and although that end is obviously undesirable in the short term, it leads to a relief of burden in the long term. Thus, we may need to revise our conceptualizations of chronic stress to include "very-long-term" stress. The cognitive and physiological correlates of such very-long-term stress have yet to be explored.
It is intriguing that Dyck et al. have noted differential relationships between two measures of caregiver adaptation and two types of symptomatology. Negative symptoms were more likely to be associated with report of burden, whereas positive symptoms were more associated with number of infectious illness (eg, upper respiratory infection) episodes. Although the association between burden and negative symptomatology (or any symptomatology for that matter) is easier to understand at first blush, the relationship of positive symptoms to infectious illness is more fascinating. In principle, we can invoke two broad classes of mechanisms that may underlie this relationship. Health changes may be mediated primarily by behavioral factors or cognitive-physiological factors.
Behavioral factors can be primary or secondary. Primary factors are those that require changes in the caregiver’s lifestyle to care for a person with a mental disorder. For example, caregivers may need to alter their schedule to take the patient to clinic visits, thereby potentially exposing themselves more frequently to the infectious illnesses of others. Secondary behavioral factors are those that represent responses to the responsibility of caregiving. They include such factors as having less time to look after oneself, eating poorly, exercising less, and smoking more. Each of these changes in health behaviors could predispose a caregiver to infectious illness.
Cognitive-physiological mechanisms refer to the more classic "stress-illness" paradigm. Thus, the behavior or state of the patient leads to a cognitive appraisal on the part of the caregiver. Depending on the nature of this appraisal, this may lead to physiological change through a cascade of cortical-limbic and limbic-hypothalamic activation. It is thought that corticotropin-releasing hormone plays a central role in this cascade and can trigger activation both of the sympathetic-adrenal-medullary (SAM) and hypothalamic-pituitary-adrenal-cortical (HPA) systems (Fig. 1). Via the SAM system, there may be increased tone of the sympathetic nervous system as well as greater release of epinephrine and norepinephrine from the adrenal medulla. Both of these catecholamines can act on ß-adrenergic receptors on immune cells to alter their activity. For example, Irwin et al. (3) demonstrated that the intracerebroventricular administration of corticotropin-releasing factor reduced natural killer cell activity in rats and that this effect was abolished by the ganglionic blocker chlorisondamine. Furthermore, in human studies, it was demonstrated that there was an inverse association between concentration of neuropeptide Y (coreleased with norepinephrine from sympathetic terminals) and natural killer cell activity in a group of Alzheimer caregivers (4). Activation of the sympathetic nervous system may also alter perfusion in mucous membranes, which may itself predispose to local viral infection.
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and interleukin 8, at wound sites, and the concentration of these proinflammatory cytokines was inversely related to salivary cortisol concentration. Although some of the molecular cascades are now theoretically "knowable," we need to define more precisely what alterations occur under conditions of chronic stress and under what circumstances. Relevant to this, our group recently observed that Alzheimer caregivers who were classified as "mismatched" (ie, were required to give far more caregiving than the amount of respite received) had 60% fewer selectin-negative CD8+ CD62L- cellular adhesion molecules than "nonmismatched" caregivers (7). Furthermore, plasma epinephrine levels were 44% higher in the mismatched group, suggesting that chronic stress in elderly caregivers leads to a decrement in cellular adhesion molecules, possibly by adrenomedullary activation. Another factor to be considered in the chronic stress model is how successfully adapted the organism is to the stressor. Selye (8) showed long ago that the HPA axis reequilibrates to a chronic stressor; indeed, there may be no apparent changes in circulating neuroendocrines during the adapted phase, and an additional challenge may be required to reveal an augmented response (eg, augmented adrenocorticotropic response to corticotropin-releasing hormone; that indicates heightened physiological arousability in a system that is partially adapted (9). In theory, unless there is superimposed added stress, the system can stay adapted without ill effect. In the presence of added challenge, dysfunction might result (Fig. 2).
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ACKNOWLEDGMENTS
This work was supported by National Institute on Aging of the National Institutes of Health Grant 9 R01AG 15301 to I.G.
REFERENCES
This article has been cited by other articles:
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  B. T. Mausbach, J. E. Dimsdale, M. G. Ziegler, P. J. Mills, S. Ancoli-Israel, T. L. Patterson, and I. Grant Depressive Symptoms Predict Norepinephrine Response to a Psychological Stressor Task in Alzheimer's Caregivers Psychosom Med, July 1, 2005; 67(4): 638 - 642. [Abstract] [Full Text] [PDF]
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I. Grant, K. A. Adler, T. L. Patterson, J. E. Dimsdale, M. G. Ziegler, and M. R. Irwin Health Consequences of Alzheimer's Caregiving Transitions: Effects of Placement and Bereavement Psychosom Med, May 1, 2002; 64(3): 477 - 486. [Abstract] [Full Text] [PDF]
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J. K. Kiecolt-Glaser, L. McGuire, T. F. Robles, and R. Glaser Psychoneuroimmunology and Psychosomatic Medicine: Back to the Future Psychosom Med, January 1, 2002; 64(1): 15 - 28. [Abstract] [Full Text] [PDF]
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CVR = change in cardiovascular reactivity; E = epinephrine; NE = norepinephrine; NK = natural killer lymphocyte; NPY = neuropeptide Y; NS = nonsympathetic; ß2 = ß2-adrenergic receptor.