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| EDITORIAL |
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| Year : 2016 | Volume
: 1
| Issue : 4 | Page : 107-108 |
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We must continue to tease out the role of stress in the development of disease
Christopher R Stone, Yuchuan Ding
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA
| Date of Submission | 19-Dec-2016 |
| Date of Acceptance | 25-Dec-2016 |
| Date of Web Publication | 18-Jan-2017 |
Correspondence Address:
Yuchuan Ding
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2468-5690.198610
How to cite this article:
Stone CR, Ding Y. We must continue to tease out the role of stress in the development of disease. Environ Dis 2016;1:107-8 |
Today, it seems remarkable that it was once possible as it was just under 10 years ago, to lament the relative lack of credence among members of the biomedical community in the connection between stress and disease. [1] The social/environmental as well as natural/environmental determinants of health have become important issues for our community. Perhaps, this should be understood as reflective of that community's self-regulatory conservatism - its unwillingness to be carried away by the plausibility of a connection absent data and a mechanism - and so accounted to its credit.
In any case, no such lack of credence persists today. The social and environmental determinants of health have become highly important in our community. If the explanation offered above is credible, then it is the veritable surge of work on this subject seen during the past decade that accounts for the change. [2] This is not, of course, to deny the enormous importance of the investigations undertaken into this subject before the past decade. Indeed, it was only due to the paradigm-setting writings of names such as Walter Cannon (who in 1928 proposed a mediating role for the hypothalamus between affective stimuli and peripheral physiological responses) [3] and Hans Seyle (whose pioneering work throughout the latter half of the 20 th century concerned the transduction between social environment and pathology effected by the hypothalamic-pituitary-adrenal axis) that contemporary work on this subject is even thinkable. [4] It is not, therefore, merely the volume of this decade's stress-disease science that has granted the connection the extraordinary acceptance and interest it currently enjoys. It is, rather, the unprecedentedly integrative nature of the new science that accounts for its consensus-promoting effect.
This new nature is due largely to the dual application of technological and theoretical advances, such as massively parallel molecular assay systems to assess the role of stress on gene expression, noninvasive imaging modalities for established biomarkers relevant in the transduction between stress and pathology, [5] elaboration through neuroimaging of the interplay between the physiological consequences of the stress response and the neural appraisals that initiate them, [6] animal models that have helped to consolidate links between adverse social circumstances and temporally distant downstream stress-mediated physiological modifications, [7] statistical techniques that permit the generalization of theoretical frameworks from broad collections of experimental results, [8] and others. Together, these advances have resulted in an integrated appreciation of the whole pathway from psychosocial causes to pathophysiological effects, to a degree beyond what was previously possible. As such, it is now uncontroversial to list stress as an important etiological factor in many of the most common diseases, some of which include asthma, rheumatoid arthritis, anxiety disorders, depression, cardiovascular disease, chronic pain, HIV/AIDS, stroke, and cancer. [9],[10],[11] This is especially true of diseases, such as atherosclerosis, NIDDM, and asthma, known to be mediated by a chronic inflammatory process. [12]
Owing to progressive empirical elucidation of connections between the different points along the chain of causality, it is fair to say that there is broad ontological consensus emerging about the nature and mechanisms by which stress exerts influence on the development of disease. This should not, however, be construed to imply that the field is free from controversy. One issue it faces is epistemic: How should stress be conceptualized, and how do the implications differ among the possible concepts? Furthermore, what challenges do competing conceptions place in the way of generating general conclusions about the pathophysiological relevance of stress, and how to mitigate its effects? If one settles on an "objective" approach [13] to defining stress, one then faces questions about the applicability of one's conclusions to subjects whose coping abilities differ from those who were studied. A "subjective" approach [14] also faces issues, in this case related to the difficulty of extrapolating concrete categories of stress experience from highly individualized affect reports. Additionally, biological investigations of stress markers, if conducted in isolation from the phenomenology of the stress experience, risk disconnect from upstream targets for psychosocial intervention. Moreover, conceptual difficulties within this field are not confined to the topic of measurement. Stress research also poses considerable temporal problems: How is the chronicity of stress related to the pathologies within which it figures? In other words, if the experience of stress can be either chronic or transient, and can vary in degree and quality over time, how can it be measured, biologically or otherwise, in a manner that yields a concrete, quantitative connection between psychological cause and physiological effect?
It should be emphasized, of course, that these are not insurmountable difficulties; on the contrary, the literature contains numerous and persuasive attempts to deal with them. Of particular interest in this respect is a paper by Cohen et al., [15] in which the disparate approaches cataloged previously are combined in a progressive model, whereby each aspect of the concept of stress is organized into a temporal continuum. According to this model, objective stressors cause stress responses to varying degrees according to differential ameliorative capacities possessed by different subjects exposed to stress. These stress responses, in turn, precipitate homeostatic disruptions through interference with neuroendocrine pathways. Finally, the dysregulation of these pathways precipitates adverse reactions in the cardiovascular, immune, and other systems with which they interface, in magnitude broadly consonant with the extent of dysregulation.
Regardless of the details of a given problem with which this field is faced, the impetus toward further and ever more complete solutions is the same. In addition to figuring in the course of many common and serious diseases, the presence of stress in non-pathological life is nearly universal. Data collected by the American Psychological Association's Stress in America [16] survey indicated that all respondents experienced stress, stress considered to be extreme is on the rise, and that average levels of stress increase as respondents decrease in age. Stress, if those survey respondents accurately represent the population they are supposed to sample, appears to be a fact of modern postindustrial life, as prevalent as cars and taxes. This then gives rise to a further line of questioning, which deserves attention that is as urgent as its range is ubiquitous: if stress is everywhere, what about risk for the pathologies with which it is associated? If the prevalence of the former exceeds that of the latter, what accounts for the insulation of the nonafflicted? How, through medical, psychological, and social intervention, can we replicate the conditions of insulation among those who are afflicted with stress-induced pathology? These are the questions the present generation of research into the stress-disease relationship stands poised to answer.
| References | |  |
| 1. | Cohen S, Janicki-Deverts D, Miller GE. Psychological stress and disease. JAMA 2007;298:1685-7.  |
| 2. | Miller G, Chen E, Cole SW. Health psychology: Developing biologically plausible models linking the social world and physical health. Annu Rev Psychol 2009;60:501-24. |
| 3. | Lane RD, Waldstein SR, Chesney MA, Jennings JR, Lovallo WR, Kozel PJ, et al. The rebirth of neuroscience in psychosomatic medicine, Part I: Historical context, methods, and relevant basic science. Psychosom Med 2009;71:117-34. |
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| 5. | Cohen S, Janicki-Deverts D, Doyle WJ, Miller GE, Frank E, Rabin BS, et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proc Natl Acad Sci U S A 2012;109:5995-9. |
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| 11. | Heidt T, Sager HB, Courties G, Dutta P, Iwamoto Y, Zaltsman A, et al. Chronic variable stress activates hematopoietic stem cells. Nat Med 2014;20:754-8. |
| 12. | Black PH. The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain Behav Immun 2003;17:350-64. |
| 13. | Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med 1998;14:245-58. |
| 14. | Cohen S, Kamarck T, Mermelstein R. A global measure of perceived stress. J Health Soc Behav 1983;24:385-96. |
| 15. | Cohen S, Gianaros PJ, Manuck SB. A stage model of stress and disease. Perspect Psychol Sci 2016;11:456-63. |
| 16. | American Psychological Association. Stress in America: The Impact of Discrimination; 2016. Available from: https://www.apa.org/news/press/releases/stress/2015/impact-of-discrimination.pdf. [Last accessed on 2016 Dec 18]. |
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