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Article

Vanessa L. Burrows

Stress has not always been accepted as a legitimate medical condition. The biomedical concept stress grew from tangled roots of varied psychosomatic theories of health that examined (a) the relationship between the mind and the body, (b) the relationship between an individual and his or her environment, (c) the capacity for human adaptation, and (d) biochemical mechanisms of self-preservation, and how these functions are altered during acute shock or chronic exposure to harmful agents. From disparate 19th-century origins in the fields of neurology, psychiatry, and evolutionary biology, a biological disease model of stress was originally conceived in the mid-1930s by Canadian endocrinologist Hans Selye, who correlated adrenocortical functions with the regulation of chronic disease. At the same time, the mid-20th-century epidemiological transition signaled the emergence of a pluricausal perspective of degenerative, chronic diseases such as cancer, heart disease, and arthritis that were not produced not by a specific etiological agent, but by a complex combination of multiple factors which contributed to a process of maladaptation that occurred over time due to the conditioning influence of multiple risk factors. The mass awareness of the therapeutic impact of adrenocortical hormones in the treatment of these prevalent diseases offered greater cultural currency to the biological disease model of stress. By the end of the Second World War, military neuropsychiatric research on combat fatigue promoted cultural acceptance of a dynamic and universal concept of mental illness that normalized the phenomenon of mental stress. This cultural shift encouraged the medicalization of anxiety which stimulated the emergence of a market for anxiolytic drugs in the 1950s and helped to link psychological and physiological health. By the 1960s, a growing psychosomatic paradigm of stress focused on behavioral interventions and encouraged the belief that individuals could control their own health through responsible decision-making. The implication that mental power can affect one’s physical health reinforced the psycho-socio-biological ambiguity that has been an enduring legacy of stress ever since. This article examines the medicalization of stress—that is, the historical process by which stress became medically defined. It spans from the mid-19th century to the mid-20th century, focusing on these nine distinct phases: 1. 19th-century psychosomatic antecedent disease concepts 2. The emergence of shell-shock as a medical diagnosis during World War I 3. Hans Selye’s theorization of the General Adapation Syndrome in the 1930s 4. neuropsychiatric research on combat stress during World War II 5. contemporaneous military research on stress hormones during World War II 6. the emergence of a risk factor model of disease in the post-World War II era 7. the development of a professional cadre of stress researchers in the 1940s and 50s 8. the medicalization of anxiety in the early post–World War II era 9. The popularization of stress in the 1950s and pharmaceutical treatments for stress, marked by the cultural assimilation of paradigmatic stress behaviors and deterrence strategies, as well pharmaceutical treatments for stress.

Article

Thomas M. Hess, Erica L. O'Brien, and Claire M. Growney

Blood pressure is a frequently used measure in studies of adult development and aging, serving as a biomarker for health, physiological reactivity, and task engagement. Importantly, it has helped elucidate the influence of cardiovascular health on behavioral aspects of the aging process, with research demonstrating the negative effect of chronic high blood pressure on various aspects of cognitive functioning in later life. An important implication of such research is that much of what is considered part and parcel of getting older may actually be reflective of changes in health as opposed to normative aging processes. Research has also demonstrated that situational spikes in blood pressure to emotional stressors (i.e., reactivity) also have implications for health in later life. Although research is still somewhat limited, individual differences in personal traits and living circumstances have been found to moderate the strength of reactive responses, providing promise for the identification of factors that might ameliorate the effects of age-related changes in physiology that lead to normative increases in reactivity. Finally, blood pressure has also been successfully used to assess engagement levels. In this context, recent work on aging has focused on the utility of blood pressure as a reliable indicator of both (a) the costs associated with cognitive engagement and (b) the extent to which variation in these costs might predict both between-individual and age-related normative variation in participation in cognitively demanding—but potentially beneficial—activities. This chapter elaborates on these three approaches and summarizes major research findings along with methodological and interpretational issues.

Article

Stephanie J. Wilson, Alex Woody, and Janice K. Kiecolt-Glaser

Inflammatory markers provide invaluable tools for studying health and disease across the lifespan. Inflammation is central to the immune system’s response to infection and wounding; it also can increase in response to psychosocial stress. In addition, depression and physical symptoms such as pain and poor sleep can promote inflammation and, because these factors fuel each other, all contribute synergistically to rising inflammation. With increasing age, persistent exposure to pathogens and stress can induce a chronic proinflammatory state, a process known as inflamm-aging. Inflammation’s relevance spans the life course, from childhood to adulthood to death. Infection-related inflammation and stress in childhood, and even maternal stress during pregnancy, may presage heightened inflammation and poor health in adulthood. In turn, chronically heightened inflammation in adulthood can foreshadow frailty, functional decline, and the onset of inflammatory diseases in older age. The most commonly measured inflammatory markers include C-reactive protein (CRP) and proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α). These biomarkers are typically measured in serum or plasma through blood draw, which capture current circulating levels of inflammation. Dried blood spots offer a newer, sometimes less expensive collection method but can capture only a limited subset of markers. Due to its notable confounds, salivary sampling cannot be recommended. Inflammatory markers can be added to a wide range of lifespan developmental designs. Incorporating even a single inflammatory assessment to an existing longitudinal study can allow researchers to examine how developmental profiles and inflammatory status are linked, but repeated assessments must be used to draw conclusions about the associations’ temporal order and developmental changes. Although the various inflammatory indices can fluctuate from day to day, ecological momentary assessment and longitudinal burst studies have not yet incorporated daily inflammation measurement; this represents a promising avenue for future research. In conclusion, mounting evidence suggests that inflammation affects health and disease across the lifespan and can help to capture how stress “gets under the skin.” Incorporating inflammatory biomarkers into developmental studies stands to enhance our understanding of both inflammation and lifespan development.

Article

Idan Shalev and Waylon J. Hastings

Stress is a multistage process during which an organism perceives, interprets, and responds to threatening environmental stimuli. Physiological activity in the nervous, endocrine, and immune systems mediates the biological stress response. Although the stress response is adaptive in the short term, exposure to severe or chronic stressors dysregulates these biological systems, promoting maladaptive physiology and an accelerated aging phenotype, including aging on the cellular level. Two structures implicated in this process of stress and cellular aging are telomeres, whose length progressively decreases with age, and mitochondria, whose respiratory activity becomes increasingly inefficient with advanced age. Stress in its various forms is suggested to influence the maintenance and stability of these structures throughout life. Elucidating the interrelated connection between telomeres and mitochondria and how different types of stressors are influencing these structures to drive the aging process is of great interest. A better understanding of this subject can inform clinical treatments and intervention efforts to reduce (or even reverse) the damaging effects of stress on the aging process.