Research on stress and health is growing at a rapid rate. Each year important new discoveries are being made about the pathways through which stress impacts physiological functioning and disease. The following list is in no way exhaustsive; rather the purpose is to highlight some of the current major findings. For those interested in finding more research, we encourage you to go databases such as Medline or PsycINFO to get a more indepth view of the current research literature covering stress and health.
Douglas Carroll et al. (2012). Increased blood pressure reactions to acute mental stress are associated with 16-year cardiovascular disease mortality. Psychophysiology, 49, 1444-1448.
This study examined 431 participants from the West of Scotland Twenty-07 Study. Participants were 63 years old at the time of the stress testing which involved measuring blood pressure during a baseline period and during mental arithmetic stress. Participants were then tracked over the next 16 years, during which time 38 died of cardiovascular disease. Blood pressure reaction to stress was positively associated with cardiovascular disease mortality; in other words, the more exaggerated the person's stress response, the more likely they would die of cardiovascular disease during the next 16 years. The authors conclude that the long term effects of exaggerated stress reactivity appears to have an erosive effect on the cardiovascular system, thereby contributing to higher cardiovascular disease risk.
Sheldon Cohen et al. (2012). Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. PNAS, 109, 5995-5999.
Two studies were conducted to examine the hypothesis that chronic stress results in glucocorticoid receptor resistance (GCR) which in turn results in failure to down-regulate the body's inflammatory response. The first study they examined 276 health adult volunteers, and the second study involved 79 subjects, in both studies participants were quarantined for 5 days after being exposed to one of two rhinoviruses. They found that chronic stress predicted GCR, and that GCR predicted likelihood of catching a cold and increased inflammatory response. The authors conclude that because inflammation plays an important role in the onset and progression of a wide range of diseases, the GCR/inflammation relationship may have important implications for understanding how stress impacts health.
Majon Bhasin et al. (2013). Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways. PLoS ONE, 8, e62817.
Article abstract: The relaxation response (RR) is the counterpart of the stress response. Millennia-old practices evoking the RR include meditation, yoga and repetitive prayer. Although RR elicitation is an effective therapeutic intervention that counteracts the adverse clinical effects of stress in disorders including hypertension, anxiety, insomnia and aging, the underlying molecular mechanisms that explain these clinical benefits remain undetermined. To assess rapid time-dependent (temporal) genomic changes during one session of RR practice among healthy practitioners with years of RR practice and also in novices before and after 8 weeks of RR training, we measured the transcriptome in peripheral blood prior to, immediately after, and
15 minutes after listening to an RR-eliciting or a health education CD. Both short-term and long-term practitioners evoked significant temporal gene expression changes with greater significance in the latter as compared to novices. RR practice enhanced expression of genes associated with energy metabolism, mitochondrial function, insulin secretion and telomere maintenance, and reduced expression of genes linked to inflammatory response and stress-related pathways. Interactive network analyses of RR-affected pathways identified mitochondrial ATP synthase and insulin (INS) as top upregulated critical molecules (focus hubs) and NF-kB pathway genes as top downregulated focus hubs. Our results for the first time indicate that RR elicitation, particularly after long-term practice, may evoke its downstream health benefits by improving mitochondrial energy production and utilization and thus promoting mitochondrial resiliency through upregulation of ATPase and insulin function. Mitochondrial resiliency might also be promoted by RR-induced downregulation of NF-kB associated upstream and downstream targets that mitigates stress.
David Mohr et al. (2012). A randomized trial of stress management for the prevention of new brain lesions in MS. Neurology, 79, 412-419.
Objectives: This trial examined the efficacy of a stress management program in reducing neuroimaging markers of multiple sclerosis (MS) disease activity. Methods: A total of 121 patients with relapsing forms of MS were randomized to receive stress management therapy for MS (SMT-MS) or a wait-list control condition. SMT-MS provided 16 individual treatment sessions over 24 weeks, followed by a 24-week post-treatment follow-up. The primary outcome was the cumulative number of new gadolinium-enhancing (Gd) brain lesions on MRI at weeks 8, 16, and 24. Secondary outcomes included new or enlarging T2 MRI lesions, brain volume change, clinical exacerbation, and stress. Results: SMT-MS resulted in a reduction in cumulative Gd lesions (p 0.04) and greater numbers of participants remained free of Gdlesions during the treatment (76.8% vs 54.7%, p 0.02), compared to participants receiving the control treatment. SMT-MS also resulted in significantly reduced numbers of cumulative new T2 lesions (p 0.005) and a greater number of participants remaining free of new T2 lesions (69.5% vs 42.7%, p 0.006). These effects were no longer detectable during the 24-week post-treatment follow-up period. Conclusions: This trial indicates that SMT-MS may be useful in reducing the development of new MRI brain lesions while patients are in treatment. Classification of evidence: This study provides Class I evidence that SMT-MS, a manualized stress management therapy program, reduced the number of Gd lesions in patients with MS during a 24-week treatment period. This benefit was not sustained beyond 24 weeks, and there were no clinical benefits.
Keely Muscatell and Naomi Eisenberger (2012). A social neuroscience perspective on stress and health. Social and Personality Psychology Compass, 6, 890-904.
Psychological stress is a major risk factor for the development and progression of a number of diseases, including cardiovascular disease, cancer, arthritis, and major depression. A growing body of research suggests that long term, stress-induced activation of the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis may lead to increases in inflammation, which is known to play a key role in the pathophysiology of a variety of diseases. Furthermore, the burgeoning fields of social neuroscience and health neuroscience have begun to identify the neurocognitive mechanisms by which stress may lead to these physiological changes. Here we review the literature examining the neurocognitive correlates of stress-induced SNS, HPA, and inflammatory responses. Specifically, we summarize the results of neuroimaging studies that have examined the neural correlates of stress-related increases in SNS, HPA, and inflammatory activity. A set of neural systems involved in threat processing, safety processing, and social cognition are suggested as key contributors to stress-related changes in physiology. We conclude by offering suggestions for future research in the exciting new field of health neuroscience.
M. Novak et al. (2012). Perceived stress and incidence of Type 2 diabetes: a 35-year follow-up study of middle-aged Swedish men. Diabetic Medicine, 30, e8-e16.
Aim To explore incident cases of diagnosed diabetes over 35 years of follow-up in relation to self-perceived stress at baseline. MethodsThis was a population-based random sample of 7251 men derived from the Primary Prevention Trial Study, aged 47–56 years at baseline and without prior history of diabetes, coronary heart disease and stroke. Incident diabetes was identified from hospital discharge and death registries as principal or secondary diagnosis. Cox proportional hazards regression was used to evaluate the potential association between stress and diabetes. Results During a 35-year follow-up, a total of 899 men were identified with diabetes. The crude incidence was 5.2 per 1000 persons-years. At baseline, 15.5% men reported permanent stress related to conditions at work or home. After adjusting for age and competing risk of death, the estimated 35-year conditional probability of diabetes in men with permanent stress was 42.6%, compared with 31.0% for those with periodic stress and 31.2% with no stress. In ageadjusted Cox regression analysis, men with permanent stress had a higher risk of diabetes [hazard ratio 1.52 (95% CI 1.26–1.82)] compared with men with no (referent) or periodic stress [hazard ratio 1.09 (95% CI 0.94–1.27)]. The association between stress and diabetes was slightly attenuated but remained significant after adjustment for age, socioeconomic status, physical inactivity, BMI, systolic blood pressure and use of anti-hypertensive medication [hazard ratio 1.45 (95% CI 1.20–1.75)]. When examining principal diagnosis of diabetes cases separately from secondary diagnoses cases, the excess risk of diabetes associated with permanent stress remained significant both in age (only) and multivariable adjusted models. Conclusion Self-perceived permanent stress is an important long-term predictor of diagnosed diabetes, independently of socio-economic status, BMI and other conventional Type 2 diabetes risk factors.
Fredrik Stenius et al. (2011). Salivary cortisol levels and allergy in children: The ALADDIN birth cohort. Journal of Allergy and Clinical Immunology, 128, 1335-1339.
Background: Pre- and postnatal stress have been related to allergy in children, but evidence from prospective studies is limited. Several environmental factors can influence the salivary cortisol level, which is used as a measure of activity of the hypothalamic-pituitary-adrenal axis. Objective: The aim of this study was to assess the association between salivary cortisol levels at 6 months of age and allergic manifestations during the first 2 years of life. Methods: Salivary samples for the analysis of cortisol level were collected at 6 months of age on 3 occasions during 1 day from 203 children. Blood samples were collected at 6, 12, and 24 months of age for analyses of specific IgE. Information on allergy-related symptoms was obtained by repeated examinations of the children. Generalized estimating equation statistics were used to calculate the overall risk for outcome measures. Results: The adjusted odds ratio for the relationship between morning cortisol level and IgE sensitization was 1.60 (95% CI,1.22-2.10, P 5 .001) and for eczema it was 1.28 (95% CI, 1.03-1.59,P 5 .026). The odds ratio for afternoon cortisol level in relation to sensitization and eczema was 1.56 (95% CI, 1.26-1.94, P < .001) and 1.33 (95% CI, 1.12-1.58, P 5 .001), respectively, and for evening cortisol level it was 1.49 (95% CI, 1.22-1.83, P < .001) and 1.37 (95% CI, 1.18-1.59, P < .001). Salivary cortisol level in the evening was associated with food allergy.Conclusion: The association between salivary cortisol levels in infancy and allergic sensitization and allergic symptoms suggests a role of an altered hypothalamic-pituitary-adrenal axis in the etiological process of allergies.
Mikael Wikgren et al. (2012). Short telomeres in depression and the general population are associated with a hypocortisolemic state. Biological Psychiatry, 71, 294-300.
Background: The hypothalamic-pituitary-adrenal (HPA) axis plays a central role in stress regulation, and leukocyte telomere length (TL) has been suggested to represent a cumulative measure of stress. Depression is intimately related with stress and frequently exhibits a dysregulated HPA axis. We aimed to study the relationships between TL and biological and psychological facets of stress in recurrent major depressive disorder and controls. Methods: Leukocyte TL was measured in 91 subjects with recurrent major depressive disorder and 451 control subjects. Stress was assessed from both a biological perspective, by assessing HPA axis function with a weight-adjusted very-low-dose dexamethasone suppression test (DST), and a psychological perspective, with self-report questionnaires. Results: TL was shorter among patients compared with control subjects (277 base pairs, p .001). Overall, short TL was associated with a hypocortisolemic state (low post-DST cortisol and high percentage of cortisol reduction after the DST) among both patients and control subjects but more pronounced among patients. This state, which was overrepresented among patients, was characterized by high familial loading of affective disorders among patients (p .001) and high C-reactive protein levels among control subjects (p .040). TL was also inversely associated with stress measured with the Perceived Stress Questionnaire (rs.258, p .003). Conclusions: Short TL is associated with depression and hypocortisolism. Because hypocortisolism has been shown to develop from chronic stress exposure, our findings corroborate the concept of TL as a cumulative measure of stress and provide novel insights into the detrimental role of stress in depressive illness and the general population.