Social Safety Theory hypothesizes that developing and maintaining friendly social bonds is a fundamental organizing principle of human behavior and that threats to social safety are a critical ...feature of psychological stressors that increase risk for disease. Central to this formulation is the fact that the human brain and immune system are principally designed to keep the body biologically safe, which they do by continually monitoring and responding to social, physical, and microbial threats in the environment. Because situations involving social conflict, isolation, devaluation, rejection, and exclusion historically increased risk for physical injury and infection, anticipatory neural-immune reactivity to social threat was likely highly conserved. This neurocognitive and immunologic ability for humans to symbolically represent and respond to potentially dangerous social situations is ultimately critical for survival. When sustained, however, this multilevel biological threat response can increase individuals' risk for viral infections and several inflammation-related disease conditions that dominate present-day morbidity and mortality.
Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of ...social-environmental adversity with internal biological processes that drive depression pathogenesis, maintenance, and recurrence. Central to this theory is the hypothesis that interpersonal stressors involving social threat (e.g., social conflict, evaluation, rejection, isolation, and exclusion) upregulate inflammatory processes that can induce several depressive symptoms, including sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. The original article describing this formulation (Psychol Bull 140:774–815, 2014) addressed critical questions involving depression onset and recurrence, as well as why depression is strongly predicted by early life stress and comorbid with anxiety disorders and certain physical disease conditions, such as asthma, rheumatoid arthritis, chronic pain, and cardiovascular disease. Here, we extend the theory to help explain sex differences in depression prevalence, which is a defining feature of this disorder. Central to this extension is research demonstrating that ovarian hormone fluctuations modulate women’s susceptibility to stress, brain structure and function, and inflammatory activity and reactivity. These effects are evident at multiple levels and are highly context-dependent, varying as a function of several factors including sex, age, reproductive state, endogenous versus exogenous hormones, and hormone administration mode and dose. Together, these effects help explain why women are at greater risk for developing inflammation-related depressed mood and other neuropsychiatric, neurodevelopmental, and neurodegenerative disorders during the reproductive years, especially for those already at heightened risk for depression or in the midst of a hormonal transition period.
Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically ...plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation.
Mindfulness meditation represents a mental training framework for cultivating the state of mindful awareness in daily life. Recently, there has been a surge of interest in how mindfulness meditation ...improves human health and well‐being. Although studies have shown that mindfulness meditation can improve self‐reported measures of disease symptomatology, the effect that mindfulness meditation has on biological mechanisms underlying human aging and disease is less clear. To address this issue, we conducted the first comprehensive review of randomized controlled trials examining the effects of mindfulness meditation on immune system parameters, with a specific focus on five outcomes: (1) circulating and stimulated inflammatory proteins, (2) cellular transcription factors and gene expression, (3) immune cell count, (4) immune cell aging, and (5) antibody response. This analysis revealed substantial heterogeneity across studies with respect to patient population, study design, and assay procedures. The findings suggest possible effects of mindfulness meditation on specific markers of inflammation, cell‐mediated immunity, and biological aging, but these results are tentative and require further replication. On the basis of this analysis, we describe the limitations of existing work and suggest possible avenues for future research. Mindfulness meditation may be salutogenic for immune system dynamics, but additional work is needed to examine these effects.
Life stress is central to many contemporary theories of human health and behavior. Despite this fact, numerous conceptual and measurement issues remain unresolved. The present article explores these ...topics by first summarizing several key definitional and conceptual matters that are important for life stress research. Second, I introduce stressnology, defined herein as the fictitiously named, but otherwise very real and problematic approach to studying life stress exposure that involves measuring only the superficial contours of this very complex construct. Finally, I review some recent methodological advancements that have the potential to move us past primitive approaches to conceptualizing and assessing life stress. Ultimately, although the influence that life stress has on human health and behavior is profound, our understanding of this construct—and how it affects wellbeing, functioning, and development—is still very limited. Using state-of-the-art instruments for assessing life stress exposure, especially across the entire life course, should therefore be a top scientific and clinical priority.
Life Stress and Health Slavich, George M.
Teaching of psychology,
10/2016, Volume:
43, Issue:
4
Journal Article
Peer reviewed
Life stress is a central construct in many models of human health and disease. The present article reviews research on stress and health, with a focus on (a) how life stress has been conceptualized ...and measured over time, (b) recent evidence linking stress and disease, and (c) mechanisms that might underlie these effects. Emerging from this body of work is evidence that stress is involved in the development, maintenance, or exacerbation of several mental and physical health conditions, including asthma, rheumatoid arthritis, anxiety disorders, depression, cardiovascular disease, chronic pain, human immunodeficiency virus/AIDS, stroke, and certain types of cancer. Stress has also been implicated in accelerated biological aging and premature mortality. These effects have been studied most commonly using self-report checklist measures of life stress exposure, although interview-based approaches provide a more comprehensive assessment of individuals’ exposure to stress. Most recently, online systems like the Stress and Adversity Inventory (STRAIN) have been developed for assessing lifetime stress exposure, and such systems may provide important new information to help advance our understanding of how stressors occurring over the life course get embedded in the brain and body to affect lifespan health.
Recent estimates suggest that more than 50% of all deaths worldwide are currently attributable to inflammation-related diseases. Psychosocial interventions may represent a potentially useful strategy ...for addressing this global public health problem, but which types of interventions reliably improve immune system function, under what conditions, and for whom are unknown.
To address this issue, we conducted a systematic review and meta-analysis of randomized clinical trials (RCTs) in which we estimated associations between 8 different psychosocial interventions and 7 markers of immune system function, and examined 9 potential moderating factors.
PubMed, Scopus, PsycInfo, and ClinicalTrials.gov databases were systematically searched from February 1, 2017, to December 31, 2018, for all relevant RCTs published through December 31, 2018.
Eligible RCTs included a psychosocial intervention, immune outcome, and preintervention and postintervention immunologic assessments. Studies were independently examined by 2 investigators. Of 4621 studies identified, 62 were eligible and 56 included.
Data were extracted and analyzed from January 1, 2019, to July 29, 2019. The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guideline was followed. Data were extracted by 2 investigators who were blind to study hypotheses and analyses, and were then analyzed using robust variance estimation. Analysis included 8 psychosocial interventions (behavior therapy, cognitive therapy, cognitive behavior therapy CBT, CBT plus additive treatment or mode of delivery that augmented the CBT, bereavement or supportive therapy, multiple or combined interventions, other psychotherapy, and psychoeducation), 7 immune outcomes (proinflammatory cytokine or marker levels, anti-inflammatory cytokine levels, antibody levels, immune cell counts, natural killer cell activity, viral load, and other immune outcomes), and 9 moderating factors (intervention type, intervention format, intervention length, immune marker type, basal vs stimulated markers, immune marker measurement timing, disease state or reason for treatment, age, and sex).
The primary a priori outcomes were pretest-posttest-control (ppc) group effect sizes (ppc g) for the 7 immunologic outcomes investigated.
Across 56 RCTs and 4060 participants, psychosocial interventions were associated with enhanced immune system function (ppc g = 0.30, 95% CI, 0.21-0.40; t50.9 = 6.22; P < .001). Overall, being randomly assigned to a psychosocial intervention condition vs a control condition was associated with a 14.7% (95% CI, 5.7%-23.8%) improvement in beneficial immune system function and an 18.0% (95% CI, 7.2%-28.8%) decrease in harmful immune system function over time. These associations persisted for at least 6 months following treatment and were robust across age, sex, and intervention duration. These associations were most reliable for CBT (ppc g = 0.33, 95% CI, 0.19-0.47; t27.2 = 4.82; P < .001) and multiple or combined interventions (ppc g = 0.52, 95% CI, 0.17-0.88; t5.7 = 3.63; P = .01), and for studies that assessed proinflammatory cytokines or markers (ppc g = 0.33, 95% CI, 0.19-0.48; t25.6 = 4.70; P < .001).
These findings suggest that psychosocial interventions are reliably associated with enhanced immune system function and may therefore represent a viable strategy for improving immune-related health.
Many of life's most impactful experiences involve either social safety (e.g., acceptance, affiliation, belonging, inclusion) or social threat (e.g., conflict, isolation, rejection, exclusion). ...According to Social Safety Theory, these experiences greatly impact human health and behavior because a fundamental goal of the brain and immune system is to keep the body biologically safe. To achieve this crucial goal, social threats likely gained the ability to activate anticipatory neural-immune responses that would have historically benefited reproduction and survival; the presence of social safety, in turn, likely dampened these responses. Viewing positive and negative social experiences through this lens affords a biologically based evolutionary account for why certain stressors are particularly impactful. It also provides an integrated, multi-level framework for investigating the biopsychosocial roots of psychopathology, health disparities, aging, longevity, and interpersonal cognition and behavior. Ultimately, this work has the potential to inform new strategies for reducing disease risk and promoting resilience.
•Social Safety Theory posits that developing and maintaining friendly social bonds is critical.•Social conflict, rejection, and exclusion historically increased risk for injury and infection.•Therefore, anticipatory neural-immune reactivity to social threat was likely highly conserved.•This multi-level response to social threat is critical for reproductive success and survival.•However, it also increases peoples' risk for viral infections and inflammatory diseases.
Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors ...can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.
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