Loneliness, Depression, and Inflammation: Evidence from the Multi-Ethnic Study of Atherosclerosis (original) (raw)
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Social Science & Medicine, 2018
Middle-aged adults who are lonely have an elevated likelihood of death. Systemic inflammation may contribute to these increased odds. Using population-level data, this study tested if systemic inflammation is associated with loneliness in a broad age range of middle-aged adults in the United States. Methods: This study used data from the Midlife in the US (MIDUS) survey Biomarker Project, which collected data on psychological, social, and physiological measures from a sample of middle-aged adults. This sample included the 927 participants who were 35-64 years at Biomarker Project data collection. MIDUS collected baseline data from 1995-1996 and a follow-up survey was conducted from 2004-2006. The baseline Milwaukee sample of African Americans was collected in 2005-2006 and the biomarker database was collected in 2004-2009. Biomarkers were obtained from a fasting blood sample. Self-reported loneliness was categorized as feeling lonely or not feeling lonely. Hierarchical regressions examined the association between biomarkers of systemic inflammation (interleukin-6, fibrinogen, C-reactive protein) and feeling lonely, adjusted for covariates. Results: Twenty-nine percent of the sample reported feeling lonely most or some of the time. There was a positive significant relationship between loneliness and the three systemic inflammation biomarkers after controlling for covariates: interleukin-6 (n = 873) (b [se] = 0.07 [0.03], p = .014); fibrinogen (n = 867) (b [se] = 18.24 [7.12], p = .011); and C-reactive protein (n = 867) (b [se] = 0.08 [0.04], p = .035). Conclusions: Feeling lonely is associated with systemic inflammation in middle-aged community-dwelling US adults.
Open Journal of Nursing, 2016
Purpose-The purpose of this study was to evaluate the effectiveness of LISTEN (Loneliness Intervention) on loneliness, depression, physical health, systemic inflammation, and genomic expression in a sample of lonely, chronically ill, older adults. Methods-This was a prospective, longitudinal randomized trial of LISTEN, a novel intervention based on theories of narrative and cognitive restructuring to target specific aspects of loneliness. Twenty-three older, lonely, chronically ill adults were recruited from a family medicine clinic in West Virginia. Participants were randomized to two groups, 13 in LISTEN group (Loneliness Intervention) and 10 in attention control (healthy aging education). Participants attended an enrollment session where they completed consent, survey data (including sociodemographics and chronic illness diagnoses), baseline physical measures, and blood sampling for gene expression analysis. After completing the 5 weekly sessions, all participants attended a 12 week post data collection meeting (17 weeks post-baseline) for survey completion, physical measures and blood sampling. Results-The results of this study show that the LISTEN intervention improves measures of physical and psychosocial health. Specifically, subjects enrolled in LISTEN showed reductions in systolic blood pressure, as well as decreased feelings of loneliness and depression. These changes may be due, in part, to a reduction in systemic inflammation, as measured by interleukin-2. Conclusion-This study provides support for the use of LISTEN in reducing loneliness in chronically ill, older adults. Further, while some of our results are inconclusive, it provides rationale to expand our study population to evaluate the relationship between loneliness and systemic inflammation. In the future, enhancing knowledge about the relationships among loneliness, chronic illness, systemic inflammation, and gene expression of these particular targets, and how these relationships may change over time with intervention will inform translation of findings to clinical settings. * Gene expression changes in lonely chronically ill older adults.
Social Isolation and Adult Mortality: The Role of Chronic Inflammation and Sex Differences
Carolina Digital Repository (University of North Carolina at Chapel Hill), 2013
The health and survival benefits of social embeddedness have been widely documented across social species, but the underlying biophysiological mechanisms have not been elucidated in the general population. We assessed the process by which social isolation increases the risk for allcause and chronic disease mortality through proinflammatory mechanisms. Using the 18-year mortality follow-up data (n = 6,729) from the National Health and Nutrition Examination Survey (1988-2006) on Social Network Index and multiple markers of chronic inflammation, we conducted survival analyses and found evidence that supports the mediation role of chronic inflammation in the link between social isolation and mortality. A high-risk fibrinogen level and cumulative inflammation burden may be particularly important in this link. There are notable sex differences in the mortality effects of social isolation in that they are greater for men and can be attributed in part to their heightened inflammatory responses.
Loneliness Promotes Inflammation During Acute Stress
Psychological Science, 2013
Although evidence suggests that loneliness may increase risk for health problems, the mechanisms responsible are not well understood. Immune dysregulation is one potential pathway: Elevated proinflammatory cytokines such as interleukin-6 (IL-6) increase risk for health problems. In our first study ( N = 134), lonelier healthy adults exposed to acute stress exhibited greater synthesis of tumor necrosis factor-alpha (TNF-α) and IL-6 by peripheral blood mononuclear cells (PBMCs) stimulated with lipopolysaccharide (LPS) than their less lonely counterparts. Similarly, in the second study ( N = 144), lonelier posttreatment breast-cancer survivors exposed to acute stress exhibited greater synthesis of IL-6 and interleukin-1 beta (IL-1β) by LPS-stimulated PBMCs than their counterparts who felt more socially connected. However, loneliness was unrelated to TNF-α in Study 2, although the result was in the expected direction. Thus, two different populations demonstrated that lonelier participan...
Social Science & Medicine, 2011
Social isolation confers increased risk for coronary heart disease (CHD) events and mortality. In two recent studies, low levels of social integration among older adults were related to higher levels of C-reactive protein (CRP), a marker of inflammation, suggesting a possible biological link between social isolation and CHD. The current study examined relationships among social isolation, CRP, and 15-year CHD death in a community sample of US adults aged 40 years and older without a prior history of myocardial infarction. A nested case-cohort study was conducted from a parent cohort of community-dwelling adults from the southeastern New England region of the United States (N = 2,321) who were interviewed in 1989 and 1990. CRP levels were measured from stored sera provided by the nested case-cohort (n = 370), which included all cases of CHD death observed through 2005 (n = 48), and a random sample of non-cases. We found that the most socially isolated individuals had two-and-a-half times the odds of elevated CRP levels compared to the most socially integrated. In separate logistic regression models, both social isolation and CRP predicted later CHD death. The most socially isolated continued to have more than twice the odds of CHD death compared to the most socially integrated in a model adjusting for CRP and more traditional CHD risk factors. The current findings support social isolation as an independent risk factor of both high levels of CRP and CHD death in middle-aged adults without a prior history of myocardial infarction. Prospective study of inflammatory pathways related to social isolation and mortality are needed to fully delineate whether and how CRP or other inflammatory markers contribute to mechanisms linking social isolation to CVD health.
Brain Behavior and Immunity, 2011
Men Inflammatory response Combination of depressed mood and social isolation a b s t r a c t Introduction: Depressed individuals not only suffer from chronic low grade inflammation, but also exhibit an inflammatory hyper-responsiveness to acute stress. We investigate whether chronic stress also induces an exaggerated inflammatory response in individuals with increased depression features. As model for chronic stress, social isolation was chosen. Methods: Interleukin (IL)-6 and hs-CRP levels were assessed in 1547 subjects (847 men and 700 women), derived from the population-based MONICA/KORA study. Standardized questionnaires were used to assess depressed mood (depression and exhaustion subscale) and social isolation (social network index). The relationship between the two inflammatory markers, social isolation and depressed mood was examined taking into account interactions social isolation  depressed mood using multivariable linear regression models, adjusted for age, BMI, smoking, alcohol, and physical activity. Analyses were performed in men and women separately. Results: We observed a significant interaction between depressed mood and social isolation regarding IL-6 and hs-CRP, respectively in men (p-value = 0.02 for IL-6 and <0.01 for hs-CRP), evidencing a substantial synergistic effect of social isolation, and depressed mood on inflammatory responses. Furthermore, depressed and socially isolated men had highly significantly elevated IL-6 levels (geometric mean: 3.76 vs. 1.92 pg/ml, p-value <0.01) and heightened hs-CRP levels (geometric mean: 2.01 vs. 1.39 mg/l, p = 0.08) in comparison with non-depressed and socially integrated men. In women, no significant associations were seen. Conclusion: The interaction of depressed mood and social isolation elicits a substantial synergistic impact on inflammatory markers in men, but not in depressed women.
Social Isolation and Adult Mortality
Journal of Health and Social Behavior, 2013
The health and survival benefits of social embeddedness have been widely documented across social species, but the underlying biophysiological mechanisms have not been elucidated in the general population. We assessed the process by which social isolation increases the risk for all-cause and chronic disease mortality through proinflammatory mechanisms. Using the 18-year mortality follow-up data ( n = 6,729) from the National Health and Nutrition Examination Survey (1988–2006) on Social Network Index and multiple markers of chronic inflammation, we conducted survival analyses and found evidence that supports the mediation role of chronic inflammation in the link between social isolation and mortality. A high-risk fibrinogen level and cumulative inflammation burden may be particularly important in this link. There are notable sex differences in the mortality effects of social isolation in that they are greater for men and can be attributed in part to their heightened inflammatory resp...
Aging & Mental Health, 2020
The effects of loneliness and social isolation on all-cause, injury, cancer, and CVD mortality in a cohort of middle-aged Finnish men. A prospective study. Objectives: Loneliness and social isolation both increase mortality and are likely to affect health via several pathways. However, information on the potential pathways remains scarce. We investigated the associations between loneliness, social isolation, and mortality, and possible mechanisms underlying these connections. Methods: The analyzed data comprised a prospective population-based cohort of Finnish men (42-61 years at baseline, n = 2588) who were followed up for an average of 23.2 years. Mortality data were obtained from the national population register in 2012. Cox proportional hazards analysis with adjustments for possible confounding factors was used to examine the associations between loneliness and social isolation at baseline and all-cause, injury, cancer, and cardiovascular disease (CVD) mortality. Mediation analysis was conducted to investigate the mechanisms underlying the associations of loneliness and social isolation with mortality. Results: Loneliness predicted all-cause mortality, even after adjustments for all covariates. Loneliness predicted cancer mortality, except after adjustments for lifestyle variables or Human Population Laboratory (HPL) depression scores, and also predicted CVD mortality, except after adjustments for HPL depression scores. Social isolation predicted all-cause mortality and injury mortality. The effect of social isolation on all-cause mortality was mediated by loneliness and HPL depression scores. Conclusions: Our findings suggest that both loneliness and social isolation increase the risk of all-cause mortality, while they have differing effects on different causes of death. Loneliness and depressive symptoms may mediate the effect of social isolation on increased mortality.