Chirantan Banerjee, MD
Nagayoshi M, Everson-Rose SA, Iso H, Mosley, Jr TH, Rose KM, and Lutsey PL. Social Network, Social Support, and Risk of Incident Stroke:Atherosclerosis Risk in Communities Study. Stroke. 2014
Man is a social animal. In the age of social networks, when dynamics of social interactions are morphing, we know very little about how social variables affect stroke risk. Association between social stress and coronary artery disease has been previously reported. But prospective data on social support and incident stroke has been scant, as most studies have focused on social support post stroke and recovery outcomes. The Atherosclerosis Risk in Communities (ARIC) is a bi-racial prospective epidemiologic study which was started in 1989 to investigate the etiology and sequelae of atherosclerosis and its variation in cardiovascular risk factors, medical care, and disease by race, sex, place, and time in four US communities–Forsyth County, North Carolina, Jackson, Mississippi, suburbs of Minneapolis, Minnesota, and Washington County, Maryland. Data from the cohort has led to several important papers in stroke risk factor epidemiology over the years.
Nagayoshi M, Everson-Rose SA, Iso H, Mosley, Jr TH, Rose KM, and Lutsey PL. Social Network, Social Support, and Risk of Incident Stroke:Atherosclerosis Risk in Communities Study. Stroke. 2014
Man is a social animal. In the age of social networks, when dynamics of social interactions are morphing, we know very little about how social variables affect stroke risk. Association between social stress and coronary artery disease has been previously reported. But prospective data on social support and incident stroke has been scant, as most studies have focused on social support post stroke and recovery outcomes. The Atherosclerosis Risk in Communities (ARIC) is a bi-racial prospective epidemiologic study which was started in 1989 to investigate the etiology and sequelae of atherosclerosis and its variation in cardiovascular risk factors, medical care, and disease by race, sex, place, and time in four US communities–Forsyth County, North Carolina, Jackson, Mississippi, suburbs of Minneapolis, Minnesota, and Washington County, Maryland. Data from the cohort has led to several important papers in stroke risk factor epidemiology over the years.
In the current study, Nagayoshi et.al tested the hypothesis that a small social network and poor social support are associated with increased risk of incident stroke. They also tested whether vital exhaustion (fatigue, irritability, and feeling of demoralization) and systemic inflammation (hsCRP was used as the biomarker) were mediators of the association. After excluding participants with stroke and incomplete data, 13,686 and 13,683 participants were included in analyses for social network and social support respectively. Social network was measured using the 10-item Lubben Social Network Scale, and perceived social support was measured using a modified version of the Interpersonal Support Evaluation List-Short Form (ISEL-SF), previously used by ARIC investigators. Vital exhaustion was measured by the 21-item Maastricht Questionnaire. Appropriate statistical models were used. Stroke incidence was 4 per 1000 person-years. Those with a very small social network had increased risk of incident stroke, despite adjustment for age, sex, demographic, behavioral and stroke risk factors, with a HR of 1.44 (1.02-2.04). Vital exhaustion and hsCRP were then added to the model to test for mediation, and only vital exhaustion changed the beta enough to justify mediation. Lack of perceived social support was not associated with increased stroke risk after adjustment for other variables.
The findings are in concordance with 2 prior studies, which also supported association between small social network and incident stroke. The effect size in this study is striking, as those who self-reported a small social network had a 40% increased risk of stroke. The fact that the authors tested hsCRP and vital exhaustion to get at the underlying mechanism of the relationship deserves praise, as it shed light on how mental stress and its somatic correlates have potential to disturb homeostatic mechanisms and cause cerebrovascular disease. There has been a plethora of literature linking chronic stress and subsequent activation of hypothalamic pituitary axis with neuroimmune and inflammatory markers. Given the observational nature of the data, only association (and not causation) can be inferred from the study. The scales used to measure social network and social support need further validation in neurologic populations, and the self-reported nature of data collection makes measurement error and big drawback. Also, the actual prevalence of small social network and poor social support was very low in the cohort (2.8% and 0.5% respectively), significantly under powering it.
These results bring into limelight the fact that while we focus most of our efforts on traditional behavioral, demographic and medical risk factors for stroke, social interventions also have an important role in stroke prevention. WHO defines health as a state of complete physical, mental and social well-being. And we should try our best to help all our patients achieve this noble goal.
