Abstract
ObjectivesThis study aimed to explore time-varying associations between social engagement, living status and loneliness and neuro-immune markers in older adults, and ascertain whether results are explained by socioeconomic position, health behaviours or depression. MethodsWe analysed blood samples from 8780 adults aged 50 and above from the English Longitudinal Study of Ageing across three waves of data collection: 2004/5, 2008/9 and 2012/2013. We used fixed effects modelling to estimate the relationship between loneliness, social isolation, living alone and levels of fibrinogen, insulin like growth factor-1 (IGF-1), white blood cell (WBC) count and C-reactive protein (CRP), whilst accounting for all time-invariant and identified time-varying confounders. ResultsHigher levels of social engagement and living with somebody were associated with lower levels of CRP, fibrinogen and WBC, while lower levels of loneliness were associated with higher levels of IGF-1. These associations were found to be independent of time-invariant factors such as gender, medical history, previous patterns of social behaviours, unobserved aspects of social class, and genetics, and time-varying factors such as income, physical health, health behaviours, and depression. ConclusionsAspects of social engagement were associated with lower levels of inflammation whilst loneliness was inversely related to the regulation of inflammation. This suggests there could be different biological pathways involved in objective and subjective aspects of social connections.
Highlights
Multiple aspects of social connection, including social engagement and loneliness have been linked to both morbidity and mortality (Steptoe et al, 2013b)
A number of psychological and biological pathways have been identified to explain this relationship (Cacioppo et al, 2015; Cacioppo and Hawkley, 2009), including a bidirectional regulatory role of inflammatory processes (Eisenberger et al, 2017). Social stressors such as social disengagement can lead to upregulation of pro-inflammatory response genes to protect against physical vulnerability (Cole et al, 2007), and this may be detected as higher levels of a range of inflammatory markers including interleukin-6 (IL-6), interleukin-1 receptor alpha (IL1Ra), fibrinogen and C-reactive protein (CRP) (Hackett et al, 2012)
The sample was drawn from households that had participated in Health Survey for England (HSE) in 1998, 1999, and 2001
Summary
Multiple aspects of social connection, including social engagement (an individual’s quantity of social contact) and loneliness (an individual’s quality of social interactions) have been linked to both morbidity and mortality (Steptoe et al, 2013b). A number of psychological and biological pathways have been identified to explain this relationship (Cacioppo et al, 2015; Cacioppo and Hawkley, 2009), including a bidirectional regulatory role of inflammatory processes (Eisenberger et al, 2017) Social stressors such as social disengagement can lead to upregulation of pro-inflammatory response genes to protect against physical vulnerability (Cole et al, 2007), and this may be detected as higher levels of a range of inflammatory markers including interleukin-6 (IL-6), interleukin-1 receptor alpha (IL1Ra), fibrinogen and C-reactive protein (CRP) (Hackett et al, 2012). Studies of social stressors have frequently considered multiple inflammatory markers simultaneously
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