Background: Few have explored associations between loneliness and healthcare use independent of health and health behaviors. Recent indication of gender effects also requires validation across health service and cultural settings. We investigated the associations among loneliness, health and healthcare use (HCU) in older adults including stratification to investigate whether associations differed by gender. Methods: Secondary analysis of a nationally representative sample of 8,309 community-dwelling adults aged 50 and over from the Northern Ireland Cohort for the Longitudinal Study of Aging. Primary outcomes were: self-reported General Practice (GP) and emergency department (ED) visits in past year. Negative binomial and logistic regression analysis were used to investigate associations between loneliness and HCU, later adjusting for potential confounders (health and health behaviors). Results: Loneliness was consistently positively associated with both GP and ED visits (with IRRs ranging from 1.10 to 1.49 for GP visits, 1.16 to 1.98 for ED visits and ORs ranging from 1.13 to 1.51 for reporting at least one ED visit). With addition of health and health behaviors, all associations between loneliness and HCU became non-significant, excepting a small independent association between UCLA score and GP visits [IRR 1.03 (95% CI 1.01-1.05)]. Stratification of models revealed no gender effects. Conclusion: All but one association between loneliness and HCU became non-significant when health and health behaviors were included. The remaining association was small but implications remain for health service resources at population level. No gender effects were present in contrast to recent findings in the Republic of Ireland. Further studies on gender, loneliness and healthcare use needed.

The susceptibility of human CD4+ and CD8+ T cells to senesce differs, with CD8+ T cells acquiring an immunosenescent phenotype faster than the CD4+ T cell compartment. We show here that it is the inherent difference in mitochondrial content that drives this phenotype, with senescent human CD4+ T cells displaying a higher mitochondrial mass. The loss of mitochondria in the senescent human CD8+ T cells has knock-on consequences for nutrient usage, metabolism and function. Senescent CD4+ T cells uptake more lipid and glucose than their CD8+ counterparts, leading to a greater metabolic versatility engaging either an oxidative or a glycolytic metabolism. The enhanced metabolic advantage of senescent CD4+ T cells allows for more proliferation and migration than observed in the senescent CD8+ subset. Mitochondrial dysfunction has been linked to both cellular senescence and aging; however, it is still unclear whether mitochondria play a causal role in senescence. Our data show that reducing mitochondrial function in human CD4+ T cells, through the addition of low-dose rotenone, causes the generation of a CD4+ T cell with a CD8+ -like phenotype. Therefore, we wish to propose that it is the inherent metabolic stability that governs the susceptibility to an immunosenescent phenotype.