Abstract
Although several studies have shown small longitudinal associations between baseline loneliness and subsequent dementia risk, studies rarely test whether change in loneliness predicts dementia risk. Furthermore, as both increase with advancing age, genetic and environmental selection processes may confound the putative causal association between loneliness and dementia risk. We used a sample of 2,476 individual twins from three longitudinal twin studies of aging in the Swedish Twin Registry to test the hypothesis that greater positive change in loneliness predicts greater dementia risk. We then used a sample of 1,632 pairs of twins to evaluate the hypothesis that effects of change in loneliness on dementia risk would remain after adjusting for effects of genetic and environmental variance. Phenotypic model results suggest that mild levels of baseline loneliness predict greater dementia risk. Contrary to our hypothesis, change in loneliness did not correlate with dementia risk, regardless of whether genetic and environmental selection confounds were taken into account. Worsening loneliness with age may not confer greater dementia risk.
Highlights
Study of the association between perceived social isolation and dementia risk has intensified over the last 10 years
We investigate whether greater increases in loneliness increases dementia risk and whether their association is more consistent with social selection hypotheses or social causation hypotheses
Previous studies have focused on linear growth in loneliness (Wilson et al, 2007), which may misfit natural change in loneliness, we examine whether differences in non-linear trajectories of loneliness predict dementia risk
Summary
Study of the association between perceived social isolation (i.e., loneliness) and dementia risk has intensified over the last 10 years. We evaluate whether effects of individual growth parameters of loneliness on dementia risk remain statistically significant after adjusting for genetic and environmental selection that might confound their association. In pairs of monozygotic twins, for example, differences in the effect of loneliness on dementia risk must be attributed to twins’ differences in environmental exposure, as they share all of their genotype and common environments These effects are regarded as quasi-causal in the sense that twin studies lack random assignment and so are vulnerable to third variable confounds like all observational studies. As the ε4 allele of the APOE gene is the single causal variant associated with late-onset Alzheimer’s disease risk and nearly 75% of all dementia cases are Alzheimer’s disease cases (Beam et al, 2018), APOE ε4 allele status was included in the current study. Both measured and unmeasured genetic influences underlying dementia risk were included in the current study
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