Article Text

Original research
Association of social isolation, loneliness and genetic risk with incidence of dementia: UK Biobank Cohort Study
  1. Marko Elovainio1,2,3,
  2. Jari Lahti1,
  3. Matti Pirinen4,5,6,
  4. Laura Pulkki-Råback1,7,
  5. Anni Malmberg1,
  6. Jari Lipsanen1,
  7. Marianna Virtanen8,
  8. Mika Kivimäki4,9,
  9. Christian Hakulinen1,3
  1. 1Department of Psychology and Logopedics, University of Helsinki, Helsinki, Finland
  2. 2Research Program Unit, Faculty of Medicine, University of Helsinki, Helsinki, Finland
  3. 3Finnish Institute for Health and Welfare, Helsinki, Finland
  4. 4Department of Public Health, University of Helsinki, Helsinki, Finland
  5. 5Institute for Molecular Medicine Finland, Helsinki Institute of Life Sciences, University of Helsinki, Helsinki, Finland
  6. 6Helsinki Institute for Information Technology and Department of Mathematics and Statistics, University of Helsinki, Helsinki, Finland
  7. 7Research Centre of Child Psychiatry, Faculty of Medicine, University of Turku, Turku, Finland
  8. 8School of Educational Sciences and Psychology, University of Eastern Finland, Joensuu, Finland
  9. 9Department of Epidemiology and Public Health, University College London, London, UK
  1. Correspondence to Dr Marko Elovainio; marko.elovainio{at}helsinki.fi

Abstract

Background Social isolation and loneliness have been associated with increased risk of dementia, but it is not known whether this risk is modified or confounded by genetic risk of dementia.

Methods We used the prospective UK Biobank study with 155 070 participants (mean age 64.1 years), including self-reported social isolation and loneliness. Genetic risk was indicated using the polygenic risk score for Alzheimer’s disease and the incident dementia ascertained using electronic health records.

Results Overall, 8.6% of participants reported that they were socially isolated and 5.5% were lonely. During a mean follow-up of 8.8 years (1.36 million person years), 1444 (0.9% of the total sample) were diagnosed with dementia. Social isolation, but not loneliness, was associated with increased risk of dementia (HR 1.62, 95% CI 1.38 to 1.90). There were no interaction effects between genetic risk and social isolation or between genetic risk and loneliness predicting incident dementia. Of the participants who were socially isolated and had high genetic risk, 4.4% (95% CI 3.4% to 5.5%) were estimated to developed dementia compared with 2.9% (95% CI 2.6% to 3.2%) of those who were not socially isolated but had high genetic risk. Comparable differences were also in those with intermediate and low genetic risk levels.

Conclusions Socially isolated individuals are at increased risk of dementia at all levels of genetic risk.

  • dementia
  • public health
  • genetics
  • geriatric medicine

Data availability statement

Data are available upon reasonable request.

Data availability statement

The genetic and phenotypic UK Biobank data are available on application to the UK Biobank (www.ukbiobank.ac.uk). Summary statistics from the meta-analysis of genome wide association studies in dementia are available from https://www.niagads.org/datasets/ng00075.

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Data availability statement

Data are available upon reasonable request.

Data availability statement

The genetic and phenotypic UK Biobank data are available on application to the UK Biobank (www.ukbiobank.ac.uk). Summary statistics from the meta-analysis of genome wide association studies in dementia are available from https://www.niagads.org/datasets/ng00075.

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Footnotes

  • Contributors ME and CH designed the study and conducted the statistical analyses. ME wrote the first draft of the manuscript. JL and AM calculated the polygenetic risk score with the help of MP. All authors contributed to the interpretation of the results and critical revision of the manuscript for important intellectual content and approved the final version of the manuscript. ME and CH are the guarantors.

  • Funding ME and CH were supported by the Academy of Finland (339390 (ME)/310591(CH)). MK was supported by NordForsk (70521), the UK Medical Research Council (MRC S011676), the Academy of Finland (311492), and the US National Institutes on Ageing (NIA R01AG056477). LP-R was supported by the Jenny and Antti Wihuri Foundation. GERAD/PERADES was supported by the Medical Research Council (Grant no. 503480), Alzheimer's Research UK (Grant no. 503176), the Wellcome Trust (Grant no. 082604/2/07/Z) and German Federal Ministry of Education and Research (BMBF): Competence Network Dementia (CND) grant no 01GI0102, 01GI0711, 01GI0420. CHARGE was partly supported by the NIH/NIA grant R01 AG033193 and the NIA AG081220 and AGES contract N01-AG-12100, the NHLBI grant R01 HL105756, the Icelandic Heart Association, and the Erasmus Medical Center and Erasmus University. ADGC was supported by the NIH/NIA grants: U01 AG032984, U24 AG021886, U01 AG016976, and the Alzheimer's Association grant ADGC-10-196728.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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