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The contribution of ADHD genetic risk to somatic health in late life
Aarhus University, Aarhus, Denmark.
Karolinska Institutet, Stockholm, Sweden.
Cardiff Univiversity, Cardiff, Wales.
Örebro University, School of Medical Sciences.ORCID iD: 0000-0002-6851-3297
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2019 (English)In: Behavior Genetics, ISSN 0001-8244, E-ISSN 1573-3297, Vol. 49, no 6, p. 514-514Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Genetic risk variants associated with ADHD have been linked to comorbid psychiatric health problems, however less is known about how these genetic factors contribute to somatic health across the life-span. The aim of this study is to assess whether polygenic risk scores (PRS) for ADHD are associated with late-life somatic health problems in a general population sample never diagnosed with ADHD.

We derived ADHD PRS for 15,701 Swedish twins born 1911–1958 using results from an independent ADHD genome-wide association study meta-analysis (Demontis et al, 2018). Somatic health outcomes in cardiovascular, metabolic, autoimmune, and neurological domains were defined via self-report in the Screening Across the Lifespan Twin study (Lichtenstein et al. 2006) and from clinical diagnoses in the National Swedish Patient Register. Associations between ADHD PRS and somatic health problems were estimated using generalized estimating equations.

Higher ADHD PRS were associated with a small increased risk of coronary heart disease based on self-report (OR = 1.11, 95% CI = 1.02–1.20) and clinical diagnoses (OR = 1.09, 95% CI = 1.02–1.16), after false discovery rate correction. We also found statistically significant associations between ADHD PRS and obesity, type 1 diabetes, arthritis, psoriasis, and migraine, although results varied by information source. Our results suggest that polygenic risk for ADHD is associated with small increases to risk of somatic health problems in cardiovascular and autoimmune domains. These findings warrant further research into mechanisms influencing long-term health outcomes in ADHD. Next, we will test for mediation via socioeconomic variables, evaluate genetic causality using twin-comparison methods, and test for replication in a younger, clinical ADHD sample.

Place, publisher, year, edition, pages
Springer, 2019. Vol. 49, no 6, p. 514-514
National Category
Psychiatry
Identifiers
URN: urn:nbn:se:oru:diva-78622DOI: 10.1007/s10519-019-09973-8ISI: 000494050500100OAI: oai:DiVA.org:oru-78622DiVA, id: diva2:1378991
Conference
49th Annual Meeting of the Behavior-Genetics-Association (BGA), Karolinska Institutet, Stockholm, Sweden, June 26-29, 2019
Available from: 2019-12-16 Created: 2019-12-16 Last updated: 2019-12-16Bibliographically approved

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Larsson, Henrik

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