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Sci Rep. 2019 Feb 27;9(1):2880. doi: 10.1038/s41598-019-39359-z.

Investigating causality in the association between vitamin D status and self-reported tiredness.

Author information

1
Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, United Kingdom. alexandra.havdahl@bristol.ac.uk.
2
Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, BS8 2BN, United Kingdom. alexandra.havdahl@bristol.ac.uk.
3
Nic Waals Institute, Lovisenberg Diaconal Hospital, Oslo, 0853, Norway. alexandra.havdahl@bristol.ac.uk.
4
Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, N-0213, Norway. alexandra.havdahl@bristol.ac.uk.
5
Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, United Kingdom.
6
Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, BS8 2BN, United Kingdom.
7
National Institute for Health Research Bristol Biomedical Research Centre, University Hospitals Bristol NHS Foundation Trust and University of Bristol, Bristol, United Kingdom.

Abstract

Self-reported tiredness or low energy, often referred to as fatigue, has been linked to low levels of circulating 25-hydroxyvitamin D (25OHD), a biomarker of vitamin D status. Although it is uncertain if the association is causal, fatigue is a common indication for testing, and correcting, low 25OHD-levels. We used two-sample Mendelian randomization to test for genetic evidence of a causal association between low 25OHD-levels and fatigue. Genetic-25OHD associations were estimated from the largest genome-wide association study of vitamin D to date, and genetic-fatigue associations were estimated in 327,478 individuals of European descent in UK Biobank, of whom 19,526 (5.96%) reported fatigue (tiredness or low energy nearly every day over the past two weeks). Using seven genome-wide significant 25OHD-reducing genetic variants, there was little evidence for a causal effect of 25OHD on fatigue (odds ratio for fatigue was 1.05 with 95% confidence interval of 0.87-1.27 per 1-SD decrease in log-transformed 25OHD). There was also little evidence of association between any individual 25OHD-reducing variant and fatigue. Our results suggest that a clinically relevant protective effect of 25OHD-levels on fatigue is unlikely. Therefore, vitamin D supplementation of the general population to raise 25OHD-levels is not likely to be useful in preventing fatigue.

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