Abstract
BackgroundWhile observational studies revealed an inverse association between serum 25(OH)vitamin D (25(OH)D) and the risk of attention deficit/hyperactivity disorder (ADHD), the causality of this relationship remains unclear.MethodsWe conducted a bidirectional two-sample Mendelian Randomization (MR) study to examine whether 25(OH)D has an effect on the risk to develop ADHD or vice versa. Information on single nucleotide polymorphisms (SNP) associated with serum 25(OH)D was obtained from a genome-wide association study (GWAS) considering phenotype data from 79,366 individuals of European ancestry. Data on risk for ADHD were derived from a GWAS analysis with 20,183 individuals diagnosed with ADHD and 35,191 controls. For our analysis, we considered effect sizes based on the European participants (19,099 cases and 34,194 controls).ResultsSingle SNP analyses showed a causal effect of vitamin D on ADHD risk for only one SNP (rs12785878, p = 0.024). The overall MR estimates did not reveal a causal effect of 25(OH)D on risk for ADHD. In the reverse analysis, neither any single nor the multi-SNP MR analyses showed a causal effect of ADHD on 25(OH)D.ConclusionResults from this two-sample MR study did not confirm a causal effect of 25(OH)D on ADHD or vice versa. Accordingly, our study does not provide evidence that improving 25(OH)D via supplementation could reduce the risk of developing ADHD.
Highlights
Considering its impact on calcium and phosphate metabolism, vitamin D had initially been discussed in particular in the context of bone health [1]
The overall estimates calculated by Inverse Variance Weighted (IVW) or Mendelian Randomization (MR)-Egger, did not reveal an overall causal effect of 25(OH)D levels on the risk of attention deficit/hyperactivity disorder (ADHD) (Table 2, Figs. 1, 2, and S1)
The main finding of this MR study was that there was no genetic evidence for a causal effect of 25(OH)D levels on the risk of ADHD
Summary
Considering its impact on calcium and phosphate metabolism, vitamin D had initially been discussed in particular in the context of bone health [1]. Results from a recent genetic look-up analysis, based on data from large-scaled genome-wide associations studies (GWAS), revealed a genetic variant which is concomitantly associated with both vitamin D insufficiency and ADHD [6]. This genetic overlap might indicate a direct association. While observational studies revealed an inverse association between serum 25(OH)vitamin D (25(OH)D) and the risk of attention deficit/hyperactivity disorder (ADHD), the causality of this relationship remains unclear. Information on single nucleotide polymorphisms (SNP) associated with serum 25(OH)D was obtained from a genome-wide association study (GWAS) considering phenotype data from 79,366 individuals of European ancestry. Our study does not provide evidence that improving 25(OH)D via supplementation could reduce the risk of developing ADHD
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