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Vitamin D and Cognition: Findings from a Mendelian Randomisation Study
Author(s) -
Maddock Jane,
Cavadino Alana,
Power Chris,
Hyppönen Elina,
Study Group Vitamin D and Cognition
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb390
Subject(s) - confounding , cognition , observational study , vitamin d and neurology , mendelian randomization , effects of sleep deprivation on cognitive performance , psychology , medicine , biology , genetics , psychiatry , genetic variants , gene , genotype
Hypovitaminosis D has been associated with poor cognitive function, but questions surrounding confounding and reverse causality remain. We used Mendelian randomisation (MR) to estimate the relationship between 25(OH)D, a marker of vitamin D status, and cognition. Since genetic variants are randomly assigned and present from birth, confounding and reverse causality are minimised. We used data from 9 European cohorts ( N =43,954). DHCR7 ( rs12785878) , CYP2R1 ( rs12794714) and their combined genetic score provided a proxy for 25(OH)D. Cognitive tests were standardised into global and memory scores. All analyses were stratified by study‐specific 25(OH)D tertiles to assess non‐linearity. Meta‐analyses assessed the observational and genetic associations between 25(OH)D concentrations and cognitive function. Random effects models were used where p heterogeneity <0.05, otherwise fixed effects meta‐analysis was applied.
Association of 25(OH)D with global cognition and memory was non‐linear, where both high and low levels were associated with poorer cognition. However neither DHCR7 , CYP2R1 nor their combined score were associated with global cognition or memory. While there was no evidence for a causal association between 25(OH)D and cognitive function in genetic analysis, the observational association was non‐linear. Analyses may be underpowered to detect small causal effects operating at the extremes of the distribution.