The vast majority of studies reported inverse associations between 25(OH)D concentration and all-cause mortality .
This association appeared to be non-linear , with progressively lower mortality with increasing 25(OH)D up to a point , beyond which there was no further decrease .
There is moderate evidence that vitamin D status is inversely associated with cancer mortality and death due to respiratory diseases , while for cardiovascular mortality , there is weak evidence of an association in observational studies , which is not supported by the data from intervention or Mendelian r and omization studies .
Epidemiological evidence suggests that vitamin D deficiency is associated with increased mortality , but it is unclear whether this is explained by reverse causation , and if there are specific causes of death for which vitamin D might be important .
Vitamin D and overall cancer risk and cancer mortality: a Mendelian randomization study
& NA ; There is considerable debate regarding the role that 25‐hydroxyvitamin D [ 25(OH)D ] concentrations play in cancer risk or mortality , with earlier studies drawing mixed conclusions . Using data from the UK Biobank ( UKB ) , we evaluate whether genetically predicted 25(OH)D concentrations are associated with overall cancer susceptibility and cancer mortality using five 25(OH)D genetic markers . Data comprised 438 870 white British UKB participants aged 37‐73 , including 46 155 cancer cases and 6998 cancer‐specific deaths . Participants with keratinocyte cancers and /or benign tumors were excluded from the analysis . Odds ratios were calculated per 20 nmol/L increase in genetically predicted 25(OH)D for cancer risk and cancer mortality . For individual cancer risks , estimates were meta‐analyzed with publicly available data using a fixed‐effect inverse‐variance‐weighted model . We demonstrated that genetically low plasma 25(OH)D concentrations were not associated with increased cancer risk nor cancer mortality . Stratification by sex or cancer types did not reveal any meaningful differences albeit wider confidence intervals . Fixed‐effect meta‐ analysis of our individual cancer risk estimates with those derived from publicly available cancer consortia data and previous studies further reinforced our null Mendelian r and omization findings on prostate , lung , colorectal and breast cancers with tight confidence intervals ; for ovarian and pancreatic cancers , our estimates were less precise despite being not statistically significant . Taken altogether , our results provide no genetic evidence for an association  between vitamin D  and overall cancer outcomes , with tight confidence intervals to exclude all but very small effect sizes
The vast majority of studies reported inverse associations between 25(OH)D concentration and all-cause mortality .
This association appeared to be non-linear , with progressively lower mortality with increasing 25(OH)D up to a point , beyond which there was no further decrease .
There is moderate evidence that vitamin D status is inversely associated with cancer mortality and death due to respiratory diseases , while for cardiovascular mortality , there is weak evidence of an association in observational studies , which is not supported by the data from intervention or Mendelian r and omization studies .
Epidemiological evidence suggests that vitamin D deficiency is associated with increased mortality , but it is unclear whether this is explained by reverse causation , and if there are specific causes of death for which vitamin D might be important .