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 .
Association of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone with mortality among middle-aged and older European men.
BACKGROUND vitamin D deficiency has been associated with an increased risk of mortality , but whether this relationship is causal or linked to co-existent comorbidity and adverse life factors remains uncertain . Our objective was to determine whether endogenous 25-hydroxyvitamin D ( 25(OH)D ) , 1,25-dihydroxyvitamin D ( 1,25(OH)2D ) and parathyroid hormone ( PTH ) levels predicted all-cause , cardiovascular and cancer mortality independently of health and lifestyle factors . SETTING : prospect i ve cohort analysis within the European Male Ageing Study . PARTICIPANTS : 2,816 community-dwelling men aged 40 - 79 years at baseline . METHODS : Cox regression was used to examine the association of all-cause mortality with 25(OH)D , 1,25(OH)2D and PTH ;  cardiovascular and cancer mortality were modelled using competing-risks regression . Results were expressed as hazard ratios ( HR ) and 95 % confidence intervals ( CIs ) for Cox models ; sub-hazard ratios ( SHR ) and 95 % CIs for competing-risks models . RESULTS : a total of 187 men died  during a median of 4.3 years of follow-up . Serum levels of 25(OH)D ( per 1 SD decrease : HR = 1.45 ; 95 % CI = 1.16 , 1.81 ) and 1,25(OH)2D ( per 1 SD decrease : HR = 1.20 ; 95 % CI = 1.00 , 1.44 ) were associated with an increased risk of all-cause mortality after adjusting for age , centre , smoking , self-reported morbidities , physical activity and functional performance . Only levels of 25(OH)D < 25 nmol/l predicted cancer mortality ( SHR = 3.33 ; 95 % CI = 1.38 , 8.04 ) . CONCLUSION : lower 25(OH)D and 1,25(OH)2D levels independently predicted all-cause mortality in middle-aged and older European men . Associations with cancer mortality were only observed among men with very low levels of 25(OH)D. These associations were only partially explained by the range of adverse health and lifestyle factors measured here
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 .