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 .
25-Hydroxyvitamin D concentration and all-cause mortality: the Melbourne Collaborative Cohort Study.
OBJECTIVE To investigate relationships between mortality and circulating 25-hydroxyvitamin D ( 25(OH)D ) , 25-hydroxycholecalciferol ( 25(OH)D3 ) and 25-hydroxyergocalciferol ( 25(OH)D2 ) . DESIGN Case-cohort study within the Melbourne Collaborative Cohort Study ( MCCS ) . We measured 25(OH)D2 and 25(OH)D3 in archived dried blood spots by LC-MS/MS . Cox regression was used to estimate mortality hazard ratios ( HR ) , with adjustment for confounders . SETTING General community . SUBJECTS The MCCS included 29 206 participants , who at recruitment in 1990 - 1994 were aged 40 - 69 years , had dried blood spots collected and no history of cancer . For the present study we selected participants who died by 31 December 2007 ( n 2410 ) and a r and om sample ( sub-cohort , n 2996 ) . RESULTS The HR per 25 nmol/l increment in concentration of 25(OH)D and 25(OH)D3 were 0·86 ( 95 % CI 0·78 , 0·96 ; P=0·007 ) and 0·85 ( 95 % CI 0·77 , 0·95 ; P=0·003 ) , respectively . Of 5108 participants , sixty-three ( 1·2 % ) had detectable 25(OH)D2 ; their mean 25(OH)D concentration was 11·9 ( 95 % CI 7·3 , 16·6 ) nmol/l higher ( P<0·001 ) . The HR for detectable 25(OH)D2 was 1·80 ( 95 % CI 1·09 , 2·97 ; P=0·023 ) ; for those with detectable 25(OH)D2 , the HR per 25 nmol/l increment in 25(OH)D was 1·06 ( 95 % CI 0·87 , 1·29 ; P interaction=0·02 ) . HR were similar for participants who reported being in good , very good or excellent health four years after recruitment . CONCLUSIONS Total 25(OH)D and 25(OH)D3 concentrations were inversely associated with mortality . The finding that the inverse association for 25(OH)D was restricted to those with no detectable 25(OH)D2 requires confirmation in population s with higher exposure to ergocalciferol
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 .