Revue d'Épidémiologie et de Santé Publique. Volume 66, Supplement 5, July 2018, Page S271, https://doi.org/10.1016/j.respe.2018.05.092
T.Waldhoera, G.Endler, .Yang, G.Haidinger, O.Wagner, R.Marculescu
Analysis of 78,000 patients at one hospital - 20 years
Measured Vitamin D levels then looked at change in death rates 3 or more years later
If < 4 ng of Vitamin D
- Diabetics 4.4 X increased mortality
- All patients 2.7 X increased mortality
If > 36 ng of Vitamin D
- 35% decreased mortality
- Mortality category listing has
201 items along with related searches
- Review of meta-analyses of non-skeletal benefits of vitamin D (Mortality, RTI, etc) – July 2017
- 5.8 X more likely to die in 15 year followup if low vitamin D and poor methylation – July 2018
- Vitamin D - at least 4,000 IU to achieve 40-60 ng and reduce risk of early death – Holick June 2018
- Twice as likely to die if Vitamin D was less than 8 ng (or low Magnesium, or low Omega-3) – May 2018
- Diabetics helped by vitamin D in 5 ways – meta-analysis June 2018
- Diabetes less likely 12 years later with Vitamin D – 50X if 30 ng of Vitamin D and intense exercise, 5X if 50 ng – April 2018
- Blacks die more often than whites of many diseases (they have less vitamin D) – 2012 Diabetes
Items in both VitaminDWiki categories of Diabetes and Mortality:
- Mortality increased: 4X Cancer, 5X Diabetes if eat a lot of meat protein – March 2014
- Diabetics were 4.4 X more likely to die if they had low Vitamin D – July 2018
- Vitamin D protects against many types of health problems – review May 2013
- Less than 30 ng vitamin D greatly increased hazard of dying and diabetes – Nov 2010
- Diabetics are 2X more likely to die if severely vitamin D deficient -May 2010
- Table of outcomes for seniors vs vitamin D level
Vitamin D deficiency, as reflected by low 25-hydroxyvitamin D blood levels (25D), is a prevalent correctable risk factor for death in most populations around the globe. The evidence ranges from numerous association studies and meta-analyses thereof, over Mendelian randomization studies, to randomized controlled trials (RCTs). However, most studies reported to date were performed in rather older populations and some of the largest association studies may have been confounded by increased vitamin D supplementation at old age, especially in women, and by the use of vitamin D2, which is fully measured by 25D immunoassays but biologically considerably less active. In addition, cause-specific mortalities and the impact of age on the 25D association with the risk of death have not been reported in detail, yet.
Data of all patients who had a 25D measurement at the Department of Laboratory Medicine, General Hospital of Vienna between 1991 and 2011 were retrieved and matched with the Austrian national register of deaths. First 3 years of mortality since 25D measurement were excluded in the analyses. Fine-Gray regression models adjusting for competing risks were used to estimate the survival time in dependence on 25D, adjusting for sex, age, year and month of blood draw. 25D was represented using a spline with 5 knots placed on the corresponding 1/6th quantiles. Age group (0– < 45, 45– < 60, 60– < 75, 75+ years) specific analyses were conducted owning to a strong interaction between 25D and age, where age was kept as a continuous variable to avoid remaining residual confounding. Using 50 nmol/L as the reference value, we estimated hazard-ratios of chosen serum vitamin D concentration levels (10 and 90 nmol/L). All analyses were conducted in SAS 9.4 (SAS Institute Inc., Cary, NC, US). The significance level was set to 1% in order to adjust for multiple testing.
Data from 78,581 patients (mean age = 51.0 years, men 31.5%) were used for analyses. During 20 years (median = 10.5) of follow-up, 11877 deaths were observed.
Among these patients, 25D ≤ 10 nmol/L had 2-3 fold increased risk of death (
- <45 years old: HR = 2.7, 95% CI:(2.1, 3.4);
- 45- < 60 years old: HR = 2.9, 95% CI:(2.6, 3.4);
- 60– < 75 years old: HR = 2.0, 95% CI:(1.8, 2.3),
Whereas 25D ≥ 90 nmol/L has shown to be associated with up to 40% reduced all-cause mortality (
- < 45 years old: HR = 0.7, 95% CI:(0.6, 0.9);
- 45– < 60 years old: HR = 0.6, 95% CI:(0.5, 0.7);
- 60– < 75 years old: HR = 0.7, 95% CI:(0.7, 0.8).
No associations were observed in the age group 75 years and older (10 nmol/L: HR = 1.1, 95% CI:[1.0, 1.2]; 90 nmol/L: HR = 1.0, 95% CI:[0.9, 1.0]). In terms of cause-specific mortality, we found only a relatively modest relationship for cancer and cardiovascular disease. The strongest association was found for other causes of death with the largest effect size for diabetes HR = 4.4, 95% CI:(3.1,6.3).
Our survival data from a large cohort, covering all age groups, from a population with minimal vitamin D supplementation at old age and negligible intake of vitamin D2, confirm a strong association of vitamin D deficiency (25D < 50 nmol/L) with increased mortality. This association is most pronounced in the younger and middle-aged groups and for causes of deaths other than cancer and cardiovascular disease. Some J-shaped curves were found only for the 25D association with cancer and cardiovascular mortality in certain age groups. Our findings strengthen the rationale for wide spread vitamin D supplementation to prevent premature mortality, emphasize the need for it early in life and mitigate concerns about a possible negative effect at higher 25D levels up to 150 nmol/L. RCTs in younger age groups are needed to confirm these findings.