New Australian study below [1].
What does "post-treatment" mean? Vitamin D samples were collected "4.9 to 8.6 years after diagnosis".
Our vitamin D resevoir is what is usually monitored: 25-dihydroxy Vitamin {aka 25-D, 25(OH)D, calcidiol}. The hormonal form, which can vary throughout the day is 1,25-dihydroxy Vitamin D {aka 1,25-D, 1,25(OH)D, calcitriol}.
We do not learn anything about deficiency levels, but at least this is Australia & not Sweden. Instead we have traditional quartiles. How low was quartile 1? How high was quartile 4? Perhaps someone has access to the full paper?
Why measure 1,25-D? One might have a high 25-D level, but calcium intake can inhibit conversion to bioactive 1,25-D. On the other hand, fructose intake can increase 1,25-D production. So there is a case for preferring 1,25-D. However, the average for samples taken at different times might have been more useful.
"... there were 198 deaths from any cause and 41 from PC in the study period ..."
"Plasma 1,25(OH)2D was inversely associated with all-cause mortality (HR for highest relative to lowest quartile = 0·45 ...), and PC-specific mortality (HR = 0·40 ...)."
"These associations were apparent only in men with aggressive PC: all-cause mortality HR = 0·28 ... and PC-specific mortality HR = 0·26 ..."
"The inverse association between post-treatment plasma 1,25(OH)2D levels and all-cause and PC-specific mortality in men with aggressive PC, suggest a possible beneficial effect of vitamin D supplementation in these men."
-Patrrick
[1] pubmed.ncbi.nlm.nih.gov/323...
Sci Rep
. 2020 May 8;10(1):7736. doi: 10.1038/s41598-020-62182-w.
Post-treatment Levels of Plasma 25- And 1,25-dihydroxy Vitamin D and Mortality in Men With Aggressive Prostate Cancer
Visalini Nair-Shalliker 1 2 3 , Albert Bang 4 , Sam Egger 4 , Mark Clements 5 , Robert A Gardiner 6 , Anne Kricker 7 , Markus J Seibel 8 , Suzanne K Chambers 9 , Michael G Kimlin 10 , Bruce K Armstrong 4 11 , David P Smith 4 7 9
Affiliations collapse
Affiliations
1 Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia. visalinin@nswcc.org.au.
2 Sydney School of Public Health, The University of Sydney, Sydney, NSW, Australia. visalinin@nswcc.org.au.
3 Department of Clinical Medicine, Macquarie University, Sydney, Australia. visalinin@nswcc.org.au.
4 Cancer Research Division, Cancer Council NSW, Sydney, NSW, Australia.
5 Karolinka Institute, Stockholm, Sweden.
6 University of Queensland, Brisbane, Australia.
7 Sydney School of Public Health, The University of Sydney, Sydney, NSW, Australia.
8 Bone Research Program, ANZAC Research Institute, and Concord Medical School, The University of Sydney, Sydney, Australia.
9 Faculty of Management, University Technology of Sydney, Sydney, Australia.
10 Health Research Institute, University of the Sunshine Coast, Queensland, Australia.
11 School of Population Health, University of Western Australia, Perth, Western Australia, Australia.
PMID: 32385370 DOI: 10.1038/s41598-020-62182-w
Abstract
Vitamin D may reduce mortality from prostate cancer (PC). We examined the associations of post-treatment plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations with PC mortality. Participants were PC cases from the New South Wales Prostate Cancer Care. All contactable and consenting participants, at 4.9 to 8.6 years after diagnosis, were interviewed and had plasma 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D) measured in blood specimens. Cox regression allowing for left-truncation was used to calculate adjusted mortality hazards ratios (HR) and 95% confidence intervals (95% CI) for all-cause and PC-specific mortality in relation to vitamin D levels and other potentially-predictive variables. Of the participants (n = 111; 75·9% response rate), there were 198 deaths from any cause and 41 from PC in the study period. Plasma 25(OH)D was not associated with all-cause or PC-specific mortality (p-values > 0·10). Plasma 1,25(OH)2D was inversely associated with all-cause mortality (HR for highest relative to lowest quartile = 0·45; 95% CI: 0·29-0·69), and PC-specific mortality (HR = 0·40; 95% CI: 0·14-1·19). These associations were apparent only in men with aggressive PC: all-cause mortality HR = 0·28 (95% CI·0·15-0·52; p-interaction = 0·07) and PC-specific mortality HR = 0·26 (95% CI: 0·07-1.00). Time spent outdoors was also associated with lower all-cause (HR for 4th relative to 1st exposure quartile = 0·42; 95% CI: 0·24-0·75) and PC-specific (HR = 0·48; 95% CI: 0·14-1·64) mortality, although the 95% CI for the latter was wide. The inverse association between post-treatment plasma 1,25(OH)2D levels and all-cause and PC-specific mortality in men with aggressive PC, suggest a possible beneficial effect of vitamin D supplementation in these men.
