Colorectal Cancer death 2.1X more likely if poor Vitamin D plus poor Vitamin D Binding protein – May 2020

Association of Pre-Diagnostic Vitamin D Status With Mortality Among Colorectal Cancer Patients Differs by Common, Inherited Vitamin D-binding Protein Isoforms

Int J Cancer. 2020 May 11. doi: 10.1002/ijc.33043.
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Items in both categories CCR and Vitamin D Binding Protein are listed here:

Vitamin D Binding Protein category listing has 138 items and the following introduction

Vitamin D Binding Protein (GC) gene can decrease the bio-available Vitamin D that can get to cells,

  • GC is not the only such gene - there are 3 others, all invisible to standard Vitamin D tests
  • The bio-available calculation does not notice the effect of GC, CYP27B1, CYP24A1, and VDR
  • The actual D getting to the cells is a function of measured D and all 4 genes
  • There is >2X increase in 8+ health problems if have poor VDBP (GC)
  • It appears that VDBP only blocks oral vitamin D,

VDBP is NOT directly detected by vitamin D blood tests
Blood Test Misses a lot (VDW 3439)
click on chart for detials


Cancer - Colon category starts with the following

 Download the PDF from Sci-Hub via VitaminDWiki


David Corley Gibbs 1, Roberd M Bostick 1 2, Marjorie McCullough 3, Caroline Um 3, Dana Flanders 1, Mazda Jenab 4, Elisabete Weiderpass 5, Björn Gylling 6, Inger T Gram 7, Alicia K Heath 8, Sandra Colorado-Yohar 9 10 11, Christina C Dahm 12, Bas Bueno-de-Mesquita 13, Aurora Perez-Cornago 14, Antonia Trichopoulou 15, Rosario Tumino 16, Tilman Kühn 17, Veronika Fedirko 1 2

Lower pre-diagnostic circulating 25-hydroxyvitamin D (25OHD)-considered the best marker of total vitamin D exposure-is associated with higher mortality risk among colorectal cancer (CRC) patients. However, it is unknown whether this association differs by the vitamin D-binding protein (GC) isoform Gc2 (encoded by GC rs4588*C>A, Thr436Lys), which may substantially affect vitamin D metabolism and modify associations of 25(OH)D with colorectal neoplasm risk. Pre-diagnostic 25(OH)D-mortality associations according to Gc2 isoform were estimated using multivariable Cox proportional hazards regression among 1,281 CRC cases (635 deaths, 483 from CRC) from two large prospective cohorts conducted in the United States (Cancer Prevention Study-II) and Europe (European Prospective Investigation into Cancer and Nutrition). 25(OH)D measurements were calibrated to a single assay, season standardized, and categorized using Institute of Medicine recommendations (deficient <30, insufficient 30 - <50, sufficient ≥50 nmol/L). In the pooled analysis, multivariable-adjusted hazard ratios (HRs) for CRC-specific mortality associated with deficient relative to sufficient 25(OH)D concentrations were 2.24 (95% CI 1.44-3.49) among cases with the Gc2 isoform, and 0.94 (95% CI 0.68-1.22) among cases without Gc2 (Pinteraction = 0.0002). The corresponding HRs for all-cause mortality were 1.80 (95% CI 1.24-2.60) among those with Gc2, and 1.12 (95% CI 0.84-1.51) among those without Gc2 (Pinteraction = 0.004). Our findings suggest that the association of pre-diagnostic vitamin D status with mortality among CRC patients may differ by functional GC isoforms, and patients who inherit the Gc2 isoform (GC rs4588*A) may particularly benefit from higher circulating 25(OH)D for improved CRC prognosis.

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