In the British Medical Journal was reporteda review on 107 systematic literature reviews, 74 meta-analyses of observational studies of plasma vitamin D concentrations, and 87 meta-analyses of randomized controlled trials of vitamin D.
The role of vitamin D in colorectal cancer prevention, and possibly in treatment, is biologically plausible as there are receptors in the colon. The enzymes responsible for the activation of vitamin D to 1,25 dihydroxyvitamin D, is presently known in vitro in animal models. Vitamin D has important effects on cell growth, cell morphology, and cell cytokinesis, a whole range of biological factors that would be relevant to the control of cancer.
The conclusion of this review was that in cancer, particularly colorectal cancer, the evidence is suggestive of benefit for vitamin D.
The authors pointed on a positive trend toward improvements in outcomes.
There is a big question about the dose of vitamin D. Should we seek to replenish and to treat toward what we think is the internationally recognized normal range? Should we be giving the recommended dose of 400-600 IU per day? Should we be going higher? There are trials of 3000-4000 IU per day.
What is interesting is that for northern population there is no doubt that there is an inverse correlation between vitamin D levels and the propensity to develop colorectal cancer.
In the southern and in the sunniest place on earth we found very high levels of hypo-vitaminosis D. That seemed to be because it is too hot to go out, and the population spent a lot of their life indoors in air-conditioned boxes, moving from an air-conditioned car; rarely they go out in the sun.
We lean toward saying that vitamin supplementation at a safe.
Along with aspirin, vitamin D might be one of those things that we should consider taking. For patients who live in the north and have had resection of colorectal cancer, it may be worthwhile.
Moreover vitamin-D supplementation not only improved insulin sensitivity but also shifted the microbiome from a prediabetes spectrum to a healthy signature. Serum markers of gut permeability were also improved in men treated with vitamin D. Taken together, the results suggest that vitamin D may modulate gut permeability and prevent low-grade inflammation associated with obesity and insulin resistance.
Notably, microbial diversity is a significant predictor of HbA1c. In addition, vitamin D appeared to play a role in delaying the development of type 2 diabetes, possibly due to improved insulin sensitivity.
In addition, it’s reported on a subgroup of 20 men in the trial in which supplementation resulting in plasma vitamin-D levels greater than 50 ng/mL was significantly associated with changes in inflammatory markers linked to gut-derived endotoxemia.
These included lipopolysaccharide (LPS), a marker of chronic low-grade inflammation, which binds to soluble CD14 (sCD14) and LPS-binding protein (LBP), both of which facilitate the intracellular transfer of LPS. Supplementation with vitamin D was associated with significantly increased levels of antibodies to LPS, indicating a decrease in the LPS-triggered inflammatory cascade.