ECC 2013 Abstract#3 - Vitamin D Status and Inflammation in Cancer and Other Diseases

Best Abstract #3:  Vitamin D Status and Inflammation in Cancer and Other Diseases P. Autier

Background: Several observational studies have identified an apparent association between 25-hydroxy-vitamin D levels and various disease states including poor bone health and malignancy.  However, what is not known is whether this is apparent effect is correlative or modifiable. 

Methods: The authors performed an analysis of systematic reviews, randomized trials and prospective cohort studies published up to December 2012 to determine if increasing vitamin D levels might be associated with a reduction in the risk of multiple health conditions including malignancy.

Results: 273 trials involving 1.2 million adult patients were identified.  High vitamin D levels were associated with a reduction in the likelihood of death from only colorectal cancer although there was a trend toward improved outcomes for patients with both pancreas and prostate cancers.  Vitamin D levels also appeared to be associated with aggressiveness of disease.  Lower levels of vitamin D were associated with conditions leading to systemic inflammation but, interestingly, supplementing vitamin D did not appear to be associated with a reduction in the inflammatory process or a reduction in the incidence or aggressiveness of malignancy.

Conclusions: Vitamin D status appears to represent a consequence rather than a cause of poor health and is likely due to underlying systemic inflammatory processes.

This was a massive review of prospective patient data that attempted to discern if vitamin D levels were associated with malignancy (among other health states) and if the effect was modifiable. While the authors did identify that elevated levels of vitamin D were associated with a reduction of colorectal cancer, this did not appear to be the case for any other malignancy. Importantly, they also identified that lower levels of vitamin D appeared to be associated with poor health states involving higher states of systemic inflammation and that this was not a modifiable effect by vitamin D supplementation. This observation led them to conclude that the observed lower levels of vitamin D and the resulting increased risk of cancer were likely a consequence of inflammation rather than a direct cause of the disease.

The suggestion that vitamin D supplementation was not able to affect the degree of systemic inflammation nor reduce the incidence or aggressiveness of cancer has definite implications for our patients attempting to modify the course of their disease. Still, vitamin D supplementation is inexpensive and lends our patients a degree of control in their cancer journey. In addition, supplementation does not appear to be associated with any ill effects and, indeed, is a necessary and important intervention to counteract the potential adverse effects of some anti-cancer therapies such as aromatase inhibitors and rank ligand inhibitors.

Moreover, these findings will have a significant implication for the design of preventative and adjuvant cancer studies and suggests that the focus of such interventions should be aimed at modifying the inflammatory process rather than via manipulation of vitamin D. Certainly, there is a suggestion that nonsteroidal anti-inflammatory medications may be effective in reducing the incidence of polyps and possibly colorectal cancer and is currently a focus of the ongoing CRC-6 clinical trial sponsored by the NCIC CTG. Interestingly however, there was a suggestion from this analysis that the vitamin D/inflammatory correlation did not appear to be dependent on COX-2 activation. This observation may affect the results of the CRC-6 trial given that the anti-inflammatory being evaluated is the COX-2 specific inhibitor celecoxib. Overall, this study highlights the importance of assessing medical observations in a prospective fashion and we will await the outcome of the CRC-6 trial with interest.
— CARE Gastrointestinal Cancer Faculty