The authors claim low levels of 25(OH)D is a marker of ill health rather than a cause. Inflammatory processes involved in disease occurrence and clinical course would reduce 25(OH)D.
http://www.thelancet.com/journals/landia/article/PIIS2213-8587%2813%2970165-7/abstract
I totally agree with the authors. Although tested several times in randomized clinical trials, results showing the lack of real benefit of vitamin D supplementation in reducing cardiovascular events or cancer strongly supports the hypothesis that vitamin D deficiency is merely a marker of disease and does not the cause . Several times the associations found in observational studies were interpreted as a cause of disease, however, in my opinion, it is the known phenomenon of reverse causality. The lack of experimental evidence demonstrating event´s reduction in similar size of the associations found in observational studies do not confirm the proof of concept. So we can not affirm that low Vitamin D is the cause of disease. Therefore, I agree that vitamin D is only one more ill health marker.
Low vitamin D status is one of the main risk factors for skeletal disorders, but is only one of many risk factors for the non skeletal problems. That is why there are so many controversies. It is quite easy to imagine that the pathologies presented in the paper can lead to low vit. D status: e.g. a person with "mood disorder" will stay mostly inside, and neglect proper food or supplements. During inflammation "white" blood cells proliferate, and they contain enzymes metabolizing 25OHD. In obesity adipocytes are very efective vitamin D sink. Etc. and for all those problems vitamin D deficiency is also a risk factor. There seems to be some negative synergy to it.
It is also important to believe the information and views published by the long standing experts in the vitamin D field and not the relative newcommers. This is a very important issue as we have more than 10 new "vitamin D" papers every day.
I personally believe that proper vitamin D status is important and is a thing which should be observed and kept at the proper level (which is easy and not expensive) even if the participation of vit. D in the non skeletal disorders is not as prominent as in the skeletal ones.
The role of Vitamin D in innate and accquiredl immunity is well established. Traditionally considered to be a vitamin involved with skeletal problems, it is now looked at as a hormone with far reaching effects. Functioning more as an immuno modulating agent it is causal in many disease conditions.
One must not forget the necessity of vitamin D for skeletal health. To leave our patients with 25(OH)vitamin D levels below 50 nmol/l even though as a result of other diseases, is in my opinion not advisable.The Institute of Medicine (IOM) states that to ensure good skeletal health in 97.5% of the population, the 25(OH)vitamin D levels needs to exceed 50 nmol/l. We thus advice substitution with vitamin D to our CKD patients when the levels are below 50.
The baby and the bath water....
I believe it is very simple:
WHO was treated in the RCTs? Surprisingly, in many vitamin D intervention trials, 25(OH)D status at baseline was either not measured or many participants were not vitamin D deficient.
This is as if in trials evaluating antihypertensives, blood pressure was not measured or everyone regardless of a diagnosis of hypertension was treated. Or antibiotics given to all patients with or without infection, or thyroxin regardless of hypothyroidism etc.. etc. ...
If a person is vitamin D replete, why and how should MORE vitamin D help?
The authors do state "....However, in many other trials, patients in intervention groups had mean 25(OH)D concentrations higher than 72 nmol/L."
Promising results were seen in RCTs in severely deficient populations, even in relatively small sample sizes (e.g. Camargo/Ganmaa 2012 or Lehouck 2012).
Vitamin D is no cure for everything and everyone. But if we concentrate on DEFICIENT populations and perform well-designed RCTs, we might well find a number of benefits.
I agree. In contrast to many other vitamins (C, B etc.) we do not need them as supplement. Most people get them enough through their food. On the contrary, vitamin D (rather a hormone than a vitamin) for some populations living close to arctic circle during winter time might not get enough vitamin D from the sun or through their food. There are also several diagnosis with a strong seasonal correlations or correlations to latitudes.
Some studies are designed to create confusion on part of the public and professionals. This is one of those studies. As others have pointed out the benefits of vitamin D for heart health or cancer prevention may not make much of a difference if the study participants are not deficient.
What I see in my clients is poor dietary choices which leads over time to deficiency diseases. This is not about taking an isolated nutrient but a systemic problem of poor nutritional choices. Vitamin D has its place but it must be consider as just one of many nutrients necessary for the proper function of the body
Anotter probleem is that vit d intake in older Parsons is mainly tested in studies toghetter with Ca. And its been proven that Ca intake has soms side-effects line increase in kidney stones.
The basic problem with most vitamin D randomized controlled trials is that they are designed and conducted using the pharmaceutical drug model, i.e., the trial provides the only source of the agent and there is a linear dose-response relation. See these papers for more information on this topic:
Biesalski HK, Aggett PJ, Anton R, Bernstein PS, Blumberg J, Heaney RP, Henry J, Nolan JM, Richardson DP, van Ommen B, Witkamp RF, Rijkers GT, Zöllner I. 26th Hohenheim Consensus Conference, September 11, 2010 Scientific substantiation of health claims: evidence-based nutrition. Nutrition. 2011 Oct;27(10 Suppl):S1-20.
Heaney RP. Guidelines for optimizing design and analysis of clinical studies of nutrient effects. Nutr Rev. 2013 Dec 13. doi: 10.1111/nure.12090. [Epub ahead of print]
Lappe JM, Heaney RP. Why randomized controlled trials of calcium and vitamin D sometimes fail. Dermatoendocrin. 2012;4(2):95-100.
Michels AJ, Frei B. Myths, artifacts, and fatal flaws: identifying limitations and opportunities in vitamin C research. Nutrients. 2013 Dec 16;5(12):5161-92.
Moser U. Vitamins - wrong approaches. Int J Vitam Nutr Res. 2012 Oct;82(5):327-32.
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