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The "report" you're mentioning regarding the H1N1 means absolutely nothing. I keep addressing these nonsensical reports and then you just keep telling me to look at all of the nonsensical reports that don't mean anything in their totality. It still means nothing, just more of it. Why do you think that randomized controlled trials are needed to see if something works?
Of course these reports are not controlled trials. However, it is not reasonable to say they are all just flukes, they all happened to be done in a year with a mild flu season or all of them just got extremely lucky and just by chance happened to demonstrate an effect of vitamin D strengthening the immune system.
You can read more about the report here:
http://www.paleonu.com/...e-immunity.html
There are certainly many variables, but I find it a very interesting "coincidence" that many cases come to the same conclusion.
The correlation between low vitamin D levels and respiratory infections isn't a fluke, at least 5 studies have demonstrated it.
http://www.ncbi.nlm.nih.gov/...pubmed/17823437
http://www.ncbi.nlm.nih.gov/...pubmed/18030309
http://www.ncbi.nlm.nih.gov/...pubmed/19237723
http://www.ncbi.nlm.nih.gov/...pubmed/15042122
http://www.ncbi.nlm.nih.gov/...pubmed/15379879
I would say this study demonstrated that there is a seasonal variance in the hosts immunity. Now, this would be explained very well by vitamin D, as we know it has an effect on AMPs. I would be interested to hear your explanation of it, why is the immune system weaker in the winter?
http://www.ncbi.nlm.nih.gov/pu...
There is a very plausible biological mechanism how vitamin D exerts its effect on the immune system. The active form of vitamin D directly stimulates the genetic expression of AMPs. When a toll-like receptor (TLR) recognizes microbial particles, it induces the expression of AMPs, the production of which is dependent on and mediated by vitamin D. Very interestingly, sera taken from African-American individuals had low vitamin D status and was inefficient in generating the expression of cathelicidin, and AMP. Remarkably, when the researches added 25-OHD to the sera and then stimulated it with the TLR2/1L, cathelicidin levels increased to levels observed in monocytes collected from whites. The TLR2/1L-induced cathelicidin mRNA levels in whites were about twice as high as in African-Americans. Now, the levels of 25-OHD in African-Americans were around 30 nmol/L, while in whites it was about 80 nmol/L. I consider this direct evidence that the increase of vitamin D levels from 30 nmol/L to 80 nmol/L enchances the expression of AMPs. Unfortunately, we do not know if the relationship is linear and at what 25-OHD levels the AMP production peaks.
http://www.ncbi.nlm.nih.gov/...pubmed/16497887
http://www.ncbi.nlm.nih.gov/...pubmed/15322146
Another study confirms that the activated form of vitamin D induces the expression of the human cathelicidin antimicrobial peptide.
http://www.ncbi.nlm.nih.gov/...pubmed/15985530
Anyhow, you've still failed to answer any of my questions. Why again did the 2,000 IU group in the vitamin D study still get 50 URI's? Why did the placebo group (which again, you've claimed had sufficient vitamin D levels) still have around the same number of URI's?
The authors of the study say it was because of the dose and length of the study. It lasted only 12 weeks, which is less than three months. For example, this study found that it takes three months for 25-OHD levels to stabilize after starting supplementation with 1000 or 4000 IU.
http://www.ajcn.org/...t/full/73/2/288
However, the vitamin D levels were increasing continuously and one would assume that there should have been at least some effect. I find it compelling that a longer study done by the same researchers, where the subjects had lower 25-OHD levels, found a dramatic effect.
I know who did the Mineola study, you don't have to tell me. I'm still not sure what your explanation is here, you just seemed to repeat what was found. So, you are or aren't saying that it's incorrect to take the results from African-American women that were clearly deficient in vitamin D and apply to people that have higher vitamin D levels? Make a point please.
I believe low vitamin D levels increase the susceptibility to colds and flu. I believe that when you have low vitamin D level, it does not matter whether you are African-American or not, however dark-skinned people do have a higher prevalence of vitamin D deficiency. Nevertheless, even in sunny places, there is a significant percentage of white people who are deficient. As an example, this study, based on a population in Florida, found that the prevalence of hypovitaminosis D, defined as 25(OH)D less than 50 nmol/liter, was 38% and 40% in men and women, respectively.
http://www.ncbi.nlm.nih.gov/...pubmed/15634725
Why do white women in the United States still get the cold and flu despite having vitamin D levels that are at the same level as the women in the Mineola study? So, you're saying they should have a drastically reduced rate of infection? White men as well I would assume?
You can still get the cold no matter what your vitamin D levels are. In a population where the average is high, there is still a proportion in deficiency. I do not believe vitamin D will make you immune to the flu or respiratory infections. Low vitamin D levels are correlated with the incidence of colds, at least 5 studies have demonstrated this. As I have said, the RECORD study did not contradict with the Mineola study, it does not contradict with my position. I have criticized the only study demonstrating that vitamin D had no effect on reported respiratory infections, mainly because of the short duration, but possibly because of the starting levels as well.
And you still seem to be missing my point. When you take out your reports of reverse causation, all you're left with is one or two reports which can be explained away by coincidence.
Ah yes, of all the reports and studies coming to the same conclusion I have referenced, some were because of reverse causation, in some the subjects were uniquely deficient, others had too many variables, some might have been because of a mild flu season, the rest were pure coincidence. Don't you think that the very plausible biological mechanism, the demonstrated effect of vitamin D increasing AMPs, one placebo-controlled trial showing a dramatic lowering effect of cold symptoms, the inverse correlation between vitamin D levels and frequency of colds, the several reports of vitamin D supplementation, cod liver oil, 60 000 IU injections and UVR reducing reported cold cases and the placebo-controlled trial showing a significant immunity to getting sick from the influenza the subjects were inoculated with in the summer make for at least a somewhat-convincing argument? I do admit that we need a couple of well-conducted placebo-controlled long-term studies to make it conclusive, but nevertheless, the evidence we already have strongly suggests vitamin D plays and important role in the immune system and the susceptibility to colds. |
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