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Yes I know. That's similar to cow's milk — cow's milk is advertised as a source of vitamin D, but raw milk has very little vitamin D. Virtually all of it is added during processing. Virtually all processed foods now have a list of ingredients as long as my arm, and many of those ingredients are simply due to "enrichment" during processing. Apparently, many in the food industry (and even in the government regulatory agencies, and medical advisory boards, etc.) mistakenly think that every food should be a complete source of nutrition. Why?
The only complete food is meat. If anyone wants a complete food that contains every essential amino acid, all they have to do is eat meat. And yet this is the very food that food "experts" in general tend to advise against eating. What's wrong with this picture?
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
So the research seems to be moving at a faster clip lately. I guess researchers realize there is money to be made in the autoimmune epidemic.
This is the most understandable and profound paper I've read on Epstein Barr Virus and autoimmunity. As far as I'm concerned, it's case closed. EBV is required to set the foundation for autoimmunity. It may not be the trigger, but it must be there, and it's worse if it was acquired in adolescence or later, when CD8 counts were lower. This creates a permanent immune system imbalance. This also explains the protective effect of sunlight and vitamin D -- it increases our precious CD8 cells!
"So the strategy EBV has developed to keep its host B cell alive but latent and hidden from attack by the immune system is by constantly poking the immune system's low level interferon response, which is akin to keeping the immune system on the edge of its seat and ready to pounce," said Horwitz, who is co-leader of the university's infection, inflammation, and immunity program.
In that hyperalert state, when the immune system detects a new threat its response could be excessive, which could push the individual over the edge into autoimmunity, he explained.
The T-Cell Connection
Many epidemiologic studies have found a strong familial component in autoimmune diseases. In a healthy host, EBV infection is tightly controlled by a subset of cytotoxic CD8+ cells, which destroy the infected cells. As Pender continued his research, he then suggested that this genetic component could be an inherited deficiency of CD8+ cells.
"Since 1980 it has been recognized that the proportion and number of CD8+ T cells in the peripheral blood are decreased and that the CD4/CD8 ratio is increased," factors that are under genetic control, he noted.
When an individual with that genetic background is infected with EBV, a greater number of B cells harboring the virus will remain in the circulation, he said. And because 20% of B cells are autoreactive, those cells could begin making potentially pathogenic antibodies that then traffic throughout the body, lodging in target organs and, in turn, producing target-specific antibodies.
His expanded hypothesis, published in 2012 in Autoimmune Diseases, proposed "that, in genetically susceptible individuals, EBV-infected autoreactive B cells seed the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis."
Age Matters
In the developing world, EBV infection is almost universal by 3 years of age, and is largely asymptomatic and lacking in clinical consequences. However, in the developed world early life exposure is less common because of improved hygiene, and in Denmark, for example, at least half of children haven't been infected by age 10, according to Pender.
And when infection doesn't occur until adolescence, it's typically much more severe, manifesting as infectious mononucleosis. The reason for this, he explained, is that healthy people have three times as many CD8+ T cells at age 2 years than at 15. Therefore, when a person already has a genetically determined deficiency in these cells and exposure occurs after the age-related CD8+ T cell decline, the autoimmune cascade can ensue.
Another contributory factor is location. "It has long been known that the further people live from the equator the more likely they are to get MS, and it seems the same may apply to rheumatoid arthritis and type 1 diabetes," Pender said.
"And we now know that if you give an extra hour of sunlight a day to a person for 2 weeks, you can increase their number of CD8+ T cells by about 35%, at least some of which occurs through the action of vitamin D," he said.
Sex also matters. Females tend to have lower numbers of CD8 T cells than CD4 T cells, which is thought to be hormonally regulated, and females are predominantly affected in the majority of autoimmune diseases, he pointed out.
Here's a huge breakthrough in understanding Lupus and probably my condition:
new treatment that boosts the ability of CD8 T cells in the immune system to fight against EBV. They believe the approach, called adoptive immunotherapy, could potentially treat MS and other chronic autoimmune diseases.
6-week course of the treatment, which appeared to produce no adverse side effects.
The treatment involves taking some of the patient's blood so the researchers can harvest some of his own T cells and grow them in the lab together with an EBV vaccine. Then, the boosted cells are transferred back to the patient intravenously.
My doctor demonstrated that my EBV titers were higher when I was flaring, and lower upon remission, so battling viruses dies seem to play a role in my autoimmune condition. I had higher titers of HHV-6 too when I was sicker.
Zizzle wrote:Could good ol' Epstein Barr be the cause of all my connective tissue issues, GI problems, skin rashes, temperature and exercise intolerance? Maybe a GI bug I picked up overseas? Or Lyme Disease?
Zizzle,
I was thinking eaxctly the same yesterday after having seen this documentary about Lyme Disease. Did MC start with a tick?
A shocking documentary, where the medical society is silent and the authorities in almost all nations, except Germany, ignore the disease.
As I have mentioned earlier, a Norwegian GP lost his licence two years ago, because he tried to treat a Lyme patient with long term antibiotics.
Zizzle wrote:My doctor demonstrated that my EBV titers were higher when I was flaring, and lower upon remission, so battling viruses dies seem to play a role in my autoimmune condition. I had higher titers of HHV-6 too when I was sicker.
That's because EBV activity is affected by the expression of T cells. Did you happen to notice my post about Magnesium, EBV, and T cell expression?
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
It's ridiculous how confused and misguided some regulatory supervisory organizations can become when the people in powerful positions have agendas to pursue.
But as always, when authorities in the medical community (or the government) abuse their power, it's the patients who suffer.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Zizzle wrote:Here's something else I read about Vitamin D (not from Dr. Ayers). I don't know the original source, but I recall some group warning that Vit D supplementation was not advised for people with Crohns, Lupus and other granulomatous autoimmune diseases. Could this be why?
Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency. Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes. The VDR dysfunction causes a decline in innate immune function that causes susceptibility to additional infections that contribute to disease progression. Evidence has been accumulating that indicates that a number of autoimmune diseases can be reversed by gradually restoring VDR function with the VDR agonist olmesartan and subinhibitory dosages of certain bacteriostatic antibiotics. Diseases showing favorable responses to treatment so far include systemic lupus erythematosis, rheumatoid arthritis, scleroderma, sarcoidosis, Sjogren's syndrome, autoimmune thyroid disease, psoriasis, ankylosing spondylitis, Reiter's syndrome, type I and II diabetes mellitus, and uveitis. Disease reversal using this approach requires limitation of vitamin D in order to avoid contributing to dysfunction of nuclear receptors and subsequent negative consequences for immune and endocrine function. Immunopathological reactions accompanying bacterial cell death require a gradual elimination of pathogens over several years. Practical and theoretical implications are discussed, along with the compatibility of this model with current research.
I know that this thread was started awhile ago and originally about EBV. But I found an article regarding what Zizzle referred to above way back at the top of the thread. You can read the article here: http://link.springer.com/article/10.100 ... 014-0755-z
Warning: this is a long and involved article. But what I wanted to point out is that it makes a very well referenced case that low vitamin D is actually caused not by a deficiency of vitamin D but by inflammation. In other words, low vitamin D (the storage form which is the one that is always measured) may not be the reason for inflammation but be the consequence of inflammation. Now this is my summary so you may want to go read the article yourself. The reader's digest version is that inflammation, probably caused by intracellular infection, dysregulates VDR. This causes an increase in the active form of Vitamin D (calcitriol which is rarely measured) which does a whole lot of things to suppress the immune system. Further, when we take Vitamin D exogenously then we further increase calcitriol and the effect is immunosuppression by way of VDR dysregulation.
The article has a lot more to say about using an angiotensin receptor blocker called olmesartan to restore VDR competence. Sure enough I looked it up and found that this is actually being done to treat autoimmune diseases.
So I found this all quite fascinating and would love to hear your thoughts if you are inclined to take a look at the article. My take away at this point is I am not so sure I want to continue to take vitamin D supplements. I can say they haven't cured me of anything that ails me yet, despite increasing my vitamin D level.
All this concerns me that maybe, like so many things, we've gotten this wrong. I am taking this information to my doctor today actually. I also plan to ask her if I can get my calcitriol tested. Calcitriol is 1,25 (OH)D and is the bioactive form of vitamin D whereas what is usually tested is 25 (OH)D which is the storage form.
No, we don't have it wrong. You (and the authors of that article) are trying to overthink it, and you're confusing yourselves. It's actually a no-brainer — the immune system uses vitamin D to fight inflammation, so naturally it's going to use up the available vitamin D to fight inflammation. If you cut off the supply of vitamin D, then you will effectively neuter your immune system, because it will run out of fuel.
I'm guessing that you haven't read my book on Vitamin D and Autoimmune Disease. I'll be happy to send you a printed copy, or email you a digital copy if you want. To email a digital copy, I need to know the type of digital reader you prefer to use (or I can sen a PDF file that can be read on a PC or most digital devices that can open PDF files).
Just let me know,
Tex
P. S. Vitamin D is not going to "cure" anything (though it will prevent many diseases) anymore than any other supplement or medication is going to cure anything. What it will do is prevent you from developing more AI diseases.
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
There is also another thread that I can't find where Tex and Polly talk about Vit D3 receptors in the cell that may be of interest.
Long story short, if the cells are deficient in nutrients, it won't use the other nutrients ie like Vit D, properly...
Vit D levels is only one chapter of a huge huge story.
Gabes Ryan
"Anything that contradicts experience and logic should be abandoned"
Dalai Lama
I didn't know you had written a book about vitamin D. I would very much appreciate it if you would email me a copy and I will read it. But I would also very much like for you to read the article that I posted and then possibly give me a little more insight on why the author's have over thought this. I truly am wanting to understanding your point of view if you have the time to elaborate. VDR regulation is highly complex and probably needs quite a lot of thought and research to understand. Their ultimate point is that intracellular infection disrupts the VDR regulation causing high calcitriol. It is plausible to me then that this disruption of vitamin D endocrine function cannot be simply fixed by taking more vitamin D. Inflammation may deplete vitamin D but it's my understanding that more is used because the action of calictriol is to metabolize more of the calcidiol (the storage form). And frankly I know enough about this I think to conclude that this can have some not so good effects like mobilization of calcium. I also realize that inflammatory diseases are associated with low storage levels of vitamin D (calcidiol) but is it necessarily accurate to say that low vitamin D causes inflammation or that taking vitamin D supplements and keeping our "number" in a certain range will alleviate inflammation? I'm not sure there is. But maybe your book will help me out here.
Also, regarding "neutering the immune system". I think this could summarize what the writer's of the article are saying that the microbes do when they hijack the VDR regulation. Anyway, it's all in the article. I was hoping someone would read it and comment.
Thank you Gabes for making that point. Also increased need for magnesium is one of the concerns I would have about taking too much vitamin D. As calcitriol mobilizes calcium our needs for magnesium increase. Our inflammed guts already leave us highly challenged to find ways to increase our magnesium levels, rubbing it on every body part and what not. And this is one thing I have noticed.....as my vitamin D blood level climbed so have my issues with muscle spasm and tightness. Is this because it indirectly depleted magnesium. I think possibly so. So, I agree that getting the Vitamin D right, however you choose to approach it, is just part of the puzzle. But if one is dealing with a latent infection, then it is possibly a huge part of the puzzle but not fixed by just taking more vitamin D.
Gigi wrote:but is it necessarily accurate to say that low vitamin D causes inflammation
No. Vitamin D deficiency does not cause inflammation, by any means. Vitamin D deficiency prevents inflammation from being resolved, so inflammation continues to accrue.
Gigi wrote:or that taking vitamin D supplements and keeping our "number" in a certain range will alleviate inflammation?
It may not be able to totally eliminate inflammation, as long as inflammation continues to be generated, but vitamin D will certainly reduce inflammation, and if the production of new inflammation is stopped (such as by changing the diet), then vitamin D will progressively resolve (eliminate) the inflammation.
You need to read the book, and especially read chapter 5 very carefully (maybe more than once, because there is a lot there to digest), in order to understand what vitamin D does for the body and the part that VDRs play.
There are many digital formats. You didn't tell me which one you want.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
What's wrong with this picture?
