Tex,
Have you come across any new info on mast cells since you addressed them in your book?
I think that some of the variability in PP symptoms/response to treatment could be due to those histamine responses other than H1 (mostly respiratory/skin effects) and H2 (mostly GI effects). Of course, we know that the standard OTC meds like Allegra and Zantac can help these two responses. Last I heard they had identified H3 (mostly central nervous system effects) and H4 (blood/bone marrow effects). As far as I know, there are no established treatments for these yet. Once available, these might help PP who do not respond to current OTC antihistamines
Your thoughts?
Love,
Polly
Paging Tex - re mast cells
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Paging Tex - re mast cells
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Polly,
I think that you're definitely on to something, because obviously mast cells play a much bigger role in this syndrome than any of us ever realized just a few years ago, and researchers have barely scratched the surface on this issue.
To be honest, even though I've been intending to do more research so that I can update the information posted about mast cell issues associated with MC, I haven't been able to devote much time to it yet. There always seems to be something else more urgent that has to be attended to first. Right now for example, the tax return deadline is bearing down on us, so I'm spending most of my spare time working on my return. And the weather is so nice here now, that it's much tougher to force myself to work on inside projects, when it's so nice outside.
And I also wonder if there might be some other class of mast cell receptors that might play a role with GI issues. Now that daylight savings time is in effect, maybe I'll be able to put that extra hour of "free" time to good use.
Thanks for the reminder, because I do want to spend some time working on this issue.
Love,
Tex
I think that you're definitely on to something, because obviously mast cells play a much bigger role in this syndrome than any of us ever realized just a few years ago, and researchers have barely scratched the surface on this issue.
To be honest, even though I've been intending to do more research so that I can update the information posted about mast cell issues associated with MC, I haven't been able to devote much time to it yet. There always seems to be something else more urgent that has to be attended to first. Right now for example, the tax return deadline is bearing down on us, so I'm spending most of my spare time working on my return. And the weather is so nice here now, that it's much tougher to force myself to work on inside projects, when it's so nice outside.
And I also wonder if there might be some other class of mast cell receptors that might play a role with GI issues. Now that daylight savings time is in effect, maybe I'll be able to put that extra hour of "free" time to good use.
Thanks for the reminder, because I do want to spend some time working on this issue.
Love,
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.
Polly,
You must be clairvoyant. When I checked out a lead in my Digestive Health Smartbrief newsletter today, low and behold, there was information on some newly-published eye-opening research concerning mast cells.
So vitamin D does indeed have the ability to suppress inflammation, by modifying IgE-based mast cell activation. Here's another paper (authored by some of the same group of researchers) first published online today, that makes a surprising observation — namely that mast cells are not always associated with inflammation. Sometimes they are associated with the suppression of inflammation. The article discusses how vitamin D enables/empowers mast cells to suppress inflammation and associated skin issues caused by ultraviolet B radiation. Zizzle, are you reading this?
Unless I'm interpreting this incorrectly, there are some far-reaching implications associated with these observations, with regard to the operation of the immune system. My take is that this could lead to something good, but maybe I'm reading too much into this.
Paint me cautiously optimistic.
Love,
Tex
You must be clairvoyant. When I checked out a lead in my Digestive Health Smartbrief newsletter today, low and behold, there was information on some newly-published eye-opening research concerning mast cells.
Mechanisms of vitamin D3 metabolite repression of IgE-dependent mast cell activation.CONCLUSION: Taken together, our findings provide a mechanistic explanation for the anti-inflammatory effects of vitamin D3 on mast cell function by demonstrating that mast cells can actively metabolize 25OHD3 to dampen IgE-mediated mast cell activation in vitro and in vivo.
So vitamin D does indeed have the ability to suppress inflammation, by modifying IgE-based mast cell activation. Here's another paper (authored by some of the same group of researchers) first published online today, that makes a surprising observation — namely that mast cells are not always associated with inflammation. Sometimes they are associated with the suppression of inflammation.
The article discusses how vitamin D enables/empowers mast cells to suppress inflammation and associated skin issues caused by ultraviolet B radiation. Zizzle, are you reading this?Evidence that vitamin D3 promotes mast cell–dependent reduction of chronic UVB-induced skin pathology in miceOur findings suggest that 1alpha,25(OH)2D3/VDR-dependent induction of IL-10 production by cutaneous mast cells can contribute to the mast cell’s ability to suppress inflammation and skin pathology at sites of chronic UVB irradiation.
Unless I'm interpreting this incorrectly, there are some far-reaching implications associated with these observations, with regard to the operation of the immune system. My take is that this could lead to something good, but maybe I'm reading too much into this.
Paint me cautiously optimistic.Love,
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.
Tex,
This is indeed fascinating stuff! I think you may be correct - that there may be far-reaching implications.
And to think we were the first ones to tout the importance of vitamin D in healing! We have definitely been cutting-edge here, on many issues.
Were they saying that locally-applied ("epicutaneous") vitamin D could treat skin inflammation due to UVB radiation? I wasn't aware of any preps like that, were you?
These studies support Gabes' recent observation that her vitamin D level dropped significantly during a period of major stress. Those mast cells were probably working overtime to suppress the IgE response to stress and therefore required more vitamin D. Interesting to think that mast cells may have a role in decreasing inflammation. If true, then we have to go back to the drawing board to find something else to blame for our underlying disease. LOL.
I am intrigued by the difference in different receptors. As we know, there is so much variability in symptoms among MCers. For example, I have never had any respiratory/skin or GYN inflammatory issues (both related to H1 receptors). Neither have I had significant nervous system problems, like nausea, vomiting, headache, vertigo, which are due to H3 receptors apparently. But many here have issues with both of these areas. I think my H2 receptors are the main problem (gastric acid secretion/cramping/diarrhea).
Thanks so much for sharing this. It is important info - perhaps of the paradigm-shift nature!
Love,
Polly
This is indeed fascinating stuff! I think you may be correct - that there may be far-reaching implications.
And to think we were the first ones to tout the importance of vitamin D in healing! We have definitely been cutting-edge here, on many issues.
Were they saying that locally-applied ("epicutaneous") vitamin D could treat skin inflammation due to UVB radiation? I wasn't aware of any preps like that, were you?
These studies support Gabes' recent observation that her vitamin D level dropped significantly during a period of major stress. Those mast cells were probably working overtime to suppress the IgE response to stress and therefore required more vitamin D. Interesting to think that mast cells may have a role in decreasing inflammation. If true, then we have to go back to the drawing board to find something else to blame for our underlying disease. LOL.
I am intrigued by the difference in different receptors. As we know, there is so much variability in symptoms among MCers. For example, I have never had any respiratory/skin or GYN inflammatory issues (both related to H1 receptors). Neither have I had significant nervous system problems, like nausea, vomiting, headache, vertigo, which are due to H3 receptors apparently. But many here have issues with both of these areas. I think my H2 receptors are the main problem (gastric acid secretion/cramping/diarrhea).
Thanks so much for sharing this. It is important info - perhaps of the paradigm-shift nature!
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Polly,
Unless I misread the article, the researchers never actually added any exogenous source of vitamin D. Vitamin D levels were measured, but apparently the vitamin D was strictly endogenous, and a product of the same UVB exposure that caused the inflammation in mast cell-deficient mice. IOW, the research involved the manipulation of the availability of vitamin D receptors (VDR), and mast cell numbers. They used VDR-deficient mice, and mast cell deficient mice. Interestingly, in order to manipulate mast cell numbers, they introduced mast cells into the ears of the mice by injecting bone marrow derived cultured mast cells (BMCMC).
So they never actually added any vitamin D (as far as I could see in the report). Basically they demonstrated that after exposure to UVB radiation (from Table 1 in the article):
1. With normal mice, (IOW normal levels of both mast cells and vitamin D receptors), inflammation was absent (0 out of 11 cases).
2. If mast cells were absent, inflammation was high (7 out of 9 cases.
3. When mast cells were added by injection to the same mast cell-deficient mice used in number 2 (with normal levels of vitamin D receptors), inflammation was absent (0 out of 9 cases).
4. If vitamin D receptors were absent, inflammation was a problem (6 out of 12 cases).
The authors noted that in the examples where inflammation was a problem (2 and 4), white cell counts were high, whereas in the groups where inflammation was controlled by adequate numbers of mast cells and VDRs, white cell counts were normal.
Here's an important preliminary finding published by the group back in 2007, and this discovery is what prompted them to search for the
mechanism that promotes the production of interleukin 10. Their investigation eventually led them to discovery that vitamin D is the key, because without vitamin D receptors, various leukocytes (white blood cells) are apparently free to promote inflammation:
Love,
Tex
Unless I misread the article, the researchers never actually added any exogenous source of vitamin D. Vitamin D levels were measured, but apparently the vitamin D was strictly endogenous, and a product of the same UVB exposure that caused the inflammation in mast cell-deficient mice. IOW, the research involved the manipulation of the availability of vitamin D receptors (VDR), and mast cell numbers. They used VDR-deficient mice, and mast cell deficient mice. Interestingly, in order to manipulate mast cell numbers, they introduced mast cells into the ears of the mice by injecting bone marrow derived cultured mast cells (BMCMC).
So they never actually added any vitamin D (as far as I could see in the report). Basically they demonstrated that after exposure to UVB radiation (from Table 1 in the article):
1. With normal mice, (IOW normal levels of both mast cells and vitamin D receptors), inflammation was absent (0 out of 11 cases).
2. If mast cells were absent, inflammation was high (7 out of 9 cases.
3. When mast cells were added by injection to the same mast cell-deficient mice used in number 2 (with normal levels of vitamin D receptors), inflammation was absent (0 out of 9 cases).
4. If vitamin D receptors were absent, inflammation was a problem (6 out of 12 cases).
The authors noted that in the examples where inflammation was a problem (2 and 4), white cell counts were high, whereas in the groups where inflammation was controlled by adequate numbers of mast cells and VDRs, white cell counts were normal.
Here's an important preliminary finding published by the group back in 2007, and this discovery is what prompted them to search for the
mechanism that promotes the production of interleukin 10. Their investigation eventually led them to discovery that vitamin D is the key, because without vitamin D receptors, various leukocytes (white blood cells) are apparently free to promote inflammation:
Mast cell-derived interleukin 10 limits skin pathology in contact dermatitis and chronic irradiation with ultraviolet B.Our findings identify a previously unrecognized function for mast cells and mast cell-derived interleukin 10 in limiting leukocyte infiltration, inflammation and tissue damage associated with immunological or innate responses that can injure the skin.
Love,
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.
Gabes,
The research didn't address excess numbers of mast cells, only extremely low levels and normal levels. And it was focused on the skin, not in the gut (where the sun don't shine). Therefore, if this article implies anything about mast cell activity in the gut (and this is just speculation on my part), it may be suggesting that when mast cells are a problem in the gut, it might be because of inadequate vitamin D receptors, not necessarily because of excess numbers of mast cells. IOW, the mast cell numbers are only a problem because of inadequate VDR expression.
Actually, a lot of the research on this already exists, so frankly I don't see why someone hasn't put most of it together by now, because it seems pretty obvious to me, that this defines the problem with mast cells, and it probably explains why mast cells (and the histamine that they release) can be such a problem with IBDs. They're a problem mostly because of the inadequate availability of vitamin D receptors. Consider this quote from the abstract at the following link:
Here's a link to the full article, if anyone is interested, maybe some clues can be found in there:
Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis
From the full article:
So now we know that both vitamin D and vitamin D receptors are depleted with IBDs. Just thinking out loud here, but could it be that VDRs become depleted because there is insufficient vitamin D to keep them active? Or does the presence or absence of vitamin D have nothing to do with the availability of VDRs? What promotes the expression of VDRs? It's known that glucocorticoids decrease the expression of VDRs, but I can't find a way to promote the expression of VDRs.
Incidentally, if the corticosteroids decrease the expression of VDRs, why does that not promote inflammation? And incidentally, if anyone is researching any of this, vitamin D receptors are also known as calcitriol receptors.
Sorry for rambling, but I'm a bit short on time today, so I don't have the luxury of enough time to allow me to more carefully edit this.
Tex
The research didn't address excess numbers of mast cells, only extremely low levels and normal levels. And it was focused on the skin, not in the gut (where the sun don't shine). Therefore, if this article implies anything about mast cell activity in the gut (and this is just speculation on my part), it may be suggesting that when mast cells are a problem in the gut, it might be because of inadequate vitamin D receptors, not necessarily because of excess numbers of mast cells. IOW, the mast cell numbers are only a problem because of inadequate VDR expression.
Actually, a lot of the research on this already exists, so frankly I don't see why someone hasn't put most of it together by now, because it seems pretty obvious to me, that this defines the problem with mast cells, and it probably explains why mast cells (and the histamine that they release) can be such a problem with IBDs. They're a problem mostly because of the inadequate availability of vitamin D receptors. Consider this quote from the abstract at the following link:
Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis.The inhibitory effects of vitamin D on colitis have been previously documented. Global vitamin D receptor (VDR) deletion exaggerates colitis, but the relative anticolitic contribution of epithelial and nonepithelial VDR signaling is unknown. Here, we showed that colonic epithelial VDR expression was substantially reduced in patients with Crohn's disease or ulcerative colitis. Moreover, targeted expression of human VDR (hVDR) in intestinal epithelial cells (IECs) protected mice from developing colitis.
Here's a link to the full article, if anyone is interested, maybe some clues can be found in there:
Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis
From the full article:
IEC stands of intestinal epithelial cells, and apoptosis is programmed cell death, which is a normal part of the immune system's role in healing. This quote says a lot about why the gut doesn't heal, when an IBD is present (because of compromised VDR signaling, due to low expression of VDRs). Unfortunately, this was published over a year after I published my book, so I wasn't able to include any of it. I may have to write an updated version, because this supports a lot of what I wrote, including some of the speculative observations, and it obviously also adds some new twists.Our results indicate that epithelial VDR signaling inhibits colitis in part by reducing IEC apoptosis in a manner independent of VDR actions in the nonepithelial immune compartment.
So now we know that both vitamin D and vitamin D receptors are depleted with IBDs. Just thinking out loud here, but could it be that VDRs become depleted because there is insufficient vitamin D to keep them active? Or does the presence or absence of vitamin D have nothing to do with the availability of VDRs? What promotes the expression of VDRs? It's known that glucocorticoids decrease the expression of VDRs, but I can't find a way to promote the expression of VDRs.
Incidentally, if the corticosteroids decrease the expression of VDRs, why does that not promote inflammation? And incidentally, if anyone is researching any of this, vitamin D receptors are also known as calcitriol receptors.
Sorry for rambling, but I'm a bit short on time today, so I don't have the luxury of enough time to allow me to more carefully edit this.
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.
-
Gabes-Apg
- Emperor Penguin
- Posts: 8332
- Joined: Mon Dec 21, 2009 3:12 pm
- Location: Hunter Valley NSW Australia
dont apologise at all Tex
i know you are busy with spring weather tasks/taxes/change of season and the like. heartfelt gratitude for replying so quickly
I am very appreciative of the links and your thoughts, this topic is VERY relevant to what I am investigating and adjusting my supplement protocol etc.
And it is a fantastic reminder to those that wonder if taking Vit D3 is worth it.
A new practitioner that I met with last week, we talked a bit about VitD3
- that Doctors in Australia are not allowed to recommend above 1000iu (they are encouraged to only recommend 600iu).
- As a nutritionist she is only allowed to recommend dosage up to 3000iu.
- my recent drastic drop in levels and the 'recommended range' and what doctors class as deficiency. Her belief is that anyone with an IBD/Immune condition/Inflammation should not go below 40 International (100 Aus measurement)
i know you are busy with spring weather tasks/taxes/change of season and the like. heartfelt gratitude for replying so quickly
I am very appreciative of the links and your thoughts, this topic is VERY relevant to what I am investigating and adjusting my supplement protocol etc.
And it is a fantastic reminder to those that wonder if taking Vit D3 is worth it.
A new practitioner that I met with last week, we talked a bit about VitD3
- that Doctors in Australia are not allowed to recommend above 1000iu (they are encouraged to only recommend 600iu).
- As a nutritionist she is only allowed to recommend dosage up to 3000iu.
- my recent drastic drop in levels and the 'recommended range' and what doctors class as deficiency. Her belief is that anyone with an IBD/Immune condition/Inflammation should not go below 40 International (100 Aus measurement)
Gabes Ryan
"Anything that contradicts experience and logic should be abandoned"
Dalai Lama
"Anything that contradicts experience and logic should be abandoned"
Dalai Lama
I certainly wouldn't argue against that. It's a shame that GI docs all over the world don't recognize the wisdom of that.Gabes wrote:Her belief is that anyone with an IBD/Immune condition/Inflammation should not go below 40 International (100 Aus measurement)
Polly,
As always, you're as welcome as a warm rain on a spring day. Thanks to your original questions, now we have something new to study, and to think about.
Love,
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.
Fascinating! I haven't read all the articles yet, but this seems to support my allergist colleague's statement that mast cells travel to and accumulate at sites experiencing inflammation. So maybe they are there to heal and ward off bad guys (food proteins, etc)? Perhaps the rapid D caused by mast cell activation is merely a temporary protective mechanism, and not the source if our chronic inflammation? Makes me think suppressing mast cell activity is simply covering up continued ingestion of foods we are sensitive to.
I wish I understood the relationship between mast cells and leukocytes. My skin condition is caused by a overproliferation of leukocytes in the blood vessels of the skin (just like the MC). I don't understand why this results in extreme sun sensitivity. Are mast cells involved in the sun sensitivity?
We still have a chicken and egg problem. Something prevented us from making enough of our own vitamin D in the first place, and I suspect supplemental D is not the answer.
I wish I understood the relationship between mast cells and leukocytes. My skin condition is caused by a overproliferation of leukocytes in the blood vessels of the skin (just like the MC). I don't understand why this results in extreme sun sensitivity. Are mast cells involved in the sun sensitivity?
We still have a chicken and egg problem. Something prevented us from making enough of our own vitamin D in the first place, and I suspect supplemental D is not the answer.
1987 Mononucleosis (EBV)
2004 Hypomyopathic Dermatomyositis
2009 Lymphocytic Colitis
2010 GF/DF/SF Diet
2014 Low Dose Naltrexone
2004 Hypomyopathic Dermatomyositis
2009 Lymphocytic Colitis
2010 GF/DF/SF Diet
2014 Low Dose Naltrexone
-
Gabes-Apg
- Emperor Penguin
- Posts: 8332
- Joined: Mon Dec 21, 2009 3:12 pm
- Location: Hunter Valley NSW Australia
Zizzle,
The practitioner I saw a week ago said that using the OTC meds to block histamines/mast cells was counter productive, as we need them.
I am now introducing/using high dose magnesium, zinc, Vit c to moderate, (calm) the mast cells/histamine.
And we hope this with other aspects we are investigating implementing , will calm the immune system...
The practitioner I saw a week ago said that using the OTC meds to block histamines/mast cells was counter productive, as we need them.
I am now introducing/using high dose magnesium, zinc, Vit c to moderate, (calm) the mast cells/histamine.
And we hope this with other aspects we are investigating implementing , will calm the immune system...
Gabes Ryan
"Anything that contradicts experience and logic should be abandoned"
Dalai Lama
"Anything that contradicts experience and logic should be abandoned"
Dalai Lama
I'm going to remember to take my D3 now!
What does this research mean for people like my MIL who have ME and chronic hives? And why do chronic hives happen to people with Hashimoto's? What's the thyroid connection?
So many questions!
What does this research mean for people like my MIL who have ME and chronic hives? And why do chronic hives happen to people with Hashimoto's? What's the thyroid connection?
So many questions!
1987 Mononucleosis (EBV)
2004 Hypomyopathic Dermatomyositis
2009 Lymphocytic Colitis
2010 GF/DF/SF Diet
2014 Low Dose Naltrexone
2004 Hypomyopathic Dermatomyositis
2009 Lymphocytic Colitis
2010 GF/DF/SF Diet
2014 Low Dose Naltrexone
I don't see that viewpoint reflected in any of these articles, but they certainly don't rule it out, either — they simply don't address that possibility. What they do emphasize, though, is that the lesions, or other centers of inflammation are devoid of vitamin D receptors. That's the key. Without vitamin D receptors, no vitamin D signaling is possible, and that allows inflammation to escalate.Zizzle wrote:Fascinating! I haven't read all the articles yet, but this seems to support my allergist colleague's statement that mast cells travel to and accumulate at sites experiencing inflammation. So maybe they are there to heal and ward off bad guys (food proteins, etc)?
The relationship that matters is the connection between vitamin D receptors and leukocytes. Whenever VDRs are in adequate supply, mast cells are calm, and inflammation is absent. If VDRs are missing, mast cells degranulate, and histamine and leukocyte numbers reach excessive levels. Consider these quotes from the last article that I cited above. The first one refers to conditions found in the intestines of typical Crohn's patients.Zizzle wrote:I wish I understood the relationship between mast cells and leukocytes. My skin condition is caused by a overproliferation of leukocytes in the blood vessels of the skin (just like the MC). I don't understand why this results in extreme sun sensitivity. Are mast cells involved in the sun sensitivity?
In most patients, VDR protein levels were dramatically decreased (by >60% on average) in the lesion relative to the adjacent normal region within the same patient (Figure (Figure1,1, E and F), whereas proinflammatory cytokine transcripts (TNFA and IL1B) were elevated in the lesion (not shown). This observation again suggests a repressive effect of local colonic inflammation on epithelial VDR expression.
.Together, our data suggest that the potent anticolitic activity of epithelial VDR signaling is derived at least in part from reducing the inflammatory status of the epithelial cells and maintaining the integrity of the mucosal epithelial barrier
And this observation about not just vitamin D, but especially vitamin D receptors, is interesting:Colonic commensal bacteria play a key role in the development of IBD. Colonic epithelial cells influence the microbiota by secreting antimicrobial peptides (61). Vitamin D has been reported to induce cathelicidin and β2-defensins (62, 63). It is conceivable that epithelial VDR can regulate colonic inflammation by regulating antimicrobial peptide production in colonocytes. Moreover, epithelial VDR signaling may also regulate autophagy, another molecular event that has been implicated in IBD (64, 65). Indeed, vitamin D/VDR signaling is known to regulate autophagy (66).
These observations suggest that vitamin D status might be an environmental determinant for IBD, whereas VDR status might be a key genetic factor influencing IBD development.
Again, it's not the vitamin D, it's the ability of the epithelia (or epidermis) to utilize it. Vitamin D receptors are the key. From one of my posts above:Zizzle wrote:We still have a chicken and egg problem. Something prevented us from making enough of our own vitamin D in the first place, and I suspect supplemental D is not the answer.
Evidence that vitamin D3 promotes mast cell–dependent reduction of chronic UVB-induced skin pathology in miceOur findings suggest that 1alpha,25(OH)2D3/VDR-dependent induction of IL-10 production by cutaneous mast cells can contribute to the mast cell’s ability to suppress inflammation and skin pathology at sites of chronic UVB irradiation.
That article is specifically about skin inflammation. You should read it. It's not easy, because of all the confusing references to the various mouse pedigrees, but at least read my comments about it, because I believe that this is very relevant to your situation with your persistent rash issues. Your vitamin D receptors are in short supply in every local area of inflammation in your skin (IMO).
Zizzle wrote:What does this research mean for people like my MIL who have ME and chronic hives?
It means that since they can't do anything about the local depletion of VDRs (at least not currently), they should keep their vitamin D levels well above normal, to make the most of the vitamin D receptors that they still have.
I think I know the answer to that question, but I can't put my finger on it at the moment. In the meantime (until I can formulate my thoughts), here's Chris Kresser take on the issue:Zizzle wrote:And why do chronic hives happen to people with Hashimoto's? What's the thyroid connection?
The Role of Vitamin D Deficiency in Thyroid Disorders
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.
Hi, Great posts. Now, I have a better understanding why so many people with FSHD have a colitis. The inability of the body to remove the toxic protein produced by the muscles. As the FSHD researchers have stated that we all have this toxic protein that is produced but 95% of the population have the mechanism to remove it. I found this connection before but now have to retrack my steps to confrim. Jon