Kickas.org Forums Ankylosing Spondylitis General Discussion #1 AS Web Support Group head on question

Hi Billy, while I am not a detractor of the NSD, I am one of those who suggest caution when approaching it. As several others have noted, we are all different and respond differently not only to our disease but to the various treatments that are available.

What works for one, will not necessarily work for someone else.

Personally, I have virtually eliminated wheat from my diet. I have also, for the most part, eliminated cow dairy. I never eat the two combined.

I also limit my intake of oatmeal, corn and potatos. However, beans/legumes, nuts and seeds are still a large part of my diet.

I believe (key word being "believe") that we could all benefit from limiting or excising our intake of wheat products, as it is the most difficult grain for our bodies to process. I also believe that limiting our intake of refined sugars and cow dairy would be beneficial. Do I maintain that it will work for everyone? No. However I believe that everyone would derive benefit from it in some way, shape or form.

Those who advocate the NSD so strongly here, do so because they believe in it. They have found that it has made an incredible difference in their lives. Often, when someone finds something that makes that great an impact on them, they want everyone to experience the benefits. Sometimes they push a little harder than we would like, but it helps to remember that they do this because they believe in it and because they care.

Ultimately, it's up to you how you handle this. And I truly hope that nobody here would condemn you for not going NSD if you believed it was not necessarily beneficial to you personally.

Hugs,

Kat



"A life lived in fear is a life half lived." - Strictly Ballroom

Hi Bilko,
I am glad to hear that the NSD theory is being researched to the point of showing stastically significant data asserting its benefits in helping reduce symptoms of AS etc.

I am reminded of the time when I was undergrad and I came across a study in which people with RA fasted for several days and their symptoms were recorded. If my memory is correct, a very high percentage of participants showed significant reduction in arthritis symptoms. Then the researchers put people back on their normal diets and , you can see what is coming... all their symptoms returned. The most astounding part of this research (although very old now) was the conclusions made by the investigators. They concluded that dietary restrictions or dietary experimentation was not a valuable avenue to explore with people with arthritis as symptoms return when food is reinstated.

I am hopeful that current research has advanced to the point that specific triggers (ie; starch) are now being investigated. My point is that if these same participants had reinstated one food item at a time, they may very well have seen value in this study as certain foods may have triggered a recurrence of symptoms.

Now, if you have followed me so far..... do you think that the participants adding in food slowly would have found the same foods irritated all participants. For example, starch added back in showed a recurrence of symptoms for a large majority of participants. Or do you think that some may have reacted to sugar, some gluten only and some starch.
That is the question. As in my opinion. further research needs to be done to prove that starch is the common denominator as the allergen as many will attest here that it still seems to be varied amongst individuals. Again, some starch others wheat, others dairy, etc...
I have enjoyed the debate. And yes, some theories have more validity than others but unfortunately all theories are theories until they became law.


Rene a.k.a Julie
Kodi

The Klebsiella molecular mimicry to HLAB27 theory is controversial in the medical literature. There are over 200 citations found in Medline when one searches "Klebsiella AND ankylosing spondylitis." While a number of studies do indeed support the Klebsiella-HLAB27 molecular mimicry theory, a number of studies do not support this theory. Here are some of the citations that fall into the second category, that is they do not support Klebsiella-HLAB27 molecular mimicry theory, either by review of the available literature, or direct evidence to the contrary, or by finding evidence of other mechanisms.

I hope that posters that respond to this post will refrain from personally attacking other posters or attacking authors of these scientific studies. It is my hope we can agree to disagree respectfully.

medline is here:
Click Here

1)
recent articles that do not support the notion of either 1) increased carriage of klebsiella in the bowels of AS patients when compared to controls or 2) increased immune reactivity to klebsiella in AS patients when compared to controls

Click Here
Stone MA, Payne U, Schentag C, Rahman P, Pacheco-Tena C, Inman RD.
Comparative immune responses to candidate arthritogenic bacteria do not confirm a dominant role for Klebsiella pneumonia in the pathogenesis of familial ankylosing spondylitis.
Rheumatology (Oxford). 2004 Feb;43(2):148-55. Epub 2003 Aug 29.
PMID: 12949256
"OBJECTIVE: Using humoral immune responses, Klebsiella pneumoniae has been implicated as a candidate microbial trigger in ankylosing spondylitis (AS) by several investigators but refuted by others….CONCLUSION: Our analysis of affected and unaffected family members in familial AS demonstrated no significant differences with respect to cellular or humoral immune responses to K. pneumoniae and three control microbes. In addition, K. pneumoniae did not exhibit a predominant immune response in affected individuals. Thus we find no supportive evidence to implicate a causal role for K. pneumoniae in familial AS."

Click Here
Stebbings S, Munro K, Simon MA, Tannock G, Highton J, Harmsen H, Welling G, Seksik P, Dore J, Grame G, Tilsala-Timisjarvi A.
Comparison of the faecal microflora of patients with ankylosing spondylitis and controls using molecular methods of analysis.
Rheumatology (Oxford). 2002 Dec;41(12):1395-401.
PMID: 12468819
"Analysis of individual bacterial groups using nucleic acid-based methods showed no differences in faecal colonization with Klebsiella pneumoniae… The concentrations of serum immunoglobulin A (IgA) and IgM antibodies reactive with klebsiella or bacteroides cells were lower in the patient group relative to the controls.

2)
recent reviews on various theories to explain pathogenesis of AS

Click Here
Turner MJ, Colbert RA.
HLA-B27 and pathogenesis of spondyloarthropathies.
Curr Opin Rheumatol. 2002 Jul;14(4):367-72. Review.
PMID: 12118169
"Although the influence of HLA-B27 on the development of spondyloarthropathies is undisputed, its role in pathogenesis remains unclear. New ideas have focused on abnormal characteristics of HLA-B27 resulting from aberrant folding, disulfide bond formation, or both, rather than a predilection for selecting arthritogenic peptides. This reflects, in part, unanswered questions about whether immunologic recognition of HLA-B27 is required for disease. Recent studies suggest that CD4 T cells, immunomodulatory killer cell Ig receptors, and Ig-like transcript receptors may recognize aberrant forms of HLA-B27. Other reports suggest that HLA-B27 expression can alter cytokine production from monocytes and T cells-effects that appear unrelated to antigen presentation. Novel bioinformatics approaches have led to the identification of HLA-B27-restricted pathogen-derived peptides and may prove useful in determining whether HLA-B27 presents arthritogenic peptides. Elucidating the role of HLA-B27 in the pathogenesis of these conditions will require an integration of information from animal models, genome-wide screens for susceptibility alleles, and translational studies using human samples."

Click Here
Colbert RA.
HLA-B27 misfolding: a solution to the spondyloarthropathy conundrum?
Mol Med Today. 2000 Jun;6(6):224-30. Review.
PMID: 10840380
"Compelling evidence indicates that HLA-B27 is directly involved in the etiopathogenesis of the spondyloarthropathies (SpAs). Several hypotheses based on its native antigenic structure, the peptides it presents and mimicry with bacterial epitopes, have been proposed. However, these potential mechanisms remain largely unsupported by human studies and transgenic animal models. Recent work demonstrating that HLA-B27 misfolds offers a novel alternative hypothesis. Here, we review this new information on the folding and assembly of HLA-B27, and discuss consequences of misfolding that could be relevant to the pathogenesis of SpAs."

Click Here
Colbert RA.
The immunobiology of HLA-B27: variations on a theme.
Curr Mol Med. 2004 Feb;4(1):21-30. Review.
PMID: 15011956
"In the thirty years since the initial discovery of a striking association between HLA-B27 and susceptibility to ankylosing spondylitis, numerous hypotheses have been proposed to explain the role of this molecule in the pathogenesis of spondyloarthropathies. In the past few years the focus has shifted from one centered largely on the physiological peptide-presenting function of HLA-B27, to include ideas based on aberrant aspects of its immunobiology. This has been driven in part by results from animal models of HLA-B27-associated disease where CD8 T cells do not appear to be playing a major role in pathogenesis. In addition, the HLA-B27 heavy chain is unusual in that it has a tendency to misfold in the endoplasmic reticulum and to form disulfide linked heavy chain dimers that can be expressed on the cell surface. Although the data suggest misfolding and cell surface dimerization are fundamentally different processes, it appears that certain structural features of the heavy chain are common to both. Potential links between these aberrant characteristics of HLA-B27 and inflammatory disease are discussed in this and other reviews in this issue. Herein we consider how protein misfolding affects cell function through the activation of an 'unfolded protein response' and/or an 'ER overload response', and the potential impact on the immune system. Despite significant advances in the treatment of spondyloarthropathies over the past few years, a better understanding of pathogenesis is likely to improve outcome by dentifying ways to provide greater and more sustained clinical responses.

Click Here
Bowness P.
HLA B27 in health and disease: a double-edged sword?
Rheumatology (Oxford). 2002 Aug;41(8):857-68. Review.
PMID: 12154202
full text here:
Click Here
"The strong association of the HLA class 1 allele HLA B27 with ankylosing spondylitis (AS) has been recognized for over 25 yr, however the pathogenic mechanism linking HLA B27 with AS and other spondyloarthropathies remains a mystery. We now know that the principal natural function of HLA B27 is an immunologic one, namely to bind antigenic peptides and then present them to T lymphocytes. I have shown that HLA B27 functions as an excellent antigen-presenting molecule in both spondyloarthropathy patients and healthy individuals. A working molecular model of how T cells recognize HLA B27 has been generated and tested. Evidence that T cells have a role in spondyloarthritis has also been found. First, expanded populations of T lymphocytes were found in both the blood and synovial fluid of patients with reactive arthritis (ReA). Secondly, a strong cytotoxic T-cell response to an HLA B27-restricted peptide epitope from Chlamydia trachomatis was found in a patient with ReA. This peptide, derived from a bacterium known to trigger ReA, is thus a candidate 'arthritogenic' peptide. We have also found evidence that HLA B27 has an unusual cell biology compared with other HLA molecules. HLA B27 demonstrates an unusual ability to form heavy chain homodimers in vitro. Dimerization is dependent upon disulphide bonding through an unpaired cysteine at position 67. Remarkably these dimers lack ß2 microglobulin, previously thought to be an essential component of all mature MHC class 1 molecules. HLA B27 homodimer formation has also been demonstrated in certain cell lines in vivo, and preliminary data suggest that significant numbers of T cells from patients with spondyloarthropathy express a ligand for HLA B27 homodimers. These findings have extended our understanding of the beneficial immunologic function of HLA B27, and have also led us to propose the testable new hypothesis that HLA B27 heavy chain dimerization may be involved in the pathogenesis of spondyloarthritis. "


3)
several older posts contain text or links that address the complexity and controversial nature of this question

Click Here

Articles with various theories to explain relationship of HLAB27 to development of AS linked here
Click Here

Links to several full text reviews here:
Click Here


Evelyn, I shortened the links to avoid page scroll, Ian

Edited by iwood51 on 11/13/04 07:08 PM (server time).

I personally do not care one whit whatsoever if "they" manage to come up with a functional theory on why certain diets aid in reducing the symptoms of the disease, because I knew long before I found this websight that diet DID and DOES affect my symptoms. This is irrefutable. It has nothing to do with any belief system in voodoo medicine. The site gave me the knowlege to expand my list of "do not consumes."

For me to blithely continue to consume things I already know upset my digestive system and flare my joints, because some doctor has been brainwashed by the pharmaceutical industry, OR because someone posting on said websight says I'm delusional says I don't have enough confidence in my own abilities to persue knowlege and use it.

I also agree with Kat that the main culprit in my case seems to be gluten, especially FRIED gluten, and most other fluffy white food products which have been fried. I've also had enough bizarre reactions to such innocuous things as caramel candies (bleeeeahhhhhhh) and commercial salad dressings/other foods containing Modified Food Diabolical Starch Product that it's not hard to motivate myself to reduce consumption of such items as much as possible.

Since the disease has a higher incidence being carried by certain tribes/countries/peoples based on geological origin,(northern european or american indigenous, for example) and has a genetic link, (majority carry a certain marker, some of us probably have another one not yet officially discovered because it's obscure) it's not hard to therefore postulate that certain peoples in the past became more grain adapted as a survival mechanism based on what foodstuffs were available, and certain others of us got left behind based on when our ancestors met the modern, grain-based, starch based diet. We do, however, have other characteristics that enhanced our survival, and may yet use those characteristics in the future.

Let us look at an organism in its enviroment. What is life? It respirates (breathes), it eats, it drinks, it metabolises, it creates waste, it ages and dies. Why is all life not EXACTLY the same? Because of differences in enviroment.....AND genetics. Why in the world would I be expected to respond to any one else's enviroment in the same way? I don't have the same genes. How do change enviroment? One way is you change the nourishment. Is this REALLY that hard to grasp?

Do I still sound like some whack job?

I haven't even begin to go into disease theory. Why wouldn't certain other living organisms seek to exploit dietary differences? The perfect disease organism, after all, does not kill the host...it just lives in it.

I would not even begin to say diet cures the disease. The disease is always there. Diet does, in my case, mitigate the disease. I offer my experiences in the spirit of sharing. If you, jcwinnie, were truly pro-science, you would be aware of the many nutritional studies being done on animals' health regarding diet, and you'd quietly slink away in embarrassment. My cat's diet has probably undergone more scrutiny than most human's.

Thanks for sharing your diet-related experiences with us here. I am happy to hear that you are able to manage AS successfully with diet. That is good news indeed!

Perhaps I'm missing something here (i.e. sometimes I need things spelled out real clearly), but what do the "many nutritional studies being done on animals' health regarding diet" have to do with discussing the benefits of the NSD diet in AS in humans ? I think jcwinnie made a valid point & I can't imagine why he'd want to "slink away in embarrassment," for expressing his opinion. I certainly hope he continues to post here often. His posts ... and of course, his illustrations, are always a welcome respite in dealing with AS.


Cat

Well all I would say is that starch is the usual culprit but if the patient has some other food intolerance then that other food type will also feed the little bu**ers.

Getting back to the fun

unfortunately all theories are theories until they became law.

I disagree, no science is law - remember what happened to Newton's laws. And for that reason there are those who will still argue that rheumatic fever is not caused by molecular mimicry with streptococci - and Evelyn could probably track those abstracts down if she so wished!

And what's he then that says I play the villain
When this advice is free I give and honest

Edited by bilko on 11/12/04 04:21 AM (server time).

Hi Bilko
Let's PLEASE not tell anyone to slink away with embarassment. This is obviously a controversial issue and it would be much better for everyone if we can state our points respectively. It seems apparent that the research you have found supports the NSD theory and the research Evelyn points to does not. So, this is the exact reason why I point out that NSD is still a theory. Noone no longer challenges the principle of classical conditioning as it has been substantiated through years of experimentation that has proved it to be a principle or law. The very nature of the controversy surrounding NSD deems it to be still a theory as it is obvious in my opinion that it has not been proved to the point of being a universally accepted principle or finding.

Rene a.k.a Julie
Kodi

Julie,

I think if you had had better results on the diets you would feel differently, all I can say is that after 16 years of repeatedly learning eat that and die within 6-18 hours, it works for me and I am grateful of that, and it is worth telling folks about because a bit of self control can save a whole load of pain and trouble. Same with NSAIDs.
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There are some holes in the original work ie B27-ve will develop Chron's and +ve will develop AS......well.....but proposing Asulphazine etc great.......and why? That's impotant because many have improved on sulphazine and the diet.
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Other groups have found kleb infections and other gram neg bugs.......esp in the countries where AS research seems to be advanced....but we will leave that out as it is contentious...... I reckon half of that is typical follow the establishment the earth is flat so the earth will be flat...
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Even the GI Dr.s now say that gut inflammation and bowel flora are linked, a few years ago (2) they stated it was an unknown cause and like asthma.......and 10-20 years ago caused by anxiety etc.....even the latest GI said she was aware of starch and IBD/AS and had heard it from some patients but she could n;t understand why it helped and it could n;t be substantiated........I can talk about probiotics as well they have some help but not enough to be fantastic successful, some IBDers actually flar eon probiotics......
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Reasoning:

Only 60% of ASers and Spa have microscopic or worse bowel inflammation.......so that may be where the other Gram negatives infections come into my thinking.

Of course we have slightly different forms of the disease and likely causes, but looking around research sites where Gram-Negaitive bugs have been used for genetic therapies in bladder cancer you have previously non-arhtritic patients getting SpA, ............I ask you as a ReA'er give a group of people a shot of modified BCG vaccine into the bladder and wonder why a percentage get SpA........BCG is a TB vaccine.......TB is a gram neg......so i would not expect a starch reduction diet to help that really....I'm actually suprised a number do not get Chron's....
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I think the big problem is that researchers are trying to group everyone into the same disease bracket when in fact there are distinct sub-types.......and we know that some here have celaics and others have lactose issues esp in chron's.............others rid themselves of Kleb and then spike on some of the others........that meat muncher...etc
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I've found some good stuff on the research by some of the top guys looking at IBD esp colitis and they are getting real close to what is happening in colitis type disease. that may well help us as a group fantstically........

There was one theory on liposacharides (?) an enzyeme that the gram negatives produce, that might be causing the immune response and "David Yu" reckons that is not possible for that to be the cause, but something that affects the expression of a certain protein involved in immune regualtion....I'll see if I can find it.
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The other genes now implicated in AS include the NOD/CARD for IBD and one called ANK.......that may be why some get AS as opposed to SpA......as it controls how bone is released and retaken up in the body.
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Sorry for writing a book and being a bit tetchy, but the proof I have is so strong, over 16 years, .....it works for me and it ain't a placebo effect. I'm only sorry it has n''t helped you as much! but I beleive Erbringer says it helps some of the other SpA's pateints......

David

Hi Billy
I know from my own experience what foods to definitely avoid, because I get such a severe reaction after eating them. I am finding my way through everything else. I would just like to say though, from a personal view, that I am not dedicated enough to go all the way with the NSD diet, and I do think that you have to be strong and have the mind-set to do it. I also think that if you are going to try it, then stick at it for at least a few months and not weeks, before saying absolutely that it doesn't work. I wish you good luck with your diet and hope that it works for you. As others have already said, it depends on the individual as to whether diet or drugs work for you. Take care.
Love
Sue

Hi David
I never once said it was a placebo effect!! There is evidence for and against. It is as simple as that. Even if I had tremendous results I still believe that it will work for some, even many, but not all. Too individual.

Rene a.k.a Julie
Kodi