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John,

In reply to:

(and keep opinion and diet separate from the scientific, how ever-valid).


Now would that be the papers that are pro-Klebsiella Konspiracy (sic: valid) or the majority of the literature (sic: invalid) on Klebsiella and Ankylosing Spondylitis?

Best regards,

Validity




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Jonathan:

If you have any papers that you have prepared in html format, I will consider making them available.

My only criteria are:

1) They must present a theory that can be reduced to practice.

2) Any proposed theory does not matter at all, but the long term remission of AS must be the outcome of the practical application of this theory.

3) Some clinical trial results would be nice, however, I certainly would not hold your presentation up to Ebringer standards: 40+ peer-reviewed and published papers directly related to AS. And his London AS Clinic where the Klebsiella hypothesis was tested on over 600 patients during a 20 year history with a nearly 94% solid remission rate with 50% of these requiring no drug intervention.


For every hypothesis there is an opposite hypothesis. When we become too liberal in our thinking, we can fool ourselves into believing that all hypotheses are equal or even deserve equal air time. This is only true at time zero: Let me tell you what time it is--26 years of empirical data in support of the Klebsiella 'Konspiracy.' This is not data that excludes all other theories...only the majority of them.

Null set debate.

Best Regards,
John


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John,

Well, as you probably have surmised already; it very much would be a dissenting view. I disagree with the rationale that you and others promulgate for reducing carbohydrates in the diet.

From person experience I agree with reducing carbohydrates. I would not generalize my personal opinion or bias as accepted scientific fact.

Another reason why I resist your challenge at this time is I have had a taste of what it is like when I disagree with your followers; I would not look forward to defending some loose hypotheses (Leaky Gut Syndromes, bacterial translocation, and lipopolysacchraride burden). I have yet to figure it out. Nor, do I believe, have you.

Right now, I'll settle on posing some questions:


  1. Why do world-renoun rheumatologists (research standards, not "Ebringer" standards) like Carlin and Khan say that the Klebsiella Konspiracy is hokum? (A scientific response, please, not vague disparagings about these practitioners.)

  2. Where is the evidence that "the Klebsiella hypothesis was tested on over 600 patients during a 20 year history with a nearly 94% solid remission rate with 50% of these requiring no drug intervention?" (Chapter and verse, please, not rhetorical assertions.)

  3. How does the Klebsiella hypothesis account for the success of the biologic modifiers? (You previously have ignored this question.) (Again, a scientific reason, please, not "vested interest" humbuggery.)

  4. When IgA is elevated and immunossay of which is used to support the Klebsiella hypotheis -- why is IgM (E. Coli) and IgG (Proteus) also elevated? (Yes, I have looked at the Ebringer articles.)

  5. With Ebringer trying to prove that Klebsiella causes AS for 25 years, why hasn't an antibiotic protocol become a standard attempt at treatment like sulfasalazine, steroids and immunosuppressants? (Please avoid the quack response; you know as well as I do that there are plenty of physicians who would want to "find a bug, use a drug.")


    As I mentioned to Ike, there already are plenty of articles about Klebisella and Ankylosing Spondylitis; PubMed lists 161 at last count. Thus, it would seem that someone else, other than the folks with whom you have an allegiance, have examined this issue. Note: these are articles about Klebsiella, not about a reduced carbohydrate diet. That has been another rhetorical ploy, to imply the research on Klebsiella supports the reduced carbohydrate diet when there has been little research on this dietary therapy.

    If you want to do something useful, why not a more diligent search for a scientific correlation between NSD and wellness for people with AS? I suspect the Klebsiella Konspiracy, which does have logical consistency, is the smoke used because other data is lacking.

    I also believe recommendations offered would on a sounder ethical foundation if offered as a complementary, rather than alternative intervention.

    Lastly, while there is an absence of support for a low carbohydrate diet therapy, there is support for the use of Omega-3 fatty acids. Without a solid scientific foundation, you advocate a diet that is counter to standard dietary practice and eschew a dietary intervention that is shown to help. Since the interventions discussed and recommended represent a change in diet, the absence of convergence with nutritional practice and research concerns me! Null set debate, does that mean you have lots of ear wax?

    Best regards,

    jcwinnie

    Another evening at Hokum Hall

    "This is not data that excludes all other theories...only the majority of them."

    "What?"



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You have looked at the Ebringer papers? If so, you mislead in reporting what you have read. For instance, in Antibodies to Klebsiella, Proteus, and HLA-B27 Peptides in Japanese Patients with Ankylosing Spondylitis and Rheumatoid Arthritis, The Journal of Rheumatology 1997, it says No antibody elevation of any class was seen against P. mirabilis in active or inactive AS patients compared to controls. Similarly, no elevation in any antibody class against E. coli was seen in active AS or inactive AS compared to controls.

The secret of this forum's success is the honesty of participants. Even though opinions can vary we can learn from each other. But only trouble results from deception.

Regarding Calin and Khan, they are practising rheumies who in the main seek to interpret the basic research of others to their fellow practitioners. They themselves are not academic scientists employed doing basic scientific research as is Ebringer. The difference between Ebringer and Calin is that Ebringer could (and did) do Calin's job but Calin couldn't do Ebringer's.

Regarding the rest of your drivel, Ebringer did indeed propose in his published work that a prescribed controlled clinical trial be undertaken using antibiotics, as he did of course for the diet. But he was denied the funds on the say so of the sort of experts you espouse.

And has it not penetrated your thick skull that the reason immunosuppressants work is because AS is an autoimmune disease?

'Pain is a state of conciousness. Understanding is not'

Edited by bilko on 07/26/02 07:15 AM (server time).

Edited by bilko on 07/26/02 09:19 AM (server time).



'Then you should say what you mean,' the March Hare went on. 'I do,' Alice hastily replied; 'at least - at least I mean what I say - that's the same thing , you know.' 'Not the same thing a bit!' said the Hatter.
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Sergeant Bilko:

Poor Professor Ebringer, 25 years on this and still can't convince them to see reason. I feel sorry for the poor chap.

Sorry, too, the 1997 article says that. I was looking at the more recent article:

Tiwana H, Natt RS, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M, Ebringer A. Correlation between the immune responses to collagens type I, III, IV and V and Klebsiella pneumoniae in patients with Crohn's disease and ankylosing spondylitis. Rheumatology (Oxford) 2001 Jan;40(1):15-23

Now in 1997, there were the following articles about elevated IgM, IgG, and IgA:


Maki-Ikola O, Hallgren R, Kanerud L, Feltelius N, Knutsson L, Granfors K. Enhanced jejunal production of antibodies to Klebsiella and other Enterobacteria in patients with ankylosing spondylitis and rheumatoid arthritis. Ann Rheum Dis 1997 Jul;56(7):421-5

Maki-Ikola O, Hallgren R, Kanerud L, Feltelius N, Knutsson L, Granfors K. IgM, IgG and IgA class enterobacterial antibodies in serum and synovial fluid in patients with ankylosing spondylitis and rheumatoid arthritis. Br J Rheumatol 1997 Oct;36(10):1051-3

Tani Y, Sato H, Tanaka N, Hukuda S.. Antibodies against bacterial lipopolysaccharides in Japanese patients with ankylosing spondylitis. Br J Rheumatol 1997 Apr;36(4):491-3


But, you probably didn't mean those?

Curious that these other titers should show up in research when normally the IgA level is so much higher:

In normal subjects the majority of the B-cells are committed to IgA synthesis (90%), the residual 10% being represented (in order of decreasing frequency) by IgM, IgG, IgE and IgD producing plasma cells. These cells, which are located diffusely in the mucosa and more organized in Peyer's patches, together with an intact mucosal layer provide an effective barrier to the antigenic food load, that passes the bowel daily.

Arnold Stronkhorst, Guido N.J. Tytgat, Sander J.H. van Deventer. Immunotherapeutical approaches to Crohn's disease in view of a possible pathogenic role of Mycobacterial antigens. http://www.iol.ie/~alank/CROHNS/RESEARCH/IMMUNMOD/immuther.htm

Ah, well, must slog on further in my drivel.

Best regards,

jcwinne

Sergeant Major (Abudefduf saxatilis), in Bermuda also called 'Cow Polly'.

"But only trouble results from deception."

"Oh, how true, how true."




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The Tiwana et al paper you refer to (Correlation between the immune responses to collagens ....) in Rheumatology 2001;40:15-23 does not discuss antibody response to P. mirabilis and E. coli, as per your original assertion. Nowhere are they so much as mentioned. Your dishonesty and bullshit continues.

'Pain is a state of conciousness. Understanding is not'


'Then you should say what you mean,' the March Hare went on. 'I do,' Alice hastily replied; 'at least - at least I mean what I say - that's the same thing , you know.' 'Not the same thing a bit!' said the Hatter.
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Hey Guys,
Is it really important if it are the IgA, IgM or IgG antibodies that play a role? In my view the articles summed up by Jonathan are not against a role for Klebsiella in our disease. Read for instance the conclusion from the first article"

CONCLUSION: There is strong direct evidence for an abnormal mucosal humoral immune response particularly to K pneumoniae in patients with AS.

Furthermore I would like to stress that the not knowing about AS in science is probably a factor hundred or more greater then the knowing (this is a wild guess but derived from the little bit of science I was able to do). So before we go throwing citations (or worse) at each other: relax, there is no absolute truth to find yet.

Finally I think Jonathan's critical views are essential for this group for not becoming a bunch of diet cult followers but becoming a group of critical persons that try to enbetter there situation in a sensible way. On the other hand I see the problem that not anyone is interested in so much discussion and we need to set up some simple diet steps and further info so that as much people as possible can benefit from our experiences.

Best regards,
Gerard

" Support bacteria - they're the only culture some people have."
-Stephen Wright-


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heres my 2 cents on the good issues brought up

1. i find the statistics john noted from ebringers clinic (94% remission rate out of 600 people) as almost too good to be true. i typically define "remission" as no disease activity with no drugs and "in control" as no disease activity with drugs. even if remission were extended to cover no disease activity with or without drugs, 94% is a huge number for n=600. i truly wish this were the case, then kickas would have reached its mission goal and the site could be shut down, as stated in the main page. if all that was needed to achieve this 94% was nsd, possibly in conjunction with sulfa, then the the case would be closed. i also find it hard to believe that 600 people could do nsd or even lsd because it is a very difficult task which only the truly headstrong would undertake.

2. there have been antibiotic trials (cipro) for spa. i remember reading an abstract on it. i think the results were positive. from an empirical standpoint, i think many people who have been put on antibiotics for other reasons found their AS improved during that time. another thing is that sulfasalazine (ssz) is an antibiotic. i read some history on it. in the 1940's some guy thought rheumatoid arthritis was caused by a form a streptococcus so he mixed the antibiotic of choice then (sulfa) with aspirin to get ssz. ssz may have other weird effects on immune system and everyone says the active mechanism of ssz is unknown, but the most obvious mechanism is antibacterial and slight intestinal nsaid. what is odd is that newer and probably more effective antibiotics have been developed since the 1940's, but i dont understand why they are not used or tested more. i read there will be a double blind trial of cipro for IBD. i personaly know of people with ibd who have responded to cipro and others who have not, again pointing to the case that there are multiple causes and everyone is different.

3. regarding the biological modifiers, the question is whether rheumatic diseases are caused by too much tnf or whether too much tnf is the result of the real root cause. i tend to believe the latter.

4. regarding the whole kleb thing, i think there is evidence for and against klebsiella. my conclusion is that both are right. for some, kleb may be the cause, for others not. this disease is weird and is really just a classification of symptoms. i think there can be multiple causes and we are all biologically unique, but i really believe the source can be traced to the intestinal tract. i think all basic reasearch into AS points in this direction. so for the laymen like us, it behooves us to try to experiment with altering the gut. diet, supplements, antimicrobial drugs etcs are all tools to experiment with.

5. fish oil EPA should be part of everyones regiment. it is a "no sacrafice" thing one can do that can only help. i find it sad that many people dont know about this, but its ones own responsibility to find out. everyone on kickas should take EPA, but i bet many do not.

lastly, continue the debate, but quit the bickering. we all must find out our way thru this maze whether it is diet, drugs, supplements, exercise, meditation or a combination of all. as the budda said, "seek your own salvation with great diligence"

-ken


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to jcwinnie,

i would like to clarify one more thing. you alluded to knowing what it "tastes" like when you question a hypothesis discussed on this board. i was involved in the discussion on leaky gut and bacterial translocation. however, i dont believe you were ever attacked on this issue. if i remember correctly, i posted a discussion on leaky gut and translocation because i could not make sense of the hypothesis and wanted others input. you equated the leaky gut hypothesis as sepsis and if anything jumped on me by saying i was out of my mind to suggest this. i took no offense to your reply because i knew they were different once one understood the leaky gut hypothesis. i have since noticed you have done research on leaky gut as i have, posted about it and may have found some potential truths and possible treatments for it.

if you viewed this thread as an "attack" on you, i would suggest you try to adjust your viewpoint. we are all here with the common goal to help each other in our quest for health and well being.

-ken




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Jonathan:

At first, I was taking you seriously...now I get the picture (thanks for your photograph).

I have argued this case by casting aspersions on the motives of the researchers, exposing logical flaws in their papers, pointing out faked research, and even placed suspicions upon their clinical methods, HOWEVER, I have never attacked the suitability, talent, or credentials of any of the researchers involved. That you have just done so speaks volumes about you. I'm sorry to have indulged your ego to the extent that I have. There is just no way to gently nudge your awareness back into the real world:

....................{ Ø } = NULL SET = That group of points in common between the generally accepted universe and jcwinnie's perception of the universe. Translation: There is no established common ground for communication/debate.

I wish you all the best in your own universe.
Goodbye,
John

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