Why hasn't there been large, substantial studies . . .

The big gatherings of medics to discuss AS (and other diseases) are financed by the drug companies. Those who organise and report the proceedings receive significant sums from the companies and unsurprisingly are not helpful to non-drug therapies. Indeed, the best known of them goes out of his way to be critical of the molecular mimicry hypothesis. He is much lauded, even here.

This morning I red in spanish daily "El Pais" (not for free in Internet)one interesting interview with Barry J. Marshall, australian, one of two doctors wich found Helicobacter pylori.

Journalist asked: "What did you feel when scientists didn't support your discovery in these days?" Answer: "10 years passed before they believed us". They isolated that bacterium in 1982, but untill 1994 the health authorities of USA didn't support them. "I was asking for money to farma-industry. Laboratories answered no, and they sent us some papers with documents and ulcer drugs advertisments".

In 1984 this doctor decided to swallow 20ml of Helicobacter Pylori: infected himself for experience!

How much money earned laboratories selling "Famotidine", "Ranitidine", etc? How many earned surgeons? And psychiatrists? 20 years later, this doctor will use money of Nobel award paying mortgage, bringing up to date the computer and repairing his car.

Pello.

Hi there, I went to PubMed and searched this. I didn't have time to look at everything that came up. However, just to dispell the myth that pharma companies control the research on this, I wanted to link you to this abstract K. Pneumoniae in familial AS, done by researchers at Toronto Western Research Institute and the University Health Network. These are teaching hospitals, just so you know, not pharma funded research facilities.

One of the researchers involved in the study, Dr. Inman, has been researching AS in families for several years. You will note that this study says that the k. pneumoniae link doesn't necessarily work in familial/genetic AS. Luckily, this was the first study to come up in my search, as I've not as much time for this right now as I would normally have.

I'm generally right in there on the pharma company agenda slate. I do believe that we are not being given the whole truth on any number of health related issues because pharma companies stand to lose money if unbiased studies are published. However, as this study shows, just because the study disagrees with Dr. Enbringer, doesn't mean it's been funded by pharma companies with an agenda. To assume that is the same as assuming that the only way the k. pneumoniae connection to AS can be proven is if Dr. Enbringer does the study himself.

And just for the record, I'm not taking sides either way on this in this post. I'm simply trying to make a specific point. Just as not all doctors are jerks who don't care, not all researchers are pawns of the pharma companies. Unfortunately, it's often left up to people like us, the laity, if you will, to do our own searching and researching to find the information that we need to make informed decisions on our treatment.That being the case, we must keep our minds open to all possibilities (until they are disproven), lest we miss out on information that might be helpful to us because of prejudicial judgements based in assumptions.

Sorry to sound preachy here.

Hugs,

QUOTE:

"Sorry to sound preachy here."

END QUOTE


Are you kidding me? Preach on, sister! Testify to the congregation, although I can tell you right now we won't be getting down on our knees in this particular church--either too hard or impossible for most of our members!

To turn serious, great post Kat. Information can come from many places, which is important to remember.

Brad

Hi, Kat:

It is VERY EASY to dispute the validity of these findings, since the study had at least one basic design flaw: We are not looking for differences in IgA levels, but it is HOW WE REACT to ANY (specific) IgA level that causes AS in the first place.

Experiment after experiment is conducted using improper DOE guidelines, and cited in attempts to discredit Ebringer's results. You are very right that not just BIG PHARMA has an interest in the status quo, but funding at the university level is a very tricky thing, also. I have seen papers that appear to contradict the 'germ theory,' co-authored by people doing some of the work both with and for Ebringer. The reason? Grant money (first I suspected this, but over a year later I confirmed it by asking some of the people directly involved).

Don't believe everything you read--even the committee at the Karolinska Instituet gets it totally wrong sometimes.

Besides, Ebringer's results are nearly a moot issue when compared with myriad other sources proving dietary connections with AS and other arthritides. More than a decade before Ebringer began using his London AS Diet in his clinic, Giraud Campbell had already published his work--with X-ray evidence that diet can reverse bone damage and eliminate AS symptoms. There are many others over the past 100 years.

I appreciate your bringing this paper to our attention; I stopped looking for them quite some time ago, refusing to toss the Philosophers' Stone back into the pond once again!

Best to You,
John

Wow! What a great group this is; so much passion, compassion, wisdom and advice. And nobody commented on my typo. Thank you for kicking some major AS!!!

These are teaching hospitals, just so you know, not pharma funded research facilities.

Here in the UK university research is funded partly by grants from government bodies (and other public sources) and partly from commercial organisations, with government contribution becoming progressively smaller making the labs increasingly dependent on commercial money. And of course if a pharmacuetical company wants to do a trial with patients it will have to work with a medical school or other hospital in any case. This has been causing such concern as to the direction academic research is taking, as well as to what gets published and what doesn't, that the medical journals like the BMJ and Lancet have tightened up their rules regarding the disclosure of authors' commercial links.

I doubt if matters are different in Canada; the idea that university research institutes are independent organisations free from commercial pressures is myth.

Testify to the congregation . . .

Would this be the feast of the asse, as celebrated by the medieval church?

hey, the ADM here is pretty tolerant...
they rarely call 'Comma Faults' so you're safe...(it's only five yards and loss of down if they see it.)

be forewarned, however, abuse of adverbs is a biggie.
aB

the group has gone through a number of rounds on these questions. I will point to some of my previous posts that contain links to medline abstracts or full text articles from the medical literature which contain information bearing on the controversial nature of the klebsiella molecular mimicry theory

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:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed

recent previous post is here
https://www.kickas.org/ubbthreads/showthreaded.php?Cat=0&Number=180018&page=&vc=1
[note that the links within this post to additional previous posts under heading number three are broken, this is the result of the move of the board to the new host; the rest of the links to medline abstracts or to full text articles should work fine]

older previous post is here
https://www.kickas.org/ubbthreads/showthreaded.php?Cat=0&Number=53351&page=&vc=1

the 1999 Ringrose review article covers aspects this controversy in some depths, and the full text of this review article is now available on line
http://ard.bmjjournals.com/cgi/content/full/58/10/598
Ringrose JH.
HLA-B27 associated spondyloarthropathy, an autoimmune disease based on crossreactivity between bacteria and HLA-B27?
Ann Rheum Dis. 1999 Oct;58(10):598-610. Review.
PMID: 10491358

Specifically on the issue of IGA levels against klebsiella in AS subjects vs controls:
http://www.ncbi.nlm.nih.gov/entrez/query...st_uids=8835503
Sprenkels SH, Van Kregten E, Feltkamp TE.
IgA antibodies against Klebsiella and other Gram-negative bacteria in
ankylosing spondylitis and acute anterior uveitis.
Clin Rheumatol. 1996 Jan;15 Suppl 1:48-51.
PMID: 8835503
"...Examination for anti-Klebsiella antibodies was performed using three different strains, isolated from patients with ankylosing spondylitis. The sera were tested on antibodies against Klebsiella K43 (BTS1) as well. The number of IgA positive sera against Yersinia, Salmonella, Shigella, Campylobacter and Klebsiella K43 (BTS1) did not differ between HLA-B27 positive patients and controls, nor among the various groups. Differences were neither observed when the Klebsiella strains from AS patients had been used as antigen. These results do not confirm a relationship between HLA-B27 associated AS or AAU and infection with Klebsiella or other Gram-negative bacteria."

Here are recent articles discussing YET A DIFFERENT form of molecular mimicry: between a viral-derived peptide and a self-peptide, and its relation to the development of AS/spondyloarthropathy:

these articles discuss or present the new observation that a peptide (RRRWRRLTV) derived from the Epstein Barr virus (EBV) - the virus associated with mononucleosis - can be bound by HLA B27 subtypes in more that one conformation, and that this may allow differential immune recognition and activation of the immune response in a HLA-B27 subtype-specific manner. It is noted that this Epstein Barr-derived peptide displays substantial homology with the self peptide (RRRWRRWHL)derived from the vasoactive intestinal peptide receptor type 1-this self peptide is also observed to bind to HLAB27 subtypes in more than one conformation.

reviews/commentaries ON THE EBV peptide or its related self pVIPR peptide:

http://www.rheuma21st.com/archives/report_050225_hlab27.html

http://immuneweb.xxmc.edu.cn/wenzhai/pdf/007205.pdf

http://www.jem.org/cgi/content/full/199/2/151

original research reports on the EBV/pVIPR peptide:

http://www.jem.org/cgi/content/full/199/2/271

http://www.jbc.org/cgi/reprint/M410807200v1

http://www.jci.org/cgi/content/full/106/1/47

Evelyn, thank you for, once again, posting this info. I have a feeling that this won't be the last time.

Zdog, the issue of dietary involvement in AS tends to be rather hotly contested here. Not so much whether or not there is dietary involvement, but, rather, whether or not dietary involvement occurs with all of us. And, yes, we are very passionate when it comes to our individual beliefs on this issue.

Personally, I believe that while diet may be a factor in some (perhaps many?) of us, it is certainly not the case for all of us. AS is a highly individual disease, affecting each person in a very different way. We all respond differently to the various treatments, diet no less than any other. This is my belief, based on personal experience, talking to people here and research. You might come to a different conclusion.

I encourage you to do your own research. Talk to people. Try the NSD or the LSD for yourself. Then form a conclusion based on your own findings about which treatments will be most beneficial to you.

Hugs,

Bill, I do not know the veracity of this in Canada. It's certainly worth looking into. However, I know Dr. Inman personally. I have talked to him about these things. He is a leader in AS research, both in Canada and internationally. He has done and is doing research on the genetic/familial factors in AS. Note that in his study, he does not discount KP involvement completely. Indeed, had he done so I would be suspicious. His study was to see if it carries through in families in which AS occurs in more than one person - generally siblings if I remember correctly. His study found that KP involvement is not consistent within families.

Am I to assume that he's lying? That would put into question all of his research. Surely, the international community at large would refuse to work with him if his research was found to be filled with lies.

Yes, pharma companies have an economic reason for wanting biased research. My main issue with this comes with the use of herbals and alternative medicines. You cannot patent the Purple Coneflower - you can only patent the distillation process that results in the Echinacea that is sold as an herbal remedy, for example.

Using implied/assumed bias as a reason for disbelieving research results could very easily be turned on Dr. Enbringer's research. Does he not have a bias to prove his theories? Could he not be padding the numbers, so to speak?

I am not saying Dr. Enbringer is doing this!!

I am saying that this argument could as easily be used to try to discredit Dr. Enbringer's results (probably has been by someone, somewhere) as it could be to discredit the results of other researchers who disagree with him (as it has been here, with the claim that other researchers are biased by a tie to pharma companies).

The logic works both ways. Which is why I would encourage anyone starting on this path to do their own reading and experimentation, and then make a decision as to what they believe or don't believe.

Hugs,

It is clear that this oddly-named condition, if we can agree to call it that, is a very complicated one. Diet may not apply to all with AS. Or, diet may be just one of several factors. What seems clear, however, is that the anecdotal evidence is powerful, that many people are clearly finding relief via this approach. What is also clear, and disturbingly so, is that significant resources are not being put into an unbiased examination of the diet-autoimmune link. It is nothing less than inflammatory.

The Arthritis Society of Canada? You mean the same folks who have their seal splashed all over my aspirin bottle?

And the same folk who have their seal on my bottle of Tylenol Arthritis.

Zdog, do not mistake endorsing a product as being helpful (which is, I believe, the case here) with getting a big payoff. The Arthritis Society raises money to fund research. In fact, I just finished a stint on the Joints In Motion marathon team on which we, the 33 team members from all across Canada, not all of whom have arthritis, raised over $151,000. This money will be used for research, education, information, support groups and various therapists (physio, occupational, counsellors) - all benefits being available free to people who live with arthritis. They also distribute a pamphlet on alternative supplements and medicines (herbals) published by The Arthritis Foundation in the States.

I can attest from personal experience that while The Arthritis Society fights for our right to pharmaceutical treatments (such as Enbrel and Remicade - competing pharma companies, by the way), they are not partisan to any particular pharma company.

So, while I understand your skepticism, I cannot back you on it. I know far too well the good work that The Arthritis Society does.

Hugs,

Hey Kat,

Being fortunate enough to be under the care of such respected researchers does give us a unique insight; they are not merely unknown names and initials on top of some abstract. One is the personable, compassionate and brilliant doc I met with only last week.

I would bet my life on the integrity of my doctor and on the high quality of this research. Her integrity is unquestionable in my opinion and her motivation to help AS patients is genuine!

Today, just for fun, I tried to get in touch with the study co-ordinator (for 3 AS research studies I’ve participated in just recently) to ask this question of funding, only to find she's unavailable until Dec. Since Evelyn was able to post the acknowledgements, the great conspiracy is revealed – none!

The referenced study found no supportive evidence to implicate a causal role for Kp in familial AS. If it had, they would've reported that finding without bias, I am sure. I recognise pressures can and do exist, but wildly unfounded conspiracy theories make me chuckle and shake my head.

The study did not investigate dietary control of AS in any way, shape or form.

Hugs,
mig

Using implied/assumed bias as a reason for disbelieving research results could very easily be turned on Dr. Enbringer's research. Does he not have a bias to prove his theories? Could he not be padding the numbers, so to speak?

I am not saying Dr. Enbringer is doing this!!

C'mon Kat, I wouldn't think that of you for a nano-second. Anyway it would be very difficult for Ebringer to have done that because his results have been replicated by other workers around the world with different ethnic groups. If Inman et al are to establish their findings they will need to do the same. It wouldn't be the first time workers have obtained findings contradicting Ebringer's but then finding their work was flawed.

When I first attended Ebringer's clinic in '77 he had a research fellowship at the Middlesex Hospital Medical School funded by one of the drug companies (Beechams?). In the later years I think he was much dependent on government grants, and it was one of his constant moans that they wouldn't give him the money he needed. And neither would the Arthritis Research Council (our arthritis charity) give him the money for a controlled dietary trial. Well Beechams or whoever never will!

And while we are on the subject - I've always wondered who Evelyn works for!

Aaaw Jeanna - what if Evelyn was to work for a drug company? Nothing to be accused of, nor is working for an academic institute come to that. But all researchers are subject to peer pressure and this must sometimes influence their stance on some things. If Evelyn is totally objective in her selection of references (irrespective of any possible involvements) then she is a saint; she is good, but not necessarily a saint. I'm not asking for the information, but it is true I do wonder!

To be completely clear I do work in an academic institution - I am on the research faculty in a basic science laboratory in a basic science departmant in a large university medical school in the US. We are strictly basic science laboratory examining cell mechanisms that are involved in one aspect of normal mammalial development. THat particular aspect of normal development comprises a field quite distinct from either immunology or rheumatology. Our laboratory is supported by two NIH (National Institute of Health) grants, one looking at the role of a specific protein phosphorylation cascade in the control of differentiation from an immature cell type to a mature cell type, and the other looking at the role of a specific docking protein in the control of the mature cell's responses to external stimuli.

What I have learned in my approximately thirty years in this research field is to be a critical reader of the medical literature. I have no problem with people seeking out different approaches for their care, the question of the diet can be separated from the question of pathogenesis.
I do have a problem with people implying that a particular hypothesis of pathogenesis has been "proven" when there is so much experimental data contradicting that hypothesis from a variety of laboratories published in well-respected peer reviewed journals.

It's funny, bilko: I didn't think it was appropriate to ask Evelyn that question, or to even express my wonder; however, I did find myself wondering the same exact thing. Maybe I should be scolding you for your bluntness, but I'll thank you for asking instead. And, I'll thank Evelyn for responding. Although I still do wonder about some things...

In all my years here at Kickas I have found the support and learning here at this site very helpful. I think the openness and friendship separates this site from other sites on the web.

The openness allows for alternatives to be discussed and a forum devoted to anyone interested in diet or alternative methods. This openness probably saved me from a life of considerable pain since the diet has been my answer after coming off meds due to liver.... no where else at the time did I find information on this diet when I was looking. That being said, since others are respectful to my views on diet and alternatives, I feel it is my responsibility to be respectful of other views as well even if I do not agree. I believe the best way for me to influence others to look into dietery measures is providing an example to follow and share my story at times.

And in all my years of posting and developing friendships, I honestly believe I have not come across anyone with what I consider a hidden agenda, only different opinions.

Tim

personally,
i've always been amazed by evelyn's posts...she's so computer literate and so well read and has marvelous
access to stuff...i've learned so much form her contributions...i've often wondered what she 'did'...
and i don't recollect a single post in which she's editorialized about any informative post she's given to us.

thank you, E.

i do love the openness here...within the surly constraints of my not normally G rated prose.
i don't subscribe to the nsd/lsd religion...not for me, but i enjoy the debate and the information
( i have insisted that h.pylori and a lyme test (all the igg/igm bands) is now a part of my regular blood work)
and i have great respect for the folks who do find relief thru the discipline of nsd.lsd...i do try
to add to the lsd/recipe forums the stuff the things i do know about food products...and i read every food label.

all the best...good kickas
aB

Thanks to Ben and Pello for your kind words, to Jeanna for your support, to Kat and Mig also, to Tim for your always kind and fair approach, and finally to Bilko- I'll take the "she is good" part from your post nicely. I am not a saint, nor do I aspire aspire to be a saint.

In regards to the information that Pello mentioned on my son: his remission was induced by a short course of metronidazole (Flagyl) for probable giardia-induced reactive arthritis. His remission is now seven years in duration.

Reactive arthritis is a member of the spondyloarthropathy family, the family of conditions which includes AS. Giardia is an intestinal parasite which is common in certain areas of the world. It is usually spread through contact with contaminated water. Giardia-induced reactive arthritis is a treatable form of spondyloarthropathy- eradication of the parasite results in remission of the associated arthritis. Giardia-induced reactive arthritis is probably underdiagnosed, since it is not often considered. Metronidazole (Flagyl ) is often used as the treatment for giardia, and in many cases only a short course is needed .

Here are links to previous posts that describe our experience in more detail and provide links re:giardia and giardia induced reactive arthritis

https://www.kickas.org/ubbthreads/showthreaded.php?Cat=0&Number=152548&page=&vc=1

https://www.kickas.org/ubbthreads/showthreaded.php?Cat=0&Number=16396&page=&vc=1

https://www.kickas.org/ubbthreads/showthreaded.php?Cat=0&Number=185050&page=&vc=1

Hi John:

I'm not even going to comment on the Erbinger/NSD/LSD/Kleb-IgA thing, bc frankly I'm just tired of it all. What I do want to comment on however is your blatant misrepresentation of the ulcer story. The story is not quite as black and white as you tell it. Personally, I believe very few things exist in our world with that sort of certainty, but again, perhaps we differ there.

I completely admit that I agree with you about how pompous beliefs in Western medicine can be, and it is something that bothers me routinely. I often cite the H. pylori story, along side the "sunlight can't cure children with Rickett's - for goodness sake they don't undergo photosynthesis" one. Yes, sometimes medicine as an institution doesn't accept things easily, or readily, but as in both incidences that are stated here, eventually gets accepted into current dogma.

So, while we're on the topic of ulcers, I just want to make a few points clear. H. pylori and ulcers are NOT synonymous. Not all ulcers are due to H. pylori. "H pylori infection occurs in 75% of gastric ulcers and 90% of duodenal ulcers.", from: emedicine - Gastic Ulcer

Futheremore, not all people with H. pylori have ulcers. In fact:

The human gastric pathogen Helicobacter pylori causes chronic gastritis, peptic ulcer disease, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma. It infects over 50% of the worlds' population, however, only a small subset of infected people experience H. pylori-associated illnesses.

(From Helicobacter pylori and gastroduodenal pathology: New threats of the old friend, Niyaz Ahmed and Leonardo A Sechi, Annals of Clinical Microbiology and Antimicrobials 2005, 4:1)

So what is it that makes only a small percentage of half of those people colonised with H. pylori succumb to gastric pathology. No one knows for certain, but there are many suggestions: NSAID or steroid use, smoking, alcohol or coffee consumption, stress, delayed gastric emptying, and duodenogastric bile reflux.

I'm just tired. Absolutely freakin' exhausted with the oversimplification of the facts. You know what's really sad about all of this, is that many of us probably share quite a few ideas, for example, that diet plays a larger role in many diseases than we can prove at this point in time, yet we'll never be able to meet in the middle because of the compulsion for fanatacism.

It never fails to amaze me that the same people who maintain the drug company/physician conspiracy to forgo the cure of AS patients with diet in lieu of lining their pockets with money are the same people who are UNABLE to explain to me how the same medical institution readily admits that the only treatment for Celiac disease is a gluten ELIMINATION diet.

Regards,
Jeanna

Fluoride, definitely too much fluoride.

i think the flouride ruminations were zapped into the ether

K-Mart, definitely NOT K-mart!!

Wapner...time for Wapner...

LMAO!! Good one JC!
Holly

Thanks for sharing and bringing up this. Great post.

I read your other threads on this parasite-induced arthritis as well.
I seiously suspect that I might also be a victim of Giardia-induced Reactive Arthritis and hopefully can be cured by Metronidazole. Water in my country(Taiwan) is generally ok although some areas are contaminated by the heavy-metal factories. Others risk factors I have is that I like swimming and went camping before my syptoms of Arthritis gradually was coming out.

My systoms are quite similar to your son.
Groin(near the sexual organ)was my first symptom and it's tender .Sometimes left groin is hurt but right side is normal.Sometimes it's the opposite. Sometimse it's both. In the following months,my knee tendon,lower back,hip,Achilles heels and cervical spine and neck were all painful to touch and move.
I also have a high incidence of Diahhera.
I was finally been referred to a Rheumy and was given
a diagnosis of AS about 4 months ago(HLAB27-positive).

I am still not sure how a diagnosis of Giardia-induced Reactive Arthritis can be given. I don't even know I am AS or Reactive Arthritis. Any difference. One of the article mentioned that Giardia-induced Reactive Arthritis is diagnosied by the fact that you don't response well to NSAIDs.In contrast, from the information I read about Reactive Arthritis, NSAIDs is the drugs to treat Reactive Arthritis.(http://www.medicinenet.com/reactive_arthritis/page3.htm) For me, I got a good response by taking Mobic and Diclofenac. Does that exclude me from infection of Giardia? From my desciptions, do you think I should be put on Metronidazole to see if I was infected with Giardia?

All the best,Charlie

Generally the diagnosis of giardiasis is made by examination of the stools. I would encourage you to seek out a doctor to do the stool examinations for giardiasis. In our case our rheumatologist chose to just go ahead and try the Flagyl as a therapeutic trial even without proof by stool exams, but not all doctors would do so.

In my son's early years of involvemnt (age eight to twelve) - his flares were moderate - he responded well to NSAIDs. When his flares became more severe (age twelve to fourteen), his severe flares did not respond AT ALL to NSAIDS.

I hope this all helps. THanks, Evelyn


Now here is more on the diagnostic tests for giardiasis:

http://www.emedicine.com/med/topic868.htm

Giardiasis:
Brooks D Cash, MD, FACP, Director of Clinical Research, Assistant Professor of Medicine, Gastroenterology, National Naval Medical Center
Coauthor(s): Mark Johnston, MD


"Lab Studies:


The traditional basis of diagnosis is identification of G lamblia trophozoites or cysts in the stool of infected patients via a stool ova and parasite (O&P) examination.
Stool examination may be performed on fresh specimens or after preservation with polyvinyl alcohol or 10% formalin (with appropriate staining).

Ideally, 3 specimens from different days should be examined because of potential variations in fecal excretion of cysts.

Stool O&P testing remains the diagnostic method with which other tests are compared.

Aspiration of duodenal contents and demonstration of trophozoites also have been used for diagnosis but this is more invasive than stool examination and, in direct comparison studies to stool microscopy, may have a lower diagnostic yield.

Stool antigen enzyme-linked immunosorbent assays also are available.

These tests are similar to the stool O&P test in terms of cost and have a sensitivity of 88-98% and a specificity of 87-100%.

These tests are best used as a screening test for high-incidence settings such as day-care centers or for identification of subjects during an epidemic, but they should not take the place of stool microscopy or other possible diagnoses may be overlooked.

Routine laboratory tests (CBC count, electrolyte levels) usually are normal; eosinophilia is an uncommon feature of infection.

In summary, stool O&P tests aid in the diagnosis of giardiasis in 80-85% of patients. If the results from the 3 O&P tests are negative and the disease is still suspected, stool antigen enzyme-linked immunosorbent assay (ELISA) may be helpful. If both of these methods result in negative findings but the patient has symptoms consistent with small bowel diarrhea/malabsorption, upper endoscopy with biopsies and duodenal aspirate is a reasonable alternative."


See also:

http://www.emedicinehealth.com/articles/17334-5.asp


Additional information on giardiasis:

http://www.emedicine.com/emerg/topic215.htm


http://www.aafp.org/afp/20040301/1161.html

I just asked the doctor about the possibility of Reactive Arthritis caused by Giardiasis. But he didn't know this. And I explained that Giardiasis is a parasite that might be why I am hurting. He answered,"You think too much. It's impossible that nowadays people still be infected by this parasite".
Apparently, he didn't bother to examine my stool ,or perhaps he didn't know how to do it.
What kind of doctors should I seek help for Giardiasis?
A Rheumy or...?

Dear Charlie, you might try consulting a rheumatologist or a gastroenterologist or infectious disease specialist. The gastroenterologists and the infectious diseases specialists will be more familiar with the diagnostic tests for giardia or other bowel parasites.

It might be helpful to print out the information from the medline abstract list or full text article describing giardia-induced reactive arthritis and bring it along with you to the doctor. The doctor that treated our son was a rheumatologist, and we brought the full text article to him, the article was this one as I indicated in other posts:
http://www.ncbi.nlm.nih.gov:80/entrez/qu...p;dopt=Abstract
Layton MA, Dziedzic K, Dawes PT.
Sacroiliitis in an HLA B27-negative patient following giardiasis.
Br J Rheumatol. 1998 May;37(5):581-3.
Full text can be downloaded-click on link at the top of the abstract-the letter starts on page 3 of the PDF file)
link to full text:
http://rheumatology.oupjournals.org/cgi/reprint/37/5/581


I cannot comment on how common parasites are in your country, the first article below suggests that giardia is at low levels in Taiwan but it has been documented to exist, according to the sources I found from medline.

Here are some references from medline on Taiwan re: giardia as well as different parasite called cryptosporidium, which has also been reported to cause a form of reactive arthritis:

http://www.ncbi.nlm.nih.gov/entrez/query...t_uids=11605804
Yeh TC, Lin PR, Chen ER, Shaio MF.
Current status of human parasitic infections in Taiwan.
J Microbiol Immunol Infect. 2001 Sep;34(3):155-60. Review.
PMID: 11605804
"...Intestinal protozoal infections with Giardia lamblia and Cryptosporidium parvum are at low levels but may be widely distributed..."

http://www.ncbi.nlm.nih.gov/entrez/query...t_uids=10376882
Hsu BM, Huang C, Jiang GY, Hsu CL.
The prevalence of Giardia and Cryptosporidium in Taiwan water supplies.
J Toxicol Environ Health A. 1999 Jun 11;57(3):149-60.
PMID: 10376882
"...The frequency of occurrence of cysts was 77.8% for Giardia and 72.2% for Cryptosporidium in 18 raw water samples. Ten out of 13 samples collected from treated water samples showed the presence of cysts..."

See also:

http://www.ncbi.nlm.nih.gov/entrez/query...t_uids=11950125

http://www.ncbi.nlm.nih.gov/entrez/query...t_uids=11206115

Evelyn, I think I owe you an apology for uttering my thoughts; saying what I think in haste then regretting it at my leisure! I'm incurable. I didn't mean to prise personal information out of you, my question was a bit deeper than that, it's because I have found your approach uncritical of the literature, but you are right to make your point and debating with you has helped teach me to say that the klebs stuff is the working hypothesis of the diet forum - even if like John you'll be able to knock me over with a feather if Ebringer is shown to have missed by a mile.

Dear Bilko, thank you for your thoughtful apology - I thought carefully about how to answer clearly and I am comfortable with the level of personal information that I provided in my answer- and I feel it is just as well to have put the information out there. I am proud of what I do, and I am proud of our laboratory.

As for the question of just which individuals are reading critically and just which individuals are reading uncritically, my conclusion to that question differs from yours. You can call the kp molecular mimicry theory a working hypothesis, and I will continue to call the kp molecular mimicry hypothesis a controversial hypothesis, and continue to note that is is only one of many hypotheses that have been put forth by researchers over the years to explain the connection of HLA B27 to AS/spondyloarthropathy.

That's exactly what I was about to ask. Having recently been diagnosed with AS, one would think the docs would give me any and all information available on how to help myself deal with this potentially debilitating disease.

Luckily, I research every bit of new information to exhaustion, and again LUCKILY I found this great site, or I wouldn't have a clue about NSD or leaky gut syndrome, or a whole host of other things that I can be wprking on myself.

I pity people who have no computer, or lack interest and/or capability to research for themselves. Doctors are good, but often we're treated like cookie-cutter patients and given only the bare minimum of information, rehearsed speeches if you will, as if we're not intelligent enough to or capable of handling more information. This needs to stop, and I intend to tell my Rheumy so at my next appointment!

Looking back, I KNOW my docs are aware of the gastro intenstinal connections to AS, because in the past few months I have endured upper and lower G.I.'s, a full colonoscopy, pelvic x-rays and MRI's - all BEFORE being diagnosed with AS. It took many complaints from me about contuinued digestive problems before these tests took place.

At least for myself, I WANT TO KNOW EVERYTHING! And if it takes more than the typical 15 minute alotted consultation time, so be it. I refuse to be treated like a mushroom (kept in the dark and fed bullsh--).

Candi

Thanks a lot for your information.
I would print out that and give it to my doc on my next appointment with my doc.
All the best,Charlie

I just returned to this, I think my first kickas post ever, and I think you will agree that it is an outstanding thread in terms of passionate presentation of information, civil debate--and most importantly--SUPPORT.

Today, after months of learning more about the A word, and also the S word, and of having gotten to better know many of the great personalities who frequent this site, I am able to doubly appreciate the wealth of information, support--and superb comic delight--which greeted my first ever foray into kickas, and which has continued to sustain me to this day.

--zdog

Zdog. I missed this thread last year which was not so bad, but now it is bumped and I feel compelled to write a reaction. I’m not as glad with it as you as I reckon it’s gonna be an extensive one and I’m about as tired from it as Jeanna. But well it’s a bit my territory so in that sense I must thank you for bumping.

Jeanna,
Nice post, as always, and yes it did give me some new information from your textbooks. I think we can learn, at least, three things from the Pylori story:

1) Narrow mindedness blocks scientific/medical/all progress
2) Objective observation can also lead to the wrong conclusion/treatment
3) There is more we don’t know then do know

The first point is already extensively discussed by others in this thread. How long it took for the medical world to accept the antibiotic cure for gastric ulcers etc. etc.

The second point can be derived from your post. When 50% of people has the Pylori bacterium and say only 2% develop a gastric ulcer somewhere in their lifetime it is not logical to blame Pylori for gastric ulcers. Yet the gastric department of my hospital had to undergo a reorganisation after the new antibiotic treatment was introduced and appeared to be so effective. When I look at myself I was absolutely convinced that it was my NSAID usage but even more the stress and inward bound emotions when loosing the love of my life to someone else (in my perspective, at that time) that caused my gastric ulcer within weeks after that happened. However I was cured with the antibiotics against Helicobacter pylori also within weeks. Just goes to show that there is no such thing as simple cause and effect.

The third point seems a platitude (is that English?). For instance Newton discovered gravity and mankind do makes good use of this but boy do we know little about what gravity really is. Surprisingly enough the Pylori story contains an intriguing twist. When 50% of mankind is infected with Pylori and only a small percentage of these people get ill at some point in their life what is then the chance of a doctor becoming ill within weeks from infecting himself. I should say pretty near zero unless there are other factors around that up till know are unknown. One obvious factor could be that he isolated the bacterium from people who developed an ulcer already. That could lead to for instance differences in the Helicobacter pylori strains that have not yet been detected but also environmental factors/adaptations or little earthgnomes having a bad temper could play a role.

Don’t think we disagree much, except for the gnomes.
Gerard

Evelyn,
In earlier posts you always cited articles contra the Klebsiella theory in accordance with pro Klebsiella theory articles. In this thread you chose to skip the pro articles probably in an attempt to get this thread somewhat more in balance. There are however some obvious flaws to the two cited articles mentioned here and in one case the article is not a contra finding but it is in fact the article that is most supportive for a role of Klebsiella.
The first article from Ringrose has the problem that Ringrose did not do any research himself accept researching the literature. Should he have done a research on the role of Helicobacter on stomach ulcers he would have found the same negative outcome depending on the year that he did the research .
The second article from the Dutch research group is such a strong pro Klebsiella article because this group made a complete turnaround two years later when they worked together with Ebringer. Now probably using a better method they were able to show a connection between anti Klebsiella antibodies and AS:

Antibodies to Klebsiella pneumoniae in Dutch patients with ankylosing spondylitis and acute anterior uveitis and to Proteus mirabilis in rheumatoid arthritis

J Rheumatol. 1998 Apr;25(4):743-7. Related Articles, Links
Blankenberg-Sprenkels SH, Fielder M, Feltkamp TE, Tiwana H, Wilson C, Ebringer A.
Netherlands Ophthalmic Research Institute, Amsterdam.

CONCLUSION: Our data support the hypothesis that Klebsiella are involved in the pathogenesis of AS and AAU and that the same might be true for Proteus in RA..

An amazing turnaround that shows that when someone can’t find an antibody reaction he probably used the wrong method. In fact as a research from Finnish researchers in cooperation with Ebringer from three weeks ago shows: the antibody reaction could well result in an early diagnostic tool for AS and arthritis. Overall I do agree by the way with your last post. It is just that the examples of the contra articles are unhappy chosen.

Gerard

Kat,
I have discussed the article you discovered from pubmed in the no starch section about as soon as it was published under the title “Not supportive Klebsiella findings”. Which at least shows that I discuss every article pro or con where Klebsiella is involved. Happily for me there are not too much of them. The reactions to that article where focused around the article that was discussed in the last part of my reaction to Evelyn: apparently negative associations can become positive if another method is used.

Apart from that I doubt the objectiveness of the researchers in line with point 1 of my reaction to Jeanna:
1) Narrow mindedness blocks scientific/medical/all progress
As one of the researchers from this Canadium consortium, not Inman himself, called any research done on dietary measures against AS “Junk science” on another ankylosing spondylitis site. When this sort of statements are made before doing the research itself I would call that, in your words “prejudicial judgements based in assumptions” and I can't help to take the research less seriously.
Pff I knew this would take some time, now off to make my weekend run.
Gerard

Dear Gerard:

I have great respect for the time, energy, and subsequent content of your posts. Thank you for replying to my post. I similarly spent a lot of time writing it, only to have it remain unanswered until now. It's particularly nice to get a straight-forward reply without riddles to interpret.

I don't have much to add, except that I agree with all the points you've listed, particularly "there is more we don't know than we do". There have been numerous times when I've brought this up with former preceptors (on un-AS related issues), much to their shock, dismay and occasionally anger. That being said, there are rare occasions when even this attitude is encouraged in medicine, which is how I found my 'mentor', a oncologist and palliative care doc, who doesn't mind to wax philosophically, and doesn't purport to have all the answers.

I'd say (if you don't mind the switch to positive phrasing) that we often agree, and I'm more than willing to hold opinion on the earthgnomes, until I've researched them more fully.

In friendship,
Jeanna

P.S. Interestingly, H. pylori and HLA-B27 have a lot in common. They're both present in a greater population of people than those they're able to affect, but in affected-individuals they're nearly (but not) always present.

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.


Dear Gerard, a careful review article is a well-established and well-accepted format to discuss a controversial set of observations. I do not concur that the Ringrose review is any less relavent to the current discussion based on being a review article rather than being a primary report. Dr. Ringrose is clearly an established investigator with immunological research expertise. A review format can serve to broach a number of differing observations and compare, contrast and analyze these observations in a much fuller way than would be available in a primary report format.

As for your second point, indeed you correctly point out that two of three authors of the original 1996 report were included in the author list of subsequent 1998 report that you cited. These two authors are:
Dr. SHD Sprenkels = Dr. SHD Blankenberg-Sprenkels, who is first author on both publications and Dr. TEW Feltkamp, who is senior author on the first publication and a middle author on the 1998 report. However I’m not sure that the story ends with the publication of the Blankenberg-Sprenkels et al. report in April 1998.

It is interesting to note that of these two authors, the first author, who is the primary author on both studies (Dr. SHD Sprenkels = Dr. SHD Blankenberg-Sprenkels) appears to have left science altogether, as there are no further Medline entries for this author for any work subsequent to that April 1998 Journal of Rheumatology citation.

Medline is here:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi

As for the other author, Dr. TEW Feltkamp, I could not find evidence that he has come to view the klebsiella molecular mimicry hypothesis as an established explanation for the pathogenesis of AS/spondyloarthropathy based on publications subsequent to April 1998. Even in 1998, several months following the publication of the cited Journal of Rheumalogy paper, Dr. Feltkamp is using rather noncomittal language to describe a “possible” role for klebsiella in the pathogenesis of spondyloarthropathy:

http://www.ncbi.nlm.nih.gov/entrez/query...st_uids=9725092
Feltkamp TE, Ringrose JH.
Acute anterior uveitis and spondyloarthropathies.
Curr Opin Rheumatol. 1998 Jul;10(4):314-8. Review.
PMID: 9725092
“…The cause of AAU and spondyloarthropathy is unknown...It is possible that Gram-negative bacteria such as Klebsiella or Yersinia are involved in the pathogenesis in a yet unknown way...”


Dr. Feltkamp has clearly remained active in research, as evidenced by his continued publications cited in Medline, however none of Dr. Feltkamp’s work subsequent to 1998 lists klebsiella as an etiological agent for spondyloarthropathy or molecular mimicry as an established etiology, as far as I can tell by searching either Medline or the ISI Web of Science citation index. According to this index, it appears that Dr. Feltkamp has not included any references to the 1998 Blankenberg-Sprenkels paper in any of his subsequent publications: The ISI Web of Science lists eleven articles that cite the 1998 Blankenberg-Sprenkels paper and none of these eleven articles include Dr. Feltkamp as an author.

ISI Web of Science citation index can be accessed through the ISI Web of Knowledge portal:
http://portal.isiknowledge.com/portal.cgi

Instead, Dr. Feltkamp served as a consultant for Dr. Ringrose on his 1999 review as indicated by the “Acknowledgements” at the end of the Ringrose review.
http://ard.bmjjournals.com/cgi/content/full/58/10/598
Ringrose JH.
HLA-B27 associated spondyloarthropathy, an autoimmune disease based on
crossreactivity between bacteria and HLA-B27?
Ann Rheum Dis. 1999 Oct;58(10):598-610. Review.
PMID: 10491358
“Acknowledgements:
Funding: this study is published with support of the Edmond and Marianne Blauw Fund for Ophthalmology.
I would like to thank (in alphabetical order) the following persons for their contributions and for critically reading the manuscript: Dr L van Alphen, Laboratory of Vaccine Development and Immune Mechanisms, National Institute of Public Health and the Environment, Bilthoven, the Netherlands; Prof dr J Dankert, Department of Medical Microbiology, Academic Medical Center, University of Amsterdam,the Netherlands; Prof dr T E W Feltkamp, Arthron, Amsterdam, the Netherlands. “

Notably Dr. Feltkamp continues to publish regularly with Dr. Ringrose, exploring other explanations for the pathogenesis of ankylosing spondylitis/spondyloarthropathy, focusing specifically on what peptides HLA B27 can bind to using its peptide binding pocket: See for example

http://iai.asm.org/cgi/content/full/72/9/5097

Dear Jeanna,
Thanks for all those kind words. I'm glad we don't have to agree to disagree but just AGREE. Personally I like point two the most but is should be better phrased as there is nothing wrong with objective observations except that we can never be sure that we do one, in line with point three. Good to hear you've found a good mentor. During my study I was at one point at a loss, being surrounded by research people I could in no way relate to. So after I finished the subject I chose to go working with a man from whom I knew he was creative, full of humour and brilliant no matter what the subject of research precisely should become. It was the best decision I made during my study.
Got the feeling you are aware of the fact that earthgnomes are best researched in the presence of some open bottles of glutenfree beer .
Gerard
P.S. I noticed the resemblance too, in fact there are numerous research areas in life sciences with similar correllations. Just goes to show that some but not all the factors that are involved are known.

Evelyn,
Thank you for the extensive answer and links. As you can guess I'm not per se interested in what is well-established and well-accepted. Einstein did not come to his ideas by making a review of the existing material, nor did Newton, Darwin or Watson and Crick. Not that I would like to compare Einstein to Ebringer of course.

Ringrose in his article first defines what he sees as an auto-immune disease and then tries to make objective standards for the researches he is studying, in particular matching age/sex controls. After applying a score list he concludes "In conclusion, there is no evident proof that SpA is an autoimmune disease attributable to crossreactivity between bacteria and HLA-B27."
But as I already stated in my reaction to Jeanna you can choose an objective standard but you never know if it is really objective. In this case it is clear that it is more difficult to find crossreactivity then not to find crossreactivity. For instance it could be that you need people in an active phase of the disease. It is obvious that it is far more difficult in this case to find a proper number of matching sex/age controls and patients.

Another example: Ringrose didn't use either of the two Feltkamp/Sprenkels researches. These two researches have a complete opposite outcome. Yet none of the standards Ringrose uses is able to select the good from the bad one as there was a flaw in the method used that can't be seen by from the outside reviewing an article.

Another example: Picture the "to be" Noble prize winner who is infecting himself with the Helicobacter bacterium, develops a stomach ulcer and cures himself with antibiotics. He states: Helicobacter is the cause of stomach ulcers. His hypothetical opponent does a research on 100 people matching sex and age from which 50% have Helicobacter in their intestines and none have an stomach ulcer. Ringrose's verdict in that case would be: "In conclusion, there is no evident proof that stomach ulcers are attributable to the existence of the Helicobacter pylori bacterium in the stomach." And yes that would be a well-accepted conclusion but if all researchers would work in such a way I would probably by now be walking around with a scar in my tummy and part of my intestines gone just like my father.

About the later publications and direction of publications of Theo Feltkamp and Mme Sprenkels: We can only guess about the reasons why one stopped and the other chose not to go that path again. Feltkamp had became a prof by the the time and will have multiple research threads and students and researchers under him. Maybe he was not too glad with the whole episode and chose to let other research groups work in that area where he didn't have his finest hour especially in comparison with the research areas he do is good at. I have by the way no problems with the conclusion of the later article:

“…The cause of AAU and spondyloarthropathy is unknown...It is possible that Gram-negative bacteria such as Klebsiella or Yersinia are involved in the pathogenesis in a yet unknown way...”

Describes in my view pretty accurately where we are by now in the Klebsiella/AS research.
Gerard

Dear Gerard, I think also you and I can come to find common ground. The point where I believe that I find common ground with you is in the realization that there are not yet "known" answers to the question of the mechanism of pathogenesis of spondyloarthropathy, and to the question of how HLAB27 contributes to the spondyloarthropathy process. Many different theories have been proposed to answer the question of HLAB27 contribution to the pathogenesis of spondyloarthopathy. Clearly the pathogenesis of spondyloarthropathy remains an open question and an area of active research.

Re: Dr. Feltkamp's followup- on your comment "Maybe he was not too glad with the whole episode.." - we can only speculate as to what Dr. Feltkamp feels about this episode. I believe it would be fair to infer based on your own words here that the possibiltiy stands that he has undergone less of a complete "reversal" of belief than what you had indicated in your previous post. He is still clearly actively involved in research on the pathogenesis of spondyloarthopathy and continues to explore a DIFFERENT proposed mechanism by which HLAB27 contributes to the pathogenesis of spondyloarthropathy.

Evelyn,
Of course there is common ground in the sense that we both don't like AS to be pictured as a solved puzzle. And though we are often opposing you do are needed on this site to keep things in line and balanced.

We differ in the appreciation of Ebringer's theory, like Bill I see it as a good working hypothesis, controversial or not. There are indeed other theories that try to explain the contribution of HLAB27 to the pathogenesis of spondyloarthopathy but they go against my gut feeling, no pun intended. That gut feeling is strenghtened strongly however by the recent progress that is made with TNF alpha inhibition and the important role that follows from that for the T cell lymphocytes. These T cells play a dominant role in the intestinal immune system and to make this circle round Klebsiella is a strong activator of these T cells. Due to the success of TNF alpha inhibition, research will be and is now concentrating in the direction of intestinal inflammation and impairment of the gut:blood barrier as the driving force for AS, while the other theories like the misfolding of HLA-B27 are getting more out of the picture.
See for instance the article below:


Dichotomy between Lactobacillus rhamnosus and Klebsiella pneumoniae on dendritic cell phenotype and function.

Braat H, de Jong EC, van den Brande JM, Kapsenberg ML, Peppelenbosch MP, van Tol EA, van Deventer SJ.

Academic Medical Center, Department of Experimental Internal Medicine, PO Box 22700, 1100 DE Amsterdam, The Netherlands. h.braat@amc.uva.nl

The reaction of the intestinal immune system to intestinal bacteria shows striking differences between various bacterial strains. Whereas Klebsiella pneumoniae induces a fierce proinflammatory reaction, the probiotic strain Lactobacillus rhamnosus has clear anti-inflammatory effect in gastrointestinal disease and allergy. The molecular basis for this dichotomy is poorly understood but is likely to involve different modulation of antigen-presenting dendritic cells (DC) by L. rhamnosus and K. pneumoniae. Hence we evaluated phenotypic and functional characteristics of DC matured in the presence of L. rhamnosus and K. pneumoniae. Monocyte-derived immature DC were cultured in the presence of live bacteria to obtain mature DC. Both micro-organisms induced maturation of immature DC as shown by CD83 and CD86 expression, but receptors involved in activation of Th1 cells were expressed predominantly on DC exposed to K. pneumoniae. In contrast to K. pneumoniae, maturation with L. rhamnosus resulted in lower TNF-alpha, IL-6, and IL-8 production by immature DC and lower IL-12 and IL-18 production by mature DC. Moreover, L. rhamnosus led to the development of T cells without a typical Th phenotype whereas K. pneumoniae induced a Th1 immune response, dependent mainly on IL-12 production. Thus our results strongly support the concept that differential modulation of DC explains the differences in the immune response to various bacterial strains and indicates that K. pneumoniae induces Th1 immune responses via DC.

Dear Gerard, it would not at all be surprising that a pathogenic bacterium such as klebsiella would induce the production of an inflammatory cytokine like TNF alpha, but of course a variety of other pathogenic organisms could also induce the production of proinflammatory cytokines.

The study you cited does not really replicate the complexity of the host-gut microorganism interaction in vivo, because as far as I could tell by looking at the abstract you cited, that study is introducing a microorganism species singly to an in vitro culture of immune cells. As you well know, the intestine has a very complex microbiological makeup - there are myriads of different types of microorganisms in the gut, and a subset of these microorganisms are pathogens or potential pathogens. Other individual bacterial species would be expected to also be capable of eliciting production of proinflammatory cytokines if they were studied in the same way - if they were introduced singly to in vitro cultures of immune cells within a similar experimental paradigm to that used by the authors in the study you cited. The focus of the study on klebsiella is because this is the particular pathogenic organism the authors used, not because it would be the only organism that would be capable of eliciting production of proinflammatory cytokines by immune cells.

More on the complexity of the microbial world present in the gut:
http://www.cell.com/content/article/fulltext?uid=PIIS0092867406001929

Evelyn,
My point was that due to success of TNF alpha inhibition the focus in AS research is getting more and more to the gut and not to the abnormal intrinsic capabilities of HLA-B27 for misfolding or similar explanations. To be honest I did a google yesterday with a few components like T-cell TNF etc and NOT with Klebsiella and was very surprised to see Klebsiella pop up as the first one in the list. That I choose to show it is because it shows that bacteria are able to trigger the same immune cells that are responsible for fuelling our inflammatory processses being the same immune cells that are inhibited by TNF alpha blocking. Another reason is that it makes a nice bridge between the sometimes opposing views and discussions here on these forums. In my view it could very well be that the success of TNF alpha inhibition and the success at least some of us have with diet have the same ground. If another pathogenic organism has the same effect on TNF alpha production that is no problem for me as this other bacterium will also respond to changes in his environment due to diet, antibiotics or probiotics.
I do by the way realise that the above could only explain part of the pathogenesis of AS, though it also could explain the positive effects and the problems having results when trying to change the indeed complex intestinal flora.
Best regards,
Gerard

Gerard, I've only just seen this now. I find myself particularly unwilling to get into a second debate this week. However, just because one author on a study has made shown a bias does not mean that all of them do. You cannot make that assumption. How many production teams have I worked on on which one of my team members has been an as$. Doesn't mean everyone on the team is an as$ and it certainly does not mean the the show being produced is going to be any less artistically valid. It just means that one teammate is an as$. Same with any research study. I rather doubt that everyone involved in a study believes exactly the same things in the same way. That would be counter to any good scientific research. It is the differences that create a more rich and thorough piece of research.

Again, you can no more colour the other authors of the study with the same paint because of the comments of one of them than you can make the statement that all of Dr. Enbringer's research is slanted because he believes the kleb p. related pathology in AS. And that is an easy assumption to make, but to do so is to invalidate every piece of his research. I certainly do not have the hubris to do that, being a lowly pleb in the grand AS scheme of things.

We also know that any one of us here does have an agenda - that being what he or she believes in any given instance. It would be very easy to say that John only posts things that agree with Dr. Enbringer and Evelyn only posts things that disagree with Dr. Enbringer. It would be very easy, but it would be untrue and unfair.

The study that I posted states only that there was no link found in the family studies that were done - from sibling to sibling. It certainly wasn't negating the entire theory. However, the accusation has been made that the research was skewed against kleb because of [insert spurious excuse here]. But research is only as skewed as our own points of view are when it comes to studying and reading the results of the research. If you firmly believe that kleb is the root cause of AS, then you're going to doubt the research. If you believe that the root cause of AS has yet to be determined, you'll be more inclined to accept the research as one more piece of a rather large puzzle.

Anyway, enough for now.

Hugs,

Dear Gerard, your note adds another area where I believe you and I could find some common ground: the intestinal flora is indeed complex, and alteration of diet could affect carriage of other pathogenic or potentially pathogenic organisms within that complex flora.

The same would hold true for use of antibiotics or introduction of probiotics: these could affect carriage of a variety of pathogens or potential pathogens within the complex flora of the gut.

Additionally gut inflammation and loss of epithelial integrity within the gut could provide exposure and loss of tolerance to food antigens that are not necessarily microbial in origin. A change in diet might potentially affect the immune response by providing a greater or lesser degree of exposure to food-derived antigens. Such a mechanism is in play in gluten enteropathy/celiac disease, and it is notable that there is a link between gluten sensitivity and arthritis.

To my understanding, the link between gut inflammation and the potential to develop AS/spondyloarthropathy is pretty broadly accepted, even though consensus on pathogenic mechanisms remains incomplete.
see:
http://ard.bmjjournals.com/cgi/content/abstract/ard.2005.047738v1

Hi there, thanks for clarifying. As an artist, I find it easier to analogize from an artistic viewpoint; hence, my specific analogy. I admire your tenacity in doing the searches at PubMed. These days I have neither the time nor the energy to do the indepth research I would like to do.

For the moment, I am content to accept what you say. And I certainly do not outright deny an involvement of kleb p in AS. I do, however, maintain that it is not necessarily true in all cases. I'm stubborn that way. Perhaps, one day, a kleb p test will be done on all potential AS cases and the results used in the same way as the HLA-B27 test - a positive result is a good indicator of AS, but a negative one does not necessarily rule out AS when the other symptoms are clearly AS related. However, I have a feeling that we are still a long way from that.

Consider my leg well stretched and my foot up (it's been propped on my hard drive while I type).

Hugs,

Hi Kat,
By reading your response I just have to know if you indeed read the latest Ebringer/Finnish research in which he suggested to use the antibody response to a particular Klebsiella peptide (piece of a protein) as a diagnostic tool. If not you have more then only the artistic talents and should become a researcher yourself, if you did you're mostly right in your conclusions except that I don't rule out that by that time we know so much more about AS that we don't consider it to be one disease any more.
Gerard

Truth be told, Gerald, I don't remember if I read it right now. I try to read research that's posted here, but sometimes by the time I'm done I feel as tho someone has presented me with the calculations for pi or E=Mc2 and asked me to present a brief on them!! In short, my eyes and head are swimming in terminology that I understand only sporadically at best and I'm like a dolphin in the middle of the Sahara.

We'll see what the future brings with regard to this. In a way, I do agree that AS is more than one disease. But the way I think of it is more in terms of a saying by Confucious (I think it was Confucious). There are as many philosophies (types of AS) as there are people in the world.

With the advent of genetic research and our growing knowledge of DNA, the ideal of treatment tailored for the individual is in our future. In the meantime...

Anyway, I've been trying to finish this post for two hours now and it's 5:20, so I'm going home.

Hugs,

AS; so it is polyphiloprogenitive? So many theories, even more words

They sell Polyfilla in our DIY stores to fill up the voids