banners
Kickas Main Page | Rights and Responsibilities | Donate to Kickas
Forum Statistics
Forums30
Topics43,801
Posts518,838
Members13,858
Most Online1,568
Jun 29th, 2016
Newest Members
Leonag, SoniaPetrowski, listart, NIMBBL, divayadharshi
13,858 Registered Users
KickAs Team
Administrator/owner:
John (Dragonslayer)
Administrator:
Melinda (mig)
WebAdmin:
Timo (Timo)
Administrator:
Brad (wolverinefan)

Moderators:
· Tim (Dotyisle)
· Chelsea (Kiwi)
· Megan (Megan)
· Wendy (WendyR)
· John (Cheerful)
· Chris (fyrfytr187)

QR Code
If you want to use this QR code (Quick Response code) just save the image and paste it where you want. You can even print it and use it that way. Coffee cups, T-Shirts etc would all be good for the QR code.

KickAS QR Code
Previous Thread
Next Thread
Print Thread
Page 3 of 11 1 2 3 4 5 10 11
Joined: Oct 2008
Posts: 758
jroc Offline OP
Magical_AS_Kicker
OP Offline
Magical_AS_Kicker
Joined: Oct 2008
Posts: 758
Quote:
It is their belief, is it not? They are entitled to believe whatever they choose whether it be correct, partially correct, or not correct at all.

in the opening post i stated that "i think that everyone is entitled to choose whatever beliefs they please."
Quote:
Also, define unhealthy.

the context in which i used the term unhealthy was where i said that "certain proponents of this hypothesis may have an unhealthy level of attachment to it." in this context i am using unhealthy to mean 'out of all proportion to the level of supporting evidence, potentially harmful to character, corruptive'. in Ebringer's case i think that his attachment to the molecular mimicry hypothesis has clouded his judgement and prevented him from being able to objectively evaluate it. i think this attachment has eventually been harmful to his scientific credibility as he keeps extrapolating single bacteria molecular mimicry theories to other diseases without adequate evidence e.g. RA-proteus, BSE-acinetobacter. in journal articles he is usually careful to state that these are only speculative hypotheses but in public makes statements such as "We have found that ankylosing spondylitis is triggered by the bowel microbe klebsiella and rheumatoid arthritis is produced following a urinary tract infection by the microbe proteus."

the BSE-acinetobacter theory has been particularly detrimental to his credibility and has led to harsh public criticism by his peers. PJ Lackman, professor of immunology at the university of cambridge commented in a letter to the editor of The Times - "Sir, William Rees-Mogg's article on BSE (July 7) is most unfortunate in that it gives prominence to Alan Ebringer's preposterous thesis that BSE is an auto-immune disease. This is comparable with Peter Duesberg's false hypothesis that Aids is not the consequence of infection with HIV, another story which had extensive coverage in the press and on television. While maverick views on science exceptionally turn out to be right, the reverse is usually the case."

he has become the scientist equivalent of the boy who cried wolf. the next time he cries 'molecular mimicry' i don't think anyone is going to come running. perhaps it will be the e coli molecular mimicry theory of schizophrenia since they have raised antibodies to e coli. in the end i think that it is a shame because if a scientist with an interest in potential links between diet and AS goes back and looks at his dietary trial they will see find that it was based on an implausible hypothesis by a scientist with a controversial track record and will be unlikely to take it seriously when it may have genuine merit via other mechanisms.

Quote:
Additionally, how is your place to decide what is healthy or unhealthy for another individual?

it's not my place at all and i don't decide what's healthy or unhealthy for other people. there's plenty of other people doing that already.

Joined: Sep 2001
Posts: 6,151
Likes: 4
AS Czar
Offline
AS Czar
Joined: Sep 2001
Posts: 6,151
Likes: 4
For jroc:


Quote:
i think it is true that modern science does not have very effective treatment answers for people with AS however that doesn't give anyone carte blanche to claim that their own implausible theories or treatments are equally valid


And exactly which theories are “implausible?” Does that include those ‘theories’ which, when actually reduced to practice produce useful RESULTS? Can we trust YOU to decide for us?

Quote:
…a disease pathogenesis that can accurately account for all aspects of the disease is not currently known


This is simply another statement that is false. Can You provide even one “aspect” of AS that is not explained by the process of molecular mimicry?

I did not think so, but wanted to give You the chance for at least a modicum of redemption.

What is becoming more and more clear, the more You pontificate, is that You have absolutely no idea what You are talking (writing) about.

That ego You are stumbling over is Your own—You want everyone else to believe You are some kind of expert in everything—a psychologist, a bioscientist, THE lone voice of reasoned discourse. But, in reality, You are just another [guy with endless questions that have already been answered] dissenter without offering any alternative viewpoint.

AS—and KickAS is not all about ME. And if You do not like my ideas or the way I present them, that is all about YOU. I am not likely to change, but You can change the channel; there are plenty of other options, even starting Your own site. Maybe You can solicit for contrary theories and find the explanations You are looking for. I hope You do find them.

Quote:
i would be interested to know why anybody should consider your knowledge of the efficacy of antibiotics in the treatment of chronic ReA to be more accurate and reliable than a meta-analysis of double blind placebo controlled trials involving thousands of patients.


In scientific studies, it is important to change one and only one thing at a time. On the surface, it seems like a logical thing to introduce antibiotics where there were previously no antibiotics before. This looks like just one thing. However, it is not that simple when it comes to a study of this nature. Consider the situation of the introduction of an antibiotic that has broad-spectrum action and has a considerable affect upon the lumen of the intestinal tract.

Now whereas the mucosal lining once covered up lesions (breeches in the epithelium), this was affected by the introduction of the antibiotics enough that those lesions are now exposed. Any arthritogenic bacteria within the gut now have direct access to the blood and lymph, making the primary disease more active and even initiating new and more types of ReAs (polyarthritis).

In fact, the first tests of antibiotics for AS not only did this and more—they created resistive colonies so that the best agent could no longer effectively be employed in the management of AS in these individuals. Diet was not also changed, so the bacterium selected-out resistive members, which then proliferated upon their favorite substrate.

Do we share this knowledge here, is that any part of our basic purpose? I am NOT an expert, and nobody should believe me over anyone else.

So the same question--why should anybody rely upon YOUR interpretation of jroc-selected existing scientific data? We can all go to our physicians and get their ‘expert’ (and sometimes equally wrong) medical opinions. Recently, their expert opinion included that ulcers were the result of “stress!” Study after study “proved” this accepted fact. You would have been a cheerleader for those studies, also, because they appeared ‘scientific.’

I make claims about good results regarding my own case of AS. And over the years, I have had correspondence with over 200 people directly and many more here at KA who have also had similar results. Some (very) few have not, and I cannot explain these, despite my belief in their valid attempts and assiduous adherence to the regimen. Well, in retrospect, I have been given some positive information on one of these cases.

Also, I have had the distinct advantage of attending the two lecture series Professor Ebringer gave here in the US (I did not see You there), and had the opportunity to ask him questions about mechanism in AS and many other diseases. He gave me results of his scientific results and also his opinions about AS and other diseases we are interested in, as well as his opinions about ‘current’ research in autoimmune conditions.

Of course, I am not shy about sharing my opinions and the caveat is that they are just my own opinions—not more valid than anyone else’s, and everyone knows they are each free to like, dislike, manufacture offense, take personally, ignore, dispute, or take as absolute Gospel anything I say; we are each all grown up and can decide for ourselves.

Quote:
… that this was done through experiments with antibiotics (as diet was initially unsuccessful), some form of NSD as well as chelation therapy.


Diet was NOT initially unsuccessful; it was only not spectacular. At that time, I had no explanation as to why my results were ‘spotty.’ But from my fasting experiences, I knew that diet was certainly a factor. Subsequently, I proved the starch connection through Bayesian calculations using key literature database retrospectives.

I added antibiotics to put the germ theory to the test. In fact those agents that have no effect against Klebsiella pneumoniae also provided no symptom relief. Sometimes I did not know which agents were viable, as I grabbed just about anything cheap, oral route, and available through those Farmacias in Mexico. And I kept very accurate records, setting aside effective agents for what I knew would eventually happen (and it did)--I got an ineffective batch of normally effective antibiotics, so returning to effective date code material provided relief expected.

When I had the chelation therapy, and for many years afterward, I did not know about the germ connection with AS, but chelation was only used for a short time to get me out of a major flare.

Quote:
it does suggest that those type of interventions may be useful to some people with AS but it is certainly not proof of any underlying mechanism and implying that it is conclusive proof and then extrapolating it to all others with the disease, and even other diseases is a giant leap of faith.


Sometimes we will decide to act upon others’ experiences, whether we call it ‘faith’ or personal research; it is our personal choice. Although I believe that a single bacterium is responsible for every case of AS, and that all AS is the result of molecular mimicry, I admit I could be wrong—that is just my opinion but it is based upon a lot more experience than You have revealed.

Quote:
my beliefs are consistent with modern science because it one of the main (although not the only) source of information that i use to arrive at them. i read all of the evidence, take into consideration any biases that different information sources may have, try to be aware of any personal biases i may have, evaluate the evidence in order to arrive at an informed opinion, and then revise and re-evaluate my position as new evidence emerges.


You have not shared Your beliefs with us, but only provided a bunch of references that You consider ‘evidence,’ and have not bothered to analyze critically. All You can do is provide more reasons for paralysis; this is neither helpful nor scientifically sound. Your opinions are the result of an unfortunate propensity to believe every scientific-looking paper You read. If You were able to synthesize anything useful from this endless collection of pap, You have not enlightened us with any RESULTS!

As I have said before, it is easy to find Ebringer detractors and for every paper he published there might be 20 that appear to contradict his data, but when properly analyzed these usually do not hold their own. Flawed DOE, statistical methodology, irrational premise, improper study groups—I have seen it all over the years, and don’t care to elaborate. Most of the researchers were not frauds, but so many managed to fool themselves, and now obviously You, also. One of the researchers, in particular, was and is a fraud, and I have named him by name before. These people have done much to set back true advances in AS research, and continue to cause harm to AS patients; their mistakes and outright frauds will long outlive them.

You pretend Your beliefs are “consistent with modern science,” but only fool Yourself—if You could just step back and look at such statements for what they are really worth; if You do not see the puffy pomposity of this, You are not quite introspective enough.

However, You are absolutely correct with Your subtle accusation against me: I certainly am NOT CURRENT. I do not have any reason to be; it is not within my field of interest anymore. Basically, by 1982 AS was explained enough that I could have resolved all of my issues, had I known about the Ebringer et al research. Regret I had relied too heavily upon my physicians to come up with the right answers, but they never had a clue. If this medium of exchange had only existed back then, the truth probably is that I would not be imprisoned in my current damaged body.


For some reason I can only speculate upon, You make very weird statements:
Quote:
in Ebringer's case i think that his attachment to the molecular mimicry hypothesis has clouded his judgement and prevented him from being able to objectively evaluate it.


I don’t know how many people You have helped personally, but Your very obvious level of jealousy is pathetic. In fact, I asked Professor Ebringer to look at this thread, but regret that now, because of Your churlish and insulting attitude. Again, You should be more introspective about the statements You make. Most thoughtful individuals reading this, regardless of their knowledge level, will correctly conclude that You are at least incredibly full of Yourself, if not here to attempt to soothe a terrible, nearly-debilitating, inferiority complex.

In general, You have not offered anything new or "current," when objecting to Ebringer's research and results, but only cite old papers that even many of the original authors now distance themselves from.

And regarding the BSE/vCJD controversy: There are to date (April, 2012) NO provable cases of prion disease. Injected "prions" cause a disease condition which should be called "Pasteur's Disease," or Experimentally Acquired Encephalopathy.

The proponents of the prion proposal originally stated that the incubation period could be from seven years up to twenty-five years. But, curiously, now that it has been MORE than 25 years and the EPIDEMIC is still MISSING, they are trying to cling to their unhealthy obsession with prions by moving the incubation period to 100 years! So a disease that shows up in cattle within two years and in humans within 10 years has morphed into a 100 year timebomb?!

Ebringer stated he is willing to consume a decent cut of steak from any certified "Mad Cow;" I will be right there with him.

So, whether or not his information will help those with MS, this has not been disproven but only remains to be studied further. If a family member were diagnosed with MS, I would not hesitate doing plenty of anti-Acinetobacter calcoaceticus measures exactly where he claims the primary lesion happens. This, in addition to but not replacing common medical practices. Just like AS diet therapy.

Now he is busy writing his book "Ankylosing Spondylitis and Klebsiella," so I wanted him to receive Your insightful inputs before he finishes. If You have something to add, I'm sure he would be very interested in the opinions of someone with Your particular experience.


Further, he writes:
"Tomorrow I am flying to Bermuda. I have been invited to give 3 lectures on
(a) Rheumatoid arthritis.
(b) Ankylosing spondylitis
(c) Crohn's disease."

And I ask You--WHO, in their right minds would ever invite Ebringer to lecture on anything?

And-
"After pressure from some NASS members, the editorial board asked Professor Paul Wordsworth, Professor of Rheumatology in the University of Oxford to review and comment on the "LOW STARCH DIET" in AS:"

[AS News, Spring, 2012--[maybe not "current" enough for You...]]

THE LOW STARCH DIET
Many people with AS express an interest in trying low starch diets to treat the condition as proposed by Professor Alan Ebringer of Kings College, London.

The original rationale for this was based on some very interesting findings by Alan and his brother Roland at the Middlesex Hospital in the early 1980s. They identified antibodies to a bacterium called Klebsiella in the blood of individuals with AS, and also found that they could culture this organism from the stools of many people with active disease. Such antibodies are typically made by the immune system in response to infections, and are one of the means by which viruses and bacteria are eliminated from the body.

Furthermore these anti-Klebsiella antibodies potentially bind not only to proteins in Klebsiella but also to certain human proteins including HLA-B27, which is one of the tissue transplant antigens that have to be matched between organ donors and recipients.

I have vivid memories of Alan and Roland carefully sifting through thousands of stool samples and blood tests from patients with AS, trying to correlate their laboratory findings with the activity of the disease. Their work led to the idea that these anti-bacterial antibodies might also bind to human proteins like HLA-B27 to stimulate inflammatory responses in some way. Subsequently the Ebringer team also reported similarities between HLA-B27 and another Klebsiella protein called pullulanase-A, which helps break down starch molecules. They also noted that pullulanase-A had some similarities not only to HLA-B27 but also some other human proteins, called collagens, found in joints and also the eye (both of which can be affected in AS).

The role of Klebsiella antibodies in AS has proved highly controversial over the years. It is now recognised that molecular mimicry between different proteins as described above is not that uncommon in nature. Whether or not Klebsiella antibodies are relevant to AS, there may well be an important role for the gut in causing AS. For example, about 10% of people with AS also have inflammatory bowel disease (IBD, Crohn’s disease or ulcerative colitis), and many people with AS without overt IBD symptoms have evidence of low-grade bowel inflammation if one looks hard enough for it. Furthermore, many of the genes that predispose to AS also predispose to IBD, including CARD9, IL23R and IL12B. This lends credibility to the idea that altering the gut flora (the population of bacteria living naturally in the gut) might have an influence on bowel inflammation and, perhaps, susceptibility to AS. Anyone who has seen the natural yoghourt adverts on TV will also be familiar with the idea that it is possible to increase the number of “good bacteria” in the gut while reducing the number of “bad bacteria”.

Various studies have found that bowel bacteria, including Klebsiella grow on undigested starch and therefore a reduction in starch in the patient’s diet might produce a reduction in symptoms by denying those bacteria the nourishment to multiply. Once starch has passed through the small intestine and enters the large bowel, it is available to feed those bacteria. There are simple starches which are sugar molecules attached together rather like a necklace or chain. Simple enzymes break up the chains and the sugars are readily available for the bacteria to grow. Some of the starch is of this simple type (20%) but most of it (80%) is hard starch and the sugar molecules are in branched structures, which appear like the branched twigs of a tree and can only be broken down by de-branching enzymes. Klebsiella has the correct pullulanase enzymes to break down the hard starch which allows the bacteria to grow and multiply, so it is very well adapted to life in the human bowel. The rationale for the Low Starch Diet is to make life less easy for the Klebsiella organisms to thrive.

There are no formal trials that have assessed the efficacy of low starch diets in AS. In common with many other inflammatory disorders the natural history of AS is rather unpredictable. It is therefore very difficult to tell whether improvements in symptoms merely reflect natural occurring fluctuations in disease severity over time rather than the influence of treatment. Some patients trying low starch diets have had very gratifying improvements in their symptoms but high quality randomised controlled studies of this type of diet in large numbers of patients have never been performed. Consequently it is very difficult to know whether the diet is truly effective. This is not an unusual position for the rheumatologist to be in when asked about unorthodox treatments and our advice is usually the same. If the treatment is not harmful there seems no reason not to give it a trial, remembering that it could be 3 months or so before you notice any difference. Furthermore even if you notice a difference this does not necessarily establish that there is a real therapeutic effect. For example, in the trials of anti-TNF drugs in AS it has not been unusual for those patients in the dummy arm to experience very significant benefit in the first 3 months – a phenomenon known as the placebo effect.

In the absence of convincing trial evidence of proven benefit it is quite impossible for a patient organisation such as NASS to endorse low starch diets as a treatment strategy. On the other hand there is some circumstantial evidence that they might have an effect – and, of course, the testimony of individuals, who have apparently had considerable benefit, can be very persuasive.


Professor Paul Wordsworth, Consultant Rheumatologist



May You find whatever it is You are seeking,
John



Last edited by DragonSlayer; 04/15/12 01:44 AM. Reason: Suggestion from Admin.
Joined: Feb 2006
Posts: 1,483
Silver_AS_Kicker
Offline
Silver_AS_Kicker
Joined: Feb 2006
Posts: 1,483
from the letter by Wordsworth

"Whether or not Klebsiella antibodies are relevant to AS, there may well be an important role for the gut in causing AS. For example, about 10% of people with AS also have inflammatory bowel disease (IBD, Crohn’s disease or ulcerative colitis), and many people with AS without overt IBD symptoms have evidence of low-grade bowel inflammation if one looks hard enough for it. Furthermore, many of the genes that predispose to AS also predispose to IBD, including CARD9, IL23R and IL12B. This lends credibility to the idea that altering the gut flora (the population of bacteria living naturally in the gut) might have an influence on bowel inflammation and, perhaps, susceptibility to AS"

pretty much what JROC is saying as well. Not much difference between the opinions really other then JROC is saying it is a maybe and we need to be open to other hypothesis (as did the doc above) and John saying it is a sure thing and settled.

Not sure I see that much conflict here wink To me the mechanism of AS is still not settled but Ebringer's thoughts sure are intriguing as the good doctor states in his letter and I don't think you can say ebringer's judgment was clouded until all the data is in and he is proven incorrect. So far I just don't think Ebringer has been proven incorrect.


No families take so little medicine as those of doctors, except those of apothecaries.

Oliver Wendell Holmes
Joined: Nov 2011
Posts: 256
Third_Degree_AS_Kicker
Offline
Third_Degree_AS_Kicker
Joined: Nov 2011
Posts: 256
I just want to say that I have much respect for everyone here, and that while I don't necessarily understand why (if it is my B27+ or some other gut connection or something else entirely,) but following Dr. Ebringer's advice has changed my life SO much for the better. I can never thank him, or KickAS enough.


Iritis first diagnosed in 1991, presently recurrent and steroid resistant.
Tested HLA B27 positive in 1996.
AS diagnosed October of 2011.

Putting most of my eggs in the NSD and exercise basket, using only TENS, massage, heat and ice, and NSAIDS (sparingly) for pain. Drops for iritis as flare necessitates. Looking back I feel I would have been diagnosed with AS years ago, if I had found a rheumy earlier than 2011.
Joined: Feb 2010
Posts: 1,046
Iron_AS_Kicker
Offline
Iron_AS_Kicker
Joined: Feb 2010
Posts: 1,046
Originally Posted By: drizzit

Not sure I see that much conflict here wink To me the mechanism of AS is still not settled but Ebringer's thoughts sure are intriguing as the good doctor states in his letter and I don't think you can say ebringer's judgment was clouded until all the data is in and he is proven incorrect. So far I just don't think Ebringer has been proven incorrect.


Well put. Even if molecular mimicry is superceded by another theory on the mechanism at some point, I'm still grateful that Ebringer and others here have helped raised awareness of the gut and diet connection for AS!

Joined: Oct 2008
Posts: 758
jroc Offline OP
Magical_AS_Kicker
OP Offline
Magical_AS_Kicker
Joined: Oct 2008
Posts: 758
Quote:
And exactly which theories are “implausible?”

as i have repeatedly stated. the theory "that all cases of AS are caused by klebsiella via molecular mimicry."
Quote:
Does that include those ‘theories’ which, when actually reduced to practice produce useful RESULTS?

absolutely it does. science has shown us that many anecdotally successful treatments are based on faulty premises e.g. the blood-type diet, homeopathy etc.
Quote:
Can You provide even one “aspect” of AS that is not explained by the process of molecular mimicry?

why it occurs more often in males than females, why some patients have raised CRP and ESR and others don't, why ERAP1 is involved in disease susceptibility, why some patients have iritis and some don't, why some people fuse and some people don't, variation in sites of disease activity etc
Quote:
I did not think so, but wanted to give You the chance for at least a modicum of redemption.

thanks for the opportunity.
Quote:
In scientific studies, it is important to change one and only one thing at a time.

you might want to tell Ebringer that as his diet study doesn't even attempt to account for any of the numerous variables that are potentially changed by his diet protocol i.e. total caloric intake, amount of fruit and vegetables, amount of junk food consumed etc
Quote:
why should anybody rely upon YOUR interpretation of jroc-selected existing scientific data?

they shouldn't. they should thoroughly investigate all sides of the issue for themselves, consider the accuracy and potential biases of different information sources, and draw their own conclusions.
Quote:
Recently, their expert opinion included that ulcers were the result of “stress!” Study after study “proved” this accepted fact. You would have been a cheerleader for those studies, also, because they appeared ‘scientific.’

once gain you demonstrate a failure to read any of the relevant literature and understand the complex interactions of host and bacteria in the pathogenesis of disease. in the case of peptic ulcers it is the combination of the presence of h pylori (which is present in 70-90% of cases) and also other environmental factors of which psychological stress is a well known contributor - "An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role.[1] Researchers are examining how stress might promote H. pylori infection. For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers.[13]"
Quote:
I added antibiotics to put the germ theory to the test. In fact those agents that have no effect against Klebsiella pneumoniae also provided no symptom relief.

did you account for the fact that klebsiella shares antibiotic resistance characteristics with many other species of enterobacteriaceae? - "All Klebsiella spp. were naturally resistant or intermediate to amoxicillin, ticarcillin and to antibiotics to which other Enterobacteriaceae are also intrinsically resistant."
Quote:
You have not shared Your beliefs with us, but only provided a bunch of references that You consider ‘evidence,’ but have not bothered to analyze critically.

and yet you don't even bother to read the 'evidence' because you say that it is not within your 'field of interest' and that your curiosity into the pathogenesis of AS is satisfied by level of understanding attained by 1982.
Quote:
Your opinions are the result of an unfortunate propensity to believe every scientific-looking paper You read.

unfortunately not true as i don't believe a lot of Ebringer's studies.
Quote:
If You were able to synthesize anything useful from this endless collection of pap, You have not enlightened us with any RESULTS!

that's a fair point. i have been able to synthesise several useful nuggets of information from that 'endless collection of pap' aka the latest scientific research published in peer reviewed journals. i will make more of an effort to share some of it in upcoming posts.
Quote:
As I have said before, it is easy to find Ebringer detractors and for every paper he published there might be 20 that appear to contradict his data

and yet you facetiously claim that it is me who is "THE lone voice".
Quote:
Ebringer stated he is willing to consume a decent cut of steak from any certified "Mad Cow;" I will be right there with him.

are you sure that you haven't already? it would explain quite a lot.
Quote:
Now he is busy writing his book "Ankylosing Spondylitis and Klebsiella,"

why does that not surprise me. the scientific community doesn't take any of his hypotheses seriously any more so he writes a book so now his audience is not trained in scientific method, only presented with half the story, and are unable to spot his mistakes and call his bluff. he doesn't need to worry about being caught out cherry picking the studies he cites in his book or omitting the huge body of evidence that contradicts his theory as the content only has to make it past an editor and not a peer-review panel.
Quote:

If You have something to add, I'm sure he would be very interested in the opinions of someone with Your particular experience.

i would love to correspond with professor Ebringer but i think that it would be much more productive if he were to consult with real experts in the field that are involved in the latest research and have them explain to him the flaws in his hypothesis and show him some of the latest research such as the influence of microbiome composition on th17/treg balance, experiments with different species of bacteria in b27 transgenic rats etc.

Quote:
And I ask You--WHO, in their right minds would ever invite Ebringer to lecture on anything?

people who only look at his qualifications and university position and not the quality of the science he presents. people who do not consult with a wide range of qualified experts in the field to discover how credible they consider him and his ideas to be.
Quote:
I have vivid memories of Alan and Roland carefully sifting through thousands of stool samples and blood tests from patients with AS, trying to correlate their laboratory findings with the activity of the disease.

that should set off major alarm bells. that doesn't sound like they were trying to objectively test their hypothesis. it sounds like they were trying to manipulate the results to confirm their hypothesis. that would make sense considering that subsequent investigations by other researchers without a vested interest in the hypothesis were not able to reproduce their results. nowadays researchers are trained to be aware of cognitive biases such as expectation bias, confirmation bias etc. it sounds like the Ebringer's could have benefited from such training.

Joined: Jan 2008
Posts: 21,346
Likes: 1
Very_Addicted_to_AS_Kickin
Offline
Very_Addicted_to_AS_Kickin
Joined: Jan 2008
Posts: 21,346
Likes: 1
reading all of this with interest.

right now, for myself, i like the following theory:

the lack of lactobacillus in my gut allows unfavorable bacteria to be there too much. or that the bad bacteria have out competed the good bacteria. as evidence by stool sample testing.

in either case, this is what has given me that lower level bowel inflammation that drizzit talks about.

and that has led to leaky gut.

and that has allowed casein to sneak through.

and casein triggers an inflammatory response in my body (as determined through blood work).

so, a similar theory, where it starts with the idea of the gut microbiome. but rather than it being a response to the bacteria, its a response to the food antigens. and instead of starch, for me, it seems to be casein and to a lesser extent, egg.

so those are the two (casein and egg) i stay away from.

and probiotics to try to change the gut flora and hopefully in the process, heal the gut.

i do seem to be better in between flares now. so maybe there is something to all of this.

though on a LSD for years due to the insulin resistance, between the blood tests and all celiac tests coming back negative, and my not having the HLA-B27 gene, the leaky gut / casein inflammatory response just makes more sense for me.

but then again, i'm undiff spondy, not AS.

interestingly, i just read today about gluten and / or casein possibly being responsible for all kinds of chronic health issues. and this article was promoting a gluten-free, casein-free diet. i'm slowly coming around to the idea that casein could have been causing so many of my problems. i'm not wed to the idea, but it does make a lot of sense for me, largely based on the tests i've had done and their results.



sue

Spondyloarthropathy, HLAB27 negative
Humira (still methylprednisone for flares, just not as often. Aleve if needed, rarely.)
LDN/zanaflex/flector patches over SI/ice
vits C, D. probiotics. hyaluronic acid. CoQ, Mg, Ca, K.
chiro
walk, bike
no dairy (casein sensitivity), limited eggs, limited yeast (bread)
Joined: Feb 2006
Posts: 1,483
Silver_AS_Kicker
Offline
Silver_AS_Kicker
Joined: Feb 2006
Posts: 1,483
While I won't thrash Ebringer like JROC is and I still think he may have been first to cue people into the Gut bacteria and AS and his idea has obviously helped many to his credit.

ERAP 1 is a wrinkle that has to be considered and it calls mimicry into question for me as well. ERAP1 problems and HLAB27 can explain AS as easily as Mimicry can.


No families take so little medicine as those of doctors, except those of apothecaries.

Oliver Wendell Holmes
Joined: Oct 2008
Posts: 758
jroc Offline OP
Magical_AS_Kicker
OP Offline
Magical_AS_Kicker
Joined: Oct 2008
Posts: 758
Quote:
While I won't thrash Ebringer like JROC is and I still think he may have been first to cue people into the Gut bacteria and AS and his idea has obviously helped many to his credit.

just to be clear i am only 'thrashing' his hypothesis why he still clings to it. as i previously stated here - "if i did make a website it would not be anti-Ebringer. it would mention his pioneering work in drawing attention to the role of gut bacteria in AS, successful dietary trials in AS, and willingness to think outside the box. in the interests of a balanced perspective it would also mention the reasons why his theories never became accepted as new evidence emerged, science progressed and the titles of his journal articles morphed from 'AS is caused by klebsiella'(1992) to 'AS is linked to klebsiella'(2007)." and here - "i salute Ebringer for his pioneering work in the gut and AS, and his willingness to experiment with dietary interventions."

Joined: Sep 2001
Posts: 6,151
Likes: 4
AS Czar
Offline
AS Czar
Joined: Sep 2001
Posts: 6,151
Likes: 4

Quote:
as i have repeatedly stated. the theory "that all cases of AS are caused by klebsiella via molecular mimicry."


This is not a theory; it is the observation that every case thus far studied has been caused by a single pathogen (albeit the confusion will remain because AS can be ‘triggered’ by myriad different agents and agencies). As Ebringer suggests in other situations, if You want to try and find a vegetarian tiger, You are fully welcome to faithfully pet them all. I try and live in the real world, one that William of Ockham once also inhabited.

Quote:
absolutely it does. science has shown us that many anecdotally successful treatments are based on faulty premises e.g. the blood-type diet, homeopathy etc.


This “science” You speak of…OH, it must be a wonderful thing!

Can You provide even one “aspect” of AS that is not explained by the process of molecular mimicry?

Well, sorry to say, this was not a trick question, and You cannot so easily lie Your way out of it, despite Your keenest efforts:

Quote:
why it occurs more often in males than females, why some patients have raised CRP and ESR and others don't, why ERAP1 is involved in disease susceptibility, why some patients have iritis and some don't, why some people fuse and some people don't, variation in sites of disease activity etc


Molecular mimicry fully explains the gender differences both in frequency as well as presentation, and also why some patients experience iritis while others do not, which is the same question as variation in sites of disease activity. It also offers the best explanation as to why some individuals fuse and others do not.

It does not explain sporadic lack of inflammatory markers any better (and absolutely no worse) than the two other competitive theories I am familiar with.

Molecular mimicry also explains the epiphenomenon of ERAP 1, which alone cannot in fact explain any of Your challenges.

Your letter grade: F
Demonstrating, once again, that You are guilty of exactly what You have accused me of—You are just not paying attention. And with every statement, You crawl farther out on the limb You are sawing off.

Quote:
you might want to tell Ebringer that as his diet study doesn't even attempt to account for any of the numerous variables that are potentially changed by his diet protocol i.e. total caloric intake, amount of fruit and vegetables, amount of junk food consumed etc


NONSENSE! You might want to re-read the study and pay attention this time. There may be a quiz at the end. Hint: It is still the “Etiopathogenesis…” paper.

Quote:
once gain you demonstrate a failure to read any of the relevant literature and understand the complex interactions of host and bacteria in the pathogenesis of disease. in the case of peptic ulcers it is the combination of the presence of h pylori (which is present in 70-90% of cases) and also other environmental factors of which psychological stress is a well known contributor - "An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role.[1] Researchers are examining how stress might promote H. pylori infection. For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers.[13]"


Q.E.D.

Quote:
did you account for the fact that klebsiella shares antibiotic resistance characteristics with many other species of enterobacteriaceae? - "All Klebsiella spp. were naturally resistant or intermediate to amoxicillin, ticarcillin and to antibiotics to which other Enterobacteriaceae are also intrinsically resistant."


No, although I was aware of this fact, it is not relevant to the primary question: Do bowel or even other germs cause AS? I resolved to my own satisfaction that a) A Gram negative germ is involved and b) That pathogen is most likely one that has already been suspected and c) Hijacks (monopolizes) the secondary immune systems of all AS patients ("all" thus far studied).

Quote:
and yet you don't even bother to read the 'evidence' because you say that it is not within your 'field of interest' and that your curiosity into the pathogenesis of AS is satisfied by level of understanding attained by 1982.


Apparently, the theory You are challenging is not within Your field of interest, either, as You are very deeply so unfamiliar with it. It would otherwise be shameful; if You possessed that particular personality characteristic.

Quote:
i will make more of an effort to share some of it in upcoming posts.


I am holding my breath!


Quote:
and yet you facetiously claim that it is me who is "THE lone voice".


But You have taken this statement so far from its original context that it must at least be speciously true...for You alone.

Quote:
Quote:
:
Ebringer stated he is willing to consume a decent cut of steak from any certified "Mad Cow;" I will be right there with him.


are you sure that you haven't already? it would explain quite a lot.


Boy-HOWDY, am I glad I edited my original response to You!

Quote:
why does that not surprise me. the scientific community doesn't take any of his hypotheses seriously any more so he writes a book so now his audience is not trained in scientific method, only presented with half the story, and are unable to spot his mistakes and call his bluff. he doesn't need to worry about being caught out cherry picking the studies he cites in his book or omitting the huge body of evidence that contradicts his theory as the content only has to make it past an editor and not a peer-review panel.


The scientific community agrees with Ebringer about three-to-one (based upon pre-election polling); it is the medical industry that ‘conveniently ignores’ Ebringer. They would otherwise have a lot of explaining to do (some legal liabilities, but hey, it only harms their patients now, and later not their pocketbooks).

Ebringer’s book is written FOR SCIENTISTS and he fully expects to be examined by real experts. It will either stand up to this level of scrutiny or it will not. I am taking bets now—care to make a donation, er I mean wager?!

Quote:
that should set off major alarm bells. that doesn't sound like they were trying to objectively test their hypothesis. it sounds like they were trying to manipulate the results to confirm their hypothesis. that would make sense considering that subsequent investigations by other researchers without a vested interest in the hypothesis were not able to reproduce their results. nowadays researchers are trained to be aware of cognitive biases such as expectation bias, confirmation bias etc. it sounds like the Ebringer's could have benefited from such training.


I don’t know how familiar You are with basic scientific methods, but Your alarm bells are duly noted.

There was something said once about the “author” Patience Worth. To paraphrase it goes something like this: If this is a HOAX—then You can go and do it, too!

So far all You have contributed is an obvious hoax, easily exposed; You shall have no pie.

Page 3 of 11 1 2 3 4 5 10 11

Link Copied to Clipboard
Who's Online Now
0 members (), 33 guests, and 67 robots.
Key: Admin, Global Mod, Mod
Recent Posts
Welcome All New Members!
by Magician - 08/09/22 10:54 PM
Chamomile tea can reduce inflammation
by L33 - 07/26/22 11:20 PM
Best Gym Equipment to have
by L33 - 07/26/22 10:10 PM
Ankylosing Spondylitis is curable
by Sudhir - 07/24/22 07:34 AM
Let Us Know You Dropped In!
by Magician - 07/15/22 05:46 AM
Numb fingers, nerve pain
by Stevenage69 - 07/12/22 11:06 AM
Benifits of Wet cupping/ Hijma
by L33 - 03/20/22 10:53 AM
Popular Topics(Views)
3,230,295 hmmm
1,245,027 OMG!!!!
648,760 PARTY TIME!
Powered by UBB.threads™ PHP Forum Software 7.7.5
(Release build 20201027)
Responsive Width:

PHP: 5.5.38 Page Time: 0.034s Queries: 36 (0.013s) Memory: 3.3487 MB (Peak: 3.5606 MB) Data Comp: Zlib Server Time: 2022-08-16 03:08:32 UTC
Valid HTML 5 and Valid CSS