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?
…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.
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.
… 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.
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.
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:
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?
"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,