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