Kickas.org Forums Treatments, Drugs and Alternatives NSD and diet-related; Two AS Sub-groups?

Loz,
When the Klebs feed on meat that doesn't have to mean that that is the meat you ate. It could also mean YOUR meat or better products from your body that are available in diseased places of the intestine. Spondyloarthropaties are characterised by Crohn like lesions in two thirds of cases and in the other third the lesions are not detected (which doesn't proof they are not there) anyway proof is gathering that there is still inflammation in this one third. Crohn like lesions means ulceration and ulcerations have a bacterial and fungal microflora of their own as the article below show. In the first article Klebs are not specifically mentioned but they fall under the "different species of opportunistic enterobacteria" that are mentioned. These bacteria have a lot activities mentioned to get their energy, for instance they break down blood cells (hemolytic) lectins (lecithinase) milk proteins (caseinolytic) etc. The second article shows how NSAID's promote ulcerization in rats and that Klebsiella is associated with this ulcer formation and thriving on it.

The microflora of ulzerous zone mucosa in patients with duodenal ulcer

[Article in Russian]

Chervinets VM, Bondarenko VM, Bazlov SN.

State Medical Academy, Tver, Russia.

Bacteriological study of the biopsies taken from gastric and duodenal mucosa of 10 healthy volunteers and 74 patients with duodenal ulcer, was carried out. In the gastroduodenal zone of healthy subjects microorganisms of 6 genera (Streptococcus, Candida, Staphylococcus, Bacillus, Helicobacter and Lactobacillus) were detected. H. pylori was isolated in 20% of cases only in biopsy specimens taken from the antral section of the stomach of healthy as monoculture or in combination with C. albicans. In patients with duodenal ulcer activation of opportunistic microflora was observed in the periulcerous zone. More often H. pylori occurred in associations with fungi of the genus Candida, streptococci, staphylococci, enterobacteria, Pseudomonas and other microorganisms (of more than 30 genera). Quantitatively the dominating microorganisms (3.8-5.7 lg CFU/g) were H. pylori, fungi of the genus Candida, bacteria of the genera Streptococcus, Peptostreptococcus, Bacteroides, Gemella, Prevotella, Veillonella, Peptococcus, Bacillus, different species of opportunistic enterobacteria, as well as bacteria of the genera Staphylococcus, Micrococcus, Corynebacterium, Neisseria, Pseudomonas, etc. Opportunistic bacteria detected in the ulcerous zone, as a rule, expressed hemolytic, lecithinase, RNAase, caseinolytic, catalase and urease activity . Sonicated filtrates of such cultures produced a cytotoxic effect on cells HEp-2. Ulcer is an infected wound that needs sanitation.

Second article:

Role of intestinal bacteria in ileal ulcer formation in rats treated with a nonsteroidal antiinflammatory drug.

Uejima M, Kinouchi T, Kataoka K, Hiraoka I, Ohnishi Y.

Department of Bacteriology, School of Medicine, University of Tokushima, Japan.

The role of intestinal bacteria in induction and repression of ulcer formation in the ileum of rats treated with one of the nonsteroidal antiinflammatory drugs (NSAIDs), 5-bromo-2-(4-fluorophenyl)-3-(4-methylsulfonylphenyl) thiophene (BFMeT), was examined in this study. BFMeT was administered by intragastric gavage once at doses of 500-1,500 mg/kg of body weight to Wistar rats treated with and without antibiotics (bacitracin, neomycin, streptomycin), germ-free rats and gnotobiotic rats, and 72 hr later their gastrointestinal tracts were examined for ulcer formation. A single oral administration of BFMeT induced ileal ulcers in specific pathogen-free rats. However, the rats given antibiotics to reduce the intestinal bacteria had no ulcers. BFMeT-treated germ-free rats and gnotobiotic rats mono-associated with Bifidobacterium adolescentis or Lactobacillus acidophilus also had no intestinal ulcers. However, the drug induced ileal ulcers in gnotobiotic rats mono-associated with Eubacterium limosum or Escherichia coli. An overnight culture of B. adolescentis or L. acidophilus or yogurt containing Bifidobacterium breve and Streptococcus thermophilus, when given as drinking water, inhibited ulcer formation in the ileum of rats treated with BFMeT. Gram staining of the ileal contents of normal rats revealed that 97.4% of the stained microorganisms were Gram-positive rods and only 1.2% were Gram-negative rods. In the group of rats with ulcers induced by BFMeT, the Gram-positive rods decreased by 56.4% and the Gram-negative rods including Escherichia coli, Klebsiella, Proteus and Bacteroides increased by 37.3%. However, in the group of rats administered the Bifidobacterium culture, the Lactobacillus culture or yogurt, the percentages of the Gram-negative rods were decreased. Although Lactobacillus was a major bacterium in the ileum of normal rats, the Gram-negative facultatively anaerobic rods E.coli, Klebsiella and Proteus were increased in the ulcerated ileum of rats treated with BFMeT, suggesting that these bacteria are associated with ulcer formation in rats treated with NSAIDs, and that Lactobacillus and Bifidobacterium inhibit it by repressing the growth of ulcer-inducing bacteria.
.


"That we become twice as old now as a century ago is the work of plumbers, not doctors" -Midas Dekkers-

Lozz,

Intestinal flora also feeds very well on FOS: Fructo-oligo-sacharrides. You can check the scdiet.com on this.

With me it shows off, eating leek or onion truly kills me, like I was not doing diet at all. If NSD alone does not work, one should try FOS as well.

Regards

Arjan

Hi John

Earlier on this thread you wrote -

"Yes, it (diet) will work for everyone with AS but it requires time and more patience than most patients have."

In your last post you wrote -

"It was not my intention to give the impression that there are no vegetarian tigers, only that Ebringer did not find any. I happen to know that there ARE diet insensitive sufferers.... "

These excerpts seem to be in conflict and I have always thought the first was closer to your position.

In discussing this matter I have avoided presenting any new information but have merely analysed the facts as presented by you and Bilko. There are reasons for this approach. Firstly I am a layman in this discussion (but that doesn't limit my capacity to reason and debate). Secondly it makes it easier for anyone reading to follow.

I have quoted several times from Bilko's earlier post (because it is pivotal to this debate) -

(A) "Ebringer's classification into two groups is really very simple; he would listen to the patient's medical history to form an opinion, then if AS was suspected test the level of klebs specific antibodies. If you had inflammation and pain but no elevated klebs IgA then it wasn't AS. Otherwise it was. Often it is extremely difficult for a clinician to diagnose with the usual criteria, and some of the people in the group who do not respond to diet will have the wrong diagnosis."

and later "It is true the IgA-Kp test is not standard path lab for AS".

You have not disputed this evidence so I have assumed I could use this as a basis of argument. Is this unreasonable? Whenever I have been wrong I have been quickly informed of this, which is as it should be. I have also assumed that when Bilko said "If you had inflammation and pain but no elevated klebs IgA then it wasn't AS.", I could assume Ebringer did not include in his studies those whom he considered did not have AS (although that is not explicitly stated). Again this assumption was not challenged.

When you wrote in your last post "He (Ebringer) was unable to 'filter out' AS volunteers without high levels of Klebsiella antibodies because such a group did not exist (as a group) ..." and "I did say before that Ebringer did not screen out ANY AS individual. " surely that conflicts with Bilko's statement. If he tested for 'klebs specific antibodies' and did not include those with 'no elevated klebs IgA' then he has screened out (or filtered out) those patients. Whether they existed 'as a group' I cannot see as significant.

Would you please clarify where you stand on the statement of Bilko labelled (A) above.

Wally

Hi, Wally:

This might be one of the sources of confusion, but could easily be resolved by reading the Ebringer papers on this site:

When a person with AS is experiencing a FLARE his IgA-Kp is greatly ELEVATED. If NOT in a flare the IgA-Kp is between (high-) normal and moderately elevated; these are classified as AS but INACTIVE.

BOTH active and inactive AS people were included in Ebringer's study groups, so I do not understand your concerns about filtering; he is a primary maths and statistics person, so is very aware of the potential errors which could have resulted in bimodal distributions, taking great pains to avoid just that.

Yes, many people with AS really do not respond to the diet very well, but there is a subjective component: 1) Do they have elevated ESR when in flare? 2) Was this measured before starting on the LSD/NSD and midpoints? Getting the subjectivity out of the equation is important. Remembering just because carbohydrates are comfort foods is enough to get a general negative review even if nothing else changes.

Other reasons (for not responding) are complicating factors we have discussed already. Deciding whether these people would have otherwise responded is academic...but that is the nature of our discourse here. I quite firmly believe that there is but one mechanism for AS, even in non-B27s because they may be B7 CREG or some other similar reactive type. Ebringer did not prove this because the only group he excluded were those with AS who were non-B27; these were so few that he felt he could not get a valid scoring on them (remembering that over half of those with AS and 'non-B27' sent to him were retested and became +B27s). There are several non-B27s at kickas who DO respond favorably to a reduced starch regimen.

The seeming inconsistency relates to the way the question is asked: Does everybody respond the same to the NSD? NO. Does that prove that there is more than one mechanism for AS? NO. None of us got sick overnight, and to expect a rapid climb backwards down the spiral ladder that got us into this mess in the first place is unrealistic; many do not have the patience to persevere.

We focus on Ebringer because he is the guy who figured it out, but others have (as mentioned before) previously had the observational capacity to ferret out the cause of AS (the Giraud Campbell work, especially) and that cause was related to starch intake. And in that particular case was not even limited to AS, but Campbell included RA and OA in his observations and X-rays to prove it--before 1980.

And today we are still stuck with the Kelloggs fools pyramid with grains so pervasive that most of us, from time-to-time will give in to temptation. The difference is that we will know what caused the flare, and can figure out how to extinguish the volcano.

Health,
John

A punk stopped me on the street and said: "You got a light Mack?"

I quite firmly believe that there is but one mechanism for AS, even in non-B27s because they may be B7 CREG or some other similar reactive type.

I'm glad you mention this and that it got some space in the Ebringer papers i read recently. I've always believed the cross-reactivity could show up for B27- people as the symptoms are still so very similar. I can think of half a dozen people on KAS who may benefit from a B7 check - it may help them feel more like a typical AS sufferer, not wishing to evangelize NSD to them of course...

Ted

Whoah Ted, if Wally has *anything* about him he'll be fully aware of the B27 sub-types that are quite openly under research at the moment...and the rest *tsk*

Don't buy into it fella!!!

Let him get on with it!!!! LOL

Hi Bilko

You said "The patients were not filtered out, faulty diagnoses were." Earlier you wrote "some of the people in the group who do not respond to diet will have the wrong diagnosis."

That's agreement that there is a group of people currently diagnosed with AS today who do not respond to diet. I am happy to accept this group includes at least those with ''the wrong diagnosis'.

Wally

Hi John

I accept you would get the message across better had I read all the Ebringer papers you sent. When this thread is finished I intend to do so. But if my questions were satisfied by reading his documents the same would not be true of others observing this discussion.

I spoke to a member of the AS rehab group tonight. He has been diagnosed AS for many years. He has previously been on NSAIDs but has stopped taking them and now takes no medication. He exercises a lot. He has not tried NSD /LSD, eats with no restrictions and remains convinced his symptoms are completely unaffected by food. His pain occurs periodically, he said 6 months or so, and he sees no connection whatsoever between this pain and what he eats. He is not opposed to those who support the use of a reduced starch diet. He simply does not see the need in his case.

Of course this is not a scientific study and there is a ‘subjective component’, but it is the type of story which has me, and I gather a lot of other people, wondering.

My 'concerns about filtering' were simply an interpretation of what Bilko wrote which was never challenged by anyone. "Often it is extremely difficult for a clinician to diagnose with the usual criteria, and some of the people in the group who do not respond to diet will have the wrong diagnosis." So did Ebringer include ALL the patients with 'the wrong diagnosis' in his studies?

Surely your approach is to use the results of a carefully controlled study group and apply them to another group with unknown and probably very varied controls.

Consider the range of competence of rheumatologists diagnosing patients with AS. If Ebringer is at the expert end, what is the quality at the other end of the range? Would Ebringer accept all patients from those doctors if some had 'the wrong diagnosis'.

Isn’t it a bit like one of the those competitions where you don’t have to choose the most beautiful but the one everyone else thinks is the most beautiful. For Ebringer’s studies to cover the full range of those diagnosed with AS today he would have to include the worst cases of mis-diagnosis by the most incompetent rheumatologist. Can you be sure he did? Because if he didn’t, the ones he left out could be the ones who don’t respond to diet. Perhaps the patient I spoke to tonight is one of them.

Wally