Kickas.org Forums Treatments, Drugs and Alternatives NSD and diet-related; diet and sulfasalazine??

A friend of my mom's asked why so many problems with the kids i grew up with: 3 have RA, 1 psa, me with prob. AS, plus others with hashimoto's, ms, lupus and the like. Auto-immune seems rampant - leads me to think environmental trigger, and definitely bad diets; mc

I tried sulfasalazine while doing low to no starch, in the beginning my stiffness got much worse; went off of it and enjoyed 2 weeks drug-free, pain-killers and all, so went back on it but ended up off. so i guess i can't really answer the question, but i'd try the fish oil first.

Hi David,

I must admit I was extremely hopeful when I read the Road Back website and desperately wanted minocycline to work. It was helpful that my rheumy had recommended I try it before trying methotrexate, which I was very resistant to at the time.

As I have been a celiac for so many years, my starch intake is fairly low. I ate quite a bit of rice for a few years but rarely eat that now. Primitive hunter/gatherers still consumed a certain amount of starch - there were plenty of roots, nuts, seeds and other foods that contain starch, just not in the same quantities as the modern grain-based diet.

If grain consumption contributed to my RA I would be surprised given that I had followed a strict celiac diet for at least 15 years before the onset of the RA.

I'm also interested in the ideas of Gabor Maté and others that early childhood trauma interferes with the healthy development of our immune systems and sets the stage for the immune system to malfunction later in life.

So it seems to me we have several key factors interacting here:

genetics
environmental triggers - dietary or other
immune system development or damage

... and there are probably more... lifestyle issues such as stress, medication use, nutrition etc.

Hi, Wendy:

Ebringer is fairly confident that RA is the result of an occlusive Proteus UTI. It is not the result of a grain-based diet but Mercola rails against grains for all arthritides. Ebringer's suggestions initially included something he called the Oslo diet but that is basically fish oil and he recommends averaging 1oz/hour grape or cranberry juice, but it is getting rid of the initial infection that is most important. I have been told that it takes 2g daily Cipro to knock this one out, so I'm reluctant to suggest this as treatment without first consulting a physician.

HEALTH,
John

Thanks John. That's new information for me that I'll follow up on.

Hi Wendy and John
I found a reference implicating Proteus mirabilis as a causative agent of RA. One important thing is that they suggested that the Proteus mirabilis was causing an 'infection' in the uppper respiratory tract. The URT has a very diverse bacterial flora in a fashion akin to the gut. I say 'infection' because to extend the argument the Proteus might in most people be considered 'normal' and not illicit a response. But RA patients are known to have a number of genetic predispositions, one of them HLA DR1 and HLA DR4 polymorphisms, and this may drive a dysregulated immune response that ultimately culminates in RA. Eliminating Pm from URT might be a similarly difficult task as elimlinating Kp from the gut, if indeed you firstly accept that Pm can cause RA or that Kp can cause AS.

Cheers David

Hi David,

As a result of John's interesting information, I'm busy researching proteus mirabilis now. It looks as though elimination of this particular bacteria would require an antibiotic regime.

Hi Wendy,
I should have added that in the thousands of throat swabs and sputums I've cultured it is very rare to get any Proteus mirabils. Even at low levels it is obvious because of it's tendency to swarm on blood agar.
Pm has a fairly standard sensitivity pattern. Stragely one of the antibiotics that Pm is always resistant to is Tetracycline (and hence Minocycline). Ironically Tetacycline was the drug of choice for Dr Brown's attack on the Mycoplasma!

Hi David,

If Pm is implicated in my RA, that would help to explain why minocycline made no difference for me. However, I haven't had a known UTI since my early 20s (and I'm in my 50s now). However, I have monthly urine tests as part of the monitoring of mtx so I might ask my doc if they'll check it for Pm seeing as they've already got a sample!

Hi Wendy,
Dr Erbringer was suggesting a sub-clincial UTI.
So probably that would mean a lowish white cell count and low numbers of Pm in a urine sample. In Urine culture we are only looking for overwhelming growth of a bacterial species and it is common to get low numbers of skin flora - which are ignored with a comment such as "No significant growth"
Microbiology (at the level of the lab bench)is as much art as science!
It's a 'profession' I suppose like many that are undervalued in terms of respect and remuneration. All the glory and remuneration goes to the doctor - who in many cases only has to do the bleeding obvious to make a diagnosis.

But I'm not bitter, who needs the stress!
Cheers David

PS Minocycline was probably never acting as an antibiotic in RA - more a DMARD through its inhibition of MM3.

Hey David,
In our lab,we work up > or = to 10 colonies of gram negative rods.We don't have to have an overwheliming amount.I guess all the labs are different.
Now with what you are saying,would there be less than 10 colonies in RA?
Just curious.I don't usually see Proteus that much in such low amounts in the urine.
We don't use the "No significant growth" comment either.We have "Mixed flora" which is usually coag negative staph,diphtheroids,etc.
And "No growth",which I thought was kinda funny because they have us say "mixed" even if it is one type of "normal flora"

Shauna