HLA-B27 some more

Well, there have been a few interesting developments in the last few days. The most interesting was being invited to lunch by Prof Ebringer. That was a very long conversation and has produced a stack of papers to read and a whole lot of ideas, plus a Drs appointment for myself to see if I can get HLA-B27 tested on the NHS. At £209 per test privately, I'm rather hoping to get my GP to fund this even if I have to offer a decent bottle of wine to cover the £20 odd it costs the practice!

The HLA-B27 discussion was very interesting. Apparently the allele is very common among the Eskimo and their descendants and very rare in people from equatorial regions. This fits nicely with the carnivorous HG in temperate or extreme climates vs more starch based gathering in the tropics. By a quirk of migration the gene is also very rare in Japan, but even there the link with ankylosing spondylitis is strong.

A medic, Dr Tani, working in Japan, was looking to publish a paper on AS and approached the Kings College group to get the Klebsiella antibody titres done. Prof Ebringer suggested sending the samples coded, plus some controls and some RA samples thrown in. This is the paper which came out of the collaboration.

The Kings College group did the same with a set of coded Dutch samples, written up here. Interestingly, two other labs failed to get the same result, using the same samples. But if Ebringer can get consistent results on both the Japanes and Dutch samples, I tend to think his group is quite good at immunology.

Obviously the AS hypothesis generates the starch avoidance protocol which seems to be in fairly widespread use in places like the KickAS site. The proof of the pudding is in the eating ie, do patients get better on a behaviour based on a hypothesis. If so that seems to support the hypothesis to me...

I think it is worth noting that AS primarily involves an IgA antibody, which suggests exposure to the trigger across a mucosal surface, typically the gut. Rheumatoid disease involves an IgG response and suggests a non surface immune response, in this case classically through a low grade chronic urinary infection. This gives a simple explanation for the response seen to minocycline and doxycycline in RA patients. Of course without antibiotics (or with them) you might approach starving the proteus which triggers RA by using a dilute urine approach (the proteus bug derives energy by splitting urea in the urinary tract) and possibly eating a low protein diet might well help too. It's worth noting that the true Optimal Diet is actually rather low in protein at around 40-50g/d, once you are well established on the diet. By eating the minimum amount necessary of the highest quality protein you produce the least quantity of waste, ie urea, which is better known as proteus fodder. I'm not down at this level of protein intake but it's another option for fighting RA. I guess getting your immune system back by dumping sugar would potentially get rid of the proteus bugs completely... There's an interesting study.

Of course we spent a lot of time talking about BSE, scrapie, CJD, vCJD and MS. There is probably a book could be written here so I'll stop until I think I understand it a bit better and have had chance to tease out a few of the more problematic features of both the prion hypothesis and the auto immune hypothesis...

Peter