Multiple Sclerosis and Hydrogen

Thanks to Stephan for getting me re started on this post. Hydrogen matters.

I've been interested in diet and MS for some time. JK has apparently treated a small number of patients and Barry Groves has an interesting section on Second Opinions, mostly discussing a small series of 15 patients treated by Dr Lutz, plus a lady who put her MS in to remission by following the dietary advice in Eat Fat Get Thin.

Lutz is very interesting and cautions against aggressive, sudden onset LC nutrition in this disease as there can be a severe flare. He also mentions this phenomenon in a number of (non MS) sections of Life Without Bread. Being a medic he has the facility to use corticosteroids under these circumstances and did so as needed. There is probably a whole post related to this idea, but I think it holds water.

Anyway, MS appears to be manageable using diet. I'm going to try and look at some of the aspects as to why, though there seem to be several related ways of developing MS, which complicates matters. Intestinal dysbiosis and hydrogen production are probably crucial to development and offer some plausible mechanism for achieveing remission.

As we all know, helicobacter gastritis is facilitated by hydrogen gas produced from carbohydrate fermentation in the colon (or the small intestine if you have adequate dysbiosis). Interestingly helicobacter appears quite happy to colonise both your respiratory system and the calculus on your teeth, presumably given enough hydrogen. The authors of the paper which looked at the role of hydrogen speculated that other infections, particularly of the respiratory tract, might also be facilitated by access to hydrogen.

One other bacterium which appears to be extremely fond of hydrogen is acinetobacter. In its free living guise, just look where you can find it. All you have to do is to give some legumes the equivalent of intestinal dysbiosis by modifying their nitrogen fixing bacteria to "excrete" hydrogen, plant them in a field and there are the acinetobacter, eating it up.

Acinetobacter bacteria are ubiquitous in soil, as commensals on skin/ mucous membranes and as pathogens. The pathogenic species love the respiratory system of critically ill patients and have an initial preference for the sinuses before generalising in to the lungs, blood stream and mortuary.

Respiratory infection, especially sinusitis, has a very long and respectable association with MS. This paper gives the picture:

"MS and chronic sinus infection were also significantly associated in the timing of attacks, in the age at which patients suffered their attacks, and in the seasonal pattern of attacks"

The p value for the association was p<0.0001, quite impressive provided you remember it's an association in a retrospective observational study, not an intervention trial.

I am interested in Prof Ebringer's work on MS and acinetobacter. Prof Ebringer has a systematic technique for seeking out peptides in bacterial proteins which might reasonably be associated with auto immune diseases in humans. Obviously, for MS, you are looking for amino acid sequences in bacterial proteins which resemble a protein in myelin, the one which is targeted for attack by the immune system to give MS. Plus a few other neurological protein targets.

Acinetobacter has such peptide sequences in several rather obscure sounding enzymes. The next question is whether patients with MS have elevated antibodies to acinetobacter bacteria. Yes, they do and they also have elevated antibody counts against synthetic peptides identical to those putative trigger sequences too.

So where does that leave diet? I'm not a great enthusiast for using antibiotics for treating chronic recurrent sinusitis. Drugs are great for acute life threatening problems, or even for acute onset severe sinusitis. Guessing the correct one is part of my job. But bacteria like acinetobacter and its close relative pseudomonas (which shares similar myelin resembling peptides) simply laugh at the pharmaceutical industry's offerings. No, reducing the pathogenicity of these bacteria requires manipulation of their environment.

As an aside on pseudomonas, I was a student in Camden Town just after the IRA bombed the Tower of London in 1974. The many burns patients from this particular episode (which made you quite uncomfortable walking past litter bins in central London) were successfully treated for potentially lethal pseudomonas infections using the vinegar and hair drier technique mentioned above, when all of the antibiotics available at the time were useless. This was cutting edge for our pharmacology lecturers and it certainly taught me something about bacteria.

Back to acinetobacter and respiratory infection. I still get colds. So do my wife and son. LC friends do too. But the chronic persistent gunky nasal discharge, chronic sinusitis or persistent cough (for weeks or even months for some) that used to be a routine sequel to colds are a thing of the past. Respiratory bacteria live in an oxygen rich environment. Hydrogen, as noted by Stephan, Kwasniewski and NASA, is a very high energy molecule in the presence of oxygen. It can power a respiratory infection just as well as it can power an Apollo rocket. No hydrogen means no fuel.

Acinetobacter live everywhere. Having them in your nose is common. We've probably always had them. Converting that balance to a chronic purulent sinus infection is arriving in the modern world.

Getting rid of sinusitis strikes me as one route to removing the most likely trigger factors for MS. Marked reduction of hydrogen production from gut dysbiosis is probably essential to this. That means minimal fibre, minimal fructose, minimal gluten, minimal flatulence. Anything else we can do to normalise our immune function after that will probably help too.

But for someone with MS and a weakness for baked beans, hmmmmmm......

Peter