Helicobacter and glucose

Helicobacter is a bad bug. Really bad. So bad that in the recent consensus conferences, like this one, the plan is clear. Hunt, find, kill. Sounds like the cholesterol consensus to me. The only good cholesterol molecule is a dead cholesterol molecule. Oops, getting a bit random there. Back to reality:

"The consensus conference boldly recommended population-based screening and treatment for H. pylori in particularly high-risk population settings"

Anyway, some time around 60,000 years ago humans walked out of Africa in to what is now the Middle East and kept going. Taking their Helicobacter pylori with them. Yes, H pylori has been around the human gut for a long time. There is a nice neat diagram and discussion of human/helicobacter co-expansion on this person's blog. The basic idea is that you can get some idea of the spread of humans by looking at the genes of their H pylori. Presumably the hunter-gatherers were dying like flies from gastric carcinoma along the way.

So, the consensus plan is to eliminate a bug which has been with us on a timescale of up to 100,000 years, and this will stop gastric cancer. Truly a bold recommendation.

If you go back to the early accounts of the missionary hospitals tending to native populations before the introduction of Western lifestyles, cancer was very very very rare. Stefansson summarises it rather well in his 1960 book Cancer: Disease of Civilisation. It's hard to get hold of a copy and rather expensive too, but it makes an interesting read. Cancer searches came back negative. I'm willing to accept that H. pylori wasn't causing cancer in human hunter gatherers, although they were all "infected", if that's the right word for a gastric commensal.

So why does helicobacter cause cancer in humans nowadays? Some light was shed on the problem by the Japanese who noticed that elevated fasting plasma glucose levels are associated with gastric cancer, but only in those patients who carry helicobacter.

Helicobacter is quite a specialised bug. This paper has some interesting snippets. H pylori appears to love glucose. It will do both aerobic and anaerobic metabolism with it, but look at this:

"Under aerobic conditions acetate was the major oxidation product from pyruvate; no evidence was obtained for tricarboxylic acid cycle activity"

H. pylori doesn't appear to use the tricaboxylic acid cycle! Certainly not in this set up. Pyruvate is converted to acetate without acetyl CoA entering the TCA. This looks to me as if fermentation might be producing the bulk of its ATP. In fact if you look further you find that helicobacter does actually run a TCA cycle of sorts, but it runs it in reverse, and it's non cyclical and it runs as a reducing system, non oxidative... I'm not sure how much this set up could do with a fatty acid! I get the impression that glucose might just be the preferred fuel...

Back in the big world there is a mass of anecdotal evidence that LC eating "sorts out" many cases of dyspepsia. I can't find any specific studies since Yudkin's open cross over diet trial detailed in chapter 12 of Pure, White and Deadly, where LC eating worked for many, but not all, dyspepsia patients.

I think it's a reasonable speculation that anything which increases blood glucose might just encourage helicobacter to have a field day and do some cancer generating. Dropping blood glucose might just do the opposite. Actually, maybe just eating the glucose non-stop is a bad idea! Certainly a LC diet might have a better long term outcome for those people currently dependent on ranitidine or omeprazole for control of the extremely unpleasant effects of dyspepsia.

Or of course we could just kill all the Helicobacter pylori in people at risk of gastric cancer, and stop them ever getting infected again. That's the consensus.

Ha ha ha.

Peter