Discussion in 'Other Health News and Research' started by leela, Oct 12, 2014.
Molecular Origins Of Eating Disorders Found In Gut Microbe | Neomatica
Few comments from me
This is about 'molecular mimicry': the idea is that a gut microbiome bacteria, E coli K12, by sheer bad luck produces a protein (ClpB) that looks very much like alpha-MSH, a human protein that helps regulate our feeding and energy levels.The anit-ClpB antibodies aimed against the bacteria take out the human alpha-MSH protein as collateral damage. And in this study, patients with more severe eating disorders have higher levels of this damaging antibody (reacting against both the bacterial ClpB protein and the human alpha-MSH one).
So far, so good. Some of the findings, however, are not so clear cut.
Some of the research was done on mice, and giving mice alpha-MSH causes anorexia (weight loss/reduced eating) as expected. Mice given the E. coli strain that makes ClpB produce antibodies against ClpB and alpha-MSH, again as expected. And these mice are immune to the effect of alpha-MSH therapy - presumably because their anti-ClpB antibodies take out the injected alpha-MSH, blocking its biological effect.
So the model is that the E coli strain plays a role in eating disorders by inadvertently taking out natural alpha-MSH, which normally leads to feeling full/ induces anorexia.
BUT, when the researchers gave mice the E coli bacteria, the mice initally lost weight (as you'd predict) but then surprisingly (at least to me) gained weight, by 5%. This suggests something more complicated is going on:
I'd be interested in @Jonathan Edwards take on this, as I think he is sceptical of the evidence for molecular mimicry.
Haven't read the article, but my understanding is that people suffering from anorexia nervosa are actually hungry all the time and obsessed by food. (At least some of them.)
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