Posted by Trotter on December 30, 2012, at 23:27:27
In reply to Re: Bifidobacteria reduce depression » Trotter, posted by rca on December 30, 2012, at 11:11:29
I've spent a bit of time analysing the two studies you referenced. It has challenged my understanding of endotoxemia. Here are some of my observations.
It seems likely the endotoxemia measured in the Ghanim study was due to LPS translocation within the small bowel.
The researchers believe the LPS came primarily from the food due to the relatively small numbers of resident bacteria in the small bowel. I'm still not 100% convinced of this, but I concede it is likely.
There was around 3x increase in plasma endotoxins after the HFHC meal, compared to the AHA meal. I think this is likely explained by three factors. Firsly, the HFHC meal had a higher fat content. Secondly, orange juice (in the AHA meal) has been shown to reduce translocation of LPS. Thirdly, the higher fibre in the AHA meal may have absorbed some of the fat.
According to the reseachers, both meals had similar LPS in spite of the fact one was vegetarian and the other meat/egg based.
In the Erridge study, the main foodstuffs linked to possible increased endotoxemia were ice cream, chocolate, turkey and pork. I agree that all these foodstuffs come from milk or meat, however other meats like beef, lamb and chicken had negligible LPS. So, yes, plant foods may have low LPS, but most animal foods were low as well.
This has been an eye opener for me. Thank you for the references.
I'm not sure how this research ties in with the high fat diet rodent studies. In these two studies (linked below) a high fat diet caused endotoxemia. However in both the endotoxemia was completely avoided by increasing bifidobacteria. In the first via feeding a prebiotic, and the second by directly feeding probiotic bifidobacteria. In the OFS fed mice, presumably the increase in bifidobacteria occured primarily in the large bowel. Bifidobacteria are anaerobic so very few exist in the small bowel. This suggests the bifidobacteria reduced translocation of LPS in the large bowel. This suggest to me two different models of endoxemia. One that occurs in the hours following a high fat meal (in the small bowel), and another that occurs in the large bowel.
http://www.ncbi.nlm.nih.gov/pubmed/17823788
http://www.ncbi.nlm.nih.gov/pubmed/21685239I find it all rather confusing. I tend to think the small bowel endotoxemia may involve ingested LPS, whereas I think the large bowel endotoxemia involves resident bacteria. Which is more important? I suspect the latter. I base this on the fact that increasing bifidobacteria was able to reverse high fat induced endotoxemia.
Here are a few other studies I found interesting regarding bifidobacteria, intestinal permeability and endotoxemia.
http://www.medbc.com/annals/review/vol_10/num_1/text/vol10n1p45.htm
http://www.ncbi.nlm.nih.gov/pubmed/16773690
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2702831/
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