Comment:

(The following is an abstract of a scientific paper.  Feel free to skim-read!)

Gut microbiota has been implicated as a pivotal contributing factor in diet-related obesity; however, its role in development of disease phenotypes in human genetic obesity such as Prader–Willi syndrome (PWS) remains elusive. In this hospitalized intervention trial with PWS (n = 17) and simple obesity (n = 21) children, a diet rich in non-digestible carbohydrates induced significant weight loss and concomitant structural changes of the gut microbiota together with reduction of serum antigen load and alleviation of inflammation. Co-abundance network analysis of 161 prevalent bacterial draft genomes assembled directly from metagenomic datasets showed relative increase of functional genome groups for acetate production from carbohydrates fermentation. NMR-based metabolomic profiling of urine showed diet-induced overall changes of host metabotypes and identified significantly reduced trimethylamine N-oxide and indoxyl sulfate, host-bacteria co-metabolites known to induce metabolic deteriorations. Specific bacterial genomes that were correlated with urine levels of these detrimental co-metabolites were found to encode enzyme genes for production of their precursors by fermentation of choline or tryptophan in the gut. When transplanted into germ-free mice, the pre-intervention gut microbiota induced higher inflammation and larger adipocytes compared with the post-intervention microbiota from the same volunteer. Our multi-omics-based systems analysis indicates a significant etiological contribution of dysbiotic gut microbiota to both genetic and simple obesity in children, implicating a potentially effective target for alleviation.

 

Source:  

eBiomedicine, August 2015, Volume 2, Issue 8, Pages 968–984 (http://www.ebiomedicine.com/article/S2352-3964(15)30064-5/fulltext)

 

My thoughts:

I might have a four-year undergraduate degree in the biologcal sciences, but it makes my head spin, reading through papers like these.  There are some very clever people out there.

For the layman,  these findings are of course a bridge too far (in fact, several bridges).

For those in between, and that is where I see myself, the fun is to extract the practical takeaways, the So-whats? .    The last line of this paper gets close:  ‘Dietary modulation of gut microbiota may become a promising strategy for being integrated into the management of metabolic diseases. ‘

But even that needs unpacking:  The food that we eat affects which bugs thrive in our gut, and that ‘mix’ affects our health, because the bad bugs produce toxins that cause inflammation.   If we want a ‘healthier structure’, we need in particular to eat more indigestible carbs.

The diet  used in this trial included ‘whole grains, traditional Chinese medicinal foods, and prebiotics’, plus ‘appropriate amounts of vegetables, fruits and nuts ‘.  For starters  I’d suggest that home-made organic sauerkraut become a staple.

And meanwhile I know that there are world-class Australian gastroenterologists who continue to dismiss the significance of diet in disease.  But then that is not where they have been trained to look.

Let the learning journey continue!