File this under: “Why aren’t we talking more about this?!”
An experiment out of the Netherlands. Title says it all: Transfer of Intestinal Microbiota From Lean Donors Increases Insulin Sensitivity in Individuals With Metabolic Syndrome.
They took 18 obese men exhibiting metabolic syndrome and gave them fecal transplants (if you aren’t familiar with what that is, well, it’s exactly what it sounds like — completely replaces your microbiota with that of a donor). HALF of the obese men received a transplant from a lean, healthy donor. The other half, however, was a control — they simply had their own microbiota reimplanted.
One of the study’s findings, even before the experiment was carried out, is pretty interesting. They found that the obese men had less overall microbial diversity, more bacteroidetes, and significantly less bacteria from Clostridia cluster XIVa. You should be familiar with cluster XIVa by now — they were the superstars of this post.
But on to the experiment. The control group? No changes in insulin sensitivity. The group receiving transplants from lean donors? Insulin sensitivity significantly increased. But you already knew that would happen within the first few seconds of reading this. The juicier part is WHY and HOW, right?
Well, in observing the differences between the lean-donor recipients and the self-donor recipients, they found a few things: lean-donor recipients had more overall diversity. But in terms of specific changes in microbiota, what stood out most was a 2.5 fold increase in the abundance of R. intestinalis. Again, R. intestinalis is one of two major butyrate-producing Clostridia XIVa species that I suspected may be at play in the Resistant Starch experiment.
They also found an increase in E. halli, another major butyrate producer in Clostridia XIVa. E. halli is significant for another reason, however: E. halli is a major utilizer of lactate from bifidobacteria. It feeds on lactate produced by other bacteria and produces butyrate from it. In studies of bifidobacteria cross feeding mechanisms, E. halli seems to be a commonly cited cross feeder. If bifidobacteria and its cross feeding effects are at the root of Resistant Starch’s effects (which I explored here), then E. halli is likely to be a part of that equation.
This study lays it all out pretty well:
However, when two E. hallii strains and one A. caccae strain were grown in separate cocultures with a starch-utilizing Bifidobacterium adolescentis isolate, with starch as the carbohydrate energy source, the L-lactate produced by B. adolescentis became undetectable and butyrate was formed. Such cross-feeding may help to explain the reported butyrogenic effect of certain dietary substrates, including resistant starch.
And via this, I now see that R. Intestinalis is also a bifidobacteria cross feeder. It requires acetate from bifidobacteria to do its thing.
The “Resistant Starch –> Bifidobacteria –> Clostridia XIVa –> Butyrate” hypothesis is beginning to gain steam.
But anyway, this transplant study didn’t have anything to say about bifidobacteria or Resistant Starch. Its conclusion was pretty straightforward — that increased butyrate production in the lean-donor recipients was likely the reason that insulin sensitivity was regained:
In conclusion, our data point toward a regulating role for butyrate derived from gut microbial metabolism leading to an improvement in insulin sensitivity.
Oh, and to address the initial question — why aren’t we talking about this more? — well that’s actually kind of obvious, isn’t it?
1) Poop transplants probably don’t represent a major new revenue stream for any particular profession, industry, or company. It’s a pretty simple, low tech procedure.
2) In fact, it may represent a financial loss. For two reasons: a) It isn’t as profitable as other treatments for metabolic syndrome — drugs, devices, surgeries; and b) curing a disease — as opposed to ongoing treatment — is sort of a financial dead-end, isn’t it?
3) It’s icky.
What a world!