Poop swaps, insulin resistance, and Resistant Starch

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!

— Heisenbug

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14 thoughts on “Poop swaps, insulin resistance, and Resistant Starch

    • Well, two things:

      1) Six weeks probably isn’t enough time to completely shift one’s microbiota one way or the other.

      2) We can’t say that diet alone led to their initial microbiota. Antibiotics and other environmental exposures/behaviors could conceivably have contributed to it.

  1. Another great post. I remember when I first was exposed to the germ theory of obesity (that some unknown and communicable pathogen caused obesity). It must have been 8 or 10 years ago. It seems to have faded since then because I’ve not heard about it much more over the years, and certainly have not seen anything on it within the last 2-4 years (not that I’m on the cutting edge of any new science; more the cutting edge of science news). Now, I’m beginning to think maybe it was valid after all, and ironically the “germs” are hiding in plain sight.

      • Now that you mention it, I _do_ remember seeing that one. I have no idea from where. Amazing that didn’t make a bigger splash. I’m starting to agree with you (well, I think this is your position 🙂 ) that RS therapy for a lot of people is, as likely as not, “simply” crowding out pathogenic bacteria with more symbiotic species.

        Sometimes I wonder in 20-40 yrs time will folks look back at us, with our statins, insulin pumps, and bariatric surgery, like we look back at 19th century doctors, with their mercury, leeches, and lobotomies.

      • Oh… and yeah, I think that Nature article sort of proves your point, RE: “Why aren’t we talking more about this?!”

  2. Good post. I am having trouble reconciling their conclusions: “In conclusion, our data point toward a regulating role for butyrate derived from gut microbial metabolism leading to an improvement in insulin sensitivity.” with one of their findings: “Also, fecal short-chain fatty acids decreased after allogenic gut microbiota infusion (median acetate from 49.5 to 37.6; P .05; butyrate, from 14.1 to 8.9; P .05; and propionate, from 18.2 to 16.3 mmol/kg feces; ns) compared with nonsignificant changes in the autologous group” Any thoughts?
    Thanks.

    • Fecal SCFA is just a measurement of how much is excreted, not produced. This just means less was excreted, and probably more taken up by epithelium. Fecal SCFA says little about concentration and production in the intestine. Usually just a reflection of absorption efficiency and fecal rate of transit.

    • I started a group on FB today for healing metabolic issues via diet and bacteriotherapy and already it’s gathering momentum. I’d appreciate it if each of you here would join us. These are such exciting times. Collectively, we’re all on the verge of figuring out the triggers and therapies for so many inflammatory conditions, from a science standpoint, but also in terms of our self-treatments, such as FMT, dietary changes, probiotics and nutritional support.

      https://www.facebook.com/groups/HealDiabetes/

      Mainstream medical Drs will join the party eventually, but for now it’s up to us. Come one, come all. 🙂

  3. Very interesting post. Thanks. I have read several studies which show that Butyrate affects metabolism and kicks it up to higher gear. But how? Does it somehow increase adiponectin? Did the obese subjects in the transplant study loose weight? Or was it just insulin sensitivity was increased without weight loss?

    There is also an interesting link to histamine in the gut, and inflammation. If you have low DAO enzyme production from endolithium, either from genetic cause or acquired gut disregulation, then histadine in foods does not fully break down as normal and you can get high histamine. The higher histamine levels may shift the microbiota in one direction or another. Low DAO is associated with IBS, Chrons, and Colitis. and there are known imbalances in microbiota in those conditions as well.

    The FDA needs to be moved in the US to approve fecal transplants for more than just C-Diff infections. There are groups online which promote a DIY approach here, desperate people not helped by conventional medicine. Google: The Power of Poop you will find their site. Many have reversed their IBS completely. It would be interesting to survey them to see if any insulin resistance was ameliorated.

    If the FDA will expand the fecal transplant authorization a non-profit must be started to facilitate. There are so many cures we do not have because the “cure” is of natural origin and non-patentable. They know with great certainty that adiponectin fixes insulin resistance and is low in diabetics. It is high molecular weight so no transdermal, and oral delivery has been difficult. But we have injectable insulin. why not injectable adiponectin? because it would kill off all of the insulin drugs.

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