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

Is this why smoking is the number one predictor of heart disease?


Smoking is the number one predictor of heart disease. It’s surprising how little known that fact is. Perhaps it’s because the usual dietary whipping boys — saturated fat & meat consumption — have sucked all the oxygen out of the room. (It’s also pretty amazing that, because there’s so little public reporting of this fact, the best I could find was a report about IQ being the number two predictor. I guess smoking taking the top spot doesn’t make for a sexy or quirky enough headline.)

With that said, here’s a fascinating study showing that gut flora shifts dramatically after a person quits smoking. The punch line:

Profound shifts in the microbial composition after smoking cessation were observed with an increase of Firmicutes and Actinobacteria and a lower proportion of Bacteroidetes and Proteobacteria on the phylum level. In addition, after smoking cessation there was an increase in microbial diversity.

While the study doesn’t say this, I think it’s reasonable to assume that smoking itself causes an initial shift in gut flora. And perhaps the cessation of smoking is a (at least partial) reversal of that shift. But that second part is a little more speculative.

As I touched on just a little bit in my last post on bifidobacteria, there’s a growing amount of interest and research into endotoxemia (driven by a permeable gut and overgrowth of gram negative bacteria) as a cause of inflammation and chronic disease. If the gut is linked to the diseases of modern civilization, endotoxemia is a major suspect as a mechanism. And if that bears out, well, this study gives us a possible glimpse into how smoking might just cause or contribute to that mechanism.

Of course, this study doesn’t go into that. In fact, the little extrapolation the study does engage in, it really sort of misses the mark. The study authors seem to focus mostly on the firmicute/bacteroidetes ratio and its shaky, not-so-established link to obesity. As I documented in this post, American Gut project founder Jeff Leach has reported that the project found no such link, and that the ratio was not correlated to BMI. And other studies have found the same.

What’m more interesting to me — which the study doesn’t get into at all — is the other ratio: Actinobacteria to Proteobacteria. If the microbiome was an old Western flick, these two phyla are about as close to a good guys/bad guys pairing as we’ll get. Here’s Jeff Leach interpreting the results of an NPR writer’s gut sequencing:

Proteobacteria includes “a lot of your bad guys,” Leach said, such as E. coli and salmonella. They are associated with inflammation that may increase the risk of heart disease, cancer and other health problems.

Leach has no proteobacteria.

And at the bottom of my bar, Leach saw something else: I have very low levels of another species called actinobacteria.

“Those are typically considered good bacteria,” Leach said. “So the more actinobacteria you have, the better.” They’re helpful, Leach said. “They’re anti-inflammatory. They’re known to suppress proteobacteria. So, those are often known as probiotics.”

Proteobacteria: bad guys. Increases the risk of heart disease. All gram-negative, endotoxin producers. Actinobacteria: good guys. Includes our beloved, junction-tightening bifidobacteria (the wonders of which I wrote about in my last post). Stop smoking and the former go down, the latter go up. Pretty reasonable to think that maybe picking up the smoking habit does the reverse of this. You know, the habit that we already know is the number one predictor of heart disease. And yet the study wants to geek out on some non-existent firmicute-obesity link. Weird.

But if that’s not enough for you, here’s a 2011 paper that takes a look at the current available knowledge on sources of persistent, low-grade endotoxemia — the kind that could cause persistent, low grade inflammation that’s strongly associated with the development of chronic disease. In its review of endotoxin sources, it kicks things off with none other than smoking. But what’s interesting is that it seems cigarettes are a direct source of endotoxin-producing bacteria:

For instance, a study in 2009 performed a microarray analysis on non-smoked cigarette samples and led to the identification of several Gram negative bacterial genuses, including Clostridium, Klebsiella, and Pseudomonas which were all identified in over 90% of the cigarette samples tested.

And other studies have found that cigarettes can provide a potent dose of endotoxins to a smoker. Whether this direct exposure to endotoxins is in any way related to the bacterial shift that smoking likely causes, who knows?

To conclude: it’s pretty early days in the study of the microbiome’s impact on chronic and metabolic disease. Mirobiome researchers are rightly staying tight-lipped and reserved about what studies like these could mean, hoping to avoid the overselling disaster that befell genome researchers in the past decade. There just isn’t enough to establish any kind of firm causality. So to say that this all constitutes a mechanism whereby smoking causes heart disease, or even that it’s one of several factors in its cause, is pretty premature and speculative. There’s no fire here, yet. Just a lot of…smoke.

So in the meantime, I wouldn’t worry too much about that daily pack of cigarettes. But please do make sure to keep those firmicutes low to keep that waistline in check. And try to avoid saturated fat at all costs, and take an IQ quiz every now and then to keep that score nice and high. Mmk?

— Heisenbug

Was I too hard on Bifidobacteria?



If you recall, my investigation into the Resistant Starch phenomenon began with the assumption that, despite what many believed, bifidogenicity could not explain (at least not entirely) the effects that people were experiencing from Resistant Starch. Why? Because bifidobacteria do not produce butyrate. Because their growth is not particularly stimulated by starch. And because they are vastly outnumbered by other commensal butyrate-producing species that do utilize starch.

But there are good reasons to revisit this assumption.

Reason #1

The gut barrier-enhancing, permeability-reducing effects of bifidobacteria are pretty well-established.

If people are experiencing metabolic improvements from RS, then intestinal permeability reduction is a major suspect as a mediator of these improvements. Why? There is a lot of reason to believe that endotoxemia — when the lipopolysaccharides from gram-negative bacteria spill out from a permeable, “leaky” gut — is what initiates the inflammatory cascade that results in many metabolic disorders (and perhaps many other disorders not often considered to be metabolic….for now).

But up to this point, we’ve been focusing on butyrate as our top gut-enhancing suspect. Butyrate tightens those junctions and seals a gut like no other. But maybe it’s the bifido’s instead?

Reason #2

Relatedly, an increase in bifidobacteria — which are lactic-acid producing bacteria  — has a ph-lowering effect in the gut. Increased acidity leads to a more beneficial environment for gram positive gut commensals (good guys), and a more hostile environment for opportunistic, not-so-beneficial gram negative bacteria. Bacteria that can cause or contribute to a leaky gut. Bacteria who can leak endotoxins and thoroughly ruin your day. This may in fact be a significant contributor to bifidobacteria’s gut barrier-enhancing abilities: the reduction of opportunistic bacteria that may be at the root of intestinal permeability.

Reason #3

Bifidobacteria are a prime cross feeding species with butyrate-producing bacteria. If they aren’t directly reducing intestinal permeability and, by extension, endotoxemia, then they may be part of a larger cross feeding community that leads to increased butyrate production. A link in the chain that leads to a strengthened gut barrier.

Which is a good time to mention: in case I’ve made all of this seem just a little too simple and straightforward, we need to remember that the microbiome is an ecosystem with untold interdependencies. It isn’t as simple as feeding one species a particular substrate, and one species another. In the case of bifidobacteria — who produce lactate and also acetate — we know that certain commensal butyrate producers consume those end products (lactate and acetate) and turn around to produce butyrate. Bifidobacteria also initiate the breakdown of and then release certain fermentable fibers that are then made available to butyrate producers. (More on these two cross feeding mechanisms here.)

Reason #4

Tatertot Tim clearly had a heck of a lot of bifidobacteria in his results. Way above average. So we can’t ignore that. It should be noted that Tim admits to have been consuming yogurt and kefir at the time of sampling, which are most often cultured with bifidobacteria (those who consume probiotics or fermented foods with bifidobacteria show elevated levels of them during consumption, and those levels drop off quickly when consumption ends). So that could be skewing the results. But nevertheless, it’s still a good reason to give the bifido’s a closer look.

Reason #5

I’ve saved the most important reason for last.

“Bifidobacteria are not particularly stimulated by starch.”

Well, that might simply be wrong. It’s a point that both Tim and I seemed to agree on. But I’ve uncovered a study , which seems to be the most thorough study of the bifidogenicity of various common prebiotic fibers in human subjects, that says otherwise. RS (albeit type 3) does quite well. Significantly boosted bifidobacteria in subjects. This study, also done with human subjects, showed significant growth of bifidobacteria on starch (RS 2 and 4), but that results were highly variable among individuals. This study showed similar results, but in mice transplanted with bugs from either Italian human donors or UK human donors. Again, significant bifidobacteria growth. And again, high variability — Italian mice saw much higher bifido growth than UK mice. So again, the flora you start out with seems to matter. (This could explain RS “responders” vs. “non-responders,” but let’s not get ahead of ourselves). And there are a few other animal studies that show the same.

So there’s definitely enough here to reconsider bifidobacteria’s role. The reason I consider this to be the most important reason for reconsidering the role of bifidobacteria in the RS experiment is that for bifidobacteria to be credited with these beneficial effects, this has to be true — RS has to stimulate growth of bifidobacteria.

Well, with just one exception.



If you’ve been following the RS saga, you know that there’s more to the protocol than just the potato starch. Specifically, potato starch is often combined with kefir. Could the answer be that many (most?) RS experimenters regularly combine RS with kefir — a fermented dairy product most often cultured with bifidobacteria? Yogurt, another fermented dairy product often cultured with bifidobacteria, is also a frequent companion to potato starch with RS experimenters. And we can’t forget that, regardless of the protocol, these products are probably regularly consumed by the type of people who would engage in this kind of experiment.

Now I’m not suggesting that this means kefir/yogurt and not RS could be responsible for these metabolic improvements. If so, people would have likely discovered this effect of yogurt/kefir a long time ago. What I am suggesting is that, just maybe, this isn’t a Resistant Starch experiment, but instead a Resistant Starch + Bifidobacteria experiment. An improvised, Do-It-Yourself, synbiotic. How? Bifidobacteria are known to adhere to Resistant Starch granules, delivering them to the colon for digestion. So that’s one way. But perhaps there are other synergies realized when consuming both Resistant Starch and Bifidobacteria.

In short:

If Bifidobacteria are at the root of these effects, then perhaps RS experimenters have simply found a way to greatly enhance the deliverability/viability/effectiveness of exogenous bifidobacteria in their guts, thus allowing bifidobacteria to have those aforementioned gut enhancing, cross feeding effects.

So the question remains: Would Resistant Starch/Potato Starch continue to have positive effects if supplemented without any exogenous, bifidobacteria-cultured foods or probiotics?

If so, then we’d need to see some more gut sequencing results of RS-only supplementers to see if bifidobacteria counts are significantly raised. If they are, then bifido’s are really in the spotlight.

But if not, then RS in the form of potato starch is something entirely different than what we thought — it’s not a super prebiotic fiber with the ability to alter gut flora on its own, but instead a way to supercharge exogenous probiotic therapy.

Which is probably a good time to mention this fun little citizen science project. And here’s the indiegogo page. I truly hope a thousand of these kinds of experiments bloom. But here’s a polite request: maybe isolate the consumption of probiotics/fermented foods to certain participants? That may tell us a little more about where and how those mysterious bifido’s play into all of this.

— Heisenbug

Gut vs. Gut: This is how & why Resistant Starch is working.


You may recall in my inaugural post that I took a deeper dive into the American Gut results of Tatertot Tim, the internet’s fiercest promoter of the benefits of Resistant Starch. In particular, I compared his results to Michael Pollan’s gut makeup as a way to postulate some theories about what we know and don’t know — particularly with regard to the optimality of Resistant Starch compared to other fermentable fibers. I concluded the post by saying that it’s all just a little too speculative to say that Pollan’s high firmicutes are a result of eating lots of fermentable plant food, and that just looking at phylum-level results wasn’t going to provide us with anything conclusive. Well, I think I’ve come upon something a little more useful.

Below, you’ll see the gut sequencing results of none other than American Gut founder Jeff Leach himself.


This is significant for a few reasons. First, Jeff is an admitted Paleo-ish eater — very little grain consumption, and moderate-to-high protein & fat. No restriction on other starchy carbs as far as I can tell. And I assume he steers clear of the usual junk (n6 oils, high fructose, etc.). This is quite close to Paul Jaminet’s Perfect Health Diet, a very popular Paleo diet variant. Well it turns out Tatertot, too, is not only Paleo, but a follower of Jaminet’s PHD. So this already makes for a great comparison. With Pollan, there are too many potential confounding factors to account for — a clean, whole foods-eating omnivore, but certainly a lot of grain consumption (with the Prevotella to show for it), and perhaps lower-than-average meat/fat consumption. Just too many unknowns.

But here is where it gets really interesting and makes this a worthwhile comparison: the one significant area where Jeff differs from Tim — and from the vast majority of people — is his obsessive focus on consuming a high and diverse load of fermentable fiber from plant foods that feed gut bacteria. Jeff professes to aim for consuming 20 to 30 species of plants a week, and claims to get up to 100g of fiber per day. He eats onions, garlic, and leeks every day — foods with a high amount of fermentable fructooligosaccharides, including scFOS. If we’re looking for the gut sequencing results of a person committed to bulletproofing his/her gut microbiome, Jeff’s are as close to a gold standard as we’ll get.

So here, again, are Tim’s results:


When we make the comparison between Jeff’s and Tim’s gut results, what do we see? There it is again, firmicutes and bacteroidetes, totally opposite ratios. Tim is all orange. Jeff is all red. Even more lopsided than when compared to Pollan. And what accounts for that? I could tell you, but why don’t I just let Jeff speak for himself. Here’s how he explains his results in a Facebook comment on the American Gut facebook page, after someone questions whether his high firmicute count is a concern because of past studies showing links to obesity:

the “firmi = obesity” doesn’t really hold up anymore. in the human microbiome project – which looked at 250 healthy and normal weight folks – ppl fell along a continuum – some were 80% firmicutes, others were 20%. we see the same thing in american gut. my firmicutes are high due to high levels of members of the family of ruminococcaceae – lots of fiber fermenters in that group.

There you have it. His high firmicutes are a direct result of eating plant foods that stimulate fiber-eating bacteria. From the expert himself. I’ll also add that in addition to Ruminococcaceae, Lachnospiraceae — another plant-chomping Firmicute group — adds to that strong Firmicute count at 11.5% (it’s his third highest group; bacteroidetes is predictably in the #2 slot). So what’s the relevance of high Ruminococcaceae and Lachnospiraceae?

Ruminococcaceae and Lachnospiraceae are synonymous with Clostridium cluster IV and Clostridium cluster XIVa. These are the same immensely important commensal Clostridium clusters I wrote about in my original post. These are the butyrate producers, and have been shown in study after study to be some of the most consequential bacteria for gut health. Cluster XIVa alone accounts for up to 60% of mucosal bacteria in the gut. And we now have proof that when you bulletproof your gut with fermentable fiber, as Jeff Leach has, it is these groups that are doing the bulletproofing. (And just to really drive it home: Michael Pollan has high levels of these groups as well. What else would you expect from Mr. Eat Mostly Plants?).

So there you have it. Tatertot Tim megadoses on Resistant Starch, but doesn’t have a whole lot to show in his firmicutes. Case closed. Resistant Starch, we hardly knew ye….

But we still have a problem. Regardless of Tim’s results, we know that Resistant Starch is working. It’s having all the effects that we expect people to have from consuming gut-feeding, butyrate-boosting fermentable fibers. People are reporting results. Improved metabolic markers, improved digestion, weight loss, better sleep, improvement in IBS symptoms. Results don’t lie. How could that be???

Well, let’s take a look again at that chart comparing fibers from my original post. If you remember, Resistant Starch was somewhere in the middle of the pack, only significantly stimulating a few specific strains:


Tak a look at those two highly stimulated buggers — Eubacterium Rectale and Roseburia intestinalis. Hmm, those sound familiar. OH THAT’S RIGHT. Remember that Cluster XIVa (aka Lachnospiraceae) I just told you about — the one that accounts for almost 60% of mucosal bacteria? You know, bacteria that have “a unique composition and potential to influence human health”? Well Roseburia intestinalis and Eubacterium rectale are the leading colonizers of Cluster XIVa! Roseburia, specifically, governs butyrate production. And that third highly stimulated bugger, R. Inulinivorans? Also in Cluster XIVa. Resistant Starch loves Cluster XIVa.

So here, I’ll make this really easy:

What Resistant starch lacks in breadth, it makes up in precision. Resistant starch is a laser-guided missile aimed at the two most important strains of mucosal bacteria in one of the most crucial clusters of bacteria in the human gut.

Want the proof? Scroll back up to Tim’s results. Check out #4 for his most abundant microbes. Lachnospiraceae, aka Cluster XIVa. A respectable 4.5%…and I’ll just bet R. intestinalis and E. rectale have something to do with it.

(Side note: Yes, Tim’s Ruminococcaceae are abundant at 14%, but all the American Gut results I’ve seen so far have Ruminococcaceae somewhere in the top 4. So I don’t think that’s hugely relevant. I think Jeff Leach is the outlier at 23.2%).

So while that sweet, sweet potato powder may not give you that full spectrum firmicute high, it hits the important guys really, really hard.

Talk about “targeted therapy.”

Add to that the fact that, unlike other prebiotic fibers, with Resistant Starch we have a cheap, high dosable, abundant supplemental source in the form of potato starch (thanks Bob!).

And that, ladies and gentlemen, is the reason Resistant Starch, in the form of raw potato starch, is officially the body hack of *maybe* the decade.

— Heisenbug

P.S. — I’ll be back with more thoughts on what this all means in terms of optimal dosing and prebiotic combinations in subsequent posts.

Hadza, Otjhimba, Greeks, and Honey

Lab experiments and scientific studies are great for putting together pieces of the microbiome puzzle, but so is anthropology: customs, rituals, dietary patterns, behaviors. In fact, anthropology may be the only way we really figure this out before it’s too late and we fully cut the cord on our ancestral microbiome. That’s why I’m enthralled with the work of anthropologist Jeff Leach, who is leading the American Gut Project.


Among other things, Jeff is doing some fascinating work with African hunter-gatherer tribes like the Hadza and Otjhimba, some of the few remaining true hunter-gatherer tribes left on the planet. His work is focusing on the make up of of their microbiome in comparison to industrialized, Western people, and how their dietary and social/behavioral patterns  contribute to their flora.

There’s a ton to talk about, obviously, and it seems like Jeff’s work with them is just getting started. For now, I just want to quickly focus on one teeny tiny piece that relates to my last post on Seth Roberts’s honey experiment.

If it’s one thing we know about the Hadza and Otjhimba, it’s that they love honey. It’s their most prized food source. From Jeff, we learn that for a part of the year, the Hadza rely on honey for up to 70% of their energy intake. 70 percent! (I don’t know about the Otjhimba, but judging from their nickname — “the honey people” — I’m betting it’s pretty darn high.)

That kind of a reliance on one single source of food is enough to send your average food pyramid nutritionist (oh, sorry, now it’s “MyPlate”) into full on panic mode. Honey is a pretty energy dense food. So from that standpoint, they’re fine — they’re getting their calories. But it isn’t a particularly nutrient dense food. Only very trace amounts of vitamins and minerals. Where’s the Vitamin B??? Vitamin K??? Dear god, some one do a fly over and drop some heart healthy grains on these poor souls.

Oh wait. That’s right. Perhaps their other half is picking up the slack. More and more, we find that when people are heavily reliant on a single source of not-so-nutrient-dense food, it’s because perhaps that food is feeding someone else, and that someone else is holding up its end of the bargain.

(Btw, honey seems particularly good at stimulating the friendly bifido’s. Might be the scFOS, which is shown to be pretty bifidogenic. But this study seems to indicate that it’s some kind of synergy between the sugars found in honey.)

Lest all this talk of African hunter-gatherers seems a little too exotic for you, I’ll just add this: In light of all this, doesn’t everyone’s favorite Greek-inspired snack — honey + yogurt — start to make a lot more sense now? History’s first probiotic/prebiotic combo. Those clever Greeks.

See? Told you anthropology was cool.

— Heisenbug

The Honey and Resistant Starch experiments: Is There a Link?


In an exchange with Seth Roberts in the comments section of this post, I postulate a possible link between the honey experiment that Seth has been blogging about, and the Resistant Starch experiment.

The main outcome of the honey experiment has been the reporting of dramatically improved sleep. Sound familiar? That’s also one of the main effects people have reported while on Resistant Starch (potato starch).

Seth has apparently been following the RS experiment and made the connection himself. But he proposed a link that isn’t probable — that both honey and RS raise blood sugar, which leads to better sleep.

That’s based on a (understandable) misunderstanding of RS. I think many who aren’t following too closely are assuming that RS is a “slow carb” that is slowly digested by the body, like many other complex carbohydrates. That couldn’t be further from the truth. RS is, if I may invent a term, a “no carb.” It’s indigestible. Skips the whole digestion process, and instead goes straight to the colon, where the “other you” (your microbiota) feeds on it. And in fact, RS’s effect on blood sugar is quite the opposite — people report a lowering of fasting BG and post-meal BG. How so? The bacteria that RS feeds in turn produce short-chain fatty acids. Specifically, butyrate. Butyrate stabilizes blood sugar.

A more plausible link: Honey contains oligosaccharides, another kind of fermentable fiber which feeds bacteria that produce SCFAs, causing blood glucose to stabilize.

Honey’s effect on blood sugar, by feeding bacteria, has been documented here and here.

Oh, and what kind of oligosaccharides does honey contain? Short-chain fructooligosaccharides (scFOS)! As I’ve shown in the last couple of posts, scFOS has been shown to have complementary, different, and sometimes superior effects to Resistant Starch.

A useful test for the honey experimenters would be to measure their morning FBG after a night without honey, and then after a night with honey. If the results mirror the RS experimenters’ outcomes, then we might be onto something.

Here we go: Resistant Starch vs scFOS, Head-to-Head

I’ll keep this short and sweet. A study published in Cancer Research, the journal of the American Association for Cancer Research, pits scFOS against Resistant Starch in mice with colon cancer.

The result? Resistant Starch did nothing. scFOS significantly reduced cancerous tumors.

But there’s more:  scFOS also resulted in the generation of lymphoid tissue in the small intestine. GALT. No, not everyone’s favorite character from one of the more overrated books of the last century. We’re talking about gut-associated lymphoid tissue. The largest mass of immune tissue in the body, defending the body against pathogens and housing T and B cells. Up to 70 percent of the body’s immune system is in the gastrointestinal system.

The scFOS diet resulted in the generation of new lymphoid nodules — Peyer’s Patches — along the small intestine. These are little warehouses of immune system activity in the gut, usually found toward the distal end of the small intestine.

Here’s how the authors explain the results:

sc-FOSs and RS are fermentable fibers that provide protection against earlier stages of colon carcinogenesis: they both reduce the number of azoxymethane-induced aberrant crypt foci in rats, in conjunction with high butyrate production.4 The inefficiency of RS in the present experiment suggests that fermentation either is not involved in the protective effect or is not sufficient by itself.

I’d add one other possibility: perhaps RS simply didn’t stimulate the same amount of fermentation, didn’t target the correct site, or didn’t target the right bacterial species.

Either way…seems like a big deal.

Short-Chain Fructo-oligosaccharides Reduce the Occurrence of Colon Tumors and Develop Gut-associated Lymphoid Tissue in Min Mice