(Edit: There is a second part follow-up to this post here.)
If you’re a follower of any paleo/ancestral health/biohacking discussions on the web, then you might be aware of the Resistant Starch/Potato Starch craze underway, largely driven by FreeTheAnimal and the research/self-experimentation of one of its readers, “TaterTot” Tim. If you aren’t familiar, a quick search for “Resistant Starch” at FTA will get you caught up. TaterTot’s guest posts over at Dr. Grace BG’s AnimalPharm are also a good primer. The subject has tipped into mainstream “professional Paleo” outlets like Mark’s Daily Apple, functional medicine phenom Chris Kresser, and biohacker extraordinaire Dave Asprey’s Bulletproof Executive. So it’s a legit phenomenon, it’s got legs, and it’s had me rapt for a while now. And Richard & TaterTot deserve a lot of credit. It’s the real deal…or at least the start of it.
But the thing is, from the last couple of posts at FTA, where we get some gut sequencing results and some new diet guidelines (you know, to get you that supercharged paleo gut in time for the summer), I’m getting a whiff of triumphalism — i.e., case closed, hang up the mission accomplished banner, our work is done. Let’s all live till we’re a hundred and twenty! Here’s why I think that’s premature, and why there’s a lot to still figure out.
The linchpin in all this, so far, is the boosting of butyrate production in the large intestine: feed the commensal good guy bacteria, and in turn they’ll produce butyrate, a short-chain fatty acid that has powerful anti-inflammatory effects both within the GI tract and probably systemically. Tangible benefits range from improved fasting blood glucose and post-prandials to improved sleep, improvement in IBS symptoms, lowered cholesterol, reduced intestinal permeability, and probably a lot of other things we’re just beginning to realize. In short, it could be a major key in fighting metabolic, inflammatory disease. If the dysbiosis theory of chronic disease has any credit, butyrate production (or lack thereof) could be a major player.
Here’s where it gets a little murky. So far, the explanation for this phenomena has largely centered around feeding a specific class of bacteria: the bifidobacteria. Feed the bifido’s some resistant starch, they multiply, go into butyrate production overdrive, and you’re on your way to a bionic gut. In TaterTot’s gut analysis post, he places his super high bifido’s (11x the average!) at center stage, citing them as proof that Resistant Starch is the path to everlasting life. But here’s the problem: when it comes to butyrate-producing commensals in the gut, bifido’s don’t even register.
There my friends, are the big guns — the major butyrate-producing commensals. F. Prasnitzii alone can account for up to 15% of the gut bacteria in a human! Together with E. Rectale and Roseburia, these bacteria can account for up to 30% of the human gut biome. Do you see any bifido’s in that chart? Nope.
But it gets better. Taking a look at this study and this one, we see that those with severe gut diseases like Crohn’s and Ulcerative Colitis actually show a HIGHER ratio of bifido’s, and LOWER F. Prausnitzii and Roseburia. (Update: Here’s another one.)
Now, don’t get me wrong. I highly doubt this means that bifido’s in some way contribute to disease or that they don’t make for a healthier gut, just that their presence or absence are probably not the major driver of dysfunction when it comes to dysbiosis-related disease. It’s much more likely that the species in the chart above, and their presence or lack thereof, are in the driver’s seat.
So let’s take a look now at TaterTot’s gut sequencing results:
Tatertot’s interpretation of his results begins thusly:
“Firmicutes and Bacteroidetes (brown and orange on bar chart) – normal gut bugs for everybody, this is the bulk of everyone’s poop. These can contain pathogens as well as beneficial microbes. Nothing special here to see.”
Firmicutes? Nothing special to see? The hell there isn’t! Guess what phyla those butyrate super producers up above belong to?! Firmicutes!!! Class Clostridia, to be exact. And as evvvvvryone knows, commensal clostridia are a very important part of the gut biome. (Want more fuel for that fire? When compared to healthy kids, kids with Type 1 Diabetes seem to have a much lower Firmicute to Bacteroidetes ratio.) So yeah, I think there might be something to see here.
And it doesn’t take a genius to look at this chart and realize one thing: TaterTot has low firmicutes! Compared to the average guy or gal, anyway. Clearly the lowest Firmicute to Bacteroidetes ratio. Slow down on that victory lap, guys.
And now, more science:
That chart is from a study measuring the fermentability of various prebiotic fibers by the major butyrate-producing bacteria. Our good friends F. Prausnitzii, Roseburia, and E. Rectale are all there. They measure the usual cast of fiber friends, including inulin, starch, and short chain fructooligosaccharides (scFOS).
The results? Starch isn’t dead last. But it’s not great. First place belongs to scFOS. Major stimulation across the board. A clear winner. Surprisingly, the most commonly touted beneficial prebiotic — inulin — does worst!
(Side note: this study uses amylopectin potato starch as it’s starch substrate instead of amylose. As you might know, it’s the amylose, not amylopectin, that survives the GI tract and feeds gut bugs in humans, while amylopectin is absorbed and digested. The reason I don’t think this matters is that both amylopectin and amylose are equally fermentable, it’s just that in humans, amylopectin doesn’t ever get a chance because it’s digested in the small intestine. Since this study is in vitro, it doesn’t matter.)
And then THIS study put scFOS to the test in mice. Conclusion? “scFOS induce profound metabolic changes by modulating the composition and the activity of the intestinal microbiota.” The study goes on to specifically state that, while scFOS did stimulate bifido’s, they “are not predominant in the faecal ecosystem and do not seem to be strongly correlated with metabolite changes.” Clostridia species (i.e., Firmicutes) were the ones associated with the metabolic improvements.
Lastly, assuming you are still with me, a study out of Aberdeen found that subjects on low carb (i.e., low fermentable fiber) diets see their butyrate production plummet. Why? Because it killed their Firmicute count. (Interestingly, this study also negated the previous research that linked high Firmicutes/low Bacteroidetes to obesity.)
Ok, so now let’s go back to TaterTot’s results:
Hey, who’s that guy over on the far right? Why it’s Mr. Eat Mostly Plants himself, Michael Pollan! You know, the kind of plants that might have a sh*t ton of scFOS? And guess what? As opposed to TaterTot, Mr. Pollan has above average Firmicutes! Highest Firmicute to Bacterioidetes ratio, looks like. Verrrrry interesting. If you were a kid with a genetic predisposition to Type 1 diabetes, or just want to keep that butyrate flowing for a healthy gut, you might want Pollan’s gut, not Tater’s.
Now, lest I fall into the triumphal trap myself, it should be said that these are all just isolated studies. The prebiotic one is in vitro, at that. And speculating that Michael Pollan’s butyrate-producing clostridia are high, and TaterTot’s are low, just by looking at firmicutes, is…speculative. I wish the analysis could go deeper than phyla. Oh well. And this study puts a little damper on scFOS’s ability to cure what ails us (then again, just 20g/day for only 4 weeks seems hardly adequate, as the study authors admit themselves).
So this is all only to say that we’ve got a lot to figure out here. I’m certainly not ready to make any final recommendations (though adding more resistant starch, scFOS, and other fermentable fibers is certainly not a bad bet to place). And we should all keep experimenting. There’s no doubt people are experiencing benefits from adding fermentable fibers to their diets. But taking the time to figure out WHOM to feed WHAT, in the right combination and dosages, could make an order of magnitude difference. And if you think we can rely on big pharma to do the heavy-lifting research on a bunch of cheap to produce, colon-massaging veggie fibers, you’re in for some disappointment. This is a major project for the distributed, citizen-science web, and we’ve only just begun.