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.
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?
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.
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.)
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.
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.
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.