Resistant Starch: Case closed? Not so fast.

(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.

Major butyrate-producing bacteria isolated from the human colon
Major butyrate-producing bacteria isolated from the human colon

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:

Tim

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:

prebiotic_comparison

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:

Tim

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.

— Heisenbug

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37 thoughts on “Resistant Starch: Case closed? Not so fast.

  1. Love it! Love it! Love it! i was hoping someone would do a more advanced hack. Pass this around, i want everyone’s input.

    A few points, though:

    A dominance of firmicutes over bacteroidetes is linked to obesity! My profile is highly non-obesogenic, Pollan’s looks bad, to me, from what i read.

    Also, Bifidobacteria do not degrade RS, and are not butyrogenic. You got that right.

    There are several keystone species and co-feeders of RS that produce all the butyrate. (google it)

    I don’t know how the bifido grow in this scenario, I assume it’s because of all the butyrate and stuff produced by the keystones and co-feeders, gives bifido a chance to grow.

    If you can’t see that having a gut filled with bifido, and 13% is basically filled! Nobody has 13% except babies shortly after weaning.

    Bifido is highly associated with: the regulation of intestinal microbial homeostasis, the inhibition of pathogens and harmful bacteria that colonize and/or infect the gut mucosa, the modulation of local and systemic immune responses, the repression of procarcinogenic enzymatic activities within the microbiota, the production of vitamins, and the bioconversion of a number of dietary compounds into bioactive molecules.[2]

    Bifidobacterium spp. are known to discourage the growth of Gram-negative pathogens in infants.[citation needed]

    Mother’s milk contains high concentrations of lactose and lower quantities of phosphate (pH buffer). Therefore, when mother’s milk is fermented by lactic acid bacteria (incl. bifidobacteria) in the infant’s GI tract, the pH may be reduced, making it more difficult for Gram-negative bacteria to grow. (from wikipedia)

  2. ok. so I’ve started the RS “protocol” as outlined in FTA.

    What is a good source of scFOS supplement ? To compliment the RS protocol.

    I found this one. Is this acceptable and at what dosage ?

    NutraFlora Prebiotic Enhancing Formula
    http://www.swansonvitamins.com/swanson-probiotics-nutraflora-prebiotic-enhancing-formula-750-mg-60-veg-caps

    I have been low carb for sometime now. close to 2 years. I do eat on occasion green leafy veggies.

    How do I rebuild my Firmicute ?

    Are there any Probiotic supplements of Firmicute ?

    Regards…..

  3. Thank you for this. The gut microbiome is kind of like the last frontier. Most experts admit that there countless types of bugs and it will take decades of research to sort it out. People like quick easy answers and i think its important not to get fixated on one piece of the puzzle. That being said, for someone who has had severe gut dysbiosis and cant tolerate many fodmaps, the RS has helped alot.

  4. @tater:

    The research on firmicute/bacteroidetes link to obesity is all over the place. There seem to be 3 or 4 studies (almost all of them from the same lab) circa 2005/6 that made the link. And then a bunch since then that discount any link, and even one showing the opposite (high bacteroidetes = obesity). I link to one of them above (the Aberdeen study). And then a couple in 2011 & 2013 that establish the link in children.

    My guess is that, if there is a link, it isn’t straightforward or linear. Maybe it’s a “u-shaped” curve, sweet spot kind of thing? Or maybe in a low fiber eating population (ie, industrialized West), the obese get more fermentable fiber than the lean by virtue of the fact that they eat more. Who knows. Probably more complicated than that. But hey, the proof is kind of in the pudding — you and Pollan are at opposite ends of this chart. But Pollan seems pretty lean to me, and you look like you could probably wrestle a grizzly to at least a draw.

    I certainly think it’s premature to recommend a “Firmicutes to Bacteroidetes diet”!

    As for the bifido’s, one of my main points is that I think there is an over-focus on them. The reason they are important in infants (and have strong/beneficial effects in them) is that they can make up to 90% of their microbiota. Strength in numbers. In adults, they are a vastly smaller player. It’s that butyrate-producing “clostridia cluster” within the firmicutes that really seems to run the show. There’s no doubt that the RS is indirectly boosting your bifido’s. But I postulate that perhaps the positive effects that people are experiencing from RS is due to its direct interaction with these clostridia species, not the bifido’s.

    And if that’s where the action is, the question should be: What do they want from us? Starch? scFOS? A little of both? What combination/dosages are optimal?

    Here’s what I would love: a test between two groups, one supplementing with scFOS, one with RS. Test metabolic markers, sequence gut, etc. before and after. One can dream.

    • I think your dream may become a reality. Dr BG is working with a new crowd-sourcing program called Kickstarter for people to do gut/RS tests they make themselves. Funding is publicly sourced, and we may have a corporate sponsor to fund all the tests we put out there!

      Keep an eye on http://www.drbganimalpharm.blogspot.com/ in the next few weeks–she should get the program going soon, she is running a beta test case now. This could be way cool and you could devise any test you like. Details soon at Dr BG’s blog!
      Tim

      • Tater,
        Any idea of the status of this kickstarter campaign?
        Offnote, do you know if the book she was working on is published?

  5. There was a study I read done in Japan in re: kefir and gut microbes. There were high bifidos while the people were consuming kefir, but three days of no kefir and the bifido level went down substantially. Possibly because Tim consumes kefir on a daily or almost daily basis, his bifidos are higher than what would be expected.

    Bifido does not appear to be a normal gut resident according to the study. If I have to go find it, I will.

    • That’s a good point — I don’t know whether Tater was consuming any fermented foods with bifido in it. Maybe he can tell us. If it was pretty close to the time of his sampling, it might have an effect. But studies show that bifido levels drop to normal fairly quickly after ceasing consumption.

      • thank you sir.

        as far as dosage is concern, tatertot posted a comment on FTA blog

        http://freetheanimal.com/2013/12/dramatic-resistant-success.html#comment-546876

        “Short-Chain Fatty Acids and Human Colonic Function: Roles of Resistant Starch and Nonstarch Polysaccharides’ Topping et al. described the role of RS on the health of humans and also discussed a ‘carbohydrate gap’. In calculating the need for SCFA in the human gut, they discovered that non-starch polysaccharides could only provide 25% of the SCFA requirement for optimal gut health and posited that oligosaccharides (OS) and RS were needed to fill the gap. They noted that humans need approximately 32-42g/day of fermentable fiber for SCFA production, and that FOS and other OS’ could only be utilized up to about 5g per day.”

  6. Does anyone have any idea of the mechanism whereby RS affects blood glucose? Maybe I missed the critical post somewhere, but I can’t imagine how gut bacteria get invoved in blood glucose control.

  7. Too much butyrate production during an pathogen infection (IBS) can be very bad…am I interpreting the following study correctly? Here’s a page from Animal Pharm on which someone with IBS-C has overgrowth of a bad bacteria, which “sends buttloads of butyric flooding the whole body due to SIBO”. So if that person were to swallow some resistant starch, yikes!

    I have IBS-C, but do not know which pathogen, if any, is causing it. Based on the following study in this link I am very hesitant to try resistant starch:
    http://www.drbganimalpharm.blogspot.com/2014/01/two-case-studies-diarrhea-ibs-and.html

    • Mary, trying to game it out and guess your way through this kind of thing without trying anything is probably not going to yield much. Personal experimentation, starting with the simplest explanation, is usually the smartest way to go. Lots of people with IBS-C or D seem to get very good results with RS, which suggests that there could be a very simple explanation — lack of fermentable fiber consumption. Exploring the possibility of a pathogenic infection, in my opinion, is further down the list.

      • Actually butyrate is the LOWEST produced scfa from resistant starch. I’m not clear why people in the Paleo community are so worshipful about it. And yes I also think it leads to colitis, as does standard medicine. For example, premature babies often die at 14-21 days of age because the amount of butyrate skyrockets at that point, and they develop necrotizing colitis. (any Google Scholar search will show the connection between butyrate and colitis, not just babies, but that’s well studied). Someone else was talking about Klebsiella spp. overgrowth. I think that might throw a monkey wrench in the works because I also have this problem, and another confounding factor is people like me who have gut issues because they are too uptight. See below I talk about my years of insomnia and resultant inability to relax, which wasn’t solved by any diet or even by starving myself. It had to be solved with a drug. Though I hope someday I can sleep without it. So there is a sleep-gut-vagus nerve connection here, which can’t be solved by taking any food or type of refined resistant starch. Finding a sympathetic doctor to discuss this with and self-education is key. A doctor who doesn’t get upset when you search the internet for answers is worth every penny. Here’s a reference to some info about resistant starch and butyrate, even scientists don’t really know, so how can we? http ://physrev.physiology (dot) org/content/81/3/1031?ref=dod-jptc.org#main-content

  8. hi Mr. H & anyone else who may know,

    re. potato flour (not starch),
    the nutrition info labels on potato Flour seem to vary a lot,
    in general i was of the understanding that potato flour should have protein in it.

    so does that mean that a product labelled as potato Flour but with zero protein per 100g, is actually potato Starch.

    anyone know or have any more info on this.

    i was actually looking for some potato Flour (not starch) the other day to try as a post workout source of ‘slow’ carbs, thinking it would be a source of a mix of carbs including some RS (just not as much as in p.starch). This is when i found a potato Flour with zero protein, which got me thinking, & hence asking this Q

    cheers all

    • Daz, why on earth would you care how much protein resistant starch has? It isn’t a major source of protein, the purpose of it has nothing to do with protein.

      • A response like this seems to me not the best way to foster open and free communication between people taking the initiative to find answers, but rather a good way to keep people out of the conversation that may actually have some great insight.
        Let’s try to be respectful

  9. Hi there,

    I am 24, F, generally healthy. I’ve been supplementing with potato starch recently (after hearing about all the supposed health benefits) and lost weight a while back eating primarily cooked and cooled potatoes.

    Though I am generally healthy, I do have a long history of unexplained bloated gut-aches. I recently got a stool test done by Genova Diagnostics, and my FNP says the culprits seem to be three types of bad bacteria present in my gut in high amounts – Citrobacter freundii, Pseudomonas aeruginosa, and Klebsiella pneumoniae. The bacteria appears to be resistant to everything but Cipro, which I am now taking for a week. Ugh.

    In particular, though, Klebsiella is described as thriving in individuals on a high starch diet. Is it possible that I threw my gut out of whack partially by supplementing with potato starch?? I otherwise eat 1/2 – 1/3 cup of sweet potato or a little bit of white rice with my meals. Nothing crazy, and certainly not “high starch”, I’d say.

    • There has been much talk of whether starch might be a problem for people with Klebsiella overgrowth. While I think that’s far from proven, I think it’s a pretty easy fix — take it easy on starch that makes it to the large intestine (ie, resistant starches: raw or cooked and cooled) and go heavier on other fibers: inulin, pectin, non starch polysaccharides. The greatest determinant of colonic environment is always going to be amount of fermentable substrate. So just flood it with something else. You can have a healthy gut without a ton of resistant starch.

  10. I cannot do paleo. But I can do resistant star he’s to keep my type 1 (jevenile diabetes) in check. I have been using whole grain and nut breads for just over 2 weeks and substituting califlower and spaghetti squash as my pseudo foods for rice and pasta. And I have seen a huge change in my blood only one day. I can leave wheat flour alone no problem. I do have celiac. I am beginning to disagree with the theory wire The strict Paleo diet. It is too restrictive on how you eat to live and too expensive. I have problems with my digestive system. I have typed diabetes and no one in the health Science seems to care for the people who lives with Type 1 and no fault of our own has to take artifical insulin. Beneifical Resistant starches are now on my menu. It can reduce you insulin intake dramatically!

  11. This is excellent. Thank you. From the replies I think people want their gut “to just work” the way they want their computer “to just work.” Which for most of us, on both subjects, involves discussing a black box system. Here’s another addition to this discussion which should not be ignored. I’m not saying this is all in people’s heads, but I have to add that I didn’t resolve any of my gut issues until I relaxed enough. Laxative does not mean “bring water into the colon” it means relax, at least for me. I went through years of not being able to sleep just as many women do at perimenopause. I got so uptight that I was hoping and praying that nothing would set me off in a public place or I’d die of shame… after I had a tantrum. Lack of sleep really does make you crazy. I’m living proof. In the end, I have to take an antipsychotic to sleep. It’s the only thing that works. I know that leads to labeling like “she’s just crazy, I’m not” but try going without sleep for 4 years and tell me how you feel, ok? So anyway, after I could sleep properly (sleep such that I wasn’t aware I was sleeping and halfway awake anyway, when I even could sleep, that is), all my gut issues calmed down. My constipation was gone (I always knew “water” wasn’t the answer as does every other person whose had serious constipation), and there was no struggle to “get it out.” I’m still affected by bad diet, especially refined carbs, but now the transit time makes it nearly immaterial what I eat.

    So what I wanted to say is, if you’re having gut issues and you feel uptight all the time, consider what happens if you relax totally. Go to a spa, do whatever you need to, but relax completely. See if that helps. If it does, then you might consider your lifestyle and stress level as part of the problem. That vagus nerve thing is not something to ignore. Neither is “hypervigilance” something only women have. I knew several soldiers who taught themselves to remain half awake because their lives depended on it. But now it no longer does. And their longevity may depend on being able to totally zonk while sleeping. As my longevity depends on that too. I may be a neurotic middle aged woman, but there are plenty of people walking around in a self created cage, afraid of being “set off” and embarrassing themselves. If that’s you, consider relaxation as a path to laxation and gut health. The connection between the two is the vagus nerve. Look into it.

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