Eczema & L. Plantarum Success Stories

Thought I’d do a roundup of some of the reader reports that popped up throughout the past month…

After not achieving any success with the standard dermatological approaches, Mary has cleared up her eczema completely using the L. plantarum probiotic:

Thank you for the advice on taking probiotics for eczema. My dermatologist prescribed creams and soap alternatives and it didn’t seem to be doing much good at all. I’d had very strong symptoms of eczema since last September – including severe itching and bleeding. Since I’ve started taking the probiotics, it’s cleared up completely. And it just took a week. Could not be more grateful to you or to the friend who directed me to your blog!

Reader Gestalt reports that he cured his girlfriend’s eczema with the L. plantarum protocol:

Just wanted to report I put my gf on the L.plantarum after reading your first post about curing eczema. She has had severe eczema on her hands arms, shoulders eyes and lips for about 1.5 years. It took 2 weeks of the Jarrow’s formula, 2 capsules a day before it started diminishing. This is the best improvement she has seen in a long time and I have you to thank for this discovery. She looks like maybe after another week or so she will fully recovered at this rate. Keep up the blogging, I look forward to your every new post.

Janet noted improvement after just two doses of the probiotic:

I took my second L plantarum this morning and it looks like my hand eczema is already improving! Definitely clearing up. No itching around the margins. Number of bumps decreasing and there is just one small “colony” left in the flare that was at least 2 inches in diameter. I haven’t been drinking my homemade kombucha because I thought that was the cause of the rash, but I have realized for awhile that it wasn’t. So hurray! I can begin my KT factory again. Also, I am ready to start some other fermentations. I am amazed.

And Janet followed up that her hand eczema is now completely clear.

Reader T.J. seems to have made a major improvement in his psoriasis. Psoriasis and eczema are not the same thing. However, like eczema, psoriasis is a skin condition with a strong immune system component:

Taking L. plantarum probiotics has much reduced the severity of my psoriasis. We’re experimenting to see if it has an effect on arthritis inflammation as well.

And now the best for last. Out of all the experimenters, reader dojodelft definitely stood out as having one of the more extreme and intractable cases of hand eczema, which has been plaguing him for years. Despite not having a taste for it at all, he decided to begin a daily sauerkraut regimen.

One non-scientific observation I’ve made is that most success cases seem to come from those using the probiotic therapy rather than fermented foods. This certainly seems to be the case with the most dramatic reversals. As I mentioned, this would make sense — given the difference in bacterial concentration, doing this with fermented foods was likely going to be a longer process. When I first made my discovery, it was after having consumed fermented foods repeatedly for months, likely building up an adequate concentration. When I stopped (and the eczema returned), I took the probiotic and noticed results almost instantaneously.

Well a few weeks ago, dojodelft did note slow progress:

Though for me it doesn’t seem to disappear over night, slow progress is still noticeable. I’m eating kraut for about 4 weeks now. My skins slowly seems to heal. It started at my fingertips, then some small patches of skin started to renew (pink and soft  )and now the deep cracks and groves are starting to fade. I haven’t had the crazy itch on and between my fingers for 4 weeks.

Well I’m now excited to see that his eczema seems to have completely cleared:

Though it is maybe early to tell… but my hand eczema has vanished… gone… as in not there any more. An end to years of torture. I can’t believe it. The skin is still a bit dry and recovering from years of insane scratching, But no more itchy patches and night time finger scratching.

Pretty incredible!

— Heisenbug

Probiotics Survive Better with Some Fat: It’s the pH

If you haven’t noticed yet, a running theme/theory on this blog is the importance of pH in determining the microbial makeup of a person’s GI. The acidity level of one’s gut is what gives rise to particular species of bacteria, and I now believe it is the main determinant of whether one maximizes the benefits of supplementing with Resistant Starch and other fibers. The human gut is full of saccharolytic (carbohydrate-degrading) bacteria, and I believe what determines which ones get fed is pretty simple: whichever ones happen to be present. And again, it’s pH that largely decides that. If a bacteria is not adapted to a particular pH, it won’t survive, plain and simple. Like putting a human on a planet that doesn’t contain any oxygen. Now, this may sound a little circular — after all, it’s fermentable fiber that lowers pH. We’ll get to that soon, I promise!

For now, I wanted to do a quickie post that I think will give another angle on pH that I think is a little more tangible, since people are quite familiar with probiotics and fermented foods.

For a while now, I’ve been aware of research showing that the survivability of probiotics is greatly increased when taken with, or just prior, to a meal. And it is particularly the fat in the meal that increases the survivability. This study showed that quite clearly:

Enumeration during and after transit of the stomach and duodenal models showed that survival of all the bacteria in the product was best when given with a meal or 30 minutes before a meal. Probiotics given 30 minutes after the meal did not survive in high numbers.


The protein content of the meal was probably not as important for the survival of the bacteria as the fat content. We conclude that ideally, non-enteric coated bacterial probiotic products should be taken with or just prior to a meal containing some fats.

I hadn’t given this a ton of thought, until recently, when it occurred to me that the same pH principle applies here. The reason Lactic Acid bacteria (LABs) in probiotics and fermented food survive better is because of the pH buffering effect of food, and particularly fat. The stomach and its acids provide a very harsh environment for bacteria, as they should — that’s how we keep a lot of pathogens out. The stomach’s fasting gastric pH is about 1.5. That’s very low, even for the acid-loving LABs. What’s ideal? Broadly speaking, it looks like survivability grows and hits its peak at around a pH of 5. L. plantarum hits its peak at 4.8, in that study. And here’s a chart of L. plantarum growth in sauerkraut, which confirms that.




How does that line up with the effect of food on stomach acidity? Like so:

Humans secrete approximately 2.5 liters of gastric juice each day, generating a fasting gastric pH of 1.5, which increases to between pH 3.0 and 5.0 during feeding.

Well would you look at that. And when you look at how fermented foods are traditionally consumed, it makes perfect sense. Fermented dairy seems like quite a probiotic package, with its protein and fat content providing what is likely a pretty good pH buffer for LABs. And in the case of sauerkraut and kimchi, we know that these foods are traditionally consumed as condiments as part of larger meals that most often include meat and fat.

So it seems that if you are looking to maximize the effect of fermented food consumption it would be wise to consume some sausage with that sauerkraut, and some Korean BBQ with that kimchi.

More broadly, I think this illustrates what an important and universal principle pH is for the gut microbiome. What I found interesting in researching this was that among LABs, L. plantarum (who we’ve talked about quite a bit) seemed to be one of the most acidophilic. Which is in keeping with what’s been argued here — that L. plantarum is a pretty important commensal, and that acidophilia is a pretty good determinant of commensalism. Looks like L. plantarum is pretty well equipped to survive GI passage (but not without a little fat!).

And of course, LABs like L. plantarum seem to return the favor. If they can make it past that harsh acidic environment, their lactic acid production has a pH-lowering effect in the gut. We’ve gone at length about immunomodulation as the primary benefit of probiotic consumption, but I have to believe that this is a major benefit as well. But probably not to the same extent as fermentable fiber consumption.

Lastly, the effect of fat on pH lines up pretty well with the research showing the darker side of that effect — that meals with fat can increase circulating endotoxins, and that the consumption of fiber along with the fat negates this effect. In other words, this isn’t an excuse for a fat free-for-all. I’ve been running a personal experiment to test out this phenomenon, and it’s been quite interesting. I’ll post on that soon. In the meantime, I’ll leave you with Heisenbug’s corollary:

Eat fat. Always with plants. Sometimes the fermented kind.

— Heisenbug

Why Medicine Dabbling In The Microbiome Scares Me

One side effect of my dive into microbiome research is the startling realization that experts in medicine and health know much, much less than we think they do. Heck, even within microbiome research, it’s amazing how researchers seem to not keep up very well — I see so many studies premised on not very solid, and often outdated, assumptions. And often premises that completely conflict with one another. Ie, “Because Firmicutes are associated with obesity, we wanted to…” and “Because Bacteroidetes are the result of an unhealthy Western diet, we wanted to see if…” It’s as if they don’t talk to each other. But that’s a discussion for another time.

I bring all of this up because I came across this report: Cancer scientists seek to stop radiotherapy’s side-effects on ‘friendly’ gut bacteria.

When I first read that headline, I expected a report about how doctors are becoming more sensitive to the effect their treatments and procedures have on the microbiome. Which is a very positive thing to see. But if you actually read the article, that doesn’t seem to be the case at all:

“One possibility is that different populations of bacteria in a person’s guts are making them more or less susceptible to radiotherapy.”


“The aim is to build up a profile of gut bacteria which will allow us to predict who will suffer side-effects that might limit the effectiveness of the radiotherapy. Then we can think of finding ways to treat people in advance of radiotherapy in future.”

Mmhmm. Please, go oooooooon……

One technique would involve administering medicines that would alter the makeup of a patient’s population of gut bacteria. Alternatively their entire population of gut bacteria could be removed and replaced with another from a donor, a technique called a faecal transplant.



Call me crazy, but this sounds to me like the opposite of what the title suggested. What these doctors seem interested in is modifying gut bacteria — perhaps drastically — in order to make radiotherapy more effective.

And that’s scary. The idea that these people will figure out the “right bacteria” any time soon, and then try to proactively alter or demolish someone’s gut based on that, is very scary. Why? Because this is the same person who, in this article, said:

“Men and women have a startling amount of bacteria in their stomachs…”

Yeah. I bet he can also see Russia from your colon. The stomach is notable for being a place in your GI that is extremely hostile to bacteria. Too acidic. It has a startlingly low amount of bacteria.

It’s truly astounding to me just how strong of a proclivity these people have toward not only intervention, but extreme intervention. You can sense how titillating it is for them. A real chance to “geek out.” Even if they do identify an enterotype that is more amenable to radiotherapy, how do they know that enterotype won’t produce other side effects in an individual? How do they know that enterotype will be compatible with that person’s genotype?

If anything, emerging microbiome research teaches the opposite lesson: We don’t know as much as we think we do, so tread lightly. But some people just aren’t built to understand that lesson, I guess. No, they’re built to get really “science-y” and bring us things from the future. Hammer, meet nail:

“The crucial point is that we are now becoming aware of how important the bacteria in our guts are to our general health – and that should help direct us to a range of new drugs and treatments for all sorts of different conditions in future,” said Dearnaley.

Thank you, doctor from the future! See? Where we’re going, we won’t need common sense and a basic understanding of human anatomy…

— Heisenbug

Gut Hacking: A Guru-Free Zone

Just a quick follow-up to the last post.

I want to make sure no one takes away the idea that I’m recommending people “put the brakes” on any experimentation, or that they should be worried about dumping a couple tablespoons of a granulated whole food into a glass of water. In fact, the intention is exactly the opposite — my hope is that people don’t become complacent with one solution, or narrowly define microbiome experimentation to just one intervention. I think there is tremendous value in having many people trying many different things. There’s no other way we’ll get to the bottom of all this.

The evolving thoughts I post on this blog are a product of the research I do to primarily figure out what I, personally, should be doing in this area of health. They are not, and are never intended to be, a prescription to others. The reason I post them is because:

1) It’s a good way to document and organize the research I come across and the ideas synthesized from them.

2) It has the side effect of exposing others to new ideas and information, and putting their own experimentation into perspective.

3) The comments and reactions help to refine, expand on, or challenge the conclusions I come to.

The reason this area of health research fascinates me so much is that, besides its tremendous potential for understanding disease and improving health, it is an area of health that is extremely amenable to personal experimentation and do-it-yourself therapy. If the hypothesis that diet is the primary modulator of the gut microbiota is correct, and that the gut microbiota do hold potential to address health and disease, then people who like to make a lot of money from sick people are going to be disappointed.

If any sort of broad guidelines or recommendations do emerge on any of this — and I hope they eventually do — it will be the product of collective experimentation and conversation. As such, I think we can do without gurus or “experts.” I think we have enough of those. Using other people’s struggle and search for health as a platform for self promotion has never much appealed to me. I hope that, as we continue to explore the other 90% of ourselves, the crowdsourced aspect of this remains front and center.

— Heisenbug

Why Resistant Starch Is Probably Not Enough

Lately I’ve been turning my attention back to one of the original lines of inquiry here on this blog — the question of what effect high dose Resistant Starch (mostly in the form of raw potato starch) is having on the gut bacterial profile in individuals. I think it’s an important question for a few reasons. Despite the many reports of positive effects gained from this experiment — digestive, sleep, mood, metabolic, etc. — I still believe it’s necessary to keep some healthy skepticism. After all, it isn’t like we’ve cured cancer just yet. Having a bunch of people who have normally been on a low fiber Western diet all of a sudden throw in high doses of one very specific type of fermentable fiber is a pretty novel thing. And there are many examples of this or that protocol having great effects at the outset, only for things to level off, or even go south, when practiced chronically for a prolonged period (vegan diet, anyone?). But most importantly, I simply have the nagging feeling that there are much greater gains to be made from finding out what is going on and what should optimally be going on.

What initially spiked my skepticism was the fact that in the one gut sequencing report we have of an individual “high dosing” on RS, the results seemed…not quite what we would expect. (By the way: I am DYING for some new data from other individuals. Hopefully we’ll seem some trickle in soon.) In these two initial posts, we wondered why Tim’s results showed higher than average Bacteroidetes, and lower than average Firmicutes, specifically from the the two important Clostridia clusters Lachnospiraceae and Ruminococcaceae. These are the plant fiber degraders and butyrate producers, and have a strong association with gut health. Bacteroidetes, on the other hand, are associated with a lower-fermenting gut, typical of the standard Western diet and its low fiber content. American Gut founder Jeff Leach and writer Michael Pollan — both enthusiastic plant eaters — had far more of these (especially Jeff). But even when compared to the average American, Tim had less of these, and more Bacteroidetes.

Tim’s report:


Jeff’s report:


Given that one of RS’s purported benefits was the stimulation of butyrate production, it seemed odd that Tim’s butyrate-producing bacteria would be lower than the average person’s. Specifically, his Lachnospiraeceae — which contain major butyrate producers like Roseburia and Eubacterium — clocked in at 4.5%, last in his “most abundant.” I’ve seen a few other AmGut reports of non RS supplementers where this group registers at the top of the list at around 40%. Heck, even Tim’s wife’s report showed slightly more of these bacteria, and I don’t think she was supplementing with RS at all at the time:

Am Gut 2 Jackie

Am Gut 1 Jackie

(By the way: Tim and I speak often and he has always been very encouraging of the use and analysis of these reports. Many thanks to him for giving us something to work with.)

Well, in the end, we concluded that RS was probably strongly stimulating a very select number of species within the butyrate-producing Clostridia groups — ones shown to have good starch degrading capability in vitro. And we left it at that.

But I’m now beginning to question whether that’s the whole story.

Since those posts, we discussed here an interesting experiment done by Leach showing pretty conclusively that Firmicute growth was a direct result of consuming fermentable fibers from plants, and that in the absence of that consumption, Bacteroidetes would rise. Below you can see the dramatic reversal.


This was presaged in a comment by Leach in a previous article:

In addition, as pH shifts away from acidic, the genus Bacteroides can also bloom as well, gaining an ecological niche in this less acidic environment courtesy of a low carb diet. For those of you keeping score, many talk about the American gut in general being dominated by Bacteroides as a function of our high fat, high sugar diet. The reality is, it might have to do with what we are not eating – dietary fiber (of all kinds). The all-important butyrate producers Roseburia spp. and Eubacterium also drop in abundance as pH shifts away from acidic as well.

So from this, we took away the idea that the acidity produced by fermentaton is the driving force and a useful, “unifying” theory of gut health. A rise in acidity favors the Firmicutes and Actinobacteria (good guys which include the Bifidobacteria), and a drop favors Bacteroidetes and the dreaded Proteobacteria. And we speculated that Bacteroidetes dominance may not be such a great thing — Bacteroidetes are all gram-negative endotoxin producers, and studies have made numerous correlations to disease (Type 1 Diabetes, IBD, Obesity, Metabolic Disease). And they seem to rise when you smoke. To be clear, they are also quite clearly human commensals and not outright pathogens (though certain species do seem to turn pathogenic in certain circumstances). The endotoxins they produce are vastly less toxic than those of Proteobacteria (though that is balanced by the fact that they vastly outnumber Proteobacteria). So it’s complicated. But the more important point is that I have yet to see any disease correlations with the Clostridia clusters who, again, are the major butyrate producers and considered by many to be a health marker of the microbiome. It is this group — along with Actinobacteria (ie, Bifidobacteria) — that seems to be the marker of fermentation, proper acidity, and gut health. And we have plenty of correlations showing disease when they are in low number.

Oh, and just in case this is all a little too N=1 for you, there was another recent study done that showed this exact same effect. In fact you may be familiar with it, as it got a decent amount of press and was featured in an NPR article. The study split people into two groups. One ate a completely animal based diet (meat, cheese). The other ate a completely plant-based diet. The results:

The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale and Ruminococcus bromii).

As you can see, the same effect. (The annoying part of this study and the media reports about it was that they predictably drew the conclusion that meat and fat caused the effect. While there may be some contribution from the animal foods, the fact that it was a “bacteria starvation” diet is far more relevant. As Leach’s experiment showed, it is more likely that it was a complete lack of plant fiber, not the meat and fat, that caused the “bile-loving” bacteroides to grow in the animal-based diet. It’s about fermentation, or the lack thereof, and the resulting pH. Why didn’t they have a meat + plant group? Because it would’ve interfered with their simple and headline-grabbing conclusion?)

So when we see lower than average butyrate-producing Clostridia and higher than average Bacteroidetes in an RS supplementer’s gut report, there are two basic facts that should give us pause when considering the purported benefits of RS supplementation:

1) The abundance of Clostridia has been found to have a direct and positive correlation with butyrate productionThis is something that definitely raises questions about the value of high dose RS supplementation. The more Clostridia, the more butyrate. And vice versa.

2) The colonic pH that is conducive to Bacteroidetes has been shown to be incompatible with a high fermentation, butyrate-producing gut. It is a pH that inhibits active fermentation and butyrate production from butyrate producers like Eubacterium and Roseburia, and instead favors Bacteroides growth and its metabolites. This, too, raises doubts about the benefits of high dose RS supplementation.

In other words, if RS supplementation results in higher than average Bacteroidetes and lower than average Clostridia, it is likely not delivering on its promise.

Or at least half of its promise.

You see, taking all of this into account, we have just one problem — Tim also had a superhuman count of Bifidobacteria, and no Proteobacteria whatsoever – the kind of thing you’d expect to see in a healthy, high fermentation gut. Pretty uncommon, and unlikely to be just a fluke. Pretty clearly the result of some outlier factor in Tim’s diet. In other words, it’s quite clearly the potato starch. The RS is doing something right. How do we explain this?

One of the foundational concepts underlying gut microbial dynamics and microbiome diversity is substrate competition. “Substrate” is just a fancy word for any food that bacteria feed on. Substrate competition refers to the idea that the outcome of what you feed your gut — what bacteria grow and what byproducts (short-chain fatty acids like butyrate) are produced — is largely decided by the competitive dynamic between bacteria in the gut.

Different bacteria are adapted to metabolize different types of plant fibers. And even if one type of bacteria is able to break down a particular type of fiber, it doesn’t mean it will. Remember, it exists in a large, competitive community, and there may be other bacteria that are much more suited to metabolize that particular type of fiber. In other words, stimulating the growth of specific groups of bacteria relies on the consumption of fiber that they can preferentially feed on — fibers that they have carved out a specific niche for degrading.

That’s why in vitro experiments looking at how well a specific type of bacteria grows on some type of fiber, and what it produces as a result, aren’t very useful. That’s sort of like watching a baseball player swing a bat really hard in training, and then predicting that he and his team are going to win the World Series.

As it turns out, starch is a pretty interesting substrate. It’s highly bifidogenic, that we know from the research, and Tim’s results show that pretty clearly. In fact I’m betting this is going to be the most common result we see in the gut reports from RS experimenters: crazy high bifido’s. And this is why: bifidobacteria are known to have a unique capability whereby they adhere to resistant starch granules, allowing them to degrade RS. It is this capability that allows bifidobacteria to compete quite well for this substrate, and this is very likely why RS has such a bifidogenic effect and why we see that in Tim’s report. (And as we’ve discussed before here and here, the degradation of RS by bifidobacteria is also crucial for its fermentation by the butyrate-producers Roseburia and Eubacterium. Cross-feeding: they seem to need bifido’s to “pre-digest” the RS, and they also feed off of the acetate and lactate that the bifido’s produce when they degrade RS.)

But starch is also preferred by one other group of bacteria. A group that has also carved out a specific niche for starch degradation.

That would be the Bacteroides.

The Bacteroides (which are the predominant genus within the Bacteroidetes phyla and are interchangeable for our present purposes) seem to have quite the sweet tooth for starch.

Below, from a brand new, page-turning, thrilling read on Resistant Starch, we find a comparison of starch-degrading ability between Bacteroides, Actinobacteria, and Firmicutes:


As you can see, Bacteroides seem to come out on top. More Bacteroides strains show starch-degrading ability than any other phylum. Actinobacteria — the Bifidobacteria — come in at second. We expected them to do well on starch. Firmicutes: last place. This table is based on some pretty old research (1977), and the analysis allows for the fact that Firmicutes may have been neglected in culturing when this study was done, so let’s keep going.

Well look at this. Looks like we’re late to the game. From a 1989 study on B. thetaiotamicron, the leading Bacteroides commensal in the human gut:

These findings indicate that starch utilization by B. thetaiotaomicron apparently does not involve secretion of extracellular enzymes. Rather, binding of the starch molecule to the cell surface appears to be a first step to passing the molecule through the outer membrane and into the periplasmic space.

It looks like Bacteroides can do something quite similar to what the Bifido’s do: bind starch, hold on tight, and munch away:

The intestinal symbiont Bacteroides thetaiotaomicron uses five outer membrane proteins to bind and degrade starch.

These starch utilization systems are presumed to help Bacteroides effectively compete for starch:

It appears that an elaborate system of starch-binding proteins and periplasmic hydrolases enables this bacterium to sequester and degrade starch molecules, presumably allowing it to compete more effectively for the available substrate.

And it seems that it isn’t just B. thetaiotamicron. These starch utilization systems seem to be shared across the Bacteroides genus. Other leading species, like B. ovatus, B. vulgatus, and B. fragilis have been found to possess the same capability.

And in one study where this competition was tested, we see how things might actually play out:

Although able to use amylopectin in pure culture, Roseburia sp. strain A2-194R competed poorly for this substrate in the mixed community.


The results of our FISH analyses show that the fermentor conditions favored the growth of Bacteroides strains; the proportion of these organisms increased from 10% in the fecal inoculum to 40 to 60% of the total bacterial count, while the proportion of gram-positive anaerobes fell.

And finally, this study wraps it all up nicely with a bow on top:

Non-adherent Bacteroides sp. and Bifidobacterium sp. have been shown to outcompete gram-positive bacteria (such as Firmicutes) for easily hydrolysable starch, while Lachnospiraceae and Ruminococcaceae persist in fibrolytic communities and are uniquely suited to degrade a wide variety of recalcitrant substrates.

Is it conceivable that starch, in a particular intestinal environment, would favor Bacteroides growth? Perhaps, in certain conditions, Bacteroides might be able to compete effectively for starch? Maybe:

Dietary intake can also affect the pH in the proximal colon, and this appears likely to be a key factor determining butyrate production. In an in vitro fermentor study with a faecal inoculum, it was found that the two major butyrate- producing bacterial groups, Roseburia/E. rectale species and F. prausnitzii, thrived at pH 5.5, whereas their population declined dramatically at pH 6.5, with Bacteroides spp. becoming dominant. In accordance with the population changes, butyrate was the main fermentation product at pH 5.5, while acetate and propionate became the main products at pH 6.5.

Ah yes, pH again. Not so optimal pH = Lots of Bacteroides = not that much butyrate. So it seems that what else is going on down there is pretty important — crucial — to how this might all play out. We’ll get back to that.

The interesting thing about Bacteroides, of course, is that while it seems they like starch, they don’t really need it. In fact, they don’t need you to feed them anything. How come? Because they’re very happy to feed on you. Your mucins, specifically:

Mucin-type O-glycans are the primary constituents of mucins that are expressed on various mucosal sites of the body, especially the bacteria-laden intestinal tract. Mucins are the main components of mucus, which is secreted by goblet cells and forms a protective homeostatic barrier between the resident microbiota and the underlying immune cells in the colon.

And Bacteroides love those O-glycans. Feel like starving them? That’s fine:

According to nutrient availability, B. thetaiotaomicron can redirect its metabolism from dietary polysaccharides to host-derived polysaccharides, including mucus, and vice versa, and further refine its niche specificity. This ability of B. thetaiotaomicron to grow on mucus contributes to its colonization and persistence in the GIT.

This study found that Bacteroides “revealed a capacity to turn to host mucus glycans when polysaccharides were absent from the diet.” Some might call that opportunistic. Me? Enterprising.


As Bacteroides species are also potent mucin degraders, one may therefore assume that mucin degradation may be a more important process in the transverse colon than in the ascending colon.

Might this mucin degradation have something to do with the Bacteroides correlation to inflammatory disease? Maybe:

Another possible mechanism by which members of the Bacteroidetes probably contribute to the pathogenesis of colitis is by the production of mucin- degrading sulphatases. Elevated levels of bacterial mucin- desulphating sulphatases have been reported for patients suffering from active UC. Furthermore, the existence of enzymes that will partially desulphate mucins has been demonstrated for B. thetaiotaomicron, B. fragilis and for Prevotella spp., suggesting that members of the Bacteroidetes could contribute to chronic inflammation by an impairment of the barrier function of the epithelial cell layer.

Now do you see why blaming the rise of Bacteroides on the consumption of animal-derived foods seems a bit…off? Bacteroides don’t need that fancy grass-fed ribeye you just scarfed down. They have you and your host-derived glycans. They love it when you starve your gut, because they have a plan B, and a lot of the other guys don’t.

As such, Bacteroides are hardy bacteria. They are survivors. It’s almost as if they are our “default” gut inhabitants. In this Wired piece, we see that 9 months after a subject is treated with antibiotics, their entire gut is populated by just one bacteria: B. thetaiotamicron. Creepy.


Alright. Time to stand back and take a deep breath before we descend into mass hysteria.

Here’s the point of all this: I think it’s clear that putting a ton of emphasis on one, sole source of fermentable fiber doesn’t make much sense for your microbiome, and never did. Why? Because the microbiome is a highly complicated ecosystem, and the idea that one can game it this way is unrealistic.

Does this mean RS intake, in general, is somehow counterproductive? Of course not. Could singling it out as a sole or predominant source of fiber with a Western diet-shaped gut perhaps induce some sort of non-ideal imbalance? Maybe. But it’s a major ancestral source of prebiotic fiber, without a doubt. And there is plenty of good research showing that RS does in fact do what it’s supposed to. This study tested starch competition between a few butyrate producing Clostridia and Bacteroides, and the butyrate producers came out on top. And here we have three in vivo human studies showing the same — resistant starch significantly boosts Clostridia and butyrate in human subjects. That’s pretty good evidence, and shows that our initial conclusion about how RS is working wasn’t off base. It was probably right. In theory, that is.

But in reality, things are more complicated. As Tim’s gut report shows, results are probably going to be highly variable. It could very well be that Tim’s gut report is a total outlier. But I sort of doubt it. I think what it probably means is that results will be all over the place, and that the gut you start out with will be a critical factor. And probably overall diet. Which brings us to our final and concluding point.

In the end, it shouldn’t really matter how one single source of fiber affects one’s microbiome, because that’s not what your gut was built for — or at least shouldn’t be. Luckily, there is one great equalizer in all this: diversity. Plant diversity. Microbial diversity. A diverse intake of fermentable fiber that feeds a diverse population of bacteria.

As we said before, substrate competition means different bacteria come to the party for different reasons. Amylolytic (ie, starch-degrading) bacteria are just one subset of the microbiome. Remember how the overall pH of the gut — determined by fermentation activity — is crucial to allowing starch-degrading butyrate producers to actively ferment? How do you expect that to happen if you only invite a few bugs — no matter how important they might be — to the party? It seems that a more diverse guest list may just tip the balance:

Since Bacteroides spp. appear to be less tolerant of growth inhibition by weak acids at reduced pH than many gram-positive species, it appears that the mildly acidic pH creates the opportunity for the gram-positive species to compete successfully with Bacteroides for the polysaccharide substrates. The consequence of these differences in pH tolerance, via their effects on the balance of the microbial community, was a four-fold higher butyrate concentration in the fermentor at pH 5.5, compared to that at pH 6.5.

But it goes even deeper than that. There’s another defining principle of gut microbial dynamics, and that’s cross-feeding. There is a mind-boggling level of interdependence down there. Did you know that the acetate formed by other bacteria is a major contributor to butyrate production from bacteria like Roseburia and Eubacterium? Much of the butyrate produced is not from direct feeding, but by feeding on acetate (an SCFA) produced by the feeding of other bacteria. And that’s probably just one of a gazillion co-feeding interactions. In other words, cross-feeding is another reason to invite everyone to the party: they all need each other, or it doesn’t work. And until that’s all figured out (and I don’t think that will happen any time soon), doesn’t it make sense to throw a fiber party down there and let the biology sort the rest out?

But hey, don’t take my word for it. People who have devoted their entire careers to this stuff seem to have come to that simple conclusion:

“Eat as many high-fiber fruits and vegetables and legumes as you can,” says Stanford University’s Justin Sonnenburg, a microbiologist who studies how diet impacts bacteria in the gut. “Our hypothesis is that a variety of plant fibers supports a diversity of gut microbes.

And if there’s one constant, non-controversial marker of gut health that I’ve come across consistently throughout the research, more than any other, it’s diversity. Likely because a diverse gut is a resilient one that is firing on all cylinders, fermenting anything and everything you throw at it — which means a healthy, low pH environment — and because diversity supports a robust, complex cross-feeding community. And that’s probably just the tip of the iceberg.

Is RS a panacea? Nah. That’s a pretty strong word. But it’s an important slice of the pie. In future posts, we’ll look at the evidence for what the rest of that pie might actually look like.

— Heisenbug