I should file my next few posts under Stuff I Got Wrong, or at least Stuff I Wish I Hadn’t Ignored. One is resistant starch. The other is “safe starch” as prescribed in Paul Jaminet’s Perfect Health Diet. Revisiting resistant starch led to me to revisit safe starch, so I’ll start with resistant starch.
I dismissed resistant starch because of how it came to my attention. Some articles hit the media praising resistant starch as a means of controlling blood sugar. Reading those articles, it was clear to me that resistant starch was being promoted by the makers of high-maize resistant starch – an industrial corn product. When I looked up the studies mentioned in the articles, it turned out researchers had replaced white flour with high-maize resistant starch in baked goods, and lo and behold, people who ate the resistant-starch versions ended up with lower blood sugar.
So it looked like the “Whole grains are good for you!” story all over again: replace total crap with less-than-total crap, and people have better health outcomes. That doesn’t mean less-than-total crap is good for you. If you want to convince me resistant starch lowers blood sugar, show me the studies where it’s added to the diet, not used to replace white flour.
Turns out those studies exist and have been around for decades. I only became aware of that after Richard Nikoley took up the subject of resistant starch with a vengeance on his Free The Animal blog. He’s become so passionate about the subject, he created a permanent, top-level page on the blog called A Resistant Starch Primer for Newbies.
That page includes this brief video, which offers a clear explanation of what resistant starch is, so give it a look:
Mark Sisson also wrote a nice summary of the benefits of resistant starch on Mark’s Daily Apple.
The bottom line is that despite being labeled as “starch,” resistant starch doesn’t turn to glucose in your body. It resists digestion (thus the term) until it reaches your colon, where it feeds your gut bacteria – and that’s where the benefits kick in. The good gut bacteria digest the resistant starch and release butyrate, a short-chain fatty acid, as a result. Yup, eating a “starch” produces good fats in your colon.
And although the exact biological mechanism isn’t known (at least according to the research I’ve read), something about the process increases insulin sensitivity and leads to lower blood sugar, both before and after meals. Let’s see … glucose control, insulin control, gut health … isn’t that what drew most of us to a low-carb paleo diet in the first place?
So after Nikoley had posted enough articles to overcome my resistance to the subject of resistant starch, I finally ordered some Bob’s Red Mill Potato Starch, which is almost pure resistant starch, and started experimenting. (I’ve since learned I can just buy the stuff at our local Whole Foods.)
I started out with two tablespoons per day and didn’t experience any of the explosive-gas problems some people reported on Nikoley’s blog, so I upped it to four. I just stir it into some warm water (warning: hot water will turn it into starch, not resistant starch) and drink it.
Like many of Nikoley’s readers, I found that my fasting glucose dropped, from around 100 in the morning to around 90. Not bad, but the more impressive result has been post-meal glucose levels. As an experiment, I ate about 3/4 cup of white rice without consuming any resistant starch for the preceeding 24 hours. My glucose peaked at 150. The next day, I swallowed two tablespoons of resistant starch around 10:00 AM and consumed the same amount of rice around noon. This time my glucose peaked at 118 and dropped to 95 an hour later. In another experiment, I pre-loaded with resistant starch and then had a baked potato with dinner. My glucose peaked at 126. Lots of Free the Animal readers have reported similar results.
I was early in the experimenting phase when Jimmy Moore invited me to participate in the 100th episode of Low-Carb Conversations, so that’s what I talked about: resistant starch. My part begins at around 1:27:00 into the episode.
Jimmy, in fact, has invited Richard Nikoley to host The Livin’ La Vida Low Carb show later this month and interview his partners in crime about resistant starch. The partners are Tim “Tatertot” Steele and Grace Liu, who together with Nikoley are writing a book on the subject.
I enjoy podcasts, but I’m also a fan of written interviews, so I asked all three of them if I could submit a long list of questions, and they graciously agreed. You’re probably familiar with Nikoley already. Here are brief bios on Steele and Liu before we get to the Q & A:
Tim Steele lives in the small town of North Pole, Alaska where he is the electrical systems supervisor of a local hospital. He retired from the Air Force in 2004 after 21 years of service as an electronics technician and combat engineer. In his spare time he hunts, fishes, gardens, and studies health and food science for simple solutions to modern problems.
Grace Liu, PharmD, AFMCP, is a functional medicine practitioner with an international functional medicine practice. In addition to hormone and digestive disorders, her clinical areas of interest are autoimmune disorders, diabesity, heart disease, cancer prevention, toxins, and nutrition. As science editor, she has an upcoming book being published on evolution, the gut microbiota and how to fuel it. She also writes about gut health and other topics on her AnimalPharm blog.
On to the interview. Like I said, I asked a lot of questions and the answers are very comprehensive, so I’ll post this in two or three parts.
Fat Head: Richard, you’ve become known as the resistant-starch blogger in the past year or so. In fact, most of your posts recently fall into one of three categories: 1) resistant starch, 2) people who piss me off, and 3) people who piss me off about resistant starch.
Richard: Heh, never really thought of it that way but it does have a nice ring to it. I suppose I might add to that, those entrenched about anything, where it becomes more about the entrenchment than whether it still makes complete sense. I’d use the word iconoclastic, but I think that’s something others call you and not something you call yourself — like being humble, or something. One just doesn’t say, “I’m so humble.”
Fat Head: True, if you call yourself humble, people tend not to believe you, especially if you’re proud of being humble. Anyway, as you’ve pointed out on your blog, research pointing to possible benefits of resistant starch has been around for 30 years. There was a bit of buzz about resistant starch three years ago, but since the articles hitting the media were about replacing white flour with high-maize resistant starch, most of us in the low-carb camp dismissed it as an attempt to sell more corn products. So what prompted you to take such a passionate interest in the subject last year?
Richard: It was also dismissed out of hand because it had the word “starch” in it, and but for Paul Jaminet — who was only coming online around that time as I recall — we’d probably still be entrenched against starch. One prominent member of the overall community even called resistant starch an “anti-nutrient,” and even though he has since admitted he was unaware of it and has expressed a willingness to look at it again, that post from way back was referenced dozens of times in various forums and comment threads all over as justification to not even bother looking.
I think that’s a bad thing and I hope I never see anything anywhere like “Well, Richard (or Tim, or Grace) said this, so that settles it for me.” Nobody deserves to be taken as an authority like that. On the other hand, take a guy like Mark Sisson who, in his Definitive Guide on Resistant Starch, just plain comes out and admits he was wrong and regrets not taking a harder look.
As for me, RS didn’t cross my radar back then, for whatever reason. I was probably too busy soaking in ice cold water whilst engaging in Internet warfare or something, and when at war, things get serious in a hurry. Pansy stuff like “resistant starch” just isn’t going to cross the attention threshold.
So, when I did begin blogging about this last April — so a year ago now, or nearly 100 blog posts and over 10,000 comments ago — it was a completely new thing for me. Tim Steele, a.k.a. “Tatertot,” brought it to me and we’d just had a pretty good run with “the potato hack,” where people were essentially doing Chis Voigt’s “20-Potatoes-a-Day” deal and virtually everyone was dropping weight very rapidly.
I tried it but stopped at about a week or so. I happen to love potatoes and don’t want that to ever change. But it was very instructive and once again, caused me to begin questioning entrenched “wisdom.” So Tim had creds with me and I heard him out. He shot me enough info to take it seriously, and there was this point where I thought that if half of this stuff is true, it’s going to be huge; and moreover, this goes way beyond resistant starch. This is about the human gut biome, so you have these news things you’re seeing every day and you have all these researchers studying resistant starch, but for the purposes of better livestock, or to help a big company get their franken-RS product into every baked good on the planet — but not for gut health, but because it’ll essentially lower GI and cause 1% fewer cases of diabetes, colo-rectal cancer, or both, or something.
But I knew the Ancestral community had a very good appreciation for gut health, was paying attention, knew why it was important, had the evolutionary context in terms of probiotics and prebiotics, and really, we’re just looking at another in a set of prebiotics. All I had to do was overcome the hurdle of the “S-word.” And that was tough. We were dismissed essentially by everyone. Ridiculed, etc. But of course, ridicule is like high-octane fuel for a true iconoclast…oops, there I go again, being all humble.
Fat Head: We appreciate your humility. For those who don’t already know, what is resistant starch? How is it different from other starches?
Tim: Normally when we think of “starch,” we think of the blood-glucose spiking stuff that is one step away from pure sugar. The “bad calories” of Good Calories, Bad Calories fame. Of course, Paul Jaminet made some of the starches “safe” for us in his Perfect Health Diet, but resistant starch is something entirely different. RS was discovered in the ‘80s when scientists were trying to measure fiber in food. Under microscopic examination of the effluent of human and animal small intestines, they kept finding a confounding element that they weren’t expecting—undigested starch granules. They termed these “resistant starch.” Resistant in this case meaning resistant to enzymes that digest food.
Grace: During my schooling and training for diabetes education, no one was aware of resistant starch or how it blunts blood sugar increases just as other fibers do — psyllium, pectin, hemicellulose, and oligosaccharides. Resistant starch is consumed by the vast majority of the ‘core members’ of the gut microbes. It is a core fuel for the core gut bugs. The evolutionary purposes of fiber and resistant starch may be threefold: 1) store carbohydrate energy from the sun and photosynthesis, 2) provide structure, and 3) act as anti-freeze and stress protectors to safeguard the plant and ‘plant babies’ against environmental extremes such as frost, acid, moisture, dryness, mold/fungi, pests, and pathogens.
What I mean by plant ‘babies’ are the progeny that contain genetic material that will be passed on to the next generation of plants: tubers, underground storage organs, legumes, grass grains, fruits, and seeds and nuts. All of these contain some degree or a lot of RS and oligosaccharides that resistant human digestion. By shielding the genetic material, the fiber and RS buffered and protected the tuber, root, legume and grain from freezing and bursting open. Plants and microbial bugs were here on Earth billions of years long before Homo sapiens emerged. It is actually speculated that the extreme Ice Ages are what largely shaped the carbohydrate and fiber content in plants and their survival. To us mammals, the vast majority of these carbohydrates are indigestible; however, for the gut critters, these carbs are their favorite feasts and fuel. Our co-evolution was inseparable. Now, perhaps our de-evolution is imminent because we are suspiciously lacking our co-evolved microbial appendages. Antibiotic over-utilization, C-sections, and phobic attempts to be sterile and super-sanitary has perhaps amputated our collective guts.
Resistant starch will not raise blood glucose, unlike starch. It behaves like other fiber. The plants that have more RS also have more protein (again protecting and nourishing future ‘plant babies’) and a lower glycemic index. All of these contribute to a lower impact on blood sugars.
Fat Head: If resistant starch isn’t digested and converted to glucose, what happens to it?
Tim: Resistant starch ends up in the large intestine where it gets fermented by gut bugs into fat (short chain fatty acids=SCFA). Sounds simple, but it’s anything but! RS is the substrate for fermentation by the prime gut bacterial players, but one of the few fibers that require numerous ‘actors’ to degrade it into its final end stages. The gut is truly an ecosystem and the apex predators take first dibs on the prime rib, then the bottom feeders and scavengers get their turns eventually. The byproducts of all these interactions feed other microbes and create an entirely different structure in the gut than when simpler fibers are eaten. Inulin, legume oligosaccharides, and glucomannan are other fibers that behave the same way. The fibers found in human breast milk (Human Milk Oligosaccharides or HMOs) also share this trait. Unfortunately, when we are weaned we usually never get a good taste of these type prebiotics again, except for the tiny bits found in a few foods and snacks.
Richard: What’s cool beyond this is that we live mostly in a symbiotic relationship with the vast majority of these gut microorganisms. Keep in mind we’re talking big numbers, 100 trillion to our 10 trillion human cells. About the size of a football if packed together. People can have up to about 1,000 different species, and while the human genome is comprised of about 25,000 genes, the total genome of all the different microbial lines in our gut are about 3 million, over 100 times more. There’s more. A human generation is about 30 years while on average, bacteria go through 6 generations in a day, and they’ve been evolving for 2 billion years longer than we have.
It makes you wonder in a chicken or egg kinda way, are we just a nice house that bacteria built for themselves? And then it takes on sci-fi alien invasion proportions when you consider that via the brain-gut connection—with more neurons outside the brain than anything, including the spinal cord—it influences behavior, mood, sleep, satiety and more. I’m just guessing, but I’ll throw out there that you want to keep your mind-control aliens well fed and content.
Fat Head: If we’re talking about NSA mind-control aliens, I’d rather keep them starved and cranky, but I see your point.
Grace: It’s great you bring up breast milk, Tim! Since the dawn of breasts and breast milk, babies have received carbs (lactose) and over 100 oligosaccharides (fiber) from mom’s milk. The lactose is for the baby, but the fiber feeds the neonate’s burgeoning societies of microbes colonizing its gut and other organs. Another misconception about breast milk was recently busted as well. Mom’s breast milk contains over 700 species of probiotics (entering the mammary glands via the gut lymph circulation). On Day One of life, our superorganism symbiosis starts. Richard loves the cyborg and Matrix motifs, and rightly so!
Fat Head: “The Dawn of Breasts” sounds like a movie I might have rented when I was single, but I digress. So as counter-intuitive as it sounds, when we consume resistant starch, the stuff is converted to short-chain fatty acids in our colons. What happens to those fatty acids? Do we burn them for energy, or do they mostly feed our gut bacteria?
Grace: The SCFAs made are butyrate, propionate (metabolized by the liver) and acetate (muscle, kidney, heart and brain). Approximately 30% of butyrate is burned for host energy and the remaining 70% is rapidly absorbed to feed the intestinal cells, which are as enormous in surface area as that of a tennis court. The gut also houses a hidden brain which is innervated by over 100 million neurons, bigger than our spinal cord. Additionally the entire gastrointestinal tube is lined by immune cells; therefore, the gut is one long lymphoid organ. For an extremely large and often overlooked organ, studies demonstrate what happens when it is not properly fueled or fed. In sterile, germ-free animals, their immunity and immune organs are blunted and intestinal organs atrophied when the gut bugs are absent.
Richard: Another thing to keep in mind is that you basically have three types of these critters: 1) the symbionts, i.e., we cut a deal and it’s win-win, 2) the commensals, those who do nothing for us, but don’t harm us, either, and 3) the parasites or pathogens. The commensals are an interesting lot, because while they may not do anything directly for us and so don’t fit technically the definition of symbiosis, some do stuff for the symbionts who do, such as produce stuff they need to eat.
Keeping the whole thing in balance by feeding them fermentable fibers, primarily, is the ideal way to keep the pathogens in check. It’s chemical warfare down there, and it’s far better to have a specifically targeted antibiotic, manufactured in a 3 billion-year-old chemical plant, than to have to resort to carpet bombing or nuking the whole thing with broad spectrum antibiotics.
Tim: The end-result with the biggest impact does seem to be the creation of SCFAs, especially butyrate. A colon flooded with butyrate has a lower pH and healthier colonocytes. The lowered pH creates an environment that favors beneficial over pathogenic microbes and the increased butyrate serves as fuel for the special cells that line the colon. When these cells are fueled by butyrate, they behave normally, self-destructing when they need to and regrowing as they should. Colonocytes can also run off glucose, but when fueled by glucose, they behave completely differently. They don’t self-destruct and they are at higher risk for cancer. A low carb/high fat diet for you is a low fat/high carb diet for your gut.
Fat Head: When the makers of high-maize resistant starch sent out press releases announcing that resistant starch doesn’t raise glucose levels, my thought was “Whoop-de-do. Neither does cardboard, but that doesn’t mean eating it will improve my health.” But resistant starch doesn’t just have a neutral effect on blood glucose; it seems to have actual positive effects. Describe what you’ve heard from people about how resistant starch affects their fasting blood sugar levels.
Tim: If you replace 50% of the wheat in white bread with sawdust, the glycemic index will be cut in half! — this is how most people read those reports. But with RS, it’s a bit different. Some of the immediate blunting of blood-sugar spikes is definitely from the same action as in the sawdust and cardboard analogies, but RS is also acting as a powerful prebiotic in your large intestine, making long-term changes that affect hormones that stimulate insulin among others. Usually within a few days, many people who have type 2 diabetes or prediabetes notice lower fasting blood glucose in the morning and post-prandial spikes that are lower than normal after a carby meal.
Some really neat experiments were done by Steve Cooksey (the Diabetes Warrior) involving a dose of RS before exercising, and he clearly demonstrates that RS increased his insulin sensitivity while exercising — which is something that diabetics struggle with continuously. RS has been shown to increase whole body insulin sensitivity … that’s huge!
Richard: For me personally, RS alone wasn’t enough to get me all the way there. For some low carbers, even clinically diabetic ones, RS just works like a champ, right off. Steve Cooksey, as Tim mentioned, is one of those. Then there are others for whom it seemingly does nothing, or works for a while then nothing. I was in the middle. So, instead of 110-120 fasting, it brought me to 100-110. And in terms of post meal, I was seeing spikes maybe 20 points less but still in the 140-160 range, often.
But I had been so used to eating low carb so much of the time that it was difficult, and I had to really force myself to eat the rice, potatoes or legumes with almost every meal. As it turns out, I now prefer a bowl of my pinto beans with a couple of over-easy eggs on top to my bacon and eggs; and anyway, I was getting pretty tired of the most Paleo food on the planet: bacon. It began tasting like a salt lick to me (just guessing) a long time ago, but I digress. So, yeah, some days it’s the beans and eggs, some days “refried wok potatoes” from previously baked and tossed in the fridge to form retrograde RS that resists degradation with mild reheating.
Long story short, by getting my starchy carbs (“safe” in every sense) up to the 100-200 range, maybe 150 average, BANG!, my BG normalized, both in terms of fasting and post meal. I understand that this is hugely inconvenient for a lot of folks to hear, entrenched in low carb doctrines, but it is nonetheless true, and I’m far from the only one to report it.
Grace: What is impressive to me is how RS and other fibers improve insulin sensitivity anecdotally and in clinical trials. We have seen a huge number of improvements in fasting BGs reported at Free the Animal. If a person has noticed fasting BGs > 125 mg/dl in the mornings, then with consumption of RS, they may report that their fasting glucoses return to the 80s range. Many of these folks at FTA noticed trending of higher glucose readings the longer that they were adapted to chronic VLC. With no other changes to diet, they noted that after eating RS, their BGs began to shift downwards. It’s not uncommon to see high fasting sugars in regards to VLC diets. It is related to normal feedback mechanisms of the body to preserve circulating glucose for the high energy organs — liver, brain and muscles — by ratcheting up insulin resistance in peripheral tissues. Under perceived starvation, insulin resistance can occur at even the muscle level — exactly where you don’t want it. If one is trying to lose body fat, this physiological insulin resistance may strongly hinder your efforts. The best ways to improve insulin sensitivity in my opinion is to not starve insulin-regulating organs of what they need (gut, fiber + RS; muscles, carbs) and use the organs that use insulin — muscles. Studies demonstrate that weight loss can depend on the glycemic index of diet, but even more predominantly the insulin-resistant status of the individual.
Fat Head: People are also reporting that if they consume resistant starch, they get less of a rise in glucose levels after eating starchy foods like beans or rice or potatoes. Is there a timing issue involved? Do we need to consume resistant starch shortly before consuming other starches for that blunting effect to occur?
Richard: It was actually first called “the lentil effect” because they noted that legumes yielded less of a spike in glucose than one would expect for the amount of carbohydrate ingested, and that the blunting persisted, often into the next day, for other starches or sugars a person ate. They had unwittingly discovered what RS and other fermentable fibers do when the gut critters get fed.
Tim: What you are referring to is the “second-meal effect.” This has been studied for many years and is a normal part of our physiology. When you embark on a diet that incorporates RS at every meal or at least every day, then every meal is a ‘second meal’ and you see long term reductions in HgbA1C as well as postprandial glucose spikes.
Grace: This effect is one of the coolest side benefits. It appears to last 2-4 hours depending on the study. Many other fibers like glucomannan, psyllium and pectin have it as well. In a way it provides even further shielding from potential high-glucose damage, because one study demonstrated for a high glycemic meal with sufficient fiber and resistant starch, glucose tolerance was maintained at the next meal. Ultimately what impacts the second meal effect is the fermentability of the indigestible carbohydrates and fiber, and this is contigent upon the right species being located in the gut, which ultimately do the magic.
Fat Head: Do researchers understand how resistant starch ends up lowering glucose levels? What’s the mechanism?
Tim: Well, it’s not so much that it lowers glucose, it’s more about increasing insulin sensitivity. Remember all those hormones that people have been talking about…Peptide YY, Glucagon-like Peptide-1, Ghrelin, and Leptin? These are all modulated by the microbes in your gut. When the right microbes are present and they are being fed enough fermentable fiber such as RS, they start producing these hormones that act together with them to increase insulin sensitivity.
Grace: In the gut, pancreas and immune system are fatty acid receptors called GPRs 41 and 43. The selective fats that bind these are the SCFAs (butyrate, etc.) made from the gut microbes metabolizing RS, oligosaccharides and other indigestible complex carbohydrates.
When GPR41/43 are activated by butyrate, they decrease body fat, increase satiety (PYY), increase insulin sensitivity and other anti-diabetic effects, reduce inflammation, power immunity, suppress and shrink cancer cells, divert oxidative DNA damage, maintain tight barrier and gut function, and many other beneficial host activities. We even double our butyrate from the gut microbiota with exercise.
Butyrate from microbial production also binds the ketone receptors known as GPR109a (formerly known as HM74A in humans and PUMA-G in animals). This was a surprising and recent discovery. I suspected butyrate would bind it, but no confirmatory studies occurred until recently. It makes sense, no? We are cyborgs and controlled in symbiosis with our microbes. Microbes maketh who we are and what we burn and store. Earlier the research showed only niacin (vitamin B3), nicotinic acid, and ketone bodies could bind HM74A with fidelity and duration. Therefore many of the health benefits that short-term ketosis affords overlaps with what is achieved by optimal gut health. This is what I observe clinically as well as anecdotally at my blog Animal Pharm and Richard’s blog Free the Animal.
Tim: Thanks, Grace…you had to go there didn’t you? As if this stuff isn’t boring enough! Now you kind of see our problem, Tom: this stuff is just so complex that everyone’s eyes sort of glaze over when we talk about the magic of RS. These GPRs that Grace talks about are an incredible piece of the puzzle, but just so hard to work into conversation or even write about. GPR stands for G Protein-coupled Receptors (the G doesn’t even seem to stand for anything). And, we haven’t even mentioned Peyer’s patches, Treg cells, and defensins! Seriously, you could write an entire book on the deep science of RS. People spend their entire lives studying it, but sometimes it’s best if we answer questions like this with, “It just works…who cares how?”
Okay, I admit it: Tim’s right — my eyes did glaze over a bit with all the chemical names. I don’t like words without vowels. But I agree … if it works, it works. So far it’s working nicely for me.
More Q & A in my next post. We have a ways to go yet.
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