On resistant starch and blood glucose control

For overall health and well-being, fermented foods like sauerkraut and kefir are great.  Especially when following a low carbohydrate diet which is generally low in the types of foods which feed the gut microbiome.

For those with gastrointestinal problems, the gut microbiota is probably involved.  Whether it is bacterial overgrowth or dysbiosis, gut bugs are usually the culprit.  Treatment options vary widely, ranging from global extermination with vinegar & a low fibre diet (as per Jane Plain), or remodeling the microbiome with a prebiotic like galactooligosaccharides.   Probiotics like bifidobacteria can help, too, if they’re administered with either prebiotics or fermented foods (they need something to nourish them in transit).  Dark chocolate is also an excellent vessel.  Resistant starch is another option, although the question remains as to whether or not this is compatible with a low carbohydrate diet.

Resistant starch has been around for a while, and when I was in school it received about 10 minutes of attention during the fibre lecture.  But Jimmy Moore and Richard Nikolay have been talking about it a lot lately so I decided to freshen up on the topic.  In brief, it can be therapeutic for GI issues, but some studies have shown mixed effects on glucose & insulin metabolism.  The former is virtually unarguable, but I found the latter interesting.  And the impact of resistant starch on ketosis is included as well.

Some studies are designed to determine the impact of including resistant starch with a meal on metabolic parameters (single-dose), others are chronic dosing studies designed to determine if resistant starch elicits lasting effects.  The first study is the latter.

Dietary fibre improves first-phase insulin secretion in overweight individuals (Bodinham et al., 2012)

In this randomized crossover study, participants were assigned to receive one of two interventions for four weeks:

Resistant starch (RS): 67 grams of Hi-maize 260, which provides 40 grams of type II RS & 27 grams of regular starch
Control: 27 grams of regular starch

The amount of “available carbohydrates” was controlled (27 grams).  Type II resistant starch is found in things like raw potatoes or green bananas.

After 4 weeks, glucose tolerance was assessed via frequently sampled intravenous glucose tolerance test.  Both groups received the same dose of glucose (the relevance of this will become apparent later) & insulin.  Closed circles = RS:

Hi Maize glucose

Four weeks of RS had no effect on insulin sensitivity.  I was mildly surprised at this because it’s not uncommon for fibre interventions to improve glucose control.  Also, the title of the study suddenly became a big red flag: “Dietary fibre improves first-phase insulin secretion in overweight individuals.”  Indeed, it did: 4 weeks of 40 grams RS enhanced first-phase insulin secretion (right, insulin; left, c-peptide):

HiMaize insulin

Since it’s a crossover study, the elephant in the room must be acknowledged: 4 weeks of resistant starch induced insulin hypersecretion , which according to Barbara Corkey will cause insulin resistance and according to Robert Lustig will cause obesity.

However, fasting glucose was modestly lower after 4 weeks of RS (5.0 vs 4.8 mM, p=0.049 <– just made it!), so I don’t think this means resistant starch will cause IR or obesity… had to include this study because it is one of the very few crossover studies with chronic dosing.  It’s also part of why I said: “mixed effects on glucose and insulin metabolism” in the intro.

Resistant starch intake at breakfast affects postprandial responses in type 2 diabetics and enhances the GIP – insulin relationship following a second meal (MacNeil et al., 2013)

Breakfast was a regular bagel or one enriched in type II RS (Hi-maize 260); both had 50 grams of “available carbohydrates,” the RS bagel had ~30 grams RS.  Lunch was a quarter of a Subway sandwich.Subway glc and insulin

More in agreement with known effects of fibre, RS modestly blunted the glycemic impact of the bagel at breakfast (statistically non-significant; note the huge error bars).  The reason we didn’t see this in the Bodinham study (above) is likely because those subjects received glucose alone, whereas in this study glucose was administered with RS.  (also, wouldn’t recommend intravenous RS; that would completely defeat the purpose and probably kill you).

After lunch, glucose & insulin levels were higher in the RS group (only the insulin 2-hour AUC was statistically significant).  I can see 3 possible explanations here.  Either: 1) RS reduced the rate of bagel carbohydrate absorption, so some of the breakfast carbs were still entering the bloodstream after lunch; or 2) some of the RS itself was digested…?  it’s called resistant starch, not impervious starch; or 3) similar to Bodinham, RS tends to enhance insulin secretion, which should’ve reduced post-lunch glucose, but didn’t…

To dispute the second option, Richard Nikolay directed me to this study, which shows that type II RS doesn’t impact blood glucose (Raben et al., 1994).  They used 50 grams of potato starch, which provides ~27 grams of RS.

potato starch glucose

Considering these data together with those of MacNeil, it’s likely that potato starch doesn’t impact blood glucose levels because digestion of the digestible portion occurs at such a low rate that glucose absorption is easily matched by glucose clearance.  This wouldn’t be expected to impact insulin levels either, similar to SuperStarch:


And another one courtesy of Richard, comparing ~60 grams of a resistant starch-enriched cornstarch (“high-amylose”) vs low-amylose cornstarch for 4 weeks, crossover (Noakes et al., 1996).  At the end of each intervention, participants were subjected to a “meal tolerance test.”  Disclaimer: this wasn’t a strong intervention; high amylose cornstarch is ~33% RS, so there wasn’t very much RS in their diets.  In other words, the results of their meal-tolerance test probably weren’t affected by the 4 week diet.  The “meal” was a muffin with 60 grams of carbohydrate, 33% of which was high or low-amylose cornstarch.  So in the figures below, we’re looking at 60 grams of regular starch vs about 50 grams of regular starch + 10 grams of RS… and we see modestly lower glucose and insulin, which is likely due to: 1) known effect of fibre on glucose absorption; and  2) the fact that there was less slightly less “available carbohydrate” in the high-amylose cornstarch group.

high amylose cornstarch

The last study on type II RS, courtesy of FTA commenter Tim: 50 grams of Hi-maize 260 (30 grams of RS + 20 grams of regular starch) vs 20 grams of regular starch for four weeks (Robertson et al., 2005).  This is one of the better chronic RS dosing studies.

Meal-tolerance test consisting of 60 grams of available carbohydrate and no resistant fiber. RS, open circles:


Insulin, 5 hour AUC, was significantly lower in RS group.  No impact on blood glucose response, possibly because there was no RS in the test meal, but less insulin means improved glucose tolerance.  This is also in contrast to Bodinham & [possibly] MacNeil.

Oddly enough, the most statistically significant finding of the entire study was increased glucose uptake by adipose tissue (p=0.007) (?).  However, they did perform a hyperinsulinemic-euglycemic clamp (the gold standard) which showed a 14% increase in insulin sensitivity (p=0.027), which may have been due to the modestly greater lean mass in the RS group <– that’s a good thing; this is a crossover study.  Another disclaimer: statistics are the bane of my existence.  I’m including “p-values” here because these are crossover studies.

Moving on to type III RS, which is found, for example, in a cooked potato after it has cooled.

Impact of short term consumption of diets high in either non-starch polysaccharides or resistant starch in comparison with moderate weight loss on indices of insulin sensitivity in subjects with metabolic syndrome (Lobley et al., 2013)

This study compared the addition of 60 grams of Novelose 330, a type III RS containing 25.4 grams of RS with a similar amount of starch coming from bran & complex carbohydrates.  This was a 3-week long weight-loss study, where weight loss was achieved by a high protein low calorie diet.  By the end of the intervention, participants lost ~5% of their body weight; >80% of it was fat mass, likely due to the relatively high level of dietary protein (~150 grams).  The only other major finding was that weight loss reduced fasting insulin levels (duh), but this wasn’t affected by the addition of type III RS.

Next on the docket is a pharmaceutical-grade type IV RS, which isn’t found anywhere in nature.

Novel resistant potato starches on glycemia and satiety in humans (Haub et al., 2012)

This is a single-dose, 5-way crossover study.  Participants were given either water or 50 grams of glucose along with 38 grams of one of two RS products.  38 grams yields approximately 30 grams of RS (and some moisture, etc.).  So the RS + glucose groups were given ~80 grams of “carbohydrate,” 30 of it being RS.

Another curveball:Potato starch

As expected, and in agreement with Raben (above), RS didn’t budge blood glucose levels.  However, surprisingly, nor did it blunt the glycemic impact of 50 grams of glucose.

Resistant Starch roundup:
Type II: Hi-maize 260 (raw potato or green banana) (Bodinham’s insulin [hyper]secretion study, MacNeil’s Subway study, and Raben & Noakes)
Type III: Novelose 330 (cooked then cooled potato) (Lobley’s 3-week high protein weight loss study)
Type IV: Pharmaceutical-grade potato starch (Haub’s single-dose GTT)

Resistant starch products ingested alone don’t affect blood glucose because the digestible portion digests very slowly, leading to a very slow rate of glucose absorption (Raben & Haub).  According to the studies discussed here (Bodinham, Noakes, & Lobley), the effects of RS on insulin sensitivity appear mixed, but this is likely due to differences in study design, subject populations, etc.

There haven’t been any studies testing the impact of RS products on ketosis, but I suspect it’s just going to be a numbers game…

Two examples.

1st one:  someone in low-moderate ketosis and weight-stable.  Adding potato starch to the diet will probably reduce ketones because: 1) it’s providing glucose & calories to the body above and beyond what’s required for weight maintenance = they’re now in a positive energy balance, so the additional glucose & calories will blunt ketosis; and 2) some of the nondigestible portion will be metabolized into SCFAs, some of which will go to liver and be used as fuel, temporarily displacing fatty acids thus reducing ketogenesis.

2nd one: someone in deeper ketosis on a hypocaloric, weight-loss diet.  Adding potato starch to the diet will probably have minimal impact on ketones because: 1) unless they’re chronically ingesting large doses, not enough glucose will accumulate to inhibit ketosis in the context of a hypocaloric diet.  And 2) energy deficit is and carbohydrate restriction are two [more important] regulators of ketosis.

Some of these concepts overlap with that of dietary protein.  Energy balance is a more important determinant than the relative level of dietary protein; Phinney 1980 showed us that a diet of 50% protein doesn’t hinder ketosis in patients who were losing weight.  (and conversely, there plenty of n=1’s who say a large hypercaloric high protein meal will blunt ketones.)

If you’re on the weight loss phase of a ketogenic diet, than a couple tablespoons of potato starch won’t hinder your progress, and it’ll probably help your bowels.  If you’re weight stable with low & variable ketones, and your goal is deep ketosis, then exercise caution.

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  • Tim Steele

    Bill – I’ll be the first to agree that the studies look less than stellar when you look only at insulin sensitivity, but you can see it’s there. The real ‘magic’ with RS lies in its ability to create a better gut microbiome, especially when combined with a good probiotic.

    In real-life, long-term experience, I have found that daily supplementation with a couple TBS of raw potato starch, eating RS rich foods, and eating a good bit of yogurt resulted in lowered hBA1C, FBG, and cleared up some long-standing issues I had with sleep, cold fingers, and digestive issues that developed over 2 years on a VLC platform.

    Thanks for your interest in RS, I think it will find a place in mainstream dieting as a stabilizer of gut microbes.

    • Hi Tim, thanks for swinging by and thanks (again) for your help with this article.

      The effect of RS on your FBG is pretty much in line with most of what I’ve seen in the lit, including the Bodinham study. And I have no doubt that dietary fibre & RS will promote bowel movements… which I suspect could be related to some of the other things you’re seeing like no more cold fingers & improved sleep… but that’s all relatively speculative at the moment.

      Gut health is important.

      • Bill

        I doubt bowel movements have much to do with it. Many RS n=1s, if you’ve been actually following them, are reporting smaller and fewer bowel movements and still have the same improved sleep and body temperature improvements.

        Just my 2¢, but It would probably be wise to look at the data from the hundreds of n=1s before jumping to overly simplistic conclusions.

        • Interesting. I haven’t seen too many data on this, but this study (randomized, double-blind, crossover) showed bigger & more frequent bowel movements after 7 days of type III RS: http://www.ncbi.nlm.nih.gov/pubmed/23388502

          Same here (randomized, double-blind, crossover), after 14 days: http://www.ncbi.nlm.nih.gov/pubmed/19688627

          Perhaps this is another one of the differences between type II & type III resistant starches…?

          • Never got the obsession with taking impressive frequent dumps, I grew up in the country with a long drop and often on long camping treks with no facilities where the fewer smaller BMs conferred a significant advantage.

            I’m with Stefansson on this, 2-3 small but firm and inoffensive smelling turds a week is plenty – most else is garbage in/garbage out.

            I did an extract of Dr Eades article from 2006 about society’s obsession with epic craps in my fibre thread, here’s the full thing:


          • johnnyv

            LOL I was gonna say the same, people seem obsessed with turds. “Most satisfying BM I ever had” I will not speculate on the implications of this observation! 😉

          • Ha!

        • Butch Pornebo

          once a day maybe BUT smaller. I doubt it. Almost everyone is reporting great BM movement. Me once daily BUT the volume makes up for it and it is the most satisfying BM I ever had since I started RS. Also, check out the Bristol Chart on wikipedia, mine is always a Type 4 unless I over did my fats and magnesium the night before.

          • Bill

            I didn’t mean to imply that everyone is having smaller less frequent BMs. Mine haven’t really changed at all from pre-RS. A few people are even experiencing short term constipation:


            The point is that it’s all over the map.

            It’s not totally inconceivable that RS could enhance nutrient absorption in some people and thus reduce the size of their BMs a bit.

            But anyway, whatever RS is doing to people in the n=1s it can’t just be due to BM changes. There is some other modulation happening in most of the reports.

  • Bill, Thank you for a reasonable and factual post tackling this issue.

    I have hypothesis that contrary to the paleo quack dogma that the obese are suffering from a dire deficiency of GI microbiota, it is more likely obesity relates to general excess of microbiota. Imbalance is less of an issue as is simply excessive intake of simple sugars and simple starches, with insufficient immune boosting nutrients, and the result is pathogenic excesses of all flora.

    I can say personally after a few weeks using prebiotic, I observed wt gain. While taking “good bacteria” seemed to suppress / help symptoms like painful gas and mental sluggishness, after awhile I was finding putting on weight more easily.

    If hypercolonization of the GI by bacteria which thrive on RS promotes insulin hypersecretion perhaps secondary to modulating GIP sensitivity, this is quite a plausable mechanism to explain why diabetics seem to do well with RS. There is a lot of literature that RS affects GIP dynamics from quick google (this is type 4 RS you mention), this incretin is good for blood sugar control and promotes insulin hypersecretion but will also promote weight gain and diet induced obesity.
    Again, we see a problem differentiating between interventions for diabetes and interventions for obesity; while these sometimes overlap this is not always the case, and very often it is true things that help diabetes do so at the expense of weight gain… and things that help weight loss (like stimulants, high SNS tone and thyroid hormone) may make diabetes worse.

    This would however explain why diabetics observe progressively lower blood sugar levels, if their GIP receptors are more sensitive, but we would also expect then perhaps easier weight gain due to higher insulin levels / increased basal insulinemia. Again this is great for diabetes but not so great for adiposity.

    Last, my thoughts on this silly RS hullabaloo is this. If you are a crash dieter who refuses or is unable to adhere to a sane low carbohydrate diet, day in and day out, you are probably better off eating cold pasta, cold potatoes, and drinking RS in the morning. Most of these RS success stories RN is bragging about go something like this:

    “I sorta low carbed for 5 years, but I kept eating massive burger king meals with crap food every few days, and my blood sugar/immune system was a total wreck. Then I tried RS , which is easy for me to stick to, and now I am doing well”.

    ^^Yea, I’m sure a half assed low carb diet is terrible compared to consistent application of a moderate carb diet with supplemented RS. However, it is a FAR jump to conclude that low carb is the inferior intervention for diabetes and obesity, simply because many people find it difficult or impossible to apply consistently day in/ day out.

    Including Richard, who has been jumping through hoop after hoop for MONTHS now , to avoid the obvious conclusion that eating carbs is making him gain weight, and all of his potato/milk crash diets are not as effective as was his basic meat and vegetable “paleo diet” he started out with.

    I understand that for normal people, vanity and a desire to be thinner is not a compelling enough reason to give up tasty corn tortillas and rice and stuff like this for life. However, let’s not pull a CARBSANE here , and orchistrate elaborate strawman to justify your personal choice to eat a varied, tasty diet, at the expense of body weight and/or blood sugar control.

    I will not tell anyone they HAVE TO!! eat low carb or else, and moderate carb + RS is better than nothing at all…but don’t come and tell wooo that I am eating an inferior diet. This is a total lolfest, my VLC diet is ten thousand times healthier, my blood work is perfect and I am quite thin. My blood pressure is like 100/60 , I have zero inflammation, if I get a cut it bleeds 4 days (will never get stroke/heart attack), my blood sugar almost never goes above 80s, after meals I only measure it at like 115, et cetera. I look 25 not 31.

    Like I said totals sympathetic that most normal ppl wanna eat some chilli and rice and don’t want to hear this crap that they are better off on very low carb… and yes, people are better “settling” for the diet htey can stick to, vs trying to do a 50 carb diet and then binging out on cake/cookies or plates of pasta and rice, and writing FTA complaining of it. Woo simply does not eat these things. I maybe have 1 cookie that is sugar free at work. That’s why wooo is healthy and thin.

    From my vantage point, I look at this RS thing just like the tato crash and the milk crash: A carbsane like self delusion to avoid the obvious conclusion one is way better off on a low carb diet, and while RS + starches is better than starches alone, NO STARCHES/LOW CARB is best for most non-athletes who are old/fat/metabolic d/o train wrecks like wooo.

    • I also want to address this persistent myth that a ketogenic low carb diet is deficient of fiber.

      I have rule 34’ed my sexy pee pee strips many times, so you all know I am in ketosis pretty much 24/7. However, my dietary fiber intake is pretty absurd, given I consume flax seeds, at least 3 ounces of almonds/peanuts per day, as well as vegetables like avocados, broccoli, celery, and leafy greens.

      The irony is my diet is probably waaaay amazing and quite prebiotic, which is probably why i ended up with such a bad case of GI dysbiosis in the context of low vit d/zinc stores, stress, and sleep deprivation from shift work.

      So, as for the STRAW MAN that low carb / keto diets “aren’t good for your GI microbiome”, this is nonsense, and I would argue my diet is way better at fostering good bugs than some diabetic fooling himself into thinking he’s doing himself a favor eating a potato with a wopping 2 or 3 grams fiber that will spike sugar 140+

      • Wenchypoo

        As I understand it, FAT moves the stool anyway–not so much fiber. Here’s an article I read about this: http://www.marksdailyapple.com/dietary-fiber-is-bad-for-sex-thats-the-only-claim-about-it-that-isnt-a-myth/

        From my own experience. it’s true.

        • Eating anything promotes peristalsis and bowel movements; high fiber low calorie dies will exhibit constipation, as will low thyroid states. Fat does promote bowel movements, but really eating in general does.

          • an old GI textbook I have says exactly that: bowel movements should follow meals. All of your meals. Kind of makes sense; may even be healthier. But not very practical.

            Also, one of the MD’s who was onsite at “The Biggest Loser” was telling me about common health complaints… bowel movements were as infrequent as 1/week in some participants. They were on very low calorie, zero-carb diets.

          • Jack Kruse

            ^^^gastocolic reflex.

          • Carol Loffelmann

            Babies demonstrate this reflex much more than non babies. Feed the baby, change a diaper.

          • Babies don’t know that 3+ bowel movements per day is socially awkward. They don’t learn this until they’re non babies 🙂

        • Stefansson said that constipation was frequent when they didn’t have access to fatty meats. Easily remedied by adding a lot of fat to meals.

          • Gašper Grom

            yes, in the past I often used protein only diet last weeks befor bb competition if in hurry. without the addition of fiber constipation is usualy.

        • Gašper Grom

          After few months on very high fat, low carb, medium protein diet I do have best bowel moments and peristalsis control ever. It takes some time to adjust (probably colon muscle strangening) but now it is perfect. I eat very little fibre, some veggies in one meal per day.

          • Fibre can be therapeutic for people with some GI issues, but it’s certainly not essential for regularity.

          • Gašper Grom

            Probably because it slows down the passage of glucose into the blood. What about the ability of removal of various toxins from the intestines. Is there anything to this?

          • I think so. I don’t know of any specific examples, but some types of fibre can bind up a lot of things – both good & bad.

          • Wenchypoo

            Nor is it required to pass colonoscopies with flying colors—Hubby and I are both proof of that. If anything, a low-fiber diet HELPS with the clean-out process!

          • Good to know!

      • Thanks. Makes sense although not entirely myth –> ASH SIMMONDS.

        But I see your point; ketogenic diet can easily accommodate adequate fibre.

        • Haha, my contention is what the term “deficient” means!

          Is someone deficient in fibre because they consume none? Well, no – because zero is the EXACT amount required.

          Can the gut microblah and colon stuff be assisted with all the fibre and other gear? For sure. That still doesn’t imply a deficiency, just that someone may require interventional methods.

          So yeah, as far as I’m concerned the idea that LC/ketards are deficient in fibre is definitely a myth.

          I’ve put my general thoughts and those of a bunch of others in here: http://highsteaks.com/forum/health-nutrition-and-science/fiber-not-good-you-198.0.html

          Basically, if you eat a junk diet or have a specific need to do something to your body that fibre does, then yes fibre is useful. Otherwise, it seems wise to limit it to “healthy” foods like veggies and fruit.

          BTW, finally finished your book yesterday, will do a bigger write-up on it soonish (still hooning around NZ), loved it (probably confirmation bias :p )..

          • I think most of us are in agreement: no such thing as dietary carbohydrate deficiency – that includes fibre.

            Awesome, let me know when/where you post it. TPMC was probably a pretty easy read for you. (did you see the fly on the cover?) (I didn’t until it was far too late)

          • Michael

            Flies, Bill. Plural. Colorblind people distinguish these much easier!
            Very nice post, btw. Always love to see your take on these topics. Thanks.

          • Michael

            Btw, remember Carol, she speculated that it was a subliminal message about the need for protein.

          • Flies PLURAL!? crap.

            Thanks 🙂

          • You use many more big words than me (reflects your science background vs my rogue research methodology), but otherwise yeah no real new concepts, just great to see nearly everything that needs to be covered to combat CICO in one handy reference.

            I’m particularly interested to explore further the stuff toward the end (spoilers?), I don’t think the role of glycogen and RQ measurements are specifically correct in the way they are currently accepted/simplified, but that’s a whole ‘nother book… The Poor, Misunderstood Glycogen? :p

          • wrt RQ & glycogen… do tell!

          • Oh and I read it on my phone, so the “cover” is like one inch tall, so no, did not notice the fly until now… Ha.

        • Wenchypoo


        • Jack Kruse
    • I definitely agree that obese microbiota is dysbiosis in part due to crap diet, but also what you said on your GI blog… seems like a “complex interplay between glucose homeostasis, immune system, microbiome, and diet.”

      Not entirely surprised about your probiotic experience, but also not entirely convinced in Jeff Gordon et al.’s theory that certain microbes induce weight gain by harvesting more energy… seems like the amount of calories would be minimal; and why wouldn’t SCFA calories influence satiety?

      Epic summary of the “hullabaloo!”
      half-assed LC improved by cleaner moderate carb + RS;
      & new strawman (assuming this is pathological RS-deficiency).


    • KM

      + 1, 100 times over.

    • persistentone

      Definitely I don’t want to get into the middle of a shooting war between you and Richard, but I will share my potato starch data points:

      * It did not lower my fasting glucose. On several occasions, it seems to have disregulated my glucose metabolism with much higher numbers. So I am keeping my doses of potato starch low for now until I figure out if this is a short-term effect or something else.

      * For me, no question potato starch induces a deeper and more restful sleep. At some level this becomes like a sedative and affects my next-day performance, but at low doses it only seems to improve sleep.

      * It affects stool volume dramatically and immediately. I have tried lots of other types of fiber and prebiotics, and nothing comes close to the effects of raw potato starch. That alone makes me think the colonic bacteria are not well fed on whatever diet I have been on, and the raw potato starch appears to be like rocket fuel for the colonic bacteria.

      Regarding your theory on obese people having an abundance of bacteria due to overeating carbs: remember that digestible carbs are largely absorbed before the colon sees any of this. That is why so many of these people have constipation issues. Their bodies are hyper-efficient at absorption of glucose from digestible carbs. What gets through to the colon is the indigestible fragments of fiber, and apparently those are in a form that are insufficient for bacteria to ferment to develop sufficient mass. The whole point of the raw potato starch is to bypass the small intestine and to directly deliver to colonic bacteria significant amounts of carbohydrate that they can easily digest.

      Regarding your weight gain: is it possible that was water weight in the colon? Did you do any kind of weight composition testing to see if your fat percentage had gone up at the same time weight went up?

      The most intriguing part of the whole potato starch thing for me is that they might be producing significant amounts of ketones by passing short chain fatty acids to the liver. I have not been motivated enough yet, but would really like to see data from someone who does ketone measurements every two hours after ingesting a large amount of raw potato starch. My guess is we might see some very measurable ketone generation there.

      • just one comment ~ the GI tract is full of microbes, and overgrowth in the more proximal parts could also be problematic for some; eg, SIBO.

        On another note, I’d also be very interested to see serial ketone measurements after a big dose of RPS.

  • Wenchypoo

    After reading an article about resistant starch types and how (or if) they affect blood glucose (over at Free the Animal), I decided to try unmodified potato starch out on Hubby, who may as well be a Type 1.5 diabetic not on insulin–I have him controlled with supplements and a VLC diet.

    The potato starch worked the first time we tried it, but after that, it didn’t do so well. The same thing happened when he tried strawberries–first time okay, second time not.

    We’ve also discovered that Omega-3 foods also raise his BG, whether they’re in meat form or veggie form.

    So far in his life, the only thing that DIDN’T move the needle is stevia (cut green leaf type), but he hates the after-taste. I’ve been seeing more and more recipes call for Swerve sweetener or stevia glycerite (supposed to not have after-taste), so we’re trying both out next week to test their claims of not causing BG to rise.

    • That’s an unfortunate side effect of omega-3 fatty acids. Not uncommon to see modestly elevated BG with fish oils.

      And congrats on keeping hubby controlled with supps & VLC!

    • Butch Pornebo

      how did you consumed the potato starch ?

      • not sure how Wenchypoo did it, but Bob’s Red Mill Potato Starch seems like a popular option. A couple tablespoons daily.

        • Butch Pornebo

          Well, there are some very important little details to make it work and unfortunately if it is consumed differently it will have a different effect. Like it must be consumed uncooked because if the potato starch is cooked it turns into digestible starch. which will spike blood sugar. Also, tried it 2 days. Is she expecting a miracle. IF she read the FTA articles it is estimated that it might take 2 to 4 weeks to see some results. Sure there are some folks who are lucky enough to see positive results.

          • right, cold & raw.

            And yeah, I tend to agree that depending on what you’re expecting it to do, it could take some time. For example,it might take a few weeks to resolve long-standing GI issues, but it could blunt a spike in blood glucose the first time you take it.

            And also, like you said, there will be some “lucky” n=1’s that respond differently.

          • Butch Pornebo

            that is true it could have an immediate effect on blunting a spike in BG and based on my own experience a “second meal effect” as described by TIM. case in point, on a High Intensity Training day I would always have a high CARB BACKLOAD meal and this usually will kick my BG to like 120+ or so BUT after doing the PS protocol for only a few days, that CARB BACKLOAD I did showed up @ 90 in the BG meter. It is even lower than my FBG. Because of the “dawn phenomenon” my FBG varies between 85 to 105. I’m hoping that the RS protocol will lower my FBG to around 75-80 once everything stabilizes.

          • That’s interesting, Butch, thanks. Glad to hear the backload protocol isn’t producing BG > 140, which is the response I suspect some are seeing (based on Kiefer’s description).

            Also, I just had the pleasure of meeting Tim; the guy really knows his stuff!

          • Butch Pornebo

            only if people realizes the simplicity of the protocol. i mean it is so stupid simple 🙂 and some other blogs stating that you will get the best RS from grains. the highest amount listed was from unrolled uncooked oats. you will get like 12g of RS PER 100 grams. You have to eat almost 3/4 lb of that just to get close to 4tbs of unmodified potato starch plus it is so cheap as of now. Another good option is to eat a whole raw plantain. get used to it or dry it out before consuming it taste like crackers.

          • Do you know Kiefer? If so, please tell him know about your strategy. I really think a lot of his followers are experiencing huge BG spikes…

    • persistentone

      Mix one part Stevia with four parts erythritol. The latter is a sugar alcohol that does not metabolize and passes through urine. In the combination I give, it tastes very close to sucrose and has zero calories.

    • Butch Pornebo

      Maybe OOT, but being in nutritional ketosis requires a ketogenic diet ?

  • Bill:

    Let me just comment on our Twitter convo just now. You asked me about the last few paragraphs.

    This is something we’ve dealt with a number of times in my comments. People get confused because of the 10g carbs per TBS on the label for potato starch. Thing is, that’s for COOKED, as that’s how people use it (baking, thickening sauces, etc).

    The cool tweak here is that we’re consuming it “off label.” The label doesn’t apply. They are handled by the gut bugs, food for them. Potato starch is 80% RS, 20% water, yet it is a very dry powder. Where’s the moisture? It’s locked inside the RS granule structure, like popcorn, and consuming it off label as we do is the equivalent of swallowing a handful of popcorn kernels vs chewing and swallowing popped popcorn. The former is going to pass through and end up in your poop and the later is going to spike your glucose.

    Accordingly, RS doesn’t give you a microgram of glucose. It MAY give you SCFAs but c’mon, how negligible is that and moreover, SFCAs would support Ketosis and probably in a number of ways. What I think is not known is how much of the SFCAs go to your cells vs other gut bugs, and what’s the downstream consequences. Hard for me to buy that that small amount of fat accounts for the feelings of satiation, though I’m certainly open for that. I’m more banking on gut/brain connection and heightened, more resolute hormonal signaling.

    • Phil Thompson

      Carbohydrates on the label are carbohydrates in the product. It says nothing about how digestible they are.

      http://ajcn.nutrition.org/content/41/6/1244.full.pdf+html Table 3 seems to show 5% or less of potato starch is not absorbed, ie 95% is absorbed, or did I misunderstand ??

      • Try it yourself, Phil. Take 60g (8 TBS – 80% “carb” 20% water) in water on an empty stomach, check your BG over 2 hours. You’ll get just normal fluctuations. Then, take the same 8 TBS, nuke it for a minute, eat the gel with a spoon after it cools. Watch your BG spike big.

        Many have done this, same result. 4 TBS would work too.

        • No need! we’ve got a couple randomized, blinded, crossover studies showing exactly that.

        • Phil Thompson

          the low GI of resistant starch is well documented and http://ajcn.nutrition.org/content/60/4/544.full.pdf reports negative AUC for resistant starch glucose response. Table 2 therein suggests RS is <80% of the dry matter in potato starch.

          • Interesting, thanks. From their analysis, 27% of the starch in cold raw potato starch proper is digestible. 54% RS.

      • Thanks for the link. It looks like they were using a baked potato as their source of potato starch… likely very different from cold raw potato starch.

        • Phil Thompson

          Mea culpa, missed the reference to the baked potato as they used “potato starch” throughout. A rework on resistant starch would be good, don’t fancy doing a DIY ileostomy to satisfy my curiosity and don’t have access to radiolabelled starch for an n=1 🙂

          • Ha! yeah, the ileostomy does provide a unique model to study digestion… but wouldn’t volunteer 🙂

    • Thanks for coming over from Twitter. Much easier to get ideas across.

      Regarding the glucose we absorb from cold raw potato starch, here are my thoughts:

      The gas & bloating reported in the Robertson study (among others) pretty much confirms that some of the stuff is indigestible. I don’t doubt this.

      On the other end of the spectrum, SuperStarch is completely digested & absorbed but doesn’t affect blood glucose levels. –> suggests glucometers are a poor indicator of glucose availability in some contexts.

      In the Raben study (as Phil pointed out), 27% of the starch in cold raw potato starch is digestible… but this doesn’t impact blood glucose levels bc it’s like SuperStarch.

      • Thomas Hemming Larsen

        Does this simply mean that there is a difference between eating a hot or cold boiled potato? What if you reheat it after it has been boiled?

        • Raw cold = type II RS.
          Cooked, hot = no RS.

          Cooked, cooled = type III RS.
          Cooked, cooled, reheated = no RS.

          • Thomas Hemming Larsen

            Sorry Bill, I realise that after reading it more thoroughly you did mention that already.

          • Bill, Tim would have a reference for this but RS3 is resistant to reheating. And in fact, particularly with legumes, each cooling and reheating, recoiling cycle actually forms more retrograde RS (RS3). However, it’s a curve. Biggest bang is the first cooling.

            You know how most Mexicans make refried beans at home (my in-laws are Mexican)? They actually start out with regular pinto beans. Leftovers go in the fridge to be reheated, recooled, reheated, etc. as part of every subsequent meal. After a while, you’ve got refried beans. 🙂

          • it doesn’t have to be cold potatoes!?

            Down the rabbit hole… now I’m curious as to the amount of digestible & resistant starch in each of the above examples (surely they’re all less than uncooked Bob’s Red Mill PS).

            Also, given the differential impact of RS isoforms on various health outcomes: type II RS from 1 potato vs. type III RS from 1 potato. (quantity & quality, predicted effects, etc.)

          • Tim Steele

            1 pound of raw potato = 4TBS of Bob’s PS

            1 pound of cooked and eaten hot potato = 1tsp of Bob’s PS

            1 pound of cooked, cooled, eaten cold potato = 1TBS of Bob’s PS

            1 pound of cooked, cooled, reheated potato = 1.25TBS of Bob’s PS

            1 pound of cooked, cooled, reheated, recooled, reheated = 1.5TBS of Bob’sPS

            See the trend? Doesn’t have to be cooked and cooled, the retrograde action keeps adding, but not much more after the first cycle. The reheating needs to be a quick, hot heat, not boiling.

            Works the same with rice.

          • Thanks! Very interesting.

          • Thomas Hemming Larsen

            Will potato starch that’s used for thickening a custard (and therefore brought to a boil) then be type III RS after it has cooled?

          • I believe so. And it will have 75% less resistant starch then when it was raw (as per Tim’s comment, below).

          • Thomas Hemming Larsen

            Yes, exactly. The benefit does diminish but I think it would still be better than corn starch for putting together a traditional Danish layer cake 🙂

          • Thomas Hemming Larsen

            It seems like the potato flour in Denmark is made from raw potatoes and therefore has the highest content of RS II.
            I’m definitely trying it – both raw and in a custard. I saw Richard say that the breakdown of the RS happens at 160F which might be high enough to thicken a custard. It woould be fun to quantify the difference between the two ways.

          • Have you been following this on Facebook? Someone contacted the people at Bob’s Red Mill… their Unprocessed Potato Starch isn’t “raw.” The potatoes are boiled at an early stage of the extraction.

          • Thomas Hemming Larsen

            Yep, I even shared some of your great wisdom 🙂
            I got some from a Danish company called KMC. I’ve written them to hear if they boil the potatoes or not.

          • Ha! awesome.

            I’d be great if these companies actually tested the RS content, instead of us having to guess based on their production methods. But testing is probably expensive… and what do they care? They’re marketing a cooking ingredient, not a health product. Oh well.

          • Thomas Hemming Larsen

            I’m sure they do – but why spend time on publishing it when only a few crazy people on a blog care about it.
            I’ve asked them about the making and how much resistant starch it has. In any case 0.5kg was only one dollar so I’ll live even if I have to give it to mom 🙂 This is the product

          • Good point.

            And that actually looks like a pretty good source of potato starch… please let me know if they respond!

          • greensleeves

            So this means actually none of the starch is resistant then, since we don’t know that it’s ever been cooled enough to form the RS3. Game over.

          • stick it in the refrigerator!

  • Bill,

    I’m interested in the effect RS (specifically PS) has on short term and longer term levels of insulin.

    I’m more interested in a study showing just the ingestion of PS vs a placebo. .

    This is a study you linked to from RN on your post. http://www.ncbi.nlm.nih.gov/pubmed/8092089 says,

    “After the R meal postprandial plasma concentrations of glucose, lactate, insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1, and epinephrine were significantly lower compared with after the S meal. ”

    I have anecdotal evidence and an N=1 from a T1 who produces -0- insulin that supports this.

    But would like to know if you have anymore info on this.



    • Hi Steve, thanks for bringing the discussion over from Facebook.

      As to the Raben study you cited: I have no doubt that PS alone won’t cause a spike in glucose, similar to your experience and that of the T1 you mentioned, especially because Raben showed the digestible starch in their raw PS to be only ~27% (w/w) and people aren’t taking 200 grams of PS at a time.

      There’s also no effect of type IV RS alone on blood glucose as per Haub’s study (PMID: 22655177).

      As to the effects PS has on insulin long-term: one of the ways RS is thought to improve glucose control is by enhancing the incretin response, which will improve insulin secretion. This is kind of like what they saw in the Bodinham study (PMID: 22815837) and in the one by MacNeil (PMID: 24195618). Also, in this rodent study: http://www.ncbi.nlm.nih.gov/pubmed/18796545.

      What do you think?

  • wooo fans

    Is “Hydroxypropyl-Distarch Phosphate” a resistant starch too? I read it refills glycogen and burns fat at the same time

  • Wenchypoo

    They’re now onto parboiled white rice as RS over at Free the Animal (http://freetheanimal.com/2013/12/parboiled-nutritious-resistant.html). I asked them if anyone considered the arsenic level in this stuff.

  • Resistant starch and IBD (from Tim)

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  • Thanks for this article.

    I just started on two tbsp Bob’s Red Mill potato starch and so far, so good. But I was thinking about cutting back to one tbsp long term, and the cautions you’ve sounded make me think this is probably wise so that’s what I’ll do.

    • Thanks for the link.

      I really don’t know what to make of the hyperinsulinemia data… if RPS enhances the incretin response, then we’d certainly expect to see greater insulin secretion. In any case, cutting back to 1 tbsp seems prudent; this doesn’t seem like a clear-cut “more is better” type of thing.

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