Resistant Starch: An Overall Primer, with References

In the process of drafting Part 2 of all the research (here's Part 1) I came across this: Resistant Starch Intakes in the United States. Its purpose is to analyze data in order to estimate average intake of RS and to provide a list of foods and how much they contain. They conclude:

The estimated intake of resistant starch by Americans is in the range of approximately 3 to 8 g per person per day. [...] By combining estimates of resistant starch intake with those of other components of dietary fiber, researchers and food and nutrition professionals will be able to more accurately estimate total intakes of carbohydrate compounds that escape digestion in the small intestine and provide nutrients and function to the large intestine.

Thing is, there was a really excellent whole initial discussion of Resistant Starch and why it's important. So, I began pulling some of the more important references for my Part 2 draft. But at a point, I thought it best to give you the whole, raw, undigested section along with the resistant references.

OK, Now Listen Up: if, so far, you've been all "meh" about this whole deal or, you're still stuck on the word "starch"...i.e., still ignorant of the fact this is not the kind that "spikes" your glucose but most often: lowers it...then take a breather, relax, put away your LC and Paleo Bibles and Catechisms, and just check it out...and cure your ignorance (e.g., "I can get all the butyrate needed eating butter.").

I've denoted my emphasis in bold, below. Some of those more important references will be included in my next post.

~~~

Dietary fiber represents a broad class of undigested carbohydrate components. The components vary in chemical and physical nature, and in their physiological outcomes. Some of the better known components include cellulose and lignin. It is now widely known that some dietary starch escapes digestion in the small intestine, and upon reaching the large intestine also acts as a component of dietary fiber in the body. This starch could potentially be a major contributor of fermentable carbohydrate in the large intestine.

Starch exists as large glucose polymers localized in granules in plants, although processing and preparation can change some of the starch to nongranular forms. Starch polymers can either be straight chain (amylose) or branched chain (amylopectin), and both are a source of dietary carbohydrate and energy (1). The structure of starch polymers and granules influences its digestibility, so consequently not all starches are equally affected by digestive enzymes (2). The starch that is not digested is called resistant starch, and the recognized definition for resistant starch is “the sum of starch and products of starch degradation not absorbed in the small intestine of healthy individuals” (3).

Four main subtypes of resistant starch have been identified based on structure or source (4). Starch that is physically inaccessible to digestive enzymes is called resistant starch type 1 (RS1). RS1 is found in whole or partly milled grains and seeds so would be present in whole-grain foods. Starch that is resistant to digestion due to the nature of the starch granule is referred to as resistant starch type 2 (RS2); this type of resistant starch is found in raw potato, unripe banana, some legumes, and in high amylose starches such as starch obtained from high amylose corn. Resistant starch that forms from retrograded amylose and amylopectin during food processing is called resistant starch type 3 (RS3). This resistant starch form is found in cooked and cooled foods such as potatoes, bread, and cornflakes. The fourth type of resistant starch, resistant starch type 4 (RS4), is produced by chemical modification.

The physiologic effects of resistant starch have been studied during the past 30 years in animals and human beings and include health effects in the large intestine and systemic effects. Health benefits in the large intestine include enhanced fermentation and laxation; increased uptake of minerals such as calcium; changes in the microflora composition, including increased Bifidobacteria and reduced pathogen levels; and reduced symptoms of diarrhea (5). Systemic effects involve plasma glucose and insulin, insulin sensitivity, and fatty acid oxidation (6).

Most early research on the health benefits of resistant starch focused on fermentation-related outcomes. Shortchain fatty acids, primarily acetate, propionate, and butyrate, are produced during resistant starch fermentation. They directly influence the large intestine environment, for example, by lowering intestinal pH, which inhibits the growth of pathogenic bacteria, increases the absorptive potential of minerals, and inhibits absorption of compounds with toxic or carcinogenic potential (7). Shortchain fatty acids also stimulate colonic blood flow, increase tone and nutrient flow, promote colonocyte proliferation, and reverse atrophy associated with low- fiber diets (7).

Consequences of resistant starch fermentation are well established in clinical studies, particularly for resistant starch from high-amylose corn, which is the most widely studied source of resistant starch. Currently there are insufficient studies to compare different types and sources of resistant starch, so it is prudent to assess consistent effects across similar sources of resistant starch. Results of nine clinical trials evaluating the effects of resistant starch from high amylose corn on measures of colonic fermentation are summarized in Table 1. Significantly increased fecal weight was found in four of the nine studies measuring this endpoint. Resistant starch doses used for fermentation-based studies are typically high, and minimum effective dose is typically not assessed. The median effective resistant starch dose for the fecal weight endpoint was 38 g, and the minimum effective dose used was 22 g. Fecal pH decreased significantly in four of the seven studies measuring this endpoint. Statistically significant increases in fecal butyrate concentrations were found in four of the five studies assessing this endpoint.

Limited studies have assessed clinical effects of other sources of resistant starch. For example, intakes of 17 to 30 g resistant starch from potato, banana, wheat, and corn resulted in significant increases in fecal weight and short-chain fatty acid excretion (17). Others have assessed the synergistic effects of resistant starch in combination with other sources of dietary fiber. Intake of 22 g/d RS2 from high amylose corn in combination with 12 g/day dietary fiber from unprocessed wheat bran increased fecal weight, decreased fecal pH, decreased fecal total phenols and ammonia concentrations, and increased fecal short-chain fatty acid concentration relative to the wheat-bran group (10).

Some short-chain fatty acids are absorbed across the intestinal mucosa with effects extending beyond the large intestine. Robertson and colleagues (18) reported increased insulin sensitivity in healthy subjects fed 30 g/day RS2 for 4 weeks, suggesting a link with nonesterified fatty acids. Higgins and colleagues (6) fed healthy subjects a single meal containing 2.5, 5, or 10 g RS2 per 2,000 kcal and noted increased meal and total fat oxidation suggesting inhibition of acetyl coenzyme-A derivation from carbohydrate relative to fat in the liver. The benefit was observed at 5 g but not 10 g resistant starch, suggesting a fermentation/excretion threshold, or possibly increased lipid excretion due to a resistant starch/ lipid association. Emerging research in animals has linked resistant starch fermentation to satiety, with increased expression of genes coding for the satiety hormones PYY and GLP-1 when rat diets contain RS2. Increased concentrations of these hormones were also measured in plasma (19,20).

Not only does resistant starch benefit health via fermentation, but because the starch does not contribute directly to blood glucose, it also helps to lower blood glucose and insulin levels. Reductions in plasma glucose and insulin responses were seen following meal-based resistant starch intakes of 11.5 g resistant starch (12), whereas postprandial blood glucose and insulin responses in adults with untreated borderline diabetes were lower after eating a meal containing 6 g resistant starch (21). Postprandial insulin responses decreased slightly but significantly in hypertriglyceridemic patients following consumption of a meal containing 5.8 g resistant starch (8). Glucose and insulin effects are less apparent when available carbohydrate is matched between test and control diets; for example Higgins and colleagues (6) reported no effects when meals contained up to 10 g resistant starch. [...]

References:

1. Mann J. Carbohydrates. In: Bowman BA, Russell RM, eds. Present Knowledge in Nutrition. 8th ed. Washington, DC: ILSI Press; 2001: 59-71.

2. Englyst KN, Englyst HN. Carbohydrate bioavailability. Br J Nutr. 2005;94:1-11.

3. Asp NG. Resistant starch: Proceedings from the second plenary meeting of EURESTA: European FLAIR Concerted Action No. 11 on physiological implications of the consumption of resistant starch in man. Eur J Clin Nutr. 1992;46(suppl 2):S1.

4. Brown IL, McNaught KJ, Moloney R. Hi-Maize: New directions in starch technology and nutrition. Food Australia. 1995;47:272-275.

5. Brown IL. Applications and uses of resistant starch. J AOAC Int. 2004;87:727-732.

6. Higgins JA, Higbee DR, Donahoo WT, Brown IL, Bell ML, Bessesen DH. Resistant starch consumption promotes lipid oxidation. Nutr Metab. 2004;1:8-18.

7. Bird AR, Brown IL, Topping DL. Starch, resistant starch, the gut microflora and human health. Current Issues Int Micro. 2000;1:25-37.

8. Noakes M, Clifton PM, Nestel PJ, Le Leu R, McIntosh G. Effect of high-amylose starch and oat bran on metabolic variables and bowel function in subjects with hypertriglyceridemia. Am J Clin Nutr. 1996; 64:944-951.

9. Jenkins DJ, Vuksan V, Kendall CW, Wursch P, Jeffcoat R, Waring S, Mehling CC, Vidgen E, Augustin LSA, Wong E. Physiological effects of resistant starches on fecal bulk, short chain fatty acids, blood lipids and glycemic index. J Am Coll Nutr. 1998;17:609-616.

10. Muir JG, Yeow EG, Keogh J, Pizzey C, Bird AR, Sharpe K, O’Dea K, Macrae FA. Combining wheat bran with resistant starch has more beneficial effects on fecal indexes than does wheat bran alone. Am J Clin Nutr. 2004;79:1020-1028.

11. Grubben MJ, van den Braak CC, Essenberg M, Olthof M, Tangerman A, Katan MB, Nagengast FM. Effect of resistant starch on potential biomarkers for colonic cancer risk in patients with colonic adenomas: A controlled trial. Dig Dis Sci. 2001;46:750-756.

12. Behall KM, Hallfrisch J. Plasma glucose and insulin reduction after consumption of breads varying in amylose content. Eur J Clin Nutr. 2002;56:913-920.

13. Heijnen ML, van Amelsvoort JM, Deurenberg P, Beynen AC. Limited effect of consumption of uncooked (RS2) or retrograded (RS3) resistant starch on putative risk factors for colon cancer in healthy men. Am J Clin Nutr. 1998;67:322-331.

14. Silvester KR, Bingham SA, Pollock JR, Cummings JH, O’Neill IK. Effect of meat and resistant starch on fecal excretion of apparent N-nitrose compounds and ammonia from the human large bowel. Nutr Cancer. 1997;29:13-23.

15. Phillips J, Muir JG, Birkett A, Lu ZX, Jones GP, O’Dea K, Young GP. Effect of resistant starch on fecal bulk and fermentation-dependent events in humans. Am J Clin Nutr. 1995;62:121-130.

16. Hylla S, Gostner A, Dusel G, Anger H, Bartram HP, Christl SU, Kasper H, Scheppach W. Effects of resistant starch on the colon in healthy volunteers: Possible implications for cancer prevention. Am J Clin Nutr. 1998;67:136-142.

17. Cummings JH, Beatty ER, Kingman SM, Bingham SA, Englyst HN. Digestion and physiological properties of resistant starch in the human large bowel. Br J Nutr. 1996;75:733-747.

18. Robertson MD, Bickerton AS, Dennis AL, Vidal H, Frayn KN. Insulinsensitizing effects of dietary resistant starch and effects on skeletal muscle and adipose tissue metabolism. Am J Clin Nutr. 2005;82:559- 567.

19. Keenan MJ, Zhou J, McCutcheon KL, Raggio AM, Bateman HG, Todd E, Jones CK, Tulley RT, Melton S, Martin RJ, Hegsted M. Effects of resistant starch, a non-digestible fermentable fiber, on reducing body fat. Obesity. 2006;14:1523-1534.

20. Zhou J, Hegsted M, McCutcheon KL, Keenan MJ, Xi X, Raggio AM, Martin RJ. Peptide YY and proglucagon mRNA expression patterns and regulation in the gut. Obesity. 2006;14:683-689.

21. Yamada Y, Hosoya S, Nishimura S, Tanaka T, Kajimoto Y, Nishimura A, Kajimoto O. Effect of bread containing resistant starch on postprandial blood glucose levels in humans. Biosci Biotechnol Biochem. 2005;69:559-566.

(Source)

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Comments

  1. Richard,

    A very thought inducing article. Many thanks.

    Cheers – Mark

  2. Rob B. says:

    Great post…I always enjoy your science write-ups.

  3. Rob B:

    35 references in tomorrow’s post, including my very unique and unusual take on the whole of it.

  4. I can certainly attest to the satiety effects. I started taking 2T of unmodified potato starch twice a day last week and I am noticing a spontaneous reduction in food intake. In fact, I am going for extended periods without even thinking about eating – not common for me.

  5. As I can’t say it on Facebook, I’ll say it on here.
    Bye, Richard!

  6. Yea, right, Nigel.

    I’ll see you when you come to me.

  7. But whose going to make a habit out of eating raw potatoes, uncooked oats and green bananas?

  8. Richard-

    I’ve become a lurker on your site and find most everything you write to be well thought out and informational. This series on RS has motivated me to try it out and to see how it works for me. Early results are that my food intake has dropped and I am not thinking about eating for hours on end. I will continue to track my results.

    Thanks to you and Tatertot for doing the heavy lifting on this topic!

  9. James Howell says:

    Cool.

    I have been a very-low-carber for about a year. I’ve known during this time that there are supposedly “safe” starches but the ones I tried spiked my blood glucose. In a normal, healthy person this may not be a big concern but as a pre-diabetic I worry about it; maybe unduly so but there it is.

    Back in January I stumbled across the idea of resistant starches then I read Nikoley’s and tatertot’s first post and decided to do an N=1 experiment. Although I hadn’t taken it to the 40 gm/day level, yet, I did find that my blood glucose did not increase. Excellent. As Nikoley says, it appears we VLC-ers are wrong about our starch phobia so I’m going to take the level of potato starch higher and see what happens.

  10. I decided to do a bit of experimenting myself but am somewhat confused by the data so far.
    For the last year and a half I’ve been eating mostly primal, targeting 100 a red flag?

    I’m open to considering boosting my carb count back to the 100 g range if I can find a way to do it without gaining some of the weight back. I initially lost 24 pounds, gained about 9 back (when I wasnt careful about portions and too much protein), then lost 4, so I’m concerned about my weight creeping back up. So far my weight loss seems to correspond to the times of lowest carb count in my diet.

  11. When my above post showed up the middle part of the text was missing! The top and bottom were there but the rest was gone and no visual indications that the post was condensed.

  12. tatertot says:

    Hey, Eric – I went from sub-100g/day carbs to full-on PHD levels of safe starch in the 150-200g range. I gained about 5 pounds over the first few weeks, but then hit a stable wall. I think if you can get over the fact that you most likely will gain a few pounds as your body soaks up the glycogen, you will be fine. It’s a long-term change. Eventually, once I settled in to a good routine of having potatoes, rice, or beans with nearly every meal I found some sources of fat that could easily be eliminated to more than make up for the extra carb calories.

  13. Still not sure what happened to the entire middle of my first post. It was about PIR.
    I started experimenting with Potato Starch and testing blood sugar and the results were confusing.
    Fasting glucose runs the gamut from 83 to 103. In the evenings usually around 114 or so.
    One time it was even 113 fasting, down to 92 two and a half hours after breakfast! Sounds like the descriptions of PIR from this blog.
    I hadnt expected my carb count to be low enough to induce PIR as it’s above Keto levels. But regardless of the reason, isnt fasting glucose > 100 a red flag?

  14. tatertot says:

    FBG of 100 isn’t that bad. Over 120 is a big red flag. The real test is the hbA1C which shows an average BG level over 3 months.

    I think that everyone on an LC, below 100g/day, diet has PIR to some extent.

  15. Eric,
    actually if you were long into deep ketosis, your FBG will fall, along with your average daily BG. Range 65-85mg/dl is usual.

    So on the contrary, it’s especially those doing ‘keto-lite’ and LC (50-100g/day, or even 150g/day for a particularly muscular man), that often get a distinct rise in the morning FBG, because they still depend to a measurable extent on ingested carbs. That rise in the morning may be due to PIR, it may also be a morning reaction to an actual hypoglycemia which sometimes happens earlier, in the wee hours of night.
    Often, it’s some of both.
    Regardless, I’ll add my two cents to tatertot’s, your particular FBG numbers are nothing to worry about if hbA1C is good.

  16. @Marie: I’d like to understand your hypoglycemic comment better. Is what you are saying might be happening is that my BG drops as I sleep and my liver overcorrects and responds with a big shot of glucose to bring it back up and that causes it to spike, thus the high FBG reading? This sounds a lot like the crash that happens after a high carb BG roller coaster. My understanding is that what is *supposed* to happen is a smooth transition to burning fat avoids the need for that sort of reaction.

  17. Eric, sure, but note that this isn’t about big dips and peaks, since the FBG isn’t above 120 (that would be noteworthy and signify a possible metabolic problem or diabetes). There’s also a ‘dawn phenomenon’ which doesn’t require hypoglycemia but seems to be a release of glucose in response to a constellation of hormones that kick-in in the morning. Meanwhile, PIR always remains a good candidate.

    However, research on these effects is mostly on diabetics, so what a healthy metabolism is doing is less clear. Then again, there’s a lot of folks with some degree of metabolic syndrome….
    So the fact remains that the reaction to any change in diet composition is very individual.
    However, since the FBG rise is something often reported in LC circles, those forums maybe a good place to look for tips on how to tell what it is, if you care to.
    It doesn’t seem bad, since it’s not hitting red flags, like 120mg/dl or staying elevated all day but does fall later in the morning.

  18. My only complaint is that this blog makes a fatal mistake in HOW the subject of resistant starch is presented, in a disorganized mass of text. Toss in overuse of acronyms, and this presentation style is fatal – fatal meaning 90% of people who stumble on this site will be so lost they will give up on the subject altogether. I had to dig and sift to find what was useful to me, and I’m a methodical, patient person willing to spend 45 minutes on one blog to see if that blog even has anything useful for me within the subject the blog is tackling.
    The millions of people who could be helped by a simple explanation of resistant starch, won’t be.

  19. You’re right M. I should have been writing about it since April, waiting until I new everything about it, publish it in a 50-page blog post and wait for a few thousand comments.

    I’m such a lousy blogger. 10 years, 3,700 posts, 70,000 comments and I can’t seen to get it right.

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  2. [...] Richard Nikoley continues to share his findings about the health benefits of having foods with resistant starch in your diet. If you are new to what resistant starch is and why you should eat it, be sure to read Richard’s primer on the subject [...]

  3. […] increasing the bioavailability of nutrients. (2) But it could also be beneficial for increasing the resistant starch content of bread (particularly rye), thereby improving insulin response and gaining prebiotic […]

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  5. […] Richard Nikoley of the blog Free the Animal is leading the way on the pro resistant starch argument. Here’s his primer on the topic. […]

  6. […] Resistant Starch: An Overall Primer, with References (21 references) […]

  7. […] in your crock, add a few tablespoons of water or broth. I have rice cooling in the fridge (go go RG-RS) so that will accompany the meal made also with a bit of tomato paste and onion. A bit of […]

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