What is Resistant Starch?
Resistant starch is a type of starch that resists digestion. Starch in general is a large complex carbohydrate used by plants such as oats, corn, potatoes, wheat, rice, nuts, legumes and some fruits such as bananas to store energy. Foods that contain starch make up a large part of many people’s diet. For many years it was believed that starch was completely digested and absorbed in the small intestine. But studies published in the 1980s, based on hydrogen breath testing, showed that oats, wheat, potatoes, corn, and beans contained 10 to 20% malabsorbed, fermentable material. Even the digestion of bread, long known as the “staff of life,” has been shown to end in malabsorption by hydrogen breath testing and symptom scoring. Starch that isn’t absorbed, known by scientists as “resistant starch,” is estimated to represent at least 10% of the total starch in a typical Western diet. Undercooked, or cooked, then cooled foods contain more resistant starch than fully cooked or hot foods. In many ways, resistant starch is similar to and behaves like fermentable fiber in the digestive tract.
Resistant starch (RS) has been assigned to four groups based on the properties that allow it to resist digestion:
RS1 – Physically resists digestion because of a protective matrix or coating surrounding the granules found in whole grains, legumes and seeds.
RS2 – Is intrinsically resistant to digestion before cooking. RS2 includes unripe bananas, uncooked potatoes, along with many other foods.
RS3 – Retrograded starch is formed when starchy foods are cooked and then cooled.
RS4 – Refers to starch that is chemically modified to resist digestion and absorption. RS4 starches are often developed for use in processed foods.
Several factors contribute to the formation of resistant starch, and, the relative amount of resistant starch in foods influences the level of malabsorption. The most important, yet often overlooked, factor is the ratio of the two molecular types of starch, amylose and amylopectin. Each type of starch possesses a unique structure and different properties that affect how easily they can be digested and absorbed.
Amylopectin starch, which is easy to digest and absorb, is a much larger molecule, containing 10,000 to 100,000 glucose units. At the molecular level amylopectin is highly branched. The large size and branching forms starch granules that are less dense and gelatinize (absorb water) easily when heated in water. Gelatinized starch is easier to digest. The branched, less dense structure also allows the digestive enzyme amylase to work more efficiently, breaking amylopectin down quickly into glucose, which is absorbed rapidly.
Amylose starch, which is more difficult to digest and absorb, is both smaller, containing only 100 to 10,000 glucose units, and less heavily branched compared to amylopectin. This linear shape allows amylose to pack more tightly into the less accessible regions of starch granules where it’s more difficult to digest. A high ratio of amylose in starch granules also makes it more difficult to gelatinize (it gelatinizes at a higher temperature), making digestion by amylase enzyme even more difficult. In general, foods that contain more amylopectin (higher glycemic index), such as jasmine rice, short grain sticky rice (also known as glutinous or sushi rice) as well as some varieties of potatoes, such as Russet Burbank, are much easier to digest and absorb than foods containing more amylose (lower glycemic index), such as basmati rice, most long grain rice (except for jasmine), pasta, most wheat, corn, oat and barley products, most potatoes and bananas.
Resistant starch escapes digestion and absorption yet is fermentable by certain bacteria common to the large intestine, such as Bifidobacterium, Clostridium and Bacteriodes species. These bacteria contain efficient starch-degrading enzymes and most can break down both amylopectin and amylose starch.
General Health Aspects of Resistant Starch
Moderate levels of resistant starch are generally well tolerated by most healthy people and, along with other indigestible or poorly digestible carbohydrates such as fiber, fructose, disaccharides, oligosaccharidies and undigested proteins feed our gut bacteria. The main function of bacteria in our large intestine is to salvage energy from these undigested, but energy –rich substances by producing short chain fatty acids (SCFAs) that we can burn, thus improving our food mileage by 30%. But harboring a diverse population of commensal microorganisms in our large and small intestine (referred to as gut microbiome) provides many other benefits including:
- Helping maintain normal gut function – recycling bile acids, water and electrolyte balance and motility.
- Protection against colonization with bad bacteria (pathogens) such as C diff.
- Production of butyrate – possible protective role in cancer and inflammatory bowel disease.
- Vitamin production – we can’t make biotin, folate and vitamin K – bacteria can.
- Immune stimulation – gut microbes help “train” our immune response.
- Degradation of toxins and carcinogens.
Reported health benefits of resistant starch linked to fermentation by gut microbes have fostered an interest in using resistant starch for improving overall health and for preventing and treating diseases. Some of the specific health benefits reportedly linked to resistant starch includes:
- Improved blood glucose levels and insulin regulation
- Lower blood cholesterol and triglyceride levels
- Improved satiation
- Reduced colon cancer risk
Note: There are a huge number of published studies on resistant starch. I acknowledge that readers may find additional studies to support or refute points made in this post. Please feel free to post these in the comment section, especially hypothesis testing studies in humans.
Though positive effects on glucose / insulin modulation have been associated with consumption of resistant starch with fiber or other indigestible carbohydrates,, low carbohydrate dieting led to greater improvements in glycemic control, and more frequent medication reduction/elimination than a low glycemic index diet (by definition has more resistant starch) in diabetics.
As for lowering cholesterol, I know there are a handful of studies in rats, but I am not aware of similar studies in people. But the bigger question is whether or not lowering cholesterol levels matters since no one can seem to agree on the significance of cholesterol levels in cardiovascular disease. Also, I don’t know of studies in people showing triglycerides are lowered by resistant starch, but I do know resistant starch stimulates the production of SCFAs which are also a form of fat.
As for improving satiation, it’s true that rats fed a diet high in resistant starch did not consume more food even though resistant starch is not broken down into glucose. But as Dr. Mike Eades mentions in his blog on resistant starch, the fatty acids produced by bacteria fermenting resistant starch still add calories to our diet, so the real question becomes does resistant starch help people lose weight? Again, I have not seen evidence for this though it may exist.
The claim that resistant starch reduces colon cancer risk is based on observational studies suggesting there may be a link between low fiber or high meat consumption and colon cancer,, possibly due to the buildup of secondary bile acids such as deoxycholic acid (DOC), believed to be carcinogenic., Another idea is that fermentation of resistant starch produces more butyrate thought to be protective for cancer. Observational study findings however, often turn out to be wrong. Ironically, two species of bifidobacterium (B. longum and B. angulatum) were “significantly associated with high risk of colon cancer”. The researchers determined that total concentrations of bifidobacteria (promoted by RS consumption and partially responsible, via cross feeding, for butyrate production) increased with higher risk of colon cancer.
A study that specifically looked at the protective effect of resistant starch in carriers of hereditary colorectal cancer found that resistant starch had no detectable effect on cancer development. While I’m not dismissing possible cancer-protective roles for resistant starch and fiber, I am interested in seeing more definitive studies relating cancer risk to resistant starch and fiber in humans, if they exist.
Clearly there is evidence that we and our resident microbes derive benefit from some level of resistant starch and / or other indigestible fibers in our diet. Whether or not we need to supplement our diet beyond what we receive from simply eating some fiber rich green leafy vegetables, avocados, nuts, and some fruit (recommended in the Fast Tract Digestion book series) is an open question. But for most healthy people, there is little down side as long as the amounts are not excessive. Excessive amounts of resistant starch (or any other indigestible carbohydrate) may backfire. Excess fermentable carbohydrates may foster potential harmful properties of gut microbes which may include:
- Small Intestinal Bacterial Overgrowth (SIBO) – described below
- Infection by disease-causing organisms – less competition for nutrients
- Excess toxin production
- Excess gas formation
- Increase in microbe – mediated formation of carcinogenic compounds.
Caution for People with GI Issues
My biggest concern is that resistant starch has the potential to cause or perpetuate digestive problems if and when excessive fermentation occurs in the wrong place, mainly the small intestine. To be on the safe side, people with Small Intestinal Bacterial Overgrowth (SIBO)-related digestive illnesses such as GERD, IBS and Celiac disease, to name a few, would be best served by consuming lower levels of resistant starch because it behaves much like fermentable fiber. If you have read my three part article on fiber, you know where I am coming from. Also find out more about SIBO on this site.
There is clear evidence in the scientific literature (summarized in the Fast Tract Digestion books) that lactose, fructose, fiber and sugar alcohols are subject to various degrees of malabsorption similar to the malabsorption of resistant starch and can promote SIBO-related digestive illness, such as IBS, GERD, Celiac disease and other functional GI conditions. SIBO can cause diarrhea, constipation, bloating, excessive gas, belching, acid reflux, vitamin and mineral malabsorption and damage the critical digestive machinery of the small intestine. Keep in mind that (overgrowing) gut bacteria produce more than butyrate and other SCFAs. They also produce a large amount of gas in the form of hydrogen, carbon dioxide and methane in some cases. That’s enough gas to cause well documented explosions during intestinal surgery. It’s these gases that are responsible for bloating, acid reflux (read about the original theory of SIBO and GERD in Heartburn Cured), abdominal pain, cramping, respiratory problems and other symptoms of IBS, GERD, asthma and other SIBO-related conditions. But the idea that fructose, lactose, fiber and sugar alcohol can feed SIBO but resistant starch can’t, makes little sense to me.
Here is some evidence (excerpted from the Fast Tract Digestion books) that led me to conclude that resistant starch should be avoided by people with SIBO-related illness until SIBO and symptoms are under control.
- In healthy people, starch which escapes digestion (RS by definition) is predominantly fermented by the bacteria residing to the large intestine, including Bifidobacterium, Clostridium, Bacteroides, Fusobacterium and Butyrivibrio. But SIBO involves many of the same types of bacteria native to the large intestine. Therefore, one might expect that SIBO would be perpetuated by the presence of resistant starch since the bacteria capable of fermenting it have moved into the small intestine. Below is a diagram from Dr. Henry C. Lin visualizing this concept.
Bacterial overgrowth and Starch Digestion.
- Studies have shown that bread and muffins which contain resistant starch known to be malabsorbed were associated with symptoms in IBS patients on an otherwise gluten-free diet. While the study was evaluating gluten, bread and muffins contain a significant amount of resistant starch, which could just as likely be the driver of symptom persistence as the patient group which did not have celiac disease. The fact that gluten-free diets contain variable levels of difficult-to-digest carbohydrates including resistant starch may help explain why 40% of the entire gluten-free group in the study continued to have symptoms.
- Diabetic drugs such as acarbose (Precose) inhibit alpha-glucosidase enzymes located on the small intestinal brush border and pancreatic alpha-amylase. Inhibition of these enzymes blocks the breakdown of starch as well as oligosaccharides. The side effects of these drugs listed on the drug package insert include abdominal pain, diarrhea, and flatulence due to undigested carbohydrates from both starch and oligosaccharides. Given the metabolic capabilities of bacteria in the large intestine also present in SIBO described above, there is every reason to believe both the oligosaccharides and the resistant starch are responsible for these side effects.
- Weight loss products that specifically block the absorption of starch are designed to inhibit amylase, the enzyme that normally breaks down starch. The idea behind these products is that blocking starch from being absorbed into the blood stream will prevent weight gain. Though industry sponsored publications downplay the issue of GI side effects, these products are similar to the diabetic drug acarbose and are associated with GI side effects.,
- Up to 80 percent of cystic fibrosis (CF) patients suffer from acid reflux compared to 15-20 percent of non-CF people. The Digestive Health Institute figured out why – read more about the connection between acid reflux, SIBO and cystic fibrosis. About the same percentage of CF patients have a well-known deficiency of digestive enzymes, including a lack of pancreatic alpha amylase, an enzyme required for starch digestion. The reason is that pancreatic amylase cannot get out of the pancreas, where it’s produced, because the pancreatic ducts are often plugged up with thick mucus, a hallmark of CF. A study of CF patients with pancreatic deficiencies showed that SIBO was diagnosed (based on hydrogen breath testing) almost three times more frequently when compared to patients without cystic fibrosis. Could the malabsorption of protein or fat (due to a lack of proteases and lipases) trigger SIBO related symptoms? This is not likely, because carbohydrates are the preferred energy source of bacteria in an oxygen-free environment. Only the glycerol backbone of lipids are fermentable in absence of oxygen and proteins are degraded more slowly in the large intestine where there are fewer carbohydrates and the pH is less acidic.
- Low carbohydrate diets that limit most carbs (except fiber), including resistant starch have shown benefit for GERD and IBS, two SIBO-related conditions.
The Fast Tract Diet for SIBO-related conditions allows up to 45 grams of difficult-to-digest carbohydrates per day, including resistant starch. The quantity of these resistant carbs per serving is available for hundreds of foods in the appendices of the Fast Tract Digestion books and can also be calculated by the Fermentation Potential (FP) formula provided in each of the Books.
Promoting a state of fermentable substrate limitation in the gut is, in my view, healthier than promoting a state of fermentable substrate excess and more consistent with Paleo diet concepts. A lean diet for our gut microbes fosters healthy competition in the gut that will favor the survival of well adapted organisms best suited to be our partners in digestion and health. We know that excess malabsorbed carbohydrates are linked to conditions associated with SIBO and there is reason to believe that resistant starch may contribute to imbalances is the gut microbiome including SIBO in susceptible people.
OK, take a break. Then you can read RS Part 2: Resistant Starch Friend, Foe or Lover.
 Anderson IH, Lavine AS, Levitt MD. Incomplete absorption of carbohydrate in all-purpose wheat flour. N Engl J Med. 1981 Apr 9;304(15):891-2. Levitt MD, Hirsh P, Fetzer CA, Sheahan M, Levine AS. H2 excretion after ingestion of complex carbohydrates. Gastroenterology. 1987 Feb;92(2):383-9.
 Hallfrisch J, Behall KM. Breath hydrogen and methane responses of men and women to breads made with white flour or whole wheat flours of different particle sizes. J Am Coll Nutr. 1999 Aug;18(4):296-302.
 Englyst HN, Trowell H, Southgate DA, Cummings JH. Dietary fiber and resistant starch. Am J Clin Nutr. 1987 Dec;46(6):873-4. Bird AR, Brown IL, Topping DL. Starches, resistant starches, the gut microflora and human health. Curr Issues Intest Microbiol. 2000 Mar;1(1):25-37.
 Macfarlane GT, Englyst HN. Starch utilization by the human large intestinal microflora. J Appl Bacteriol. 1986 Mar;60(3):195-201. A A Salyers, J R Vercellotti, S E West, and T D Wilkins Fermentation of mucin and plant polysaccharides by strains of Bacteroides from the human colon. Appl Environ Microbiol. 1977 February; 33(2): 319–322. Wang X, Conway PL, Brown IL, Evans AJ. In vitro utilization of amylopectin and high-amylose maize (Amylomaize) starch granules by human colonic bacteria. Appl Environ Microbiol. 1999 Nov;65(11):4848-54.
 Nilsson AC, Ostman EM, Holst JJ, Björck IM. Including indigestible carbohydrates in the evening meal of healthy subjects improves glucose tolerance, lowers inflammatory markers, and increases satiety after a subsequent standardized breakfast. J Nutr. 2008 Apr;138(4):732-9.
 Behall KM, Scholfield DJ, Hallfrisch JG, Liljeberg-Elmstahl HG (2006) Consumption of both resistant starch and beta-glucan improves postprandial plasma glucose and insulin in women. Diabetes Care 29: 976–981.
 Westman EC, Yancy WS Jr, Mavropoulos JC, Marquart M, McDuffie JR.The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond). 2008 Dec 19;5:36. doi: 10.1186/1743-7075-5-36.
 Armstrong B, Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int J Cancer. 1975 Apr 15;15(4):617-31.
 A. Cassidy, S. A. Bingham, and J. H. Cummings. Starch intake and colorectal cancer risk: an international comparison. Br J Cancer. 1994 May; 69(5): 937–942.
 Nagengast FM, Grubben MJ, van Munster IP. Role of bile acids in colorectal carcinogenesis. Eur J Cancer. 1995 Jul-Aug;31A(7-8):1067-70.
 Bernstein C, Holubec H, Bhattacharyya AK, Nguyen H, Payne CM, Zaitlin B, Bernstein H. Carcinogenicity of deoxycholate, a secondary bile acid. Arch Toxicol. 2011 Aug;85(8):863-71. doi: 10.1007/s00204-011-0648-7.
 Pryde SE, Duncan SH, Hold GL, Stewart CS, Flint HJ. The microbiology of butyrate formation in the human colon. FEMS Microbiol Lett. 2002 Dec 17;217(2):133-9.
 Moore WE1, Moore LH. Intestinal floras of populations that have a high risk of colon cancer. Appl Environ Microbiol. 1995 Sep;61(9):3202-7.
 Mathers JC, Movahedi M, Macrae F, Mecklin JP, et.al. Long-term effect of resistant starch on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial. Lancet Oncol. 2012 Dec;13(12):1242-9.
 Dener IA, Demirci C. Explosion during diathermy gastrotomy in a patient with carcinoma of the antrum. Int J Clin Pract. 2003 Oct; 57(8):737-8. Bigard M-A, Gaucher P, Lassalle C. Fatal colonic explosion during colonoscopic polypectomy. Gastroenterology 1979; 77: 1307-1310.
 Macfarlane GT, Englyst HN. Starch utilization by the human large intestinal microflora. J Appl Bacteriol. 1986 Mar;60(3):195-201. Wang X, Conway PL, Brown IL, Evans AJ. In vitro utilization of amylopectin and high-amylose maize (Amylomaize) starch granules by human colonic bacteria. Appl Environ Microbiol. 1999 Nov;65(11):4848-54.
 Bouhnik Y, Alain S, Attar A, Flourié B, Raskine L, Sanson-Le Pors MJ, Rambaud JC. Bacterial populations contaminating the upper gut in patients with small intestinal bacterial overgrowth syndrome. Am J Gastroenterol. 1999 May;94(5):1327-31). Ghoshal U, Ghoshal UC, Ranjan P, Naik SR, Ayyagari A. Spectrum and antibiotic sensitivity of bacteria contaminating the upper gut in patients with malabsorption syndrome from the tropics. BMC Gastroenterol. 2003 May 24;3:9.
 Lin HC. Small intestinal bacterial overgrowth: a framework for understanding irritable bowel syndrome. JAMA. 2004 Aug 18;292(7):852-8.
 Hallfrisch J, Behall KM. Breath hydrogen and methane responses of men and women to breads made with white flour or whole wheat flours of different particle sizes. J Am Coll Nutr. 1999 Aug;18(4):296-302.
 Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, Gibson PR. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 Mar;106(3):508-14; quiz 515.
 Boivin M, Zinsmeister AR, Go VL, DiMagno EP. Effect of a purified amylase inhibitor on carbohydrate metabolism after a mixed meal in healthy humans. Mayo Clin Proc. 1987 Apr;62(4):249-55.
 Mitchell, Richard Sheppard; Kumar, Vinay; Robbins, Stanley L.; Abbas, Abul K.; Fausto, Nelson (2007). Robbins basic pathology. Saunders/Elsevier. ISBN 1-4160-2973-7.
 Fridge JL, Conrad C, Gerson L, Castillo RO, Cox K. Risk factors for small bowel bacterial overgrowth in cystic fibrosis. J Pediatr Gastroenterol Nutr. 2007 Feb;44(2):212-8.
 Austin GL, Dalton CB, Hu Y, Morris CB, Hankins J, Weinland SR, Westman EC, Yancy WS Jr, Drossman DA. A very low-carbohydrate diet improves symptoms and quality of life in diarrhea-predominant irritable bowel syndrome. Clin Gastroenterol Hepatol. 2009 Jun;7(6):706-708. Yancy WS Jr, Provenzale D, Westman EC. Improvement of gastroesophageal reflux disease after initiation of a low-carbohydrate diet: five brief cased reports. Altern Ther health med. 2001. Nov-Dec; 7(6):120,116-119. Austin GL, Thiny MT, Westman EC, Yancy WS Jr, Shaheen NJ. A very low-carbohydrate diet improves gastroesophageal reflux and its symptoms. Dig Dis Sci. 2006 Aug;51(8):1307-12.