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. […]
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