Resistant Starch: Now We’re Getting Somewhere, Part 2 (35 links to research)

Part 1: Resistant Starch: Now We’re Getting Somewhere.

As I mentioned in the first post, I cut it short, actually chopping a bunch of additional links from the end. Wanted to keep a sane intro length to it, but at the same time I want a bunch of the research to be available for easy reference.

So let’s get right to it. Tons of stuff—about 35 references I think; and there’s much, much more but I had to draw the line somewhere. I haven’t looked closely for corporate interests this time, as in the previous post, so buyer beware, as always. If you missed it, I posted a short but very nice Primer on Resistant Starch yesterday, which I highly suggest you read as a prerequisite so that you’re generally familiar with the critical importance of this in the realm of general health for the 100% of you, and not just the 10% of you that are your human cells. Note that if you just skim through the research (skim, read, dig, engage rabbit holes…it’s all up to you), make sure you carefully read my wrap up at the end.

Again, the easiest and cheapest way to dose resistant starch is via unmodified potato starch. Many people are reporting good results with 4 tablespoons, spread throughout the day. Most use Bob’s Red Mill Potato Starch.

~ Insulin-sensitizing effects of dietary resistant starch and effects on skeletal muscle and adipose tissue metabolism (human study—full text). “…insulin sensitivity was higher after resistant starch supplementation than after placebo treatment…insulin sensitivity during the meal tolerance test (MTT) was 33% higher…. …muscle glucose clearance during the MTT was also higher after resistant starch supplementation…glucose clearance adjusted for insulin was 44% higher. …nonesterified fatty acid (NEFA; P = 0.02) and glycerol (P = 0.05) release were lower with resistant starch supplementation. Short-chain fatty acid concentrations (acetate and propionate) were higher during the MTT…as was acetate uptake by adipose tissue. Fasting plasma ghrelin concentrations were higher with resistant starch supplementation. Measurements of gene expression in adipose tissue and muscle were uninformative, which suggests effects at a metabolic level. The resistant starch supplement was well tolerated.”

~ Resistant starch consumption promotes lipid oxidation (human study—full text). “These data indicate that replacement of 5.4% of total dietary carbohydrate with RS significantly [by 23%!!! -Ed] increased post-prandial lipid oxidation and therefore could decrease fat accumulation in the long-term.”

~ Starches, Resistant Starches, the Gut Microflora and Human Health (review paper—full text, lots of charts & pictures). “Starches are important as energy sources for humans and also for their interactions with the gut microflora throughout the digestive tact. Largely, those interactions promote human health. In the mouth, less gelatinised starches may lower risk of cariogensis. In the large bowel, starches which have escaped small intestinal digestion (resistant starch), together with proteins, other undigested carbohydrates and endogenous secretions are fermented by the resident microflora. The resulting short chain fatty acids contribute substantially to the normal physiological functions of the viscera. Specific types of resistant starch (e.g. the chemically modified starches used in the food industry) may be used to manipulate the gut bacteria and their products (including short chain fatty acids) so as to optimise health. In the upper gut, these starches may assist in the transport of probiotic organisms thus promoting the immune response and suppressing potential pathogens. However, it appears unlikely that current probiotic organisms can be used to modulate large bowel short chain fatty acids in adults although resistant starch and other prebiotics can do so. Suggestions that starch may exacerbate certain conditions (such as ulcerative colitis) through stimulating the growth of certain pathogenic organisms appear to be unfounded. Short chain fatty acids may modulate tissue levels and effects of growth factors in the gut and so modify gut development and risk of serious disease, including colo-rectal cancer. However, information on the relationship between starches and the microflora is relatively sparse and substantial opportunities exist both for basic research and food product development.”

~ Effects of high-resistant-starch banana flour (RS2) on in vitro fermentation and the small-bowel excretion of energy, nutrients, and sterols: an ileostomy study (human study—full text). “Results: In study A, the dry weight of the ileostomy effluents and the ileal excretion of energy, iron, and chenodeoxycholic acid, but not total sterols, were higher after the addition of RBF than of CBF to the diet. In vitro fermentation of the ileal effluents obtained after the addition of RBF to the diet showed higher concentrations of acetate and butyrate. In study B, the ileal excretion of starch was lower than the amount calculated from earlier studies by use of the intubation technique. […] The addition of RBF containing RS2 to the diet of ileostomy subjects did not interfere with small-bowel absorption of nutrients or total sterols, except for a small increase in iron excretion. The ileostomy model seems to give reliable results for in vivo measurement of RS.”

~ Absorption of starch by healthy ileostomates: effect of transit time and of carbohydrate load (human study—abstract). “…starch from a radiolabeled solid meal containing 50 g potato starch was measured under control conditions and after altering transit time with either loperamide, or magnesium citrate. Loperamide significantly decreased the amount of unabsorbed starch in all six ileostomates (p less than 0.05), while magnesium citrate significantly increased starch malabsorption in all six subjects (p less than 0.05). Third, starch absorption was measured after single solid meals containing 25, 50, 75, and 100 g potato starch. There was a linear relationship between starch input and output. Mean output expressed as a percent of input remained constant. We conclude that the degree of starch malabsorption by the small intestine of ileostomates may be less than that estimated by indirect methods in intact humans. The amount of unabsorbed starch is directly related to the quantity ingested and to the small intestinal transit time.”

~ Digestibility of  raw rice, arrowroot, canna, cassava, taro, tree-fern and potato starches (1922 human study—full text). “In tests previously reported it was found that raw wheat and corn-starch, when eaten in quantity, were completely assimilated without any noted physiological disturbances and no starch was detected in the feces. Raw potato starch was much less completely digested, about one-fourth of the amount eaten being found in the feces on an average, and in many instances the subjects experienced pain or other physiological disturbances. […] It seemed desirable to extend the work on the digestibility of raw starches to see whether complete digestibility was characteristic of other starches and to determine whether the less complete digestibility of potato starch (78.2 per cent on an average) was influenced by the amount eaten and also whether it was characteristic of the starch from other roots, tubers, and similar sources.”

Comment: It’s really a doll of a paper, from 1922. Basically, they discovered resistant starch but didn’t know what it was. Of note, raw Canna starch appears to have even more resistance to rapid digestion (or digestion at all) than raw potato starch. I wonder who traditionally eats Canna, in what form, and what their health was on their traditional diet was.

~ Resistant starch is effective in lowering body fat in a rat model of human endocrine obesity (rat study—full text). “Although RS was not effective in lowering body weight or body fat in the first study, the data indicates that resistant starch may lower body weight and fat in postmenopausal women.”

~ Resistant Starch Intakes in the United States (data analysis with lots of good RS discussion—full text). “Findings from this study suggest that the estimated intake of resistant starch by Americans is approximately 3 to 8 g per person per day. These estimates of resistant starch intake provide a valuable reference for researchers and food and nutrition professionals and will allow for more accurate estimates of total intakes of carbohydrate compounds that escape digestion in the small intestine.”

~ Effects of resistant starch, a non-digestible fermentable fiber, on reducing body fat (rat study—abstract). “Energy dilution resulted in decreased abdominal fat in all studies. In Study 2, rats fed fermentable RS had increased cecal weights and plasma PYY and GLP-1, and increased gene transcription of PYY and proglucagon. In Study 3, RS-fed rats had increased short-chain fatty acids in cecal contents, plasma PYY (GLP-1 not measured), and gene transcription for PYY and proglucagon. […] Inclusion of RS in the diet may affect energy balance through its effect as a fiber or a stimulator of PYY and GLP-1 expression. Increasing gut hormone signaling with a bioactive functional food such as RS may be an effective natural approach to the treatment of obesity.”

~ Peptide YY and Proglucagon mRNA Expression Patterns and Regulation in the Gut (rat study—full text) “The gene expression patterns for PYY and proglucagon are similar to their peptide distribution patterns in the gut. Also, PYY and proglucagon mRNA expression were up-regulated in the cecum and colon in resistant-starch—fed rats. Butyrate increased PYY and proglucagon gene expression in a dose-dependent manner in vitro. […] Our data provide evidence that the distal part of the gut has the ability to sense nutrients such as butyrate, resulting in the up-regulation of PYY and proglucagon gene expression.”

~ Plasma glucose and insulin reduction after consumption of breads varying in amylose content (human study—abstract). “Consumption of a meal high in amylose starch (70%) decreases peak insulin and glucose levels and area under the curve (AUC). The objective was to determine the amount of amylose necessary in a meal for the beneficial decrease in glucose or insulin to occur. Design: …glucose alone (1 g glucose/kg body weight) and five breads (1 g carbohydrate/kg body weight) made with 70% amylose cornstarch, standard cornstarch (30% amylose), and blends of the two starches (40, 50 and 60% amylose starch). […] Peak glucose response was lowest after the breads containing 50-70% amylose starch. AUC was significantly higher after the glucose load than after all bread loads. The lowest AUCs occurred after the 60 and 70% amylose starch breads. Insulin response and AUC were significantly lower after the 60 and 70% amylose starch breads than after the glucose or the other breads. […] Results indicate that the amylose content of the starch used in the acute meal needs to be greater than 50% to significantly reduce plasma glucose and insulin in men and women.”

~ Effect of bread containing resistant starch on postprandial blood glucose levels in humans (human study—abstract) “We examined the inhibitory effect of a single ingestion of bread containing resistant starch (bread containing about 6 g of resistant starch derived from tapioca per 2 slices) (test food) on the postprandial increase in blood glucose in male and female adults with a fasting blood glucose level between 100 and 140 mg/dl. Bread not containing resistant starch (placebo) was used as the control. The study was conducted in 20 subjects (9 men and 11 women with a mean age of 50.5+/-7.5 years) using the crossover method, with a single ingestion of either bread containing resistant starch or the placebo. Blood glucose and insulin were measured before ingestion, and at 0.5, 1, 1.5, and 2 h after ingestion. The blood glucose level before ingestion was stratified into a borderline group (blood glucose level >/= 111 mg/dl) and a normal group (blood glucose level </= 110 mg/dl), with the upper limit of the normal range defined as 110 mg/dl. Postprandial increases in both blood glucose and blood insulin were significantly inhibited in subjects in the borderline group who took the test food in comparison with the placebo group (blood glucose: p<0.05 and p<0.01 at 1 and 1.5 h after ingestion respectively; insulin: p<0.05, p<0.01 and p<0.05 at 1, 1.5, and 2 h after ingestion respectively). These results indicate that bread containing resistant starch is useful for prevention of lifestyle-related diseases such as diabetes mellitus, and as a supplementary means of dietetic therapy.”

~ Effect of high-amylose starch and oat bran on metabolic variables and bowel function in subjects with hypertriglyceridemia (human study—full text) “We compared the effects of a diet in which
25% of the carbohydrate was replaced by high-amylose starch with those of a similar diet high in oat bran or low-amylose starch in 23 hypertriglyceridemic subjects who were overweight mostly because of abdominal adiposity. Each diet was consumed for 4 wk in random order and in a crossover fashion. Overall, the diets were high in carbohydrate (> 55% of energy) and low in fat (< 30% of energy); the amount of resistant starch in the foods containing high-amylose starch was 17 g in women and 25 g in men. The metabolic effects of specific starches on plasma lipids, fasting and postprandial glucose and insulin profiles, and bowel function were assessed at the end of each intervention. Plasma triacylglycerols (triglycerides) were significantly lower after the oat bran diet than after the other two diets.”

~ Postprandial effects of resistant starch corn porridges on blood glucose and satiety responses in non-overweight and overweight adults (human study—full text) “…mean plasma glucose at peak time-point 30 minutes was significantly lower in subjects consuming 28.9% RS treatment compared to the other treatments. Baseline-adjusted plasma glucose AUC was also significantly lower in subjects consuming the 28.9% RS porridge compared to the other porridges.”

~ Feeding resistant starch to Goto-Kakizaki (GK) diabetic rats improves glucose status (rat study—abstract). “Dietary prebiotics have shown potential in the anti-diabetes field. Our group has worked on resistant starch (RS), one type of prebiotic. We showed that dietary resistant starch possesses favorable impact on gut hormone profiles, including promoting GLP-1 release consistently, an potent anti-diabetic incretin (Zhou et al, 2006). Also we demonstrated dietary RS reduces body fat (Keenan, 2006; Shen, 2008). The current project is to determine if resistant starch can improve glucose status in a genetic animal model of diabetes. We hypothesize that dietary resistant starch can improve glucose metabolism in a type 2 diabetic rat model. The Goto-Kakizaki (GK) rat is a non-obese Wistar substrain which develops Type 2 diabetes mellitus early in life. In this study GK rats were fed a diet containing 30% resistant starch that was isocaloric and isonitrogenous when compared to the control diet. After 10 weeks of treatment, fasting blood glucose was reduced by feeding the resistant starch diet. It is proposed that altered gut fermentation and microbiota are the initial mechanisms by which RS improves diabetes and that enhance serum gut peptides (ie., GLP-1, PYY and GIP) are secondary mechanisms involved in improve beta cell function and insulin sensitivity in this model of diabetes. This dietary approach is potentially of great therapeutic importance in the treatment of diabetes.”

~ Changes in Bowel Microbiota Induced by Feeding Weanlings Resistant Starch Stimulate Transcriptomic and Physiological Responses (rat study—full text). “…In a synecological study, weanling conventional Sprague-Dawley rats (21 days old) were fed a basal diet (BD) or a diet supplemented with resistant starch (RS) at 5%, 2.5%, or 1.25% for 28 days. Pyrosequencing of 16S rRNA genes and temporal temperature gradient electrophoresis (TTGE) profiles in the colonic digesta showed that rats fed RS had altered microbiota compositions due to blooms of Bacteroidetes and Actinobacteria. The altered microbiota was associated with changes in colonic short-chain fatty acid (SCFA) concentrations, colonic-tissue gene expression (Gsta2 and Ela1), and host physiology (serum metabolite profiles and colonic goblet cell numbers). Comparisons between germ-free and conventional rats showed that transcriptional and serum metabolite differences were mediated by the microbiota and were not the direct result of diet composition…”

~ Short-Chain Fatty Acids and Human Colonic Function: Roles of Resistant Starch and Nonstarch Polysaccharides (review—full text) “Resistant starch (RS) is starch and products of its small intestinal digestion that enter the large bowel. It occurs for various reasons including chemical structure, cooking of food, chemical modification, and food mastication. Human colonic bacteria ferment RS and nonstarch polysaccharides (NSP; major components of dietary fiber) to short-chain fatty acids (SCFA), mainly acetate, propionate, and butyrate. SCFA stimulate colonic blood flow and fluid and electrolyte uptake. Butyrate is a preferred substrate for colonocytes and appears to promote a normal phenotype in these cells. Fermentation of some RS types favors butyrate production. Measurement of colonic fermentation in humans is difficult, and indirect measures (e.g., fecal samples) or animal models have been used. Of the latter, rodents appear to be of limited value, and pigs or dogs are preferable. RS is less effective than NSP in stool bulking, but epidemiological data suggest that it is more protective against colorectal cancer, possibly via butyrate. RS is a prebiotic, but knowledge of its other interactions with the microflora is limited. The contribution of RS to fermentation and colonic physiology seems to be greater than that of NSP. However, the lack of a generally accepted analytical procedure that accommodates the major influences on RS means this is yet to be established.” (emphasis added) […]

“Although NSP resist digestion by intrinsic human intestinal digestive enzymes completely, their intakes do not account for calculated human SCFA production (the “carbohydrate gap”). Some of the deficit may be filled by oligosaccharides (OS), but starch and products of small intestinal starch digestion are thought to contribute the most. This fraction is termed resistant starch (RS). This review aims to examine the relative contributions of RS and NSP to SCFA production in the context of the epidemiological and other data linking complex carbohydrates to improved colon function and lowered disease risk. […]

“The “carbohydrate gap” is the discrepancy between NSP intakes and calculations of bacterial activity of the large bowel microflora and supports a significant contribution by RS. Individuals in affluent westernized countries may consume up to 28 g NSP/day. However, much larger quantities, possibly as much as 80 g, of fermentable carbohydrate are needed to sustain the biomass and account for SCFA production, and NSP may only provide 25% of that requirement. […]

“In humans, RS and OS could close the carbohydrate gap, but consumption of OS appears to be self-limiting due to osmotic effects and may contribute only 5–10 g/day.”

~ Effect of resistant and digestible starch on intestinal absorption of calcium, iron, and zinc in infant pigs (pig study—abstract). “The first nonmilk foods that are given to infants contain high levels of starch, a fraction of which is resistant to enzyme hydrolysis. Incomplete digestion of starch may interfere with the absorption of certain minerals. A fraction of dietary starch which is resistant to in vitro enzymatic hydrolysis has been termed resistant starch. The aim of this study was to compare the intestinal apparent absorption of calcium, phosphorus, iron, and zinc in the presence of either resistant or digestible starch. Twelve 7-10-d-old piglets were fitted with a T-tube inserted into the intestine approximately 3 m distal to the duodenum. Animals received in random order 200 mL of a test meal of cooked, cooled, high amylose corn starch (16.4% resistant starch), or cooked rice starch (digestible starch) administered by an orogastric tube. Both meals contained the same amount of calcium, phosphorus, iron, and zinc. The test meal also contained tracer amounts of 59Fe and 65Zn, as well as polyethylene glycol 3350, as a nonabsorbable marker. Intestinal apparent absorption of starch was greater the meal with digestible starch (71.0 +/- 17.0%) than after the meal with resistant starch (49.2 +/- 10.3) (p < 0.001). After feeding the meals with resistant and digestible starch, mineral apparent absorption was, respectively: calcium, 40.2 +/- 11.8% versus 28.1 +/- 16.4% (p < 0.05); phosphorus, 73.2 +/- 14.0% versus 67.8 +/- 18% (NS); iron, 24.1 +/- 12.2% versus 12.6 +/- 10.6% (p < 0.01), and zinc, 35.0 +/- 13.0% versus 30.6 +/- 8.22% (NS). In conclusion, a meal containing 16.4% resistant starch resulted in a greater apparent absorption of calcium and iron compared with a completely digestible starch meal. If this finding holds true for the whole bowel, administration of resistant starches could have a positive effect on intestinal calcium and iron absorption.”

~ Impact of Resistant Starch on Body Fat Patterning and Central Appetite Regulation (mice study—full text). “Forty mice were randomised to a diet supplemented with either the high resistant starch (HRS), or the readily digestible starch (LRS). Using 1H magnetic resonance (MR) methods, whole body adiposity, intrahepatocellular lipids (IHCL) and intramyocellular lipids (IMCL) were measured. Manganese-enhanced MRI (MEMRI) was used to investigate neuronal activity in hypothalamic regions involved in appetite control when fed ad libitum. At the end of the interventional period, adipocytes were isolated from epididymal adipose tissue and fasting plasma collected for hormonal and adipokine measurement. Mice on the HRS and LRS diet had similar body weights although total body adiposity, subcutaneous and visceral fat, IHCL, plasma leptin, plasma adiponectin plasma insulin/glucose ratios was significantly greater in the latter group. Adipocytes isolated from the LRS group were significantly larger and had lower insulin-stimulated glucose uptake. MEMRI data obtained from the ventromedial and paraventricular hypothalamic nuclei suggests a satiating effect of the HRS diet despite a lower energy intake. […] Dietary RS significantly impacts on adipose tissue patterning, adipocyte morphology and metabolism, glucose and insulin metabolism, as well as affecting appetite regulation, supported by changes in neuronal activity in hypothalamic appetite regulation centres which are suggestive of satiation.”

~ Dominant and diet-responsive groups of bacteria within the human colonic microbiota (human study—full text). Time to give a little love to North Pole Tim aka “Tatertot” who did the bulk of the yeoman work, here. His summary of that study:

This study used a low-carb weightloss platform to compare the differences on individual populations of gut microflora when fed either high RS, high NSP, or a low carb control diet in humans, over 10 weeks. I think this study shows that a high-fiber diet does very little in altering the composition of gut flora, while a high RS diet makes immediate changes, favoring butyrate producers, and creating an environment hostile to pathogenic species.

I will try to pick out a few statements from the study in the hopes I can get your interest:

• ‘blooms’ in specific bacterial groups occurred rapidly after a dietary change. These were rapidly reversed by the subsequent diet.
• Relatives of Ruminococcus bromii (R-ruminococci) increased in most volunteers on the RS diet
• Relatives of Eubacterium rectale increased on RS (to mean 10.1%) but decreased, along with Collinsella aerofaciens, on [low carb control] diet.
• Members of the E. rectale group are…major producers of butyrate in the large intestine, and may therefore contribute to the butyrogenic effect of RS.
• In contrast to these responses to RS, there was little evidence that the high NSP diet resulted in major alterations in the composition of the faecal microbiota.

~ Psyllium Shifts the Fermentation Site of High-Amylose Cornstarch toward the Distal Colon and Increases Fecal Butyrate Concentration in Rats (rat study—full text). “Cummings et al…. indicated in human studies that an interaction between dietary [resistant] starch and fiber occurred in large bowel fermentation and that [RS] was fermented in preference to fiber, suggesting that [RS] might exert a sparing effect on certain dietary fibers. Also, the present study clearly showed the interactive effects of RS and [Fiber] on large bowel SCFA and suggests that it is possible to maintain relatively high butyrate concentration in the distal large bowel by dietary manipulation. The amounts of RS and [Fiber] used in the present study were conservative … 25 g RS and 7.5 g Fiber intake/d, within the range recommended for adults to consume in a healthy diet. These findings might have an important implication for large bowel physiology since there [are] strong inverse associations between the incidence of colorectal cancer and starch intake or the sum of dietary fiber and RS intake, while dietary fiber alone did not show any significant relationships. Given that fermentation in the colon is the mechanism for achieving colorectal cancer protection, via the specific contribution of n-butyrate to reduction of proliferation and induction of differentiation of the mucosal cells (Cummings 1981), it is probable that dietary manipulations which slow the fermentation rate of [RS] and dietary fiber would be of benefit in cancer protection in the distal colon and rectum.”

~ Banana and Plantain: the Earliest Fruit Crops? (focus paper). “On the African continent a hundred or more different cultivars of Plantain grow deep in the rainforest. In the countries bordering the Great Lakes region in Africa, more than sixty different cultivars of the Highland Bananas – also called “Mutika/Lujugira” group, can be found (INIBAP, 1995). Cultural history and tradition point to the presence of the crop in these areas since time immemorial.” (note: I still recall Art DeVany: “I would never eat a banana.”)

~ Gut microbe battles obesity (medical article). “Akkermansia muciniphila is one of the many microbes that live in our intestines. This bacterium, which feeds on the intestine’s mucus lining, comprises between 3 and 5 percent of the gut microbes of healthy mammals. There is an inverse correlation between body weight and abundance of A. muciniphila in mice and humans. In a paper published in the Proceedings of the National Academy of Sciences, Patrice Cani of the Catholic University of Louvain in Belgium and his colleagues reveal that levels of this bacterium are very low in mice genetically predisposed to obesity. Restoring Akkermansia to normal levels leads to fat reduction and reduced insulin resistance.

“Cani and his team found that genetically obese mice had 3,300 times less A. muciniphila in their intestines than healthy mice. When they fed mice, regardless of body weight, a high-fat diet, levels of the bacterium fell 100 times.

“The researchers were able to restore normal Akkermansia levels to mice on a high fat diet by feeding them live Akkermansia or by giving them oligofructose prebiotics.

“When normal levels were established, the mice lost weight and developed a better fat to lean mass ratio. Insulin resistance and adipose tissue inflammation, all associated with obesity and type 2 diabetes, also decreased. Metabolic endotoxemia, another related condition, was abolished, while fasting hyperglycemia was reversed. There was an increase in levels of endocannabinoids, which help control blood glucose levels, the gut barrier and inflammation.

“Intestinal mucus, which normally erodes with weight gain, became thicker. The mucus that lines the intestines acts as a barrier to harmful microbes, so A. muciniphila could play an important role in preventing inflammation and other disease triggers.” […]

“We also observed that prebiotic feeding normalized A. muciniphila abundance, which correlated with an improved metabolic profile. In addition, we demonstrated that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance. A. muciniphila administration increased the intestinal levels of endocannabinoids that control inflammation, the gut barrier, and gut peptide secretion.” (emphasis added)

~ High dietary intake of prebiotic inulin-type fructans in the prehistoric Chihuahuan Desert (review article). North Pole Tatertot, again:

Basically, they examined preserved poopage of hunter-gatherers living in the Chihuahuan Dessert and found they were consuming tons of fiber and prebiotics.

I think this is very relevant because the biggest argument I get is : ‘Grok didn’t eat potato starch.’ I think increasing RS, even if it means potato starch, is a simple way to even the gap between modern and ancestral diets. We have been doing 4TBS (30-40g/day), this examination of ancient stool showed an intake of 3-4 times that amount! And consider the average paleo dieter gets about 2g of total prebiotics and maybe 20g of fiber.

• …the average male hunter – forager from this population would have consumed about 135 g prebiotics per day
• …the overall dietary intake of fibre from all sources ranges from about 150 to 225 g/d for an adult male.
• …Even though about 135 g/d is difficult to comprehend in the context of our modern diet, it is also useful to remember that the total dietary fibre component for this prehistoric population, as with most ancestral groups before the widespread adoption of agriculture, was characterised by an extraordinary diversity of fibre sources… This is the nutritional landscape upon which our genome and symbiotically evolved microbiome were selected.

~ Gut Microbes Affect Weight After Gastric Bypass (medical article). “A study in mice suggests that gastric bypass surgery may result in weight loss in part by altering microbes in the gut. The finding may lead to a better understanding of how microbes influence energy balance.

“Gastric bypass is a type of surgery used to treat severe obesity. In a procedure known as Roux-en-Y gastric bypass (RYGB), part of the stomach and small intestine are removed. The procedure results in significant weight loss as well as improvements in associated conditions such as type 2 diabetes. Decreased calories, however, can’t fully account for all these effects.

“The digestive tract is home to trillions of microbes, both helpful and harmful, that outnumber the body’s cells by 10 to 1. A team of researchers led by Dr. Alice P. Liou and Dr. Lee M. Kaplan from Massachusetts General Hospital and Dr. Peter J. Turnbaugh from Harvard University wondered whether some of the benefits of RYGB surgery might come from changes in digestive tract microbes.”

~ Resistant Starch – A Surprising New Helper in the Battle for Health (article—Dr. LaValle). North Pole Tim-Tot, again:

First, it extolls the virtues of RS, then it recommends the UCan Superstarch as the best source, at $49.95 for a 2 week supply [Bob’s Red Mill Potato Starch will set you back $15 for a couple of months -Ed].

I’d like to think the takeaway from all this effort we have been doing will be:

1. RS is a valid tool for health (gut and overall).
2. RS doesn’t mean Hi-Maize, SuperStarch, or unobtainable levels of vegetables.

~ Hunter-gatherer Use of Small Animal Food Resources: Coprolite Evidence (research paper—full text). “Faunal remains are commonly found in coprolites and provide direct evidence of animal consumption. An evaluation of hunter-gatherer coprolites from the Southwest United States shows that animal bone in coprolites can be used to assess patterns of hunting, food preparation, and general importance of small animals in diet. This is demonstrated by a comparison of faunal assemblages between two hunter-gatherer sites with respect to small animal hunting strategies. The sites are Dust Devil Cave on the Colorado Plateau, an Archaic winter habitation, and Hinds Cave, a warm season Archaic habitation in the lower Pecos of Texas. The results indicate that small animal hunting varied regionally and seasonally. […]

“Plants recovered from the midden of Dust Devil Cave include the dry fruits or seeds of Juniperus, Ephedra (mormon tea), Pinus edulis, grass, Chenopodium (goosefoot), Quercus, and Opuntia. Fleshy fruits recovered from the cave midden include Cucurbita spp. (non-cultivated squash), Shepherdia (buffalo berry), Astragalus (vetch), Amelanchier, Celtis, and Yucca. Pot herbs and stems from the midden include Allium (wild onion), Eriogonum (wild buckwheat), and Apiaceae (parsley family) (Richard H. Hevly, unpublished data). Many of these plants become available for consumption in the autumn.

“Compared with the Dust Devil Cave midden, only a limited number of pollen and macrofossil types were recovered from the coprolites. The plant foods from the coprolites consist mainly of Opuntia pad fragments, Chenopodium seeds, fibers from desert succulents, parched Sporobolus (drop-seed) caryopses, sunflower achenes, wild onion bulbs and piñon pine nuts (Van Ness, 1986; Hansen, 1994: 104). Very few background pollen types were present (Reinhard, 1985a). These data suggest that the dietary remains from the coprolites reflect a diet low in plant food diversity. Such a diet would be consistent with a cooler season occupation from late autumn through to early spring. The poor representation of background pollen in the coprolites supports this inference. It is our opinion that the Dust Devil Cave coprolites represent a cool season diet with low food diversity both in plants and animals.”

[Translation: not exactly all steak & bone broth.]

~ Some of My Best Friends Are Germs (Michael Pollan gets a clue). “His comment chimed with something a gastroenterologist at the University of Pittsburgh told me. ‘The big problem with the Western diet,’ Stephen O’Keefe said, ‘is that it doesn’t feed the gut, only the upper G.I. All the food has been processed to be readily absorbed, leaving nothing for the lower G.I. But it turns out that one of the keys to health is fermentation in the large intestine.’ And the key to feeding the fermentation in the large intestine is giving it lots of plants with their various types of fiber, including resistant starch (found in bananas, oats, beans); soluble fiber (in onions and other root vegetables, nuts); and insoluble fiber (in whole grains, especially bran, and avocados).”

~ Fecal Butyrate Levels Vary Widely among Individuals but Are Usually Increased by a Diet High in Resistant Starch (human study—full text) “Butyrate and other SCFA produced by bacterial fermentation of resistant starch (RS) or nonstarch polysaccharides (NSP) promote human colonic health. To examine variation in fecal variables, especially butyrate, among individuals and the response to these fibers, a randomized cross-over study was conducted that compared the effects of foods supplying 25 g of NSP or 25 g of NSP plus 22 g of RS/d over 4 wk in 46 healthy adults (16 males, 30 females; age 31–66 y). Fecal SCFA levels varied widely among participants at entry (butyrate concentrations: 3.5–32.6 mmol/kg; butyrate excretions: 0.3–18.2 mmol/48 h). BMI explained 27% of inter-individual butyrate variation, whereas protein, starch, carbohydrate, fiber, and fat intake explained up to 16, 6, 2, 4, and 2% of butyrate variation, respectively. Overall, acetate, butyrate, and total SCFA concentrations were higher when participants consumed RS compared with entry and NSP diets, but individual responses varied. Individual and total fecal SCFA excretion, weight, and moisture were higher than those for habitual diets when either fiber diet was consumed. SCFA concentrations (except butyrate) and excretions were higher for males than for females. Butyrate levels increased in response to RS in most individuals but often decreased when entry levels were high. Fecal butyrate and ammonia excretions were positively associated (2 = 0.76; P < 0.001). In conclusion, fecal butyrate levels vary widely among individuals but consuming a diet high in RS usually increases levels and may help maintain colorectal health.”

~ Resistant starch and “the butyrate revolution” (review—abstract) “Early epidemiological studies indicated that populations that consume a high proportion of non-starch polysaccharide (NSP) dietary fibre (DF) in their daily diet suffer less from gastrointestinal diseases, in particular colorectal cancers, than populations that consume diets that are high in fat and protein but low in NSP fibre. In this respect, diet, by increasing the amount of vegetables and NSP DF’s, has been suggested to contribute as much as 25–35% to risk reduction for colorectal cancer. A reduction of fat intake may further reduce the risk by 15–25%. Based on these observations, DF’s and substances that are part of the fibre complex such as antioxidants, flavonoids, sulphur containing compounds and folate have been proposed as potentially protective agents against colon cancer. However, results from controlled prospective studies in which beta-carotene and vitamin E or isolated dietary fibres were given to high risk groups showed disappointing results. There are recent indications that the regular consumption of certain subclasses of highly fermentable dietary fibre sources result in gut associated immune and flora modulation as well as a significant production of short chain fatty acids. In vitro studies as well as animal studies indicate that in particular propionate and butyrate have the potential to support the maintenance of a healthy gut and to reduce risk factors that are involved in the development of gut inflammation as well as colorectal cancer. A suggestion put forward is that beneficial effects may be obtained in particular by the consumption of resistant starch (RS) because of the high yield of butyrate and propionate when fermented. These SCFA are the prime substrates for the energy metabolism in the colonocyte and they act as growth factors to the healthy epithelium. In normal cells butyrate has been shown to induce proliferation at the crypt base, enhancing a healthy tissue turnover and maintenance. In inflamed mucosa butyrate stimulates the regeneration of the diseased lining of the gut. In neoplastic cells butyrate inhibits proliferation at the crypt surface, the site of potential tumour development. Moreover, models of experimental carcinogenesis in animals have shown the potential to modify a number of metabolic actions and steps in the cell cycle in a way that early events in the cascade of cancer development may be counteracted while stages of progression may be slowed down. The present review highlights a number of these aspects and describes the metabolic and functional properties of RS and butyrate.” (emphasis added)

~ Diet of Resistant Starch Helps the Body Resist Colorectal Cancer (article). To Tim, once again:

I love that article you linked…so much misinformation it’s funny, but all based on the way the author interpreted a really good study. The author makes all the wrong assumptions and even gets the name wrong:

“Even more importantly, starch resistant foods and flours have been found to improve colon or bowel health, curb cancer, and prevent adult onset diabetes 2.”

The study they are talking about is here:

http://www.sciencedaily.com/releases/2013/02/130219140716.htm

“A University of Colorado Cancer Center review published in this month’s issue of the journal Current Opinion in Gastroenterology shows that resistant starch also helps the body resist colorectal cancer through mechanisms including killing pre-cancerous cells and reducing inflammation that can otherwise promote cancer.

“Resistant starch is found in peas, beans and other legumes, green bananas, and also in cooked and cooled starchy products like sushi rice and pasta salad. You have to consume it at room temperate or below — as soon as you heat it, the resistant starch is gone. But consumed correctly, it appears to kill pre-cancerous cells in the bowel,” says Janine Higgins, PhD, CU Cancer Center investigator and associate professor of Pediatrics at the University of Colorado School of Medicine.”

Dr. Oz did a show on RS, calling it ‘Resistant Carbs’ the whole time and also gave very bad advice on where to get it.

The deal with ‘cooked and cooled’ foods is in the different types of RS. RS-2 is the RS found in raw potato starch. RS-3 is formed when you cook a potato, destroy all the RS-2, but when it cools, it crystallizes and re-forms into a retrograded RS-3 starch. Read this for more info: http://en.wikipedia.org/wiki/Resistant_starch. It’s all pretty straightforward.

What amazes me is that EVERYONE, from researcher to reporter to consumer misses the obvious low-hanging fruit…just eat raw potato starch (Bob’s Red Mill Potato Starch). It’s the highest content of RS you can buy, it’s cheap, it’s used as the control in most of the studies, it’s easy to eat, it’s about tasteless, it mixes well with everything.

If there could be one point to this entire show I have been putting on, it’s this:

If and when you decide that you should be getting more RS in your diet. It can be had from real foods, ie. cooked and cooled potatoes/rice, green bananas, dried plantains, and legumes. These sources may net you 10-20g/day if you are diligent about consuming them all every day. If you see a gap in your intake and want to ensure a steady supply of RS, then use raw, unmodified potato starch–it contains about 8g per TBS. Use as you wish to get however much RS you want.

~ Encapsulation Technology to Protect Probiotic Bacteria (bullshit). Totmeister:

You are 100% correct about kefir + potato starch. Pro and Pre-biotics in one. I found a lot of studies during all of this where they are trying hard to figure out a way to package RS with probiotics such as kefir and yogurt—the problem is, the live cultures eat the RS. It is a challenge to pre-mix them as they then have a very short shelf-life and produce some strange gasses in the package. There have been some successes with frozen yogurt and Hi-Maize, the key is keeping it cold enough to slow down the digestion.

This is one of those areas that since there is no money in it, nobody talks about it. I try to mix potato starch with kefir or yogurt every day.

Another strange thing that occurs when you mix the two: the RS encapsulates the probiotic microbes and gives them safe passage through the stomach and small intestine, where many probiotics would normally perish. When eating yogurt or kefir alone, most of the probiotic microbes are killed by normal digestive processes—resistant starch protects them. This is a feature unique to RS, typical plant fibers do not have this protective encapsulation property.

Just look at that paper on how they are ‘micro-encapsulating’ pre and probiotics, and smugly know that you can do it at home with a spoon and a glass!

~ Gut Microbiota in Health and Disease (review—full text). “Virtually all multicellular organisms live in close association with surrounding microbes, and humans are no exception. The human body is inhabited by a vast number of bacteria, archaea, viruses, and unicellular eukaryotes. The collection of microorganisms that live in peaceful coexistence with their hosts has been referred to as the microbiota, microflora, or normal flora. The composition and roles of the bacteria that are part of this community have been intensely studied in the past few years. However, the roles of viruses, archaea, and unicellular eukaryotes that inhabit the mammalian body are less well known. It is estimated that the human microbiota contains as many as 1014 bacterial cells, a number that is 10 times greater than the number of human cells present in our bodies. The microbiota colonizes virtually every surface of the human body that is exposed to the external environment. Microbes flourish on our skin and in the genitourinary, gastrointestinal, and respiratory tracts. By far the most heavily colonized organ is the gastrointestinal tract (GIT); the colon alone is estimated to contain over 70% of all the microbes in the human body. The human gut has an estimated surface area of a tennis court (200 m2) and, as such a large organ, represents a major surface for microbial colonization. Additionally, the GIT is rich in molecules that can be used as nutrients by microbes, making it a preferred site for colonization.”

~ Resistant Carbs: The Secret Weapon to Fight Cancer? (bullshit: absolute proof that Dr. Oz can’t be bothered with properly informing himself, even to the extent of getting the name correct) To wit:

~ Dr Oz Resistant Carbs | List of Foods Very High in Resistant Starch (bullshit). So, Tothead, from the North Pole:

His advice is completely crap. The only thing he got right is green bananas, but then he advises you boil and mash them. He talks about using sorghum and plantain flour in place of wheat flour in baking. All of his advice destroys the RS. He couldn’t even get the name right!

~~~

Alright folks. I’m calling it a wrap for that, and here’s my final thoughts. It’s to Low Carbers, Paleos and what the hell…me too:

U BEEN PWNED!

Let me put it in concrete, practical terms: the LC books, the Paleo books—including my own—are wrong or at best…incomplete. The books account for 10% of us, only, with the other 90% of us almost unaccounted for or, at least, given pretty short shrift (take a probiotic, eat some onions and jerusalem artichoke blalala). Read or skim the post again, if you don’t believe me. Then tell me that shpeel about how starch per se is bad bad bad, and that “there’s no essential carbohydrate.” Gimme a ‘Gluco-neo-genesis, Gluco-neo-genesis, and Gluco-neo-genesis One. More. Time!!!’

…OK, I’ll grant it. There is no “essential carbohydrate” and you don’t need any starch. Repeat: there is no essential carbohydrate and you don’t need any starch. At all. …But, I gotta say: it’s pretty slim to base all that on what’s only 10% of you. Skim the above research, again, if you don’t immediately understand that. Or, go ahead and remain ignorant, clutching your favorite text. And see if I care.

So go ahead: starve the other 90% of you, and see if I care about that either. One way to look at all of the studies and articles is that ignoring the all of your human animal nature comes with effects that manifest in big ways.

All that said, I am truly intrigued with the idea of a sort of bifurcated diet: the one that’s only for yooz guise—the 10%—and the other one for the critters…the other 90% of you. How about VLC—even ZC—but supplemented with about 4T of potato starch per day minimum—and perhaps more, given little other fiber. That will maybe net you about 20-30ish-g carbs, digested slowly by your starving colonic bacteria.

…That’s just a thought, though, because more prescient is my suspicion that the LC diet is an effect of a wholly misinterpreted cause. In other words, the misinterpreting of cause is the cause of the effect that is the LC diet phenomenon—along with the simpler amelioration left wholly unconsidered (because, with fingers raised to the sign of the cross: ‘STARCH!!! …and “resistant” means NOTHING to me!’). I’ve no problem giving props for the LC intervention in the face of the general and specific ignorance of the gut and its feeding requirements—born of an evolution where all kinds of stuff was eaten raw we wouldn’t even consider food now—so long as anyone is open to having been wrong or incomplete. But c’mon, man… resistant starch has been on the radar for 30 years. It’s never, ever talked about in LC circles that I’m aware of—other than out-of-hand dismissal—because….IT’S STARCH!!! I’ve even seen it called an “anti-nutrient.”

So a simple question: how come it’s so easy to make distinctions between kinds of protein (e.g., animal vs. plant vs. dairy) and kinds of fats (e.g., saturated vs. monounsaturated vs. polyunsaturated), but all carbs are really just sugar and all starch is just starch and it all ends up as glucose which is TOXIC and SPIKES INSULINZ!?

The rather hilarious thing, though, is that all of that research points to the likelihood that it’s precisely a form of starch—a completely different kind than the DEVIL’S SPAWN kinda starch—that feeds the gut biome (that other 90% of you), which in turn produces things like those ANGEL’S SPAWN short chain saturated fatty acids you love so much. And it does it in a place your cubes of butter can’t reach, producing the general effect of regulating apetite, satiation, glucose levels and by direct consequence: insulin requirements. And it’s starch that does this in the very face of the fact that an enormous plate of brisket spikes insulin.

This is the nature of the pitfalls whenever you like or love something: you like and love it too much. It’s our nature. BUT DOKTORS—EVEN LATE, GREAT DOKTORS—WERE INVOLVED! Newsflash: so are those studying RS, probably a few late greats, too.

The one bright spot is this: the Paleos have it fundamentally right, because if they’re really true to what evolution informs us about the human diet, it ought already be built in that we change as we incorporate and integrate new information and data. We’ve already seen that, as Paleo has gone from pretty much an Inuit diet to a far more varried one…to the general consterantion of LCers, in fear that our train will leave the station without them.

But in truth, I want them on board. I do. LCers have a claim to fame we don’t, and that’s that they’ve been stalwart in the stand against generally accepted dogmatic, authoritarian, agriculture and pharmaceutical industry-backed dietary practices since the early 1970s (thanks the the late, great, DOKTOR Atkins and others).

Please think, people. This is where the evolution really meets the road. Bacteria evolve far more rapidly than humans.

…Here’s a final shout out to Tim aka Tatertot from way up there in Alaska. He’s been out for the last few days on a fishing trip and just got in last night. That’s him on the right.

Halibut, Bass and Goldeneyes

Thanks for all the help, Tim, and especially for making me take the time to hear you out on all of this.