Feeding the Microbiota: Non-Starch Polysaccharides (NSP), Resistant Starch (RS) and Mucous

RESISTANT STARCH GRANULES

"During the co-evolution of man and microbes, the human intestinal tract is colonised by some thousand species of bacteria. Gut borne microbes outnumber the total of body tissue cells by a factor of ten. Recent metagenomics analysis of the human gut microbiota has revealed the presence of some 3.3 million genes, as compared to the mere 23 thousand genes present in the cells of the human body tissues."

--Rijkers et al, Gut Microbiota in health and disease: a personalised summary of 
the 3rth workshop

Everything Our Microanimalia Do For Us

How Shall We FEED THEM?

Flint et al Nature 2012

Seed, Weed and Feed the GUT

I've talked already about many ways to seed the gut (fermented foods, SBO probiotics, dirt, etc) to complement the existing microbiota and weed the gut -- removing toxins, mercury, pathogenic overgrowth, parasites and worms.  How should we properly water and feed the gut?

The primary foods are fiber, mucous and starch that resists small intestine digestion. If the gut is diseased, crowding out pathogens and removing parasites is also important. If the microbiota lacks diversity, then diversity needs to be cultivated and nurtured.  Studies show the obese, inflamed, autistic and heart diseased lack microbiota diversity of species and phyla.

Feeding and nourishing the microbiota isn't a special skill... our ancestors thrived and survived in special microecological as well as macroecological niches... and so did the gut microbes.  How did ancestrally derived foods benefit the microbes and what do they specifically provide for us?  Do we rely on them for immunity? For activation of important immune factors (glutathione, our #1 master antioxidant)?  For activation of plant-derived antioxidants like lignans, etc?  For removal of toxic and carcinogenic bile acids?  To balance the steroid hormone pool?

Yes to all.

I like ancestral diets. They must've worked I figured because we are here...

Being Asian I enjoy starches and after regaining insulin sensitivity (after being 50 lbs overfat), I burn starches adequately during glycolytic activity. With VLC/ketosis, I had cortisol dysregulation and to heal metabolism fully I had to eat carbs regularly. Being previously metabolically broken and still recovering from some toxicity (heavy metals, contraceptive endocrine disruption), however, I don't overdo the starches because I'll notice that I regain bodyfat mega fast.  Typically intake may be 1/4 of plate at most meals).

Our family eat certain starches regularly -- carrots, radishes, steamed pumpkin, bamboo shoots, fermented sauerkraut/carrots/radishes, tubers (yellow, purple, white, small potatoes, yams), flours (tapioca, sweet potato) and soaked grains/seeds (psyllium, millet, sorghum, black sesame, rice (purple, brown, white, glutinous)).   The variety depends on what is in season and carried by the organic farms -- Mahota, FIELDS, BioFarm/Cityshop, etc.  All the above contain both fiber and resistant starches (RS) which the microbiota feed on.  Ultimately, both types of microbial food benefit us on many levels.

In fact some studies show synergism when both fiber and RS are consumed together compared to fiber alone (beta-glucan) or RS alone for insulin and glucose reduction and regulation. Behall, et al:  synergism -- MEN and WOMEN. Below is the outcomes from the female study examing the impact on BG and insulin with intake of beta-glucan + RS. The levels of both were modulated low v. high and vice versa. Higher beta-glucan and higher RS produced the most marked improvements in metabolism. High amounts of either were satisfactory as well (see yellow/insulin,  orange/glucose lines and green circles).  Low amounts of either fiber or RS, not nearly as wonderful metabolic outcomes in this study.

Behall, et al 2006

Beta-glucan is a special soluble fiber (NSP)-- it's not made by mammals. It's found in yeast cell walls, whole grains, and mushrooms.  It's been shown to not only affect the microbiota but also improve immune function, wound healing, metabolic dysregulation, cancer/tumour sizes, and inflammation.  A recent study tracked the fate of beta-glucan in the gut and immune lymphoid tissues.  Researchers found "these large -1,3-glucans were taken up by gastrointestinal macrophages and shuttled to reticuloendothelial tissues and bone marrow. Within the marrow, the macrophages degraded the -1,3-glucan and secreted small soluble biologically active fragments that bound to CR3 of mature bone marrow granulocytes. Once recruited from the bone marrow by an inflammatory stimulus, these granulocytes with -1,3-glucan-primed CR3 could kill iC3b-coated tumor cells."

Resistant starch (RS) is found to be quite as plentiful as beta-glucan and plant fibers however cooking breaks it down to a form that we can digest (enzymatic, mastication, acidic).  The amount remaining in a food that escapes our digestive juices varies by many factors -- species, maturity of the plant, cooking/cooling methods, food acidity, to name just a few. RS is different from beta-glucan and fiber due to its tightly bound double helical glucose polymer structure.  Yes it is coiled up like DNA....  Solubilization in cooking water 'releases' the starches into a gelatin matrix which our spit amylases and pancreatic carb-ases can breakdown to glucose for absorption in the stomach and small intestine.  Any undigested amounts enter the caecum and colon.  The amount of SFCA produced upon caecal and colon fermentation varies as well depending on an individuals microbiota species, large intestine health status, etc.

The average intake of RS in China is 14.9 g/day from wheat, rice and starch products (mung bean, sweet potato noodles); compared with average USA 3-8 g/day intake it is about 2 to 5 fold increased. However, I don't think this holds true any longer for Chinese urban dwellers. When my parents grew up in a small rural village in Taiwan (with pigs and 'home organic' e.g. subsistence farms), they were poor and only ate potatoes, yams, mung beans, rice, and vegetables with very scarce meat/fish/pork belly or chicken or eggs. I believe their childhood intake fiber and RS intake were far more than currently, if not triple or quadruple.

Combined with veggies, most people's diets contain a mix of carbohydrates: rapid digesting (simple sugars, disaccharides), slow digesting (complex carbohydrates), nonstarch polysaccharides (FIBER = b-glucan, xylan, glycan, gums, pectin, mucin, cellulose, hemi-cellulose etc), and resistant starches (RS) to fuel both our human cells and the microbiota.  Our microbiota in the large intestines will eat and ferment fiber, RS, and the mucous produced in the protective layer of the gut.

Most Dietary Starches Contain Both b-Glucan or other soluble fiber + RS

Source: Behall et al

For SIBO and intestinal permeability, it's actually healing to minimize fermentation if it is occurring pathogically in the small intestines... where it shouldn't be.  The surface of the small intestines is not designed to support extensive networks of microbial growth which requires thick mucous.  The integrity of the small intestines can easily be compromised and fail to serve its function (digestion and absorption) when inappropriate growth manages to perpetuate whether it's 'good' v 'pathogenic' bacteria, yeasts or mycobacteria or parasites/worms.

The ONE (optimal nutri eval) is one of the best tools to measure the microbial/fungal metabolic by-products in the urine by opportunistic and pathogenic species in the small intestines.  The GDX/Metametrix GI function stool test is unique to identify microbial overgrowth, dysbiosis, pancreatic digestive enzyme capacity, small intestinal fat/fiber/protein malabsorption, and parasites/worms as well as assess microbial sensitivity to herbal and pharmaceutical antimicrobials.

Diet absolutely shifts bacterial communities in the gut ecology -- simple sugars lowers the good, raises the bad. More fiber and RS both raise the good (in Bacteroidetes -- Prevotella, etc), lowers the bad (in Firmicutes -- virulent strains of clostridas, E. coli's, enterococci, streps).  This is borne out in pig, children and human studies.  Flint et al do a great review here which includes a raffinose study (fiber from legumes) that enriched and ↑ F. prausnitzii, Bifidobacterium spp.  Like many of the good gut flora, Bifidobacter tightens up the intestinal tight junctions as super tight as a nun's **ss, which is enteroproctive and immunoprotective again gastroenteritis, intestinal permeability and necrotizing enterocolitis in trials. Guess what?  Magnesium deficiency compromises Bifidobacter and intestinal permeability (or which came first?).  Bifido appears to enjoy magnesium. In rodent studies fed a mag-deficient diet, intestinal permeability and quantitative changes to cecal bifidobacteria were associated.

My kids and I have scr*wed up Bifido (not bad but could be far better -- 3.2; Brent Pottenger's Bifodobacter is over 20% more and rocks at 3.9)... and we have low mag...  Brent has also has had zero cavities and therefore zero mercury amalgams.  Perhaps my fam and I need to forage us  some raw unpasteurized human breastmilk because it is enriched with Bifido?

Below is a human study n=10 on the microbiota shifts comparing RS2 and RS4 intakes (55 grams/day x3wks, then 2 wk washout).  Even among resistant starches, there is selective species enrichment.

The authors state in the results:  "Ten human subjects consumed crackers for three weeks each containing either RS2, RS4, or native starch in a double-blind, crossover design. Multiplex sequencing of 16S rRNA tags revealed that both types of RS induced several significant compositional alterations in the fecal microbial populations, with differential effects on community structure. RS4 but not RS2 induced phylum-level changes, significantly increasing Actinobacteria and Bacteroidetes (+++)while decreasing Firmicutes(-). At the species level, the changes evoked by RS4 were increases in Bifidobacterium  adolescentis and Parabacteroides distasonis, while RS2 significantly raised the proportions of  Ruminococcus bromii and Eubacterium rectale when compared to RS4. The population shifts caused by RS4 were numerically substantial for several taxa, leading for example, to a ten-fold increase in bifidobacteria in three of the subjects, enriching them to 18–30% of the fecal microbial community. The responses to RS and their magnitudes varied between individuals, and they were reversible and tightly associated with the consumption of RS."


Similar enrichment in enterocytes occurred in a rat weanling study feeding either basal diet or RS 5% for 28 days. I like this study because it demonstrated increased glutathione (our #1 master antioxidant; I have a GSTT1 deletion so mine is mildly compromised) by over 2-fold and improved pancreatic elastase secretion (digestive enzymes) in the RS fed groups.  [***Personally I eshew all rat studies unless they're vegetarian studies because (1) rats don't have a gallbladder and (2) they're not as omnivorous as humans or pigs so the data is incomparable, particularly the (ludicrous) meat/colon ca/nitrosamine studies.]



Shifting Microbiota Communities: GI Fx Stool Test and Optimal Nutri Eval (ONE)

Brent Pottenger's case:  Recall his Prevotella, Bacteroidetes and Firmicutes are quite stunning and no biomarkers of dysbiosis.  He has likely very little mercury (no history of cavities). His diet: near carnivory, fermented full fat Greek + some veggies both raw/cook (per Pottenger's cats).  The microbiota sequencing reveals a beautiful display of healthy guts.  Previously he c/o acne and migraines which are signs of SIBO and intestinal permeability.

My case: The Prevotella, Bacteroidetes and Firmicutes (2013) are impressively improved and robust compared with the initial 2011 when I had CFS, fogginess, fraility (sarcopenia), rank mood, and on/off body fat.  The SIBO is gone except for residual dysbiotic biomarkers from a parasite and Morganella. [yes wtf I dunno where the origin was but my children also have pathogenic overgrowth or parasites but we all different. I suspect I got it from one the irresistable poopers, see below]

Would you like to do a GI fx stool test and see your microbiota and do a ONE to evaluate nutrient deficiencies, dysbiotic markers and 8OHdG (DNA damage)?  Let me know and show me!  (Cost $99 and $129, respectively, plus admin fee $50).  Let's conduct paleo gut experiments.



What had I done?
--for two years

• gluten free, casein free, exercise/yoga (some barefoot on soil/lawn)
• removed mercury, gold, titanium parts and oral chelation on/off
• sleep, adrenal/gut support, antioxidants incl pycnogenol, omega-3, minerals
• Prescript Assist, FloraMend
• whole food diet (rainbow tubers, veggies, organic meat, lard/ghee)
• fermented pao cai, Beijing radishes, carrots

--for two months prior to the GI fx stool test

• Seed: Raw unpasteruized sauerkraut at nearly every meal and drank the brine, SBO probiotics
• Weed: charcoal and bentonite clay; removed gut irritants (alcohol -- studies here and here)
• Feed: Kraut and fiber rich foods (basmati rice, vegetables, potatoes, etc)

Energy Flux and Metabolism in Superorganisms

I consider this formula for energy flux:

Calories In (SUPERORGANISM) = Calories Out (MICROBIOTA) + Calories Out (HUMAN) + HEAT*Fluxxx

Rapid and slow digesting starches (RDS, SDS) impact blood sugars and insulin sensitivity by raising BG. The effect on insulin sensitivity and how they burn fat in the mitochondria actually depends on the individual, their insulin sensitivity and the carb/glycemic load.  See Major Paleo De-Mything.

On the other hand, insoluble or soluble fiber and RS do not raise insulin or blood sugars. In fact fiber and RS have been shown in several trials to behave like protein and omega-3 fats by raising insulin sensivity.  Both fiber and RS naturally have glycemic indices of 'zero', 'bulk' up food, increasing fecal transmit time as well as fecal microbial biomass. Combined with digestible carbs, RS and fiber both tend to prevent spiking of glucoses, thus blunting the effects of high GI (glycemic index) foods and sweets. Both fiber and RS definitely lower inflammation but appear to do so via routes which are intimately tied to the microbiota.

Role of the Gut Microbiota in Nutrition and Health

(Flint, Nature, 2012.)

The mouth and stomach digest ~10% of our carbs and the rest 90% is digested in the small intestines if all is functioning (pancreas, gallbladder, oral amylases, GI acidity, microvilli brush border enzymes, pepsin secretion, bile, peristalsis).  What escapes small intestinal degradation is later fermented by the microbiota in the large intestines (caecum, appendix, colon) to volatile organic acids, known as short chain fats -- acetate, proprionate and butyrate.  Although microbial byproducts provide some fuel to us  and the local enterocytes in the gut ecosystem (~10% of our total energy requirements compared with ~30% in other omnivores), actually much of the butyrate and other SCFA goes to provide energy to the microbiota . See above diagram 'Fermentation -- energy for bacterial growth'.  From my reading this amount varies. The SCFA collected at the colon depends on inflammation, IBD status, diabetic v. nondiabetic, etc.  I think it reflects SIBO and intestinal permeability factors which affect the microbiota.

SCFA play a role in the immune system and metabolic pathways by as binding fat-sensor receptors such as PPAR alpha, gamma, delta and GPR41/43.

How we chew the food and shear the particle sizes of resistant starch granules determines how much may be broken down in the small intestines. The first, top diagram above shows how digestive amylases 'etch' granules of resistant starches recovered in the intestines.  Food preparation also transforms the digestibility, crosslinks and polymerization of the starch matrix.  Longer heat, higher boiling/gelatinization, and maturity of the plant are all factors that predispose to higher digestibility and potential blood sugar impacts.   Cooling the starch and adding acidity (lemon, vinegar, fermentation) all lower small intestine digestibility by changing the coagulation of starches and protecting the starch granules from enzymatic degradation. Both refridgeration and autoclaving (high moist heat) polymerize the starch chains and raise RS.

So certain foods will have more RS as a result of food prep compared to the original food:
Fried rice or 'al dente' rice versus rice boiled in large volumes of water
Cold chinese rice ball snack rolled in lard/oil and seaweed versus warm steamed white rice
Sushi rice (room temp rice, sweetener +vinegar) versus warm steamed white rice
German cold potato salad with vinegar versus a boiled LARGE American monoculture GMO potato
Whole grain wheat pasta versus overboiled white pasta

Fermentation breaks down RS
Boiled poi (more) vv. Fermented poi (less)
Unfermented cooked rice v. Fermented Indian dosa rice or idli (less)

Autoclaving polymerizes amylose so raises RS
Processed (heating/reheating process) Uncle Ben's rice (but beware of the endocrine disrupting plastic it's encased in) v. freshly cooked long grain rice (less)

Evolution of RS

The amount of resistant starch appears to me to be related to the amount of protein in the tuber or grain/seed, on cursory review. I've tried to dig further but can't find anything.  The food sources which appear to have the most RS are the starch containing foods with intact cell walls and higher protein content legumes (9.5-11.1% dal, lentils, beans), whole grains (4.5-6%), or complete proteins (2% potato; 4.8-5.9% processed non-modified PS; steamed/cooled potato 31% and roasted/cooled potato 52.5%).  Perhaps amylose and other RS protect the peptides embedded in the starch matrix for tuber and grain/seed winter storage to buffer the Ice Age chill? Sprouting and germinating grains/seeds raise protein and nutritional content, but lowers RS.  Additionally, fermentation of starches is a trade-off -- fermentation lowers RS but raises protein/vitamin content.

I GAVE HER PROBIOTICS SINCE
THE FORMULA DIDN'T HAVE

ADORABLE POOPER