Part I: Bifidobacteria longum, Roseburia, F. prausnitzii (and Akkermansia) Made Us Human (NONE OF THESE EAT RAW POTATO STARCH) NSFW
Part II: HADZA GUTS HAVE THE ANCESTRAL CORE MICROBIOTA IN ABUNDANCE; High Dose RAW Starch Can Suppress Bifidobacteria, Roseburia, F. prausnitzii That Make Us Human
Part III: PALEO MAG HOT TONY FEDERICO HAS THE ANCESTRAL CORE MICROBIOTA IN ABUNDANCE; Citizen Science; Cautions with RPS-RUMPS; High Dose RAW Starch Appears to Suppress Christensenella, Akkermansia, and B longum That Make Us LEAN
Part IV: High Dose Potato Starch Can Make You Fatter, Insulin Resistant, Feed Vipers in Your UPPER GUT If You Are MISSING Bifidobacteria longum and Akkermansia mucinophila, aka SAD Microbial Fingerprint  NSFW
Part V: High Dose Potato Starch Can Make You Fatter, Insulin Resistant By Lowering GLP-1 AND ESPECIALLY If You Are Missing  Bifidobacteria longum and Akkermansia mucinophila, aka SAD Microbial Fingerprint NSFW

Diabetes Warrior: Gut Experiment with Amped-Up Bionic Fiber

Our fearless low-carber Diabetes Warrior, Steve Cooksey, and I are doing a little n=1 experiment with an amped-up version of Bionic Fiber and the 7 Steps.  Bionic Fiber  replenishes the ancestral phylogenetic core microbiota which are damaged by SAD diets, antibiotics and high-dosage potato starch (raw resistant starch, type 2). These are the gut flora that also happen to regulate insulin and body fat storage.

Steve uses a VLC (very low carb) diet to control blood sugars and successfully reversed obesity and complications related to diabetes. As 1/8 Cherokee Native American Indian, the VLC diet suits him well though he eats starches occasionally. Steve works out frequently and his diet includes a lot of greens including dandelion salads which are rich in inulin-FOS.

Steve’s results so far show reduction in weight prior to the holidays and no gains during the festivities. He was very pleased to see the blood glucoses (BG) improve from 70 – low 90s to 59 – 80s. Stools improved within 1-2 wks going from 3 times per week to daily.

PROBLEM WITH POTATO STARCH? RAISES BLOOD GLUCOSES: FOLZ FAMILY

In the Folz Family RUMP/raw potato starch experiment, the family members all observed higher blood glucoses with 1 TBS potato starch except for Child 1 who was taking 1 TBS PSYLLIUM which has been shown to reduce body weight and blood glucoses. The n=1 are small but the point of the experiment was to measure BG as a metric of gut health. Adult 2 was trying to lose weight but no body fat losses or weight loss were reported during or after the 6 week experiment.

HERE Allan Folz:

First, our blood glucose measurements marginally went up, especially for my wife and me who were taking the largest doses. 

Before beginning the experiment I measured our BG first thing after waking up across three consecutive days. These were taken on January 15, 16, and 17.

[PRE RESISTANT STARCH, RS2]
For myself: 96, 89, 88
For my wife: 89, 93, 101
For child 1: 96, 91, 109
For child 2: 84, 90, n/a



After six weeks of RS I repeated taking some morning measurements. These were taken on March 26, April 1, 2, and 4.

[POST RESISTANT STARCH, RS2]
For myself: 97, 114, 94, 98
For my wife: 116, 95, 92, n/a
For child 1: n/a, 92, 85, 89  [+ 1 TBS PSYLLIUM=IMPROVED BLOOD GLUCOSES]
For child 2: 87, 90, 79, 100

RAW STARCHES ARE NOT ANCESTRAL?

Tigernut man was the last hominid that studies show consumed a high RS2 diet — and he and his pre-human lineage expired 1.2 million years ago. The hunter-gatherers who learned to cook and use routine fire dominated the plains, steeps, and gallery forests during the hundreds of thousands of years that followed. Our diet and gut flora have likely adapted and reflects vast changes in the fiber and diversity of resource allocation since then. The flora that feed and crossfeed from raw starches (Bacteroides, Clostridium) are not the dominant immunoprotective nor body fat controlling ones (Bifidobacteria longum, Akkermansia, Christensenella, Roseburia, Faecalibacterium, etc) which consume a variety of fiber but not raw starches well or at all. The raw starch eating bacteria help make us human compared to chimps but they are not the powerful anti-inflammatory gut flora that help our bodies to efficiently utilize fats and complex carbohydrates and by cycling body fat back into ready energy brain energy (glucose or ketones).  In that respective it explains why in human and pig studies (prior post), raw starches (RS Type 2) such as high-amylose maize and raw potato starch fail to appear to perform well metabolically and may even raise fasting insulin and insulin resistance. Body fat doesn’t improve or even gets worse. Gut researchers cannot reconcile the differences between the good hamster/rodent studies and the lack of translation in human studies and human subjects.

Rats lose body fat on their native diet — raw starch — but humans do not appear to (or even get fattier organs, higher BP and higher insulin, Bodinham et al 2012 and 2014), and perhaps this is related the fact that no current human society consumes large dosages of raw starches in their regular daily diet or at least not without being accompanied by an upwards of 150 grams of dietary fiber (Hadza).  So is raw starch part of the natural food for our gut flora? What adverse shifts in the gut flora happen when unnatural ‘fiber’ becomes a large component of dietary fiber for humans and fuel for our 100 trillion gut inhabitants? The research seems pretty clear that our gut flora are maladapted, and, worse, the gut shifts affect metabolism and insulin sensitivity by lowering keystone anti-inflammatory gut species that are associated with leanness and insulin sensitivity.

Gut scientists Geurts et al recently stated:

“Resistant starches (RS) are also fermentable non-digestible
carbohydrates (Bird et al., 2010; Robertson, 2012). Although
they are not regarded widely as a prebiotics, most forms
of RS induce changes in gut microbiota composition
(Flint, 2012). In rodents, data suggest that chronic RS
feeding upregulates proglucagon expression (i.e. GLP-1
precursor) in the colon with concomitant increases in
neuropeptide expression in the hypothalamus (Shen et
al., 2009; Zhou et al., 2008). These effects result in weightloss and improvements in glycaemic control. However, todate there is no evidence for this in humans (for review see Robertson, 2012).” 

SHIFTING GUT FLORA WITH BIONIC FIBER

Cooksey tried potato starch but it didn’t lead to permanent changes in body composition — sometimes he gained weight, sometimes he lost weight. Blood sugars and stools initially improved then plateaued, so after a few months he gave up and noticed no change afterwards in glycemic control.
Like all the gut profiles I’ve reviewed, I would strongly suspect the lack of permanent improvements were related to adverse shifts in Cooksey’s guts a result of high dosage potato starch induces on the gut. 
–suppression of Bifidobacteria longum, the keystone immunity and gut guard (depletion is associated with nearly all human diseases studied so far) 
–reductions in Akkermansia(higher the better, the lower the blood sugars and disease in human trials)
–reductions in Christensenella(higher the better, the lower the body fat and disease in human trials)
–reductions in Roseburia and F. prausnitzii particularly for those on lower carb diets (these are the large butyrate producers of Clostridia XIVa and IV and are immunoprotective)

How To Boost
Bifidobacteria longum, Roseburia,
Akkermansia muciniphila,
and Faecalibacterium prausnitzii
For Fat Loss, Satiety,
Reversal of NASH/fatty liver,
Improved Glycemic Control and Insulin Sensitivity

Geurts et al 2013

To fill in the gaps that are missing in the microbial fingerprints of most modern and damaged guts, Geurts et al advise several fibers and prebiotics to increase Akkermansia, Bifidobacteria longum, Roseburia and F. prausnitzii including chitin-beta glucan, arabinoxylan (psyllium, grains), oligosaccharides and inulin-FOS. Amped-up bionic fiber contains a variety of these to promote diversity in the gut — low doses of several fibers that all increase acetate, propionate, butyrate and long term raise GLP-1, an anti-inflammatory gut hormone that promotes fat burning and leanness.  Geurts et al discusses GLP-1 in detail. These fibers that raise GLP-1 are found in a variety of foods including the below. Steve Cooksey loves to forage for dandelion roots and greens, wonderful sources of inulin-FOS which are nuclear powerhouses that enrich Akkermansia and B. longum and which are both shown in human trials to lower blood sugars,  improve fat loss and potently fix glycemic control.

Preferentially Feeding Bifidobacteria longum, Akk, Roseburia, and FP (Avoid Raw Starch)

Many plant foods contain these below special fibers and prebiotics that selectively feed B longum, Akk, Roseburia, F prausnitzii:

  • mushrooms — chitin-glucan (hat tip Dr Lagakos)
  • beans — GOS (hat tip Dr Lagakos)
  • raw dairy — GOS and other oligos
  • whole GF grains, gums and psyllium — oligos, FOS, AXOS, inulin, acacia, pectin, lignins, etc
  • low carb, non-starchy tubers (dandelion root, chicory, sunchokes, beets, rutabagas, konjac, etc) — FOS, inulin, XOS, pectin, hemicellulose, etc


Leanness Related Gut Flora
Depletions Associated with Human Clinical Disease
Leanness Gut Flora, Prebiotics, and Human Studies
Damaging Gut Effects of High Dose Raw RS2 Resistant Starch 
(Potato Starch)

N=1s

Gut Diversity
Diseases are Associated with Low Gut Diversity
Increases Diversity If Diverse Fibers
Reduced by 10-36%
–Folz family 10-20% loss of genera or phyla with RS2
Bifidobacteria longum

B.longum and bifido depleted in chronic liver disease, fatty liver/NASH, obesity, T2D

–often undetectable
–depletions of 100-fold to 2000-fold for relative bifido typically for potato starch
–B.animalis or B. adolescentis majority colonizer
Akkermansia
Depleted in metabolic disorders and gut conditions: diabetes, obesity, fatty liver/NASH, IBD, IBS

“A. muciniphila is important for a healthy host as its decreased abundance is associated with compromised health including acute appendicitis, ulcerative colitis, autism and atopic diseases. Finally, the abundance of A. muciniphila is inversely correlated with obesity …plays a pivotal role in obesity as its duodenal delivery regulates fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance” Source
reductions in Akkermansia
— 2-fold to 17-fold depletions from normal



Christensenella

Christensenellaceae bacteria might be a “keystone” species, “one that wields a disproportionate influence upon the world around it.”’
— 2-fold enrichment of Christensenella with high fiber, non-starchy tubers and vegetables
— 5-fold enrichment compared with controls of family Christensenellaceae
reductions in Christensenella
–2.5 to 10+ times depleted below controls
–Stopping raw potato starch increases Christensenella from undetectable to detectable levels
— 4-fold decreases in family Christensenelleae

B. ANIMALIS AND B. LACTIS ARE NOT AS EFFECTIVE AS GUT SPECIALIST BIFIDOBACTERIA LONGUM

Several bifido probiotics exist on the market but none work as effectively to improve immunity, improve gut disorders and reverse diseases as the ones native to humans: B. longum, B bifidum and B breve. In healthy guts and breastmilk of healthy, disease-free mothers, B. longum is the dominant species (see above table).

“In this context recent clinical studies as well as murine-based trials involving supplementation of probiotic bifidobacteria belonging to the B. animalis subsp. lactis taxon coupled with metagenomics investigations, highlighted the lack of any effect in terms of modulation/modification of the gut microbiota composition upon intake of such probiotic bacteria,41,42 thus reinforcing the notion that the use of bifidobacterial strains that do not have a human origin, such as members of the B. animalis subsp. lactis species, may be limited in their ability to interact with other members of the gut microbiota or with the host.” (Ventura, Turroni et al 2014)

Bifidobacteria in healthy subjects’ human guts (Turroni et al AEM 2007)

Fecal bifidobacteria:
B longum 43.5%  (non-starch eater, prefers oligos, arabinoxylanOS & mucin)
B lactis 23%
B adolescentis 12% (starch eater)
B pseudocatenulatum 8%
B bifidum 6% (non-starch eater)
B breve 4% (starch eater)
B pseudolongum 2%
B dentium 1.5%

  • P1

    My experience taking raw potato starch was much higher glucose levels. Your analysis of this looks right.

  • P1

    I saw immediate resolution of higher blood glucose to my “normal” prediabetic levels after I stopped raw potato starch.

    What is really strange to me is that I saw my blood sugars go lower to a more normal range when I stopped eating disaccharides and starch, and focused on a diet very similar to specific carbohydrate diet. My fruits are primarily berries, which are monosaccharides and very low sucrose / disaccharide levels. I eat LOTS of leafy green vegetables. I’m almost like a mountain gorilla eating a whole head of butter lettuce in morning and a huge pack of arrugula in evening.

    As an extension of your ideas, I wonder if those of us with gut issues similar to SIBO are getting an effect like you describe from *any* carbohydrate source that is high calorie and does not fully digest? If your sucrase enzymes are either insufficient or inactive because of compromised gut villi, can the undigested disaccharide also feed the same sorts of pathogens that raw potato starch is feeding?

    I’ll try to probiotics you suggest.

    A year ago if someone had told me I would clear brain fog, lower blood glucose, and digest food better by eating monosaccharides glucose and fructose separately instead of in sucrose, I would have thought they were crazy. But in my body that seems to be the case.

  • P1

    Yes starch and FODMAP intolerances get worse and worse in dysbiotic guts (SIBO/SIFO). Sifo is common — because antibiotics wipe out bifido and Akk which have potent antifungal spectrums. I bet Christensenella also is powerfully antifungal — this is perhaps the beauty of Tony Federico’s stellar gut profile. Never seen anything that high and correlates to his disease-free, lean, sarcophilic, high muscle mass status.

    When I was very ill, CFS, I couldn’t tolerate any FODMAP or starch. Now I eat everything almost without retribution (back to pre-gut damage days).

    Soil probiotics + B longum + Akk + Christensenella are the keys for nearly everyone. All need to be present and the uppergut needs clearance from ‘weeds’.

    Many still have alcohol/toxin secreting yeasts, E coli, Enterobacter and/or Clostridum in the uppergut — super common and these lead to intolerances of FODMAPS and carbs. People need to go lower and lower carb (to starvation) to be able to digest. If you are able to clear these out properly with probiotics/prebiotics and the bionic fiber combo, then you shall see great gut yields IMHO. Ihad to do all these to ‘repair’ the RPS induced reflux, but eventually it all worked. Glad it happened!

    Yes to all your questions.

    Other good antifungal probiotics (if not immunocompromised or surgery or chemo/rad)
    S boulardii
    Prescript Assist
    Bacillus laterosporus
    Bacillus licheniformis
    Bacillus subtilis
    Bacillus coagulans
    Bifidobacteria bifidum
    Lactobacillus plantarum
    etc

    ALL THE ABOVE MAY HAVE SUCRASE and other digestive enzymes 😉 particularly for lactose, casein and gluten/gliadin and they are all commensals to healthy human guts except S boulardii and B laterosporus

  • Interesting! How does one get Akkermansia & Christensenella? I have never heard of those before!

  • P1

    I noticed that your original post had tablespoon-ish doses of the bionic fiber mix:
    http://drbganimalpharm.blogspot.com/2013/11/how-to-cure-sibo-small-intestinal-bowel.html

    The most recent post is backing down to around a teaspoon of each fiber. Are you recommending starting at a teaspoon and then working up to larger doses? Or has experience shown that the smaller dose is sufficient?

  • One more question….is potato starch constipating?

    • Old Road ~Were you constipated? Try the bionic fiber which in clinical human trials, individually, relieve either constipation or diarrhea

  • P1

    It’s a low dose titration if you go to Cooksey’s website, instructions are there. Glucomannan however is max 1/2 tsp but Cooksey really enjoys it and has increased to 1 tsp daily while the others are 1 TBS daily each.

    Old Road Primitives — not yet! soon probably!

  • Hey Grace Sweetie, Hope all is going well with you, family, and being back in the States. I was checking out the Hawaiian Libertarian website when I saw a link to Richard-still-the-fat-boy’s site with some comment about the Gut Goddess . . . did a quick link and read some—F*ck him, what a looser. So looser Richard to lash out at anyone who doesn’t support his beliefs. Grace-Hakka-Honey: I’ll always have a sweet place for you, so it’s my nature to defend you. Wishing you the best always–XOXO . . .

    • Calvin~ That’s sweet and ur too funny — don’t exert too hard lol. Hugs and stay well!

  • Dr B G,
    About your comment above on, January 23, 2015 6:09 PM, which commercial probiotic preparation has either of the following?
    Bacillus laterosporus
    Bacillus licheniformis

    BTW, Watched your one of the old videos, that brought me here (last year or from 2013), you mentioned you are in the process of publishing a book. If its already out, mind linking it here?

    Thanks in advance.

  • Anonymous

    To each their own. Every time I try psyllium I crap out neon yellow and green mucus. It’s quite disturbing. I tried Acacia once for a couple weeks and gained 10 lbs. Green banana flower (RS2) on the other hand has been great. Down to 10% body fat (with no exercise) and fasting BG ~70.

  • Anonymous

    You said “people may still have…clostridium in the upper gut.” I thought this was one of the ancestral core? Should we not be taking the AOR if we are trying to avoid clostridium?

    • GCBC — yes but there’s ‘good clostridium, bad clostridium’ to borrow Taubes. Some fiber distinguishes, but potato starch doesnt. No AOR ‘trains’ the bad to be better 😉 and promotes the helpful and ‘cleansing’ Bifidobacteria longum (not B animalis — not helpful or even harmful because it is not specialized for human guts, only #hamsterguts)

      A couple of strains super feed or ultra ferment raw starches — these are implicated in SIBO, NASH/fatty liver, obesity, diabetes, reflux, autoimmunity, Hashimoto’s, RA, AS, Sjogren’s, cancer, etc — we don’t want them overgrowing: toxic strains of Clostridium, Bacteroides, E coli, Klebsiella, Enterobacter cloacae (seen a ton of this lately on gut profiles), ? yeast, Bifidobacteria adolescentis/animalis (too much of a good things = pathogenicity), etc.

      Look at fig 2, Krause et al 2010 — ‘bad’ E coli in the uppergut are all superfed by raw potato starch and they overgrow. Only probiotics fix this. We can simulate repair by feeding Akkermansia, Christensenella and Bifidobacteria longum (and soil SBOs) to take care of the bad E coli, just like bad clostridia.

      http://drbganimalpharm.blogspot.com/2014/12/high-dose-potato-starch-can-make-you.html

      http://4.bp.blogspot.com/-MbMl9jfWFUI/VMPH8Shkm1I/AAAAAAAAB5s/N_Tn09fcXWU/s1600/Nursery%2Bpigs%2Beradicate%2Btoxic%2BE%2Bcoli%2Bon%2Bprobiotics.png

  • P1

    Which gut profile test do you recommend to profile the bacteria you are discussing in this blog post? Is that test using DNA analysis?

    • P1 ~ ubiome or Genova stool/urine testing. Yes — DNA for both.

  • Question about if “cooked whole beans and beta-glucan/arabinoxylan/RS3-inulin-containing cooked barley (here, here) raise GLP-1 in human trials.” while “raw starch lowers GLP-1 in human trials” have any influence on insulin-manipulating diets?

    Does that make RS2 compatible with insulin-minimizing diets, while RS3, inulin is not compatible with insulin-minimizing diets?

    http://en.wikipedia.org/wiki/Glucagon-like_peptide-1
    http://emrc.tums.ac.ir/upfiles/143555871.pdf

    According to the articles GLP-1 can increase insulin production, although the exact amount is dependant on glucose levels. So my question is about the diets that explicitly avoid insulin or increase insulin at certain times.

    For example Carb Backloading by John Kiefer forbids having high levels of insulin and cortisol simultaneously, as cortisol is a hormone that releases fat from fat tissues, while insulin is a hormone that tries to store energy in the fat tissues. So in the morning, when cortisol is naturally high according to the daily rithms the practicioners of Carb Backloading eat low-carb, low-protein food. This of course raises the question of gut health, as this leaves no fuel for the bacteria. So if RS2 has this effect of not promoting GLP-1 that can increase insulin – isn’t it a prebiotic of choice for such scenarios? Notice that VLC mornings might some starchless, leafy vegetables.

    Then like 3 times a week the practicioners of Carb Backloading do a pigging out on high glycemic index carbs in the evening in order to increase insulin to the maximum. But this is preceded by intense strength excercise in order to empty the glycogen stores. At night the cortisol is low, so little combination of insling and cortisol occurs. Most of the body is insulin resistant, but the muscles aren’t thanks to the excercise: so the carbs go there, and there’s insulin – so the muscles grow (it’s a bodybuilding diet). I guess gut bacteria would get some leftovers from such pigging out. I don’t know what to think about inulin and so on such occasions – on one hand they would give more insulin via GLP-1, on the other – decrease insulin resistance.

    So does potato starch make sense as a supplement for such dieters in the mornings or on non-training evenings, perhaps with some non-starchy vegetables? How about inulin on training/feeding evenings?

    The author of the Carb Backloading diet seems dissmissive of the whole gut biome concept, at least of importance of it.

    • tomR

      You said ‘Does that make RS2 compatible with insulin-minimizing diets, while RS3, inulin is not compatible with insulin-minimizing diets?’ Inulin-FOS is compatible and part of the ancestral diet as inulin is the 2nd most common carb in nature. RS is the first — and humans have cooked for millennia making RS3 the preferred resistant starch for humans and human gut flora.

      I think the insulin effects are diff for different gut biomes — to me it appears VLCers see lower BG with RS2 however the longterm consequence is increased insulin resistance in the periphery. The liver does not improve because it is getting a high dose of ‘starch’ though raw. the by products of bacterial/fungal fermentation worsen liver function actually though the colon gets a lot of butyrate/SCFAs. THis is the paradox that gut researchers haven’t reconciled except to conclude that potato starch is not ‘prebiotic’ because it lowers the good flora.

      RS2 can raise GLP-1, very acutely immediately after ‘dosing’ however again this is not ancestral to consume 8 or more grams in one single sitting. Over time and longterm, GLP-1 actually decreases which leads to the suboptimal metabolic effects, higher fatty organs, increased blood pressure and worsening insulin sensitivity.

      For insulin sensitivity — I concur with Kiefer and Lagakos. You need carb backloading and the appropriate exercise to stimulate insulin. Use it or lose it! For women and those insulin resistant, eating small frequent meals that are ‘balanced’ for complex carbs/prot/fats is key too. These feed also the gut microbiota best, make sense? Low GI helps those with high insulin resistance, but if one has sensitivity, high GI is not that big a deal. Ludwig et al has done the studies. Low GI concurs with Geurts et al and their observations for prebiotics and the gut flora associated with improving leanness and inflammation — Akk, B longum, Roseburia, F praus, etc. Read the Geurts article again.

      Those who use pot? They get fatter and fatter often… they have high eCB tone. The prebiotics Geurts et al discusses lowers eCB tone by increase GLP-1 and GLP-2, which incidentally seal and heal the gut integrity (via stimulating the gut guardians Akk, B longum).

  • Anonymous

    Hahahah, so choice.

    Maybe first blogger ever to delete a comment with a link to her very own writing.

    Have fun, sycophants.

  • This is a great, generous blog entry getting into the nitty gritty of probiotics and prebiotics, identifying the true beneficial strains of microbes to address to bring balance via lowering pathogenic gram-negative proteobacteria. And honing the list of fibers specific to these strains, putting it all together. Seems a lot of people would benefit, especially diabetics, if they took the time and made the effort to understand this construct. This is how people should be treating diabetes, a matter of microbial overgrowth in the small intestine which is connected to the liver via the portal vein where microbes send fatty acids to the liver resulting in high blood glucose via gluconeogenesis (leaky gut not required!).

    I’d like to see a future blog devoted to lactic acid bacteria (LAB) including bifidobacteria and lactobacillus as the crucial element in regulating gut pH instead of all the focus on alkalizing diets. We need LAB to create a high acid gut which then sends bicarbonate into blood for a healthy alkaline system (inverse relationship). Diet is secondary to flora, yet the field of Nutrigenomics is largely sterile. The word ‘bacteria’ doesn’t appear on this page as if food magically alters gene expression without microbial involvement: http://en.wikipedia.org/wiki/Nutrigenomics

    This blog is about prevention as much as treatment.

  • Duck Dodgers

    Grace,

    You know I have a lot of respect for you, but your assertion that raw starches are not ancestral is extremely weak and is in no way supported by the anthropological literature. It’s sloppy.

    For instance, using 5 “ancestral” species of bacteria that are inherited from non-starch eating primates as proof that raw starch is not ancestral is a logical fallacy. It’s very misleading.

    Humans eat starch. Primates do not. Therefore, raw starch is not ancestral? I’m afraid you will need to do better than that.

    It’s well known that USOs are extremely important to human evolution, for millions of years, and it’s more than a little odd that you would try to claim that only “cooked” USOs were eaten when they were perfectly safe to eat raw.

    Tiger nuts are just one example of a sedge tuber that has had a close relationship with humans since the dawn of humankind. The tiger nut is safe to eat raw and was one of the first cultivated plants in Ancient Egypt. Even today, kids in Europe snack on raw tiger nuts as candy and the Valencians drink their raw horchata as a medicinal superfood.

    Paleo Indians at Mashantucket were shown to have yellow nutsedge (weedy tiger nut) starch all over their tools. To suggest that these sedge tubers, which were perfectly safe to eat raw, were somehow only eaten cooked will require far more assertive evidence than a short poorly-researched paragraph engineered to needle your ex-collaborators.

    Not only is there overwhelming evidence showing the importance of sedge consumption by our distant ancestors, but there are plenty of studies showing a variety of different sedge tubers consumed by H. Sapiens.

    For instance, here is a study that was published last week!

    Nuts for dinner? Cladium mariscus in the Middle Stone Age at Sibudu, South Africa

    The Middle Stone Age ended ~50–25,000 years ago. To suggest that sedge tubers were only eaten cooked is like suggesting that pecans were only eaten roasted. It’s preposterous.

    As you can see, there are a wide variety of raw sedge tubers besides tiger nuts out there. I hope you don’t plan on trying to discount the raw consumption of every USO that’s ever been classified.

    Cheers.

    • Hey Duck

      What do you think the rs2 of horchata to relative total dietary fiber? 1:10? 1:20? What’s ancestral in your opinion and the gut flora effects?

      Thanks for your thoughts and history lessons lol

  • P1

    Should the bionic fiber be taken before/after meals, with food, and does the time of day matter?

  • Duck Dodgers

    I dunno Grace. It’s an “ancestral” beverage and it has been traditionally believed to provide benefits to those who drink it. I certainly don’t think it deserves to be demonized, with loose assertions and “hawt” muscle-heads, in a six-part series. That’s for sure. One could probably say the same exact things about “high doses” of any food or fiber.

    Do you suppose that Paranthropus boisei—one of the most successful and longest-surviving population of hominids ever—was obese and insulin resistant from eating too many tiger nuts? I think you and I both know that’s highly unlikely.

    And furthermore, why does RS2 need to be cooked but for some reason the “bionic fiber” must be served raw? Makes no sense whatsoever. It’s a double-standard.

  • JC

    Hi Dr. B G

    I am using 1 tsp Inulin/FOS 3 times a day, and one sachet (5.5 g) GOS. I am on PHD. I am much better than before but I still have gas and bad smelling flatulence. I ordered everything in your bionic fiber. I will keep posting the results.

    I have a question on probiotic: What do you think about Jarro-Dophilus EPS? I ordered it because it is room temperature and stomach acid stable.
    Is LEF Bifido GI Balance acid and room temperature stable? I also want to use that one.

  • Hey Duck, nice writing! PS might lower pH in the colon by raising butyrate while causing microbial overgrowth in the small intestine, raising pH there leading to GERD, diabetes, fatty liver . . . mental illness.

    And some microbes really are better at preventing (consuming) yeast overgrowth than others. Though it’s probably a team effort, as you describe, with all the crossfeeding necessary.

  • P1

    I am more low carb, and I am probably around 100 grams of carb a day and except for some fruit in morning that is all low glycemic index. The fruits are typically berries.

    I just started the specific carbohydrate diet (SCD) within the last month and that has made it pretty clear to me that I have significant starch, disaccharide, and possibly fructose impairment. All of those foods do not digest well.

    If I eat berries (which are mostly glucose and fructose), I seem to tolerate those fairly well. If I instead get the same sugars from honey, I get a lot of gas and upset from that. That tends to make me think I may also have a fructose intolerance and when I take in a whole food like a berry not as much fructose gets through and the rest is for the benefit of bacteria. When I take it as honey I’m probably making more of it available to bugs in the small intestine. Still testing all of this, but I’m very tired of being so intolerant to food.

  • P1

    Duck, the secret to honey is that the bees predigest sucrose for us, and then convert it to the monosaccharides glucose and fructose. Honey is not the same as sucrose, even though it is the same after your do the conversion of sucrose. Metabolically in a compromised gut you either do not have enough sucrase to do the conversion, or alternately your intestinal villi are not functioning in a way that allows the sucrase to function efficiently.

    Use of honey is actually extremely consistent with the advice to avoid RS2 and potato starch. Honey would quickly absorb in the small intestine (unless you have a fructose intolerance, which one in three Northern Europeans do have). That effectively starves bacteria that might feed off of undigested sucrose, or starch.

    There is a kind of intellectual nihilism in some of these responses criticizing Grace’s cogent observation that RS2 feeds many bad bacteria and does not feed many good ones. At minimum, it is not a defense of potato starch to say the world is complex. I’m not going to take a kind of starch in large dose because the world is complex. I’ll take it when studies show it has the kinds of health effects I am chasing in human population studies. And potato starch fails to do that. With my n=1, it gave me much higher blood glucose readings, quickly.

    I don’t have any problem with Grace pointing out what types of fiber feed the good bacteria she knows about, along with some references from studies to demonstrate that. That’s more science than most potato starch blogs have going for them.

  • Duck Dodgers

    P1, your response gave me a chuckle. You have a lot more reading to do on honey. I’ll apologize in advance, but I’m being as polite as I possibly can when I say that you haven’t even found the iceberg, let alone the tip of it. Keep swimming.

    P1 said: “There is a kind of intellectual nihilism in some of these responses criticizing Grace’s cogent observation that RS2 feeds many bad bacteria and does not feed many good ones. At minimum, it is not a defense of potato starch to say the world is complex.”

    You must be joking. It’s one thing to point out a few negative aspects of eating “high doses” of any food or fiber (true of any food, by the way). It’s quite another to write a never-ending multi-part series clamoring for weak evidence to spite former collaborators. The latter is what is happening here if you were unaware and it does nothing to serve readers.

    I have a lot of respect for Grace, but when she decided to claim that ancestral starches were only eaten fully cooked, I had to speak up. It’s a ridiculous assertion at best.

    • Duck

      Why did you stop raw potato starch? Didn’t it cure all your ails?

      One second you fail to see the benefit of keystone species in the gut for either health or harm, yet later you quickly assert ‘For instance, beneficial yeast likely protect against bacterial overgrowth’? Let me point out that that is illogical

  • Duck Dodgers

    Keith Bell said: “Hey Duck, nice writing! PS might lower pH in the colon by raising butyrate while causing microbial overgrowth in the small intestine, raising pH there leading to GERD, diabetes, fatty liver . . . mental illness.”

    Keith, I’m unclear how fermentation of anything would raise pH. Can you explain? And wouldn’t most of the starch granules move through the SI faster than bacteria can detach from them? After all, PS granules are some of the largest in the plant kingdom.

    Even if I’m wrong on all counts (which I don’t mind, by the way…I’m always happy to learn), I think it’s easy to get caught up in the world of X=bad, and therefore we must totally avoid it—when in fact it may in fact take a balance of good and bad to promote a beneficial homeostasis. For instance, beneficial yeast likely protect against bacterial overgrowth. This is a difficult concept to learn when immersed in the Western world of all things being “good” or “bad.” A change in perspective helps.

  • Anonymous

    K. Bell said: “PS might lower pH in the colon by raising butyrate while causing microbial overgrowth in the small intestine, raising pH there leading to GERD, diabetes, fatty liver . . . mental illness. “

    Hold the phone…so PS is the only one of the prebiotic fibers that will do this dastardly deed?

    Inulin, GOS, all those are perfectly fine, but PS is the bad guy? And this is backed up where?

  • Duck Dodgers

    “Why did you stop raw potato starch? Didn’t it cure all your ails?”

    I’ve simply moved on to getting my RS2 from green bananas. I just prefer whole foods. And then I usually eat beans and figs, dates, whatever other fiber-rich plants I can find on any given day. I like to mix it up.

    Grace said: “One second you fail to see the benefit of keystone species in the gut for either health or harm, yet later you quickly assert ‘For instance, beneficial yeast likely protect against bacterial overgrowth’? Let me point out that that is illogical”

    Grace, this whole six-part series is teaming with logical fallacies and willful misinterpretations of data.

    And, of course, you’ve missed my point. My point is that we need a balance of things to keep everything in check. You can’t just stuff your face with things that feed keystone species and expect to have perfect health. If that’s what you’re selling, you’re misleading people.

  • Duck Dodgers

    Grace said: “But Duck, you don’t believe in keystone species? So why would you care which ones you are feeding or not? Again, that is illogical to me and your arguments.”

    Sure. I believe in them. I never said keystone species weren’t important, Grace. You’re clearly not listening to what I’m saying.

    All I said was, “one does not need a specific microbe in place to prevent candida overgrowth.” And it’s true. Just because you are missing or low in a single keystone bacteria does not mean you automatically get candida overgrowth. I hope you don’t diagnose candida that way.

    Grace said: “How is your chronic fatigue lately?”

    Um.. Excuse me? I don’t have CFS. And I never did. I had candida and taking PS saved my life. And who the F are you to try to divulge medical history like that? Who does that?

    Grace said: “It appears to me from the CFS Phoenix Rising boards, the best result has so far been Asklipia”

    Asklipia cured her CFS long before PS came onto the scene. And, once again you’ve rewritten history as Asklipia in particular was extremely grateful for learning about PS and other fibers. Most people on that forum were thrilled by the progress that a spoonful of cheap PS gave them, even if it didn’t solve all their problems.

    But, I can see what you’re doing. Take any n=1 you can find and rewrite it to discredit others. Very nice, Grace.

  • Duck Dodgers

    Ah.. I see I’m being censored now.

    Sorry P1. You’re on your own. Good luck.

  • And, Duck, I like what you’ve said here about “balance of good and bad to promote a beneficial homeostasis. For instance, beneficial yeast likely protect against bacterial overgrowth.”

    Did you know yeast are prebiotic? Chitin in the cell wall of yeast is food for commensal bacteria including butyrate-belching clostridia, bifidobacteria and lactobacillus:
    http://www.jnutbio.com/article/S0955-2863(10)00263-9/abstract
    http://www.sciencedirect.com/science/article/pii/S1075996403000301

    I tend to think LAB may be the main consumers of fungal chitin, crossfeeding lactate and acetate to clostridia for butyrate production.

  • Anonymous

    Hi Grace, Where oh where in:
    “http://www.ncbi.nlm.nih.gov/pubmed/?term=nash%2C+probiotic
    http://www.ncbi.nlm.nih.gov/pubmed/?term=nash%2C+akkermansia
    http://www.ncbi.nlm.nih.gov/pubmed/?term=fatty+liver%2C+akkermansia
    does it actually state “The literature supports that the above microbial fingerprint is implicated in NASH-fatty liver and ironically when probiotics of bifido or Akkermansia are given, NASH-fatty liver resolves.” In onr it says ‘RESULTS AND DISCUSSION: …..Akkermansia was highest with the fibre-free diet.’No mention of RS anywhere.

    Cheers, Adrian

  • Duck Dodgers

    Keith,

    Another study showing RPS isn’t burned quickly:

    Slower Fermentation Rate of Potato Starch Relative to High-amylose Cornstarch Contributes to the Higher Proportion of Cecal Butyrate in Rats.

    Where’s the study showing RPS contributes to SIBO? Did anyone fact check any of these assertions?

  • Anonymous

    For better understanding I am combining my two earlier comments.

    Hi Grace,
    With regards to:
    “–lower keystone Bifidobacteria longum
    –non existent depleted Akkermansia
    –depleted Christensenella”
    “Where oh where in:
    “http://www.ncbi.nlm.nih.gov/pubmed/?term=nash%2C+probiotic
    http://www.ncbi.nlm.nih.gov/pubmed/?term=nash%2C+akkermansia
    http://www.ncbi.nlm.nih.gov/pubmed/?term=fatty+liver%2C+akkermansia
    does it actually state “The literature supports that the ABOVE MICROBIAL FINGERPRINT IS IMPLICATED IN NASH-FATTY LIVER and ironically when WHEN PROBIOTICS OF BIFIDO OR AKKERMANSIA ARE GIVEN, NASH-FATTY LIVER RESOLVES.”
    In one it says ‘RESULTS AND DISCUSSION: …..Akkermansia was highest with the fibre-free diet.’
    Where does it mention?
    1. Bifidobacteria longum is keystone
    2. depleted Christensenella
    Where????

    Cheers, Adrian

  • Duck

    How is fatty liver related to gout? What is the link and where are your studies?

    thx

  • P1

    I didn’t spend more than five minutes reading the links Grace provided, but easily found for example in this one:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064083/

    the following quote:
    “For instance, a decrease in Akkermansia muciniphila causes a thinner intestinal mucus layer and promotes gut permeability, which allows the leakage of bacterial components.”

    Doing a Pubmed search on nash and longum, I immediately turn up:
    http://www.ncbi.nlm.nih.gov/pubmed/?term=nash%2C+longum

    which contains the conclusion:
    “Bifidobacterium longum with Fos and lifestyle modification, when compared to lifestyle modification alone, significantly reduces TNF-α, CRP, serum AST levels, HOMA-IR, serum endotoxin, steatosis, and the NASH activity index.”

    I think no one is being served well by cheap shots at Grace. If you want to absorb the literature she has posted (and there is a lot there to read through) and then make a case that the literature does not support a conclusion, that would be helpful. Simply asking abstractly “where does that research say what you claim” makes it look like you just don’t want to spend time reading it. I have no opinion about whether she is right in specific details. I simply point out I had no problems converting the links she posted into research that supports some conclusions similar to what she made, and that tells me people are not reading those links before commenting.

  • P1,

    That is an awesome citizen science experiment and I have several recruits! Will let you know how that rolls out soon

    The results will be similar to Delzenne, Geurts, Cani et al published data or better hopefully

  • duck said: “..For instance, something that seems “bad,” in isolation, may not be so bad in the context of a balanced diet.”

    when anyone starts talking about that great generality the ‘balanced diet’, i stop listening.

    remember- everything in moderation! be balanced! yin and yang! ——–yawn

  • Duck, you’re welcome for the explanation about how microbial overgrowth of the small intestine raises small intestinal pH.

    But, I agree, is there evidence that PS feeds overgrowth in the small intestine other than people complaining of GERD and other symptoms? The science of the small intestine is pretty sparse, it’s like inner outer space. Even the mighty Human Microbiome Project hasn’t gone there much.

    Here’s an interesting abstract showing significantly raised alkaline phosphatase activity in the small intestine in rats on PS, a surprise to authors:
    http://www.ncbi.nlm.nih.gov/pubmed/20579526
    Might this have something to do with gram-negative bacteria such as E. coli?
    http://en.wikipedia.org/wiki/Alkaline_phosphatase#Bacterial

    Here’s a paper showing a decline in diversity in the colon associated with digestive abnomalities on the higher RPS diet, but not a lot to say about the upper gut, duodenum and jejunum:
    http://www.prairieswine.com/pdf/36381.pdf
    http://www.ncbi.nlm.nih.gov/pubmed/18952739

    It’s not easy finding any information about RPS in the small intestine, thanks for the inspiration to research. People assume it passes through undigested, but maybe that’s no longer true in today’s world where a toxic environment has shifted flora, attacking vulnerable species and allowing gram-negative overgrowth along with opportunistic fungi known to produce ethanol from PS:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC239172/
    They’re not waiting for it to arrive in the colon, meaning you don’t have to drink to become rapidly drunk, known as auto-brewery syndrome.

  • Duck wouldn’t potato starch cause SIBO to worsen if there was a Klebsiella infection since it is one of its preferred “meals?” If someone does not have Klebsiella overgrowth it would probably be fine because it is not a FODMAP, therefore it is not easily fermentable by a lot of bacteria (including Grace’s Ancestral Core).

  • Anonymous

    Hi Grace,

    “Particularly the Family of Folz for citizen science:
    –higher blood glucoses on only one tablespoon of potato starch 8 grams alone daily
    –failure to lose weight (Adult #2 — desire was wt loss, didn’t happen, just like published trials Bodingham et al 2012)
    –worsening in all metrics for healthy gut health: lower Christensenella, increased non-human bifido which is connected to atopy and IBD, depletion of Akkermansia the keystone for leanness and fat loss”

    Another conclusion that could be drawn from Folz Family i.e.child 1 is that as soon as you mix RS with other prebiotic fibres E.g. psyllium it all starts to balance out..??
    Did we ever get results for B. Longum from Folz family?
    Going through your latest article I find 2 studies that actually link to something strongly relevant to your thesis.
    Bifidobacterium longum with fructo-oligosaccharides in patients with non alcoholic steatohepatitis – which basically says B. Longum is good for you.
    AND
    Role of gut microbiota and Toll-like receptors in nonalcoholic fatty liver disease – which states ‘Akkermansia muciniphila residing in the mucus layer of the intestine, which represents 3%-5% of the microbial community of healthy humans[81,82]. Recent studies showed that the proportion of Akkermansia muciniphila was decreased in the obese and was inversely correlated with body weight in rodents and humans[75,83-85]. Cani et al[75] intensively investigated the role of Akkermansia muciniphila in obese mice. Probiotic treatment significantly increased the abundance of Akkermansia muciniphila and improved metabolic parameters in obese mice models. In addition, Akkermansia muciniphila treatment reversed fat gain, serum LPS levels, gut barrier function, and insulin resistance by increasing endocannabinoids and gut peptides.’
    One part I would highlight is that they state that there is a range of 3% to 5% in healthy humans.

  • Duck Dodgers

    John Brisson said: “Duck wouldn’t potato starch cause SIBO to worsen if there was a Klebsiella infection since it is one of its preferred “meals?””

    No idea, John. If PS takes hours to ferment and often shows up undigested in feces, I honestly couldn’t tell you what that does to bacteria in the small intestine. That’s yet another obvious problem with this entire series, given that there isn’t really any good evidence that PS ferments quickly in the first place.

    I don’t doubt that PS causes problems for people with some gut issues. In fact, that’s always been one of the diagnostic aspects of raw PS. If you eat it and you feel worse, it probably means there’s something very wrong with your gut. (Pretty much what Keith is saying, no?).

    In fact, Grace told Dave Asprey this when she was on his podcast. How we forget so easily. She told him that the fact that he had trouble with raw RS is indicative of a gut problem.

    Newsflash…If you have significant gut issues, use prebiotics with caution or avoid them altogether. And if prebiotics cause you digestive problems, you may have a gut issue. Use your head people.

  • Anonymous

    “One part I would highlight is that they state that there is a range of 3% to 5% in healthy humans. “

    So, to recap, the headline should have been: “Raw Potato Starch Corrects Akkermansia Overgrowth!”

    As Mr. Folz went from a dysbiotic 15% akkermansia to a normal 5% after 6 weeks of 4TBS/day RPS.

  • Duck Dodgers

    Keith,

    Interesting studies. But, in the first study, the potato starch was gelatinized:

    “The 2 types of potato starch were gelatinized and crushed by the same procedure as that used for the cornstarch.”

    Therefore, it’s meaningless in an RS2 debate. (Grace will have to decide if the esterified P is an issue with RS3.)

    The second study (full text), has too many problems to even mention. But, I’ll list a few:

    – Compared against PC (positive control) diet containing antibiotics.
    – The two RS diets were 7% or 14% RPS, that is 7 and 14% by weight of food eaten. What is the equivalency in a human diet?
    – The 14% RS diet, looked worse when compared to antibiotic diet, but 7% was equivalent to antibiotics. Therefore the 7% is ‘better’.
    – The 14% RPS diet also had less whey powder, less wheat, but more soybeans…see Table 1. The diets weren’t equal!
    – The conclusion is that 7% RPS is just as good as antibiotics, but 14% RPS is inferior to antibiotics.
    – The pigs fed 14% seem to have gotten diarrhea, and may have been given therapeutic antibiotics:
    — “The occurrence of scours in the 14% RPS diet correlated strongly with the decline in richness and di- versity of microbial species in the colon.”
    — “Callesen et al. (2007) demonstrated that pigs fed diets containing 7.39% potato starch without the inclusion of antibiotics tended to result in better performance and reduced scours. However, the potato starch pigs also received more treatments of therapeutic antibiotics. We demonstrated that the inclusion of RPS at 7% reduced scouring, but at 14% the effects were negative.”
    – Really, just too much going on here to compare this to RS2, in a sane amount, for humans.

    The last study, (full text), concerning RPS and ‘autobrewery syndrome’ simply describes an industrial process to make ethanol from potato starch using bacteria and fungus selected for the purpose. No implications for human health.

    “Use of such a synergistic combination of organisms allows elimination of the enzymatic starch hydrolysis step as currently used in many commercial processes for ethanol production from starchy biomass, thereby significantly improving the economy of starch fermentation to ethanol.”

    Cheers.

  • Anonymous

    @John B – How is Raw Potato Starch NOT a FODMAP? Does it not fit the definition of “Fermentable?”

    I love you stance on SBO/HSO, don’t let up! They are pure poison. My mom took PrescriptAssist and almost died.

    Honey is just a bad…that’s why babies can’t have honey. Full of so-called ‘healthy’ SBOs. yuk

    Jenny

  • Duck Dodgers

    P1 said: “I didn’t spend more than five minutes reading the links Grace provided”

    Well, there’s your problem. No wonder.

  • P1

    P1 said: “I didn’t spend more than five minutes reading the links Grace provided”

    Duck said: Well, there’s your problem. No wonder.

    Duck, if you have specific references provide those. You keep making posts where you just allude to your vast knowledge of all subjects, but you never actually provide real content.

    It’s fine if the links provided by Grace contain studies that invalidate her conclusions. Read the research. Post the links to the relevant studies. Then copy the relevant text.

    Rather than deal with specific research she cites, and the specific research I cited, you just make cheap shots. How does anyone benefit from that?

  • lol, here Alan Folz himself on how he took the samples, and on my beloved Akkermansia:

    “…but how you gather the sample makes a big difference. Well, as I’ve subsequently learned, Akker primarily populates the intestinal wall lining. I have to assume this means it is going to be over-represented in the outer circumference of the stool. Well, without getting into too much detail, for reasons not entirely my own fault, I sampled directly from the stool’s surface. Did that push my Akker all the way to 8x typical? I have no idea. Could it have pushed it from 2x or even 4x to 8x? Seems possible.”

    and

    “No, that sample was unique in its swabbing technique.

    (I guess I gotta say it…) AmGut suggests swabbing soiled T.P. For that sample, the T.P. was inadequately soiled; so the stool was swabbed directly. At the time, I was worried it would come back with strange results indicating bacteria associated with municipal water supplies. 17% Akker was totally off my radar. I’d never even heard of Akker until I got my results. HTH.”

  • Also, Duck, to suggest using RPS as a diagnostic tool (“use your head people”) seems an irresponsible walk off the deep end.

    Let’s say someone has a gram-negative bacterial or clostridial overgrowth of the small intestine. Why fan the flames?

    A better tool would be PCR stool testing prior to treatment, but even then there are shortcomings when trying to discern small vs. large intestine issues. And breath testing in SIBO is in complete disregard of hydrogen gas produced by fungi, treating SIBFO with antibiotics only to create further imbalance. We obviously need better tools.

    I like Grace’s detective work in this blog revealing B. longum and B. Bifidum as non-starch eaters. It so happens these are the main strains of Bifido in the healthy breastfed infant gut comprised of up to 90% bifidobacteria. They’re probably reigning in the small intestine in and around Peyer’s patches regulating immune response. Feed and seed them to displace the starch-lovers in the small intestine.

  • “The genus Bifidobacterium currently comprises 37 species [38], [39]. However, the dominant bifidobacterial species detected in the investigated infant faecal samples were Bifidobacterium longum and Bifidobacterium bifidum at 56.2% and 10.7%, respectively (Fig. 2e).”
    “Diversity of Bifidobacteria within the Infant Gut Microbiota”
    http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0036957

  • Maybe this why Bob’s Red Mill Potato Starch is giving people problems in the small intestine, overgrowth leading to GERD, etc.: it’s made from cooked potatoes, boiled not raw. It’s not RPS.
    http://blog.bobsredmill.com/featured-articles/getting-gastrointestinally-groovy-prebiotics-and-probiotics/

  • P1

    This comment has been removed by the author.

  • P1

    I read the entire thread Keith posted, and at this point I have no idea what Bob’s is selling. Their customer service rep didn’t do the thread the justice of finding the right answer.

  • P1

    Grace, do you have any opinion on taking supplemental butyrate as sodium butyrate or sodium-potassium-butyrate? I have a bad reaction to both: gas and loose stool. This is in spite of my having high butyrate levels on GI Effects, but that might just reflect my having a lot of bad fermentation going on in general.

    I found there is also a triglyceride version of butyrate named tributyrin that is better-absorbed. Any thoughts on whether that one is worth supplementing? I’m sure not many people have tried it, although I find research where it seems to be safe for human consumption.

  • Anonymous

    I think Bob’s Red Mill knows who the expert is:

    Tara
    November 24, 2013 at 11:22 am

    Tim and Cassidy,
    Since the potatoes are boiled before the starch is extracted, wouldn’t that dramatically reduce the amount of resistant starch in the final product?

    Wouldn’t it be much higher in resistant starch if it was extracted from raw potatoes?

    Cassidy Stockton
    November 25, 2013 at 9:55 am

    Tara,

    You’re delving out of our knowledge zone and we’re not sure what to tell you. Perhaps Tim can enlighten you.

  • P1

    Does anyone have an opinion on supercharging a B Longum probiotic by letting it ferment for a while before eating it? For example:

    * Mix a glass of bionic fiber, then mix in a B Longum probiotic and let sit for a few hours

    * Blend a cup of blueberries, add in a B Longum capsule, and seal and allow to ferment for a few days

    The idea is to let the B Longum population really grow before you ingest it. Has anyone tried something similar? I have never fixed any fermented foods.

  • “That’s going to cause a scandal…. “

    lol

    Et tu, Keith?

  • We do know raw starch is digested in the small intestine of cattle. Perhaps this is studied as a way to fatten-up cattle, similar to antibiotics since we also know RPS lowers microbial diversity. But what about humans and our magically sterile duodenums? They’re not digesting raw starch, are they? Of course not, they want the colon to have all of it, so they skip a meal. Who’s in your small intestine? Altruistic microbes.

    “Small intestinal starch digestibility was 34% when 1.5 kg/d raw cornstarch was continuously infused into the duodenum.”
    https://www.animalsciencepublications.org/publications/jas/articles/92/9/4047

    http://gradworks.umi.com/35/51/3551021.html

    Everyone loves a marbled steak. Except the cattle themselves and people who don’t eat meat.

    Throw in some glutamate and casein, that helps starch digestion in the small intestine. Not so good for the brain though (glutamate toxicity causes seizure and damages cells):
    http://animalsci.highwire.org/content/early/2014/07/22/jas.2014-7909.abstract

    How about the jejunum and ileum, second and third sections of small intestine in rats? Apparently, it depends on rat enzyme activity where RPS is digested at higher rates in the ileum:
    http://www.ncbi.nlm.nih.gov/pubmed/6470834

    HMG-CoA is inhibited by statin drugs, so if you want to consume RPS, perhaps it’s best you’re on statins to avoid SIBFO.

  • How interesting statins affect starch digestion.
    Of course, statins are also known to cause diabetes. I’d have to research the mechanism. Perhaps it’s about changes in cholesterol as precursor of bile acid leading to flora shift.

    Meanwhile, we know statins are only as good as the microbes they’re acting on:
    http://www.medicalnewstoday.com/articles/236068.php
    “They found that those whose LDL levels went down the most after taking Zocor (simvastatin), a statin medication, had higher levels of bacterial-derived bile acids from three specific gut bacteria – lithocholic acid (LCA), taurolithocholic acid (TLCA), and glycolithocholic acid (GLCA) – compared to those whose LDL levels did not drop as much.”

    Are these the same bacteria digesting raw starch in the small intestine? People don’t generally consider statins inhibiting the enzyme activity (HMG–CoA reductase) of microbes, a matter of collateral damage:
    http://www.sciencedirect.com/science/article/pii/S0959440X01002767
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2279991/

  • Regarding casein speeding-up starch digestion in the small intestine, it’s probably not a good idea to consume RPS in milk or risk onset of schizophrenia:
    http://www.ncbi.nlm.nih.gov/pubmed/21376538
    http://www.ncbi.nlm.nih.gov/pubmed/7264771
    http://www.ncbi.nlm.nih.gov/pubmed/25023803
    http://kellybroganmd.com/article/two-foods-may-sabotage-brain/

    Not kosher.

  • Duck is missing the whole point. You want inulin to be digested in the small intestine because it feeds the right microbes for that environment, lactic acid bacteria (LAB). Does RPS? Apparently, RPS is feeding the wrong set of microbes in the small intestine.

    There seems to be plenty of hard evidence RPS is digested in the small intestine leading to microbial imbalance. At least in rats and cattle . . . if you believe RPS is bypassing the human small intestine, that’s a choice disconnected from the web of life.

  • Duck Dodgers

    Keith said: “Apparently, RPS is feeding the wrong set of microbes in the small intestine”

    Ah, yes, that must be it. Never mind that even the very study you posted shows PS is degraded very slowly—literally invalidating your previous criticisms of PS supposedly being fermented rapidly. Funny how you didn’t notice that.

    Keith said: “You want inulin to be digested in the small intestine because it feeds the right microbes for that environment, lactic acid bacteria (LAB).”

    Keith, are you suggesting that Lactobacilli in SI have no amylase enzymes able to deal with RS2, and only ferment inulin? What about RS3? What is the difference?

    The fact that you still reference cattle as proof of anything relating to humans is just laughable. Seriously, what were you thinking with that one? Humans are not ruminants. They are not even remotely applicable.

    The rat study confirms very poor digestion in the small intestine, and isn’t surprising to anyone. Why? Because PS is just a very slow digesting starch. Humans actually secrete the proper alpha amylase enzymes to break it down but it’s just too tightly packed for the enzymes to degrade most of it. So, you’re not telling us anything we don’t already know.

    I’m finding your position to be more desperate with every post. Any fiber will feed “bad” bacteria. It’s funny how you used to buy into the “Weed, Seed and Feed” philosophy just a few months ago, but suddenly you’ve decided that it can only be applied to the fibers you want it to apply to. Oh the hypocrisy.

  • Duck, you’re a fantastic foil, thanks. Trying to bring you into the 24th and-a-half century like your namesake.

    Starch degradation is a matter of microbial predisposition. What kind of microbes are present in the small intestine dictates whether an individual reacts negatively.

    I choose to believe Grace when she states PS gave her GERD along with all the other folks who suffered. What makes them different? Higher levels of proteobacteria in the small intestine such as klebsiella, E. col and other gram-negatives? There’s also such thing as lactobacillus overgrowth in the small intestine associated with obesity.

    I’ve always found it more than curious how EIGHT OF THE TOP TEN most obese nations on Earth are in the Pacific islands where generations were raised on a starchy tuber staple diet:
    http://en.wikipedia.org/wiki/Obesity_in_the_Pacific

    Combine that with islands being closed environmental systems prone to poor sanitation where people consume E. coli-packed, poopy water and this is what you get:
    https://www.youtube.com/watch?v=V1bFr2SWP1I

    Diabetes and other gut disorders such as ulcerative colitis appear to be a matter of gram-negative bacterial overgrowth, so hitting them with RPS seems contraindicated.

    Not just any fiber will feed “good” bacteria; that’s what this blog entry is about . . . feeding the good to displace the overgrowth. Add life.™

  • P1

    Keith, I have read that glutamate in the diet does not enter the brain. See for example:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136011/

    Of course you wonder if the blood brain barrier is leaky does that apply.

  • P1

    Duck, do you have any studies you can reference that show health benefits to humans – or increases in beneficial bacteria – when consuming high dose potato starch?

    The most frustrating thing about this conversation is that Grace posts studies and you post none. I post studies and you post none. Keith posts studies and you post none. All you do is play defense and you never actually assert a case for high dose – or ANY dose – of RS2, in human beings.

  • Anonymous

    Ill save duck the trouble..

    Duck Dodgers said:

    Still, no one on the planet is currently advocating “high doses” of potato starch. So, for the upteenth time… why the hell are we debating something that nobody is advocating??

  • P1, there’s also such thing as endogenous glutamate and glutamate receptors in the small intestine where vagal nerves connect the gut to the brain:
    http://pharmrev.aspetjournals.org/content/63/1/35.full
    http://ajcn.nutrition.org/content/90/3/832S.full

    90% of the fibers in the vagus go from gut to brain, not from brain to gut.

  • Duck Dodgers

    P1 said: “you never actually assert a case for high dose – or ANY dose – of RS2, in human beings.”

    Well, I shouldn’t have to, P1. After all, if you’re curious about the benefits of raw potato starch, all you need to do is go back a few months on this blog and you can see a whole bunch of them yourself.

    But, I’ll bite, P1 – Here’s five studies right off the bat and a little tip of the hat for our Pharmacist-in-chief.

    1) Langworthy et al. described bloating and discomfort with 180g of potato starch and none with 60g. It was also noted that when human subjects were fed over 40g of potato starch, a portion was found in feces [1], indicating that microbiome may only be able to process up to 40g of potato starch in a single feeding. You just poop out the excess.

    2) 17-30g/day of raw potato starch in 15 day human trials increased SCFA. [2]

    3) Studies show that the prebiotic effects of potato starch are as, or more, effective than RS from other sources. Raw potato starch is a preferred substrate by bifido bacteria over starches from pea and wheat. [3]

    4) When compared with wheat or barley starches, potato starch induced greater amounts of satiety and post-prandial glucose control and was on par with experiments measuring lipid metabolism, glucose control, and insulin response. [4]

    5) When compared with maize, wheat, and pea starch raw potato starch provided more butyrate than other starches studied. [5]

    Plus, and I’m sure Grace knows this:

    The US Pharmacopeial Convention also uses unmodified potato starch in numerous drug manufacturing and packaging processes. The technical specifications for USP Potato Starch are the same as for food grade potato starch, indicating that potato starch is a pure, safe product. USP Tech Spec

    That AOR Probiotic-3 probiotic we hear so much about? Guess what’s in it…RPS.

    Anyway, I didn’t come here to sing the praises of PS, since I don’t advocate “high doses” of PS (hello? is this mic on? test, test…)

    However, when I see sloppy and misleading conjecture in an effort to fear-monger as well as to discredit others unfairly, I’m happy to shed light on it. I’m sure you’d like to think that’s a “cheap shot”—to point that out—and that’s your choice.

    Anyhow, I’m not here to do all your homework for you. If you want to learn more about the potential benefits of PS, just look in the archives of this blog.

    Cheers.

    • Actually Duck RPS is the cheaper cryogenic, inulin is better or equally but obviously more expensive.

  • P1

    Hi Keith. Only the ajcn study suggests a neurological impact from gut-based glutamate receptors. But it does not explicitly say that the neurological effect would be to have increased endogenous production of glutamate in the brain.

    It’s still a very interesting study and I’ll keep a bookmark.

  • Here’s another study detailing PS digested in the small intestine (first section, duodenum) of rats at quite a high rate:
    http://www.ncbi.nlm.nih.gov/pubmed/15461280

    Who’s eating it? Not you! E. coli loves RPS:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008263/

    The problem is gram-negative overgrowth such as E. coli in the small intestine (where it doesn’t belong) consuming RPS.

    How interesting they used a probiotic strain of E. coli to displace a pathogenic strain of E. coli as this is also done with pregnant horses with strep where E. coli is injected into the horse vagina to displace strep. Then the E. coli is dealt with as it doesn’t pose the same problems with foals as would strep.

    But in people without small intestinal imbalance, it appears the effect of RPS may be more limited to the caecum and proximal colon:
    http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2672.2003.01836.x/abstract

    Clostridia also consume RS where clostridium overgrowth of the small intestine is a huge health crisis, i.e., C. perfringens, botulinum and difficile:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC92288/
    http://www.atsu.edu/faculty/chamberlain/Website/lectures/IntoxicationsandInfectionsoftheSmallIntestine.htm

    C. diff used to be considered as limited to the colon, but that’s changed, now also about the small intestine:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4288864/
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664326/

    Here’s another paper about RS digested in the small intestine at high rate, about 50%:
    “Digestion of so-called resistant starch sources in the human small intestine1,2,3”
    http://ajcn.nutrition.org/content/72/2/432.long
    It’s about corn starch, but if you don’t believe PS is digested in the small intestine dependent on microbial strains present, you’re delusional.

  • Duck Dodgers

    Honestly, Keith. Let’s give this a rest. Even if you find evidence of “bad” bacteria eating RS (true of any fibers) you’ve still not answered why the “Weed, Seed Feed” philosophy once promoted here no longer applies to RPS. It’s a double-standard. And frankly it’s tiresome.

    • Let’s give it a rest Duckie — my last comment for you is sincere thanks for your FYI on acacia. It is a wonderful prebiotic which totally fixed my gut last year! Keith told me a lot about it and hearing your thoughts brought it to my attention.

      Acacia does everything that RPS ruins and skews in the gut microbiota! I am not surprised Asklipia at the the Phoenix forum did so well and is one of the only individuals able to recover from Chronic Fatigue Syndrome there.

      By lowering both upper gut and lower gut pathogens, Acacia powers up the keystone immunological species, Bifidobacteria longum. It also builds a strong fat burning gut microbiota! When I developed raw-potato-starch induced GERD/reflux, it was after fixing my gut and losing 10 lbs of fat with Acacia and this amped up bionic fiber blend. During potato starch, all fat loss and lean muscle gains took break. After stopping RPS and resuming Acacia, inulin-FOS and glucomannan, then my muscle gains resumed and I lost another 5lb

  • JC

    Does anyone know how much time it takes for acacia gum to reach to the colon? I have read that for FOS it takes around 30 min. What about psyllium? My guess for psyllium is around 4 hours. Because after 4 hours I started to have gas.

  • JC

    OK. An update from me. 3rd day on acacia gum, feeling great. I increased the doses gradually and felt even better.
    Psyllium on the other hand gives me gas after four hours. It dehydrates me, it makes me drink a lot of water.
    Haven’t started probiotic yet, I wanted to see how I would react without probiotic. Let’s see after probiotic if I’ll manage psyllium.

  • P1

    Interesting discovery: if you make coconut milk – and if leave a small layer of the coconut shell on the coconut meat – this grinds up in the blender to a gritty fiber. You can then eat the grounded coconut meat, mixed with some of the coconut milk, as a type of breakfast cereal. It’s quite tasty, and my body seems to react very well to this fiber.

    Note I am NOT grinding up the hard coconut shell! I am just peeling off the coconut meat and leaving a paper thin layer of the shell intact on the backside of the coconut meat. Before I used to cut this off.

    Have you ever hear of someone using any part of the coconut shell as an ingestible fiber? How does it compare against other elements in the bionic fiber combination?

  • P1

    Do you have any opinion about the value of these bacteria:
    S.thermophilus
    L.Bulgaricus

  • Anonymous

    Hi there! Thank you, Grace, for all the information! I can’t imagine how I could ever find this much info without this blog!

    I was wondering if you, Grace, or somebody else would know if all the probiotics and prebiotics are safe to consume while pregnant?

    For example acacia fibre seems to be very confusing: some sources say it’s safe while some other say it’s not. What to believe?

    Also, even though this is not about gut, I was wondering if you have an opinion on iodine and pregnancy? In my country (Finland) the officials say one should not eat any sea vegetables while pregnant because of the iodine. I, however sometimes eat sushi, including Wakame, and just realized it contains quite a bit of iodine. I got a little worried but then started wondering if Japanese women really stop eating Wakame and other iodine-rich seaweeds when they get pregnant. I doubt that. And I suppose their babies are at least as healthy as anobody else’s. So, any thoughts on this? 🙂

    Thank you in advance! 🙂

    Kaisa

  • Anonymous

    DR B G, up in your comment on the ramped up BIONIC fibre, you list the Now brand(of what)? – the LEF bifido longum…what is the NOW brand product you list there?

    I’m trying to put together my own bionic fibre blend following your recommendation but wonder if I’m missing something from the NOW brand…also, should the probiotics be taken with the Bionic Fibre or at different times(hours apart?) like its usually suggested when taking fibre.

  • Guest

    Asklipia has not recovered from ME/CFS. She’s improved a lot, but still posting as of a week ago.