Friday, January 23, 2015

Lose Weight, Body Fat, Improve Blood Glucoses and Insulin Sensitivity; Repair the Gut Flora That Potato Starch (Raw RS2) Damages (Part VI)

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.


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.

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.

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


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)." 

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)
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

suppression of Bifidobacteria longum
--often undetectable
--depletions of 100-fold to 2000-fold for relative bifido typically for potato starch
--B.animalis or B. adolescentis majority colonizer
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


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


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%

Wednesday, January 21, 2015

PART II: Gut Guardians Podcast Episode 11 – Reinforcing Tribal Connections w Tony Federico

Gut Guardians Podcast: Episode 11 – Reinforcing Tribal Connections w Tony Federico

Part 2 of Dr. Grace’s and Matt’s talk with Tony Federico.

While most point to diet and exercise as key markers of achieving good health, Tony brings up another great aspect of living well: being apart of one’s community. A discussion on how tapping back into our roots can play an integral part of ones health. by helping and developing a sense of community with the ones surrounding gives us the same tribal setting as our ancestors.

Gather some tubers, and huddle a group of your closest friends around the fire for this podcast!

Show Notes

Tuesday, January 13, 2015

Gut Guardians Podcast: Episode 10 – Tackling Resistant Starch and the Paleo Diet w Tony Federico

Tony Federico, host of the Paleo Magazine Radio show, joins Dr. Grace and Matt to talk about his uBiome results. A possible beneficial strain Christensenella was abundant in Tony’s gut, which Dr. Grace goes into further detail. Tony talks beyond just Paleo, bringing insight to his day to day life, and how he maintains his healthy living. Tony asks Dr. Grace’s opinion on the potential effects of resistant starch and avoiding too many starches on a paleo diet.

Enjoy Part 1!

Photo Credit

Show Notes

  • Human Genetics Shape the Gut Microbiome (Ley et al, Cell 2014)
    • Christensenellaceae associates with a lean BMI
    • Christsenella reduce weight gains in germ-free transplant experiments
  • Tony Federico's
    • Christensenellaceae 4.35% (5-fold higher; ubiome avg=0.844%)
    • Christsenella 0.0224% (2-fold higher; ubiome avg=0.0120%)

Wednesday, December 24, 2014

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 (Part V) NSFW

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


Bodinham et al 2014. Let's review. High dosage 40 g/day RS2 (high amylose maize) for 12 weeks increased resistance (HOMA) and lowered the fat-burning gut hormone known as GLP1. Post prandially, HAM-RS2 made a tiny spike in GLP1 however longterm it decreased by 33% compared with the control arm (p=0.0049). The drop in the gut hormone GLP1 was quite significant and was one of the few parameters that met statistically significance in this study.  

Optimal gut health is supposed to yield better fat burning, leanness and metabolic improvements, no? Not high dosage RS2 it appears. Why?

I have low gut diversity like most people and for me each time high dose RPS caused problems; it halted fat loss besides giving me reflux and GERD when I took it for over 4weeks. 

Results Tab 1:
--increased fasting TG (p=0.039)
--increased LDL cholesterol
--increased HOMA% (aka insulin resistance) wtf??!
--~35.2% increased pancreas fat  wtf? (13.7 v. 10.5, NS)
(Body fat depots determined by MRS scanning (n=14).)
--increased fat mass (32.2 kg v 31.8 kg)
--increased BMI
--increased weight
--reduced GLP1 (11.4 v. 17.0, p=0.049)
--increased IL6 (but lower TNFa)
--lower butyrate (p less than 0.001) 
--lower propionate (p = 0.021)
--no improvements in glucose, insulin, Hgba1c

GLP-1 (the Gut-Fatness Hamster Connection)

In the Bodinham et al 2014 study, GLP1 was found to significantly decrease by 33% (p=0.049). The well controlled subjects with T2 diabetes also gained on average about a pound of fat in 12 wks compared with the controls. Apparently the researchers examined the fat depots and body fat and found that pancreas fat increased 35.2% on average. Fatty pancreas. Is this synonymous to fatty liver and NASH/NAFLD? 

The authors don't clarify or discuss but it is.  

The results were unpredicted but if we understand how the gut hormones GLP1 and microbial fingerprint became 'worse' on a high dosage non-ancestral 'fiber' and diversity was compromised, then it makes sense. Though the stool butyrate decreased, it is obvious there was butyrate in the colon because glucose handling improved a tiny bit. Insulin resistance however tanked as shown by various indicators: increased TG (p=0.039), increased LDL-chol, increased BMI and body fat, and lastly increased HOMA at both the pancreatic beta cells and traditional measurements. Hgba1c and blood sugars didn't change or improve at all, as the researchers were hoping for. They talk nothing at all about the gut microbiota. Their other study showed the same metabolic disruptions with high dosage RS2.

The same thing and worse trends were seen in overweight subjects with high dosage 40 grams daily of HAM-RS2: Bodinham et al 2012

Table 1:
--increased TG
--increased body fat (Tanita bioimpedance scales, 28.1% v. 27.8%, NS)

--increased systolic BP (wtf)
--increased diastolic BP (wtf)
--boatload of insulin increased with 40 g HAM-RS2 acute dosing
--increased fasting insulin (88.6 v. 85.4 pmol/L, NS) wtf

Fasting glucose this time decreased but that is because all the spikes in post-prandial insulin is shoving all the glucose into adipose cells now and making them fatty which is clear by the increased TG and higher insulin-related consequences: higher systolic and diastolic blood pressures. wtf. I bet it lowered GLP1 where it is already low and lame in overweight and T2 diabetes subjects.

What is GLP1? 

I love GLP-1. 

It helps us to burn and remodel fat. "Glucagon-like peptide 1 (GLP-1), a gut-derived peptide, has been reported to have profound effects on metabolism and to reduce insulin resistance (Yang et al 2013)."  High protein diets raise GLP-1 and satiating PYY gut hormones to cause nice fat burning. It appears that high dosage raw starches causes a downward trend of this fat-burning molecule. Ruh-OH. This time it does not depend on either the pre-existing gut or what human gut symbions are missing. It happens in healthy human subjects in several trials so far. 

Both GLP-1 and GLP-2 are vital for the gut. They seal and heal the gut barrier and much much much more. A healthier barrier leads to healthier leanness and body fat composition because inflammation is reduced.

So test your gut, fix your flora and consider the fibers that are (a) ancestral and (b) burn fat by improving metabolic gut pathways and hormones, not potentially worsen them.


The biggest problems I've had with RS2 #HAMSTERFOOD is the lack of translation from hamster studies to human. Like statins, RS2 looks beautiful on paper until you dig deeper... look at the downstream consequences... see what it disturbs or benefits.  RS2 definitely helps colon butyrate, but what does it do for the upper gut where there is no butyrate? Can it disturb the upper gut flora? How does lowering B longum and Akkermansia affect the host? Does it increase intestinal permeability and inflammation if they are not present? 

Raw starch RS2 (and artificially produced RS4) in several human studies is associated significant reductions in GLP-1 or lack of improvements (here, here, here). 

But... not in many rodents............ Boy rodents low raw starches and so do their guts. What about humans? Ruh-OH? Lost in gut translation from hamster to humans? Vastly different gut flora? 

Bodinham et al 2014 may appear confused but I don't think so; the authors wrote: 
"Animal studies have consistently shown that RS improves glucose and insulin metabolism through increased postprandial GLP1 secretion due to stimulation of the colonic enteroendocrine cells (8, 9). This can result in improved insulin secretion. Most recently our own data has shown restored first-phase insulin secretion in metabolic syndrome (10); however, the lack of translational work has recently been highlighted (11)."
Yesssiree. We are humans, not hamsters. So are our special human gut flora that made us big brained and brilliant fat-burning machines .  Our human gut flora eat cooked starches and the whole spectrum fiber. These researchers can see the contradictions, no? As a fiber, high dose RS2 fails to induce fat loss (it appears to raise it) and fails to improve glycemic control and Hgba1c (it in fact worsens fasting insulin and HOMA). On paper, in rodents, high dose RS2 looks decent. 

(not unlike rabbits + low cholesterol diets + human omnivorous/carnivorous heart disease =  animal pharm fallacy)

How and why did this poor metabolic outcome occur? 
Why did raw potato starch and a 'good gut biome' not prevent it?  
Does high dosage potato starch incur a gut profile that is inherently more vulnerable to GERD, reflux, chronic inflammation, and fatty liver/NASH?  
When high dosage potato starch lowers diversity and Akermansia, Bifidobacteria longum and Christensenella, what are the effects for the host?


Cooked whole beans and beta-glucan/arabinoxylan/RS3-inulin-containing cooked barley (herehere) raise GLP-1 in human trials. Don't worry, legumes and small seed grains are certainly paleo for many.

Non-starchy roots/plants like agave, Jerusalem artichokes/sunchokes, yucca, yacon, endive, and dandelion roots are rich in a special immunoprotective fiber similar to breastmilk (inulin-like oligosaccharides). Inulin-type prebiotics significantly improve GLP-2 in human studies (here).  Green vegetables also have small but additive amounts of inulin-oligosaccharides. Inulin is the 2nd most dominant fiber on earth, next to starches.

What's GLP2? GLP-2 is GLP-1's gut hormone cousin and shown to seal the gut, fix intestinal permeability and lower inflammation.

Why are GLP-1 and GLP-2 important? Because the right fiber and combo of fiber modulates and maximizes these gut hormones which basically control our health, body fat storage mechanisms and fat burning metabolism. 

GLP-1: Studs and Science
Hamster or Fat Burning Studly Ham?

VIPER IN SICK GUTS: RPS-RUMPS FFEDS Escherichia coli, an Alcohol Producing Gut Flora

Another problem with high dosage RS2 is what are you feeding and what is one potentially losing? Is RS2 an 'anti-prebiotic' meaning does it substantially lower beneficial gut flora that protect and maintain our health and leanness? Does potato-starch-induced reduction or extinction of beneficial flora such as Christensenella, Akkermansia and human-specific Bifidobacteria longum have certain health consequences?  I believe so, all the above.

E coli is part of the Proteobacteria clade which are overgrowing in several disease microbial fingerprints. We have good non-pathogenic E coli and 'bad toxic' adhesive E coli. After antibiotics, more of the 'bad toxic' and adhesive, pathogenic E coli are selected. An example of good E coli is the European Nissle 1917 E coli strain.  

Several gut flora produce alcohol -- yeasts, E coli, Clostridium asparagiforme (XIVa), Dorea longicatena (XIVa), to name a few (Duncan, Louis, Flint 2007). The XIVa are part of Lachnospiraceae. These are versatile fermenters and eat both raw and cooked starches. 

Clostridium and E coli are rapid fermenters of both raw and cooked starches, therefore if they are overgrowing in the upper gut or with triggers (holiday binge-eating, sweets, lack of sleep, etc lol) AND there is a depletion of the gut guardians -- what can happen? They will overgrow in the upper gut and produce more alcohol than the body can handle. The alcohol can harden your arteries, pancreas, liver and the brain, and make them appear 'fatty'.
"Ethanol and acetaldehyde:  Microorganisms in the small intestine have the capacity to endogenously produce ethanol which enters the bloodstream and is metabolized in theliver (reviewed in [73]). Indeed, microbial synthesis of ethanol is elevated in obese mice and may play arole in the pathogenesis of fatty liver disease [74].In turn, consumption of ethanol can promote bacterial intestinal overgrowth and has the potentialto alter the composition of the microbiota with an attendant increase in Proteobacteria [73]. Ethanol is proposed to disrupt the barrier integrity of the small intestine, and healthy human volunteers exhibit a transient increase in duodenal permeability following the consumption of alcohol [73,75] with a likely influence upon epithelial tight junctions[73].Microorganisms of the intestine can metabolize ethanol to acetaldehyde through alcohol dehydrogenase(ADH) activity [73]. Acetaldehyde has been shown to significantly disrupt cellular junctions, E-cadherin and to induce profound rearrangement sof actin [76,77]. Certainly, current data suggest arole for the microbiota both in the production and metabolism of ethanol in the small intestinewith a potential impact upon gastrointestinal permeability." (Joyce, Gahan 2014)

What raises or lowers pathogenic E coli?
  • RPS (raw potato starch) may raise E coli, including the toxic ETEC strain (travelers' diarrhea), adhesive-invasive E coli (found in gut infections and IBD), and pathogenic E coli often found in urinary tract infections.  In the pigs receiving a diet of 14% raw potato starch (RPS), substantial log growth increases of toxic ETEC E coli in every portion of the pig gut (small intestines/ileum; colon and feces) were observed compared with control and probiotic-fed pigs. Probiotic-fed pigs had dramatically less ETEC E coli in all parts of the GI tract. See below Krause et al 2010. The K88 probiotic had activity against pathogenic E coli and specially selected growths of non-pathogenic 'good', protective E coli (see green box, below).
  • Probiotics and the beneficial flora/guardians in our upper gut work to dramatically lower toxic E coli in every part of the gut (see below green box), particularly the upper gut, aka small intestines (ILEUM) which is the heart of the control center for the immune system -- see  step #3 on soil and bifido probiotics.  (Pubmed)  Probiotics like LABs (bifido, lacto) and Akkermansia produce lactic and acetic acids, respectively, which are strongly antimicrobial and antifungal. Soil probiotics (including E coli), LABs, Bifidobacteria longum and Akkermansia line our gut mucosa from where the stomach begins to the end of the rectum and protect the entire gut and modify immunity.
  • Prebiotics alone work too to lower toxic E coli.  Every prebiotic appears to work, EXCEPT RAW POTATO STARCH (Pubmed).  
  • Avoid RPS if there is too much pathogenic E coli. Raw potato starch is a prebiotic for pathogenic E coli. This Russian researcher states RPS are 'prebiotics for E coli (Ivchenko et al 2006).' (the good and the bad strains).

Krause et al 2010
Higher Toxic ETEC E coli in Raw Potato Starch Alone Arm
v. Controls and v. Probiotics

Intrepid gut explorer.    I love Tim S. and his intrepid gut testing. Several weeks ago, all the contents for this series and the past series (Parts 1-5) were run by and approved by Tim to discuss publicly. I brought up my many observations and concerns very early on. He gave his approval to discuss all my concerns, precautions and problems for adverse effects generated by high dosage RS2 including concern for his liver, his high liver tests, SIBO/upper gut dysfunction, recent bout of fatty liver/NASH in June 2014, depletions of gut guardians including Akkermansia, and possible connections to the gut obesity fingerprint that is created with high dosage raw potato starch/RS2, the studies, the other N=1s, etc.

He is a bold citizen of science and declined the three times that I asked him if he wanted me to omit his data and fatty liver/NASH.  His liver tests are better. One month ago, his liver test was still 35 and recently he reported it's now 15. He said "Grace has been privy to all of my gut tests, labs, and health concerns as a friend, not a doctor. I gave her express permission to discuss them how she sees fit. I think that this information needs to be shared freely. If I had a problem with any of this, Grace would be the first to know. I don't have a problem with her discussing me or my experiments. They are out there for everyone to see and interpret as they wish."

My potato-starch induced GERD: Recently I had GERD/reflux after several weeks of 20-40 grams RPS, raw potato starch. Several other people have reported this too. I was previously using Version B (inulin + acacia) and psyllium and had fantastic gut results such as the best flattest tummy in 7 to 8 years and improved digestion and gut health. I gave the RPS one last try and initially no problems that I had had earlier (immunosuppression). 

Tim S. had also had GERD last winter on sedentary days and didn't think much of it until I had reflux myself. In the past, I've never had reflux except a couple times after drinking pots of coffee or when I was pregnant in the 3rd trimester. Reflux was super annoying but fortunately went away with resuming probiotics (bifido/lacto and soil) and taking some gut support (ACV, enzymes, etc) temporarily. Besides RPS, I think no B longum was a factor; I had stopped the B longum supplements several months earlier and never resumed. Stress from moving from Shanghai back to USA likely lowered the bifido and lacto more than I had thought.  Potato starch lowers the populations of non-starch eating bifido which make up huge portions of our fecal and mucosa-associated bifido microbiota (see prior post):
B longum 43.5%
B pseudocatenulatum 8%
B bifidum 6%
B dentium 1.5%

Recently what made me rethink the downstream effects of high dosage potato starch was how Tim S. had a bout of fatty liver again this past summer, after over one year and a half on high dosage potato starch -- high liver functions tests, tender and painful liver on touching, gained body fat and took several months for the ALT, AST to reduce to normal again. 

Fatty Liver/NASH = COMBINATION Alcohol-Producing Gut Flora + Akkermansia Depletion

Several studies now show a unique microbial fingerprint for GERD,  NASH/fatty liver and several other chronic conditions.

GERD/reflux (me):
  •  high colon bugs in the stomach and uppergut
  •  low human bifido/lacto (I was taking prebiotics, but had stopped B longum probiotics)

NASH/Fatty liver
  • high E coli (produce alcohol)
  • high starch eating Enterobacter (produce alcohol and endotoxins)
  • high Roseburia/XIVa (Lachnospiraceae) (some are alcohol producing)
  • high yeasts, Candida (produce alcohol)
  • low human bifido
  • low B longum (high dose RPS may lower B longum, favoring starch-eating-bifido)
  • low Akkermansia (high dose RPS may lower Akk)

Obesity/diabetes/autoimmunity (most of American and industrialized nations): 
  • high starch-eaters including E coli, yeasts/Candida, etc
  • low human bifido
  • low B longum (high dose RPS may lower B longum, favoring starch-eating-bifido)
  • low Roseburia/XIVa (high dose RPS lower, fail to sustain Roseburia in low carb diets)
  • low F. prausnitzii/IV (high dose RPS may lower)
  • low Akkermansia (high dose RPS may lower Akk)


After several citizen science N=1 experiments, we can observe now how high dosage potato starch may re-inforce these 'chronic illness' gut profiles by its anti-prebiotic effects where it lowers beneficial flora in the gut that are integral and vital for protecting the upper gut from pathogens like E coli and other alcohol producers, increases leanness, GLP1, revving up fat burning and carbohydrate metabolism:
--Bifidobacteria longum 
--Akkermansia (see prior post: high dosage raw potato starch tanks Akkermansia)

In human studies, several studies show that prebiotics (GOS, FOS, inulin) reverse NASH/fatty liver and lower liver function tests by raising Akk and B longum (and GLP-1 and GLP-2).  Probiotics that contain bifido work also.

What is curious to me is that scientists can restore and alleviate fatty livers and intestinal permeability by giving live probiotics of Akkermania to rodent models (Everard et al 2013). By giving prebiotics (FOS) to fatty liver/diabetes/obesity rodent models, reversal of all the hallmark biomarkers of these conditions rapidly occurs. Restoration and reversal of intestinal permeability happens, LPS decreases, metabolic endotoxemia reverses, inflammatory markers reduce, and insulin/blood sugars normalize. 
"For instance, a decrease in Akkermansia muciniphila causes a thinner intestinal mucus layer and promotes gut permeability, which allows the leakage of bacterial components. Interventions to increase Akkermansia muciniphila improve the metabolic parameters in obesity and NAFLD. In children, the levels of Escherichia were significantly increased in nonalcoholic steatohepatitis (NASH) compared with those in obese control. Escherichia can produce ethanol, which promotes gut permeability. Thus, normalization of gut microbiota using probiotics or prebiotics is a promising treatment option for NAFLD." (Miura et al 2014)


Bodinham and other studies fail to account for the gut microbiota effects of the 'fiber' that they are studying and the metabolic consequences. That's too bad. We are what we eat and our health is determined by our gut microbiome. We can shift and shape this, and we and the researchers are doing it all the time now.  

In several human studies, body fat ('fat mass') and upper gut permeability significantly improve with FOS and inulin-type fructans. The obese subjects in the below trial were never diagnosed with fatty liver, but with intervention with inulin-FOS, weight, BMI, insulin resistance, butyrate, SCFA and  LPS/endotoxemia (proxy for permeability) and other metabolic parameters all improved. Per personal communication with one of the researchers, as can be predicted, Akkermansia significantly increased in the below trial.

"The species Bifidobacterium longum, Bifidobacterium pseudocatenulatum and Bifidobacterium adolescentis were significantly increased at the end of the treatment in the prebiotic group (p less than 0.01) with being B. longum negatively correlated with serum lipopolysaccharide (LPS) endotoxin (p  less than 0.01). Total SCFA, acetate and propionate, that positively correlated with BMI, fasting insulinemia and homeostasis model assessment (HOMA) (p less than 0.05), were significantly lower in prebiotic than in placebo group after the treatment period."


Yacon is an ancestral non-starchy root. It can be boiled down and produce a nice syrup which has little energy for humans but fiber and prebiotics for our gut flora including Akkermansia and Bifidobacteria longum. Oligosaccharides in whole foods (see below) and yacon help boost the species lost by high-dosage-raw-potato-starch. The game-changers: Akkermansia and B longum specifically.

The Folz family experiment -- I briefly reviewed earlier here. Gut diversity dropped in each person on high dose potato starch -- particularly for the leanness building gut species.

Child 2 had the least Akkermansia, then high dose potato starch mowed it down to 24-times below normal.  Not hard to rebuild: stop RPS, take Akk-building fiber/foods. 
Gut Microbe



uBiome Normal

LC paleo
beans daily


Child1 pre

Starches grains, yogurt
Child1 post

1 TB RUMPS in water + 1 TSP Psyllium husk
Child2 pre
Child2  post

1 TB RUMPS in water
(psyllium, inulin-FOS, GOS, yacon, onions, leeks)


5-fold below normal
Little change
11-fold below normal
24-fold below normal

Tim S.'s Akkermansia and B longum on high dosage RPS. Mowed down? Never replenished? Risk factor for reflux or NASH/fatty liver? 
Gut Microbe

Genus Level
uBiome Healthy Subject
N=1 TS

High Dose
20-40g RS2 potato starch

10-20g RS3

N=1 TS

20-40g RS3
10-20g inulin

(no RPS but high doseage for 1.5 years earlier)
below healthy avg
below healthy avg
B longum


Recently my buddy Justin told me he stopped potato starch (no changes) after a few weeks, then took yacon syrup for 2months.

He was surprised to see his high liver tests (fatty liver) ALT improved from 50 to 26 and AST to as low as 23 (healthy optimal levels less than 15 (male); less than 12 (female). Thanks Justin!
ALT 50-->26, ALP 101-->66, AST-->23. Getting there.

  • Test your gut species, don't guess  (Genova, uBIOME, etc). Stop potato starch until verification of decent levels of Akkermansia, Bifidobacteria longum and other vital gut guardians.
  • Akkermansia and Bifidobacteria longum are gut game-changers and guardians
  • Consider amplifying the gut guardian species associated with leanness and longevity for optimal health: B longum and Akkermansia by seeding (probiotics), weeding (probiotics, botanicals) and feeding.
  • Feed well (inulin, acacia, FOS, yacon, onions, leeks, sunchokes, GOS, psyllium, hemicellulose, cellulose, chitin-glucan (mushrooms), lignins, gums, beta glucan (oats), pectin, arabinoxylan, arabinogalactan, xylans, etc). See chart below.
  • Consider adding in foods and prebiotics that weed out pathogenic E coli and select good, beneficial E coli.
  • Everyone appears to have low B longum and Akkermansia which are risk factors for chronic inflammation according to new human gut microbiota. Studies show their replenishment yields many health benefits and control of inflammation and disease. If you don't have FODMAP intolerances, consider both Version A and B of bionic fiber in the 7 Steps to rebuild these.  

Whole Real Food

100g = ~ ½ cup

Inulin-Oligosaccharide Content

RS3 Content
Chicory root
Jerusalem artichoke
Dandelion greens
Onion (raw)
Yacon syrup, 2 TBS
Garlic (raw)
Cowpea, White Lupin
Lentils, Chickpeas, Hummus
Pinto Beans (cooked/cooled)
Purple Potato (roasted/cooled)
Yams (boiled/cooled)
Potato (boiled/cooled)
Rice (cooked/cooled)
Long grain Rice (cooked/cool)
Sushi Rice (cooked/cool)