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



Intrepid gut explorer. Gut Tests Show Depletions of Akkermansia After Long Use of RUMPS, Which Appears to Correlate With Recent Bout 10 Lb Fat Gain/High Blood Sugars/Gout/Fatty Liver:    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 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 10 lb weight gain, gout, and 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's the only person I know how has taken potato starch for over 1.5 years and his gut profiles are known with major depletions of vital 'Peacekeepers' (Faecalibacterium prausnitzii) and other immunoprotective species. Human and animal studies depletions of these gut species predispose to the conditions he developed: carbohydrate sensitivity, fat gain, fatty liver/NASH. Gut researchers have concluded that RS2 (type 2, raw; not cooked RS3) are not prebiotics and do not translate to humans. Metabolic function worsens in human randomized controlled trials.

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 carbohydrate/fruit related 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."

How does the gut microbiota and what we feed it affect our health?
Why does diet and dietary additions like supplements change in the composition and function of the gut?
How does loss of diversity with a high dosage of a single source of 'fiber' adversely affect health?




HIGH DOSAGE RAW STARCHES INCREASES BODY FAT IN T2 DIABETES SUBJECTS

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.



RAW STARCH RS2 LOWERS GLP-1 IN HUMAN TRIALS (BUT OF COURSE NOT RODENT ONES)

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?



HUMAN FOOD IMPROVES AND RAISES GLP1

Cooked whole beans and beta-glucan/arabinoxylan/RS3-inulin-containing cooked barley (here, here) 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. 

• Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics. Geurts et al 2014. (MUST READ lol)

Popsugahhhh
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
HEART OF IMMUNITY  = SMALL INTESTINES
Higher Toxic ETEC E coli in Raw Potato Starch Alone Arm
v. Controls and v. Probiotics

Intrepid gut explorer. Gut Tests Show Depletions of Akkermansia After Long Use of RUMPS, Which Appears to Correlate With Recent Bout 10 Lb Fat Gain/High Blood Sugars/Gout/Fatty Liver:    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 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 With RUMPS: 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).

In healthy controls, Bifidobacteria longum is a gut specialist and found in the majority:
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)

RPS (RAW POTATO STARCH)  = BLOCKER OF FAT BURNING?

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:
--Christensenella 
--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.

• Fecal microbiome and volatile organic compound metabolome in obese humans with nonalcoholic fatty liver disease. 
• Prebiotic approach alleviates hepatic steatosis: implication of fattyacid oxidative and cholesterol synthesis pathways. [not potato starch/RS2]
• Probiotics and synbiotics may improve liver aminotransferases levels in non-alcoholic fatty liver disease patients. [not potato starch/RS2]

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)

VERY DIFFERENT FROM HUMAN BODINHAM ET AL 2012 and 2014 STUDIES

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.

• Inulin-type fructans modulate intestinal Bifidobacterium species populations and decrease fecal short-chain fatty acids in obese women. 
• Free PDF

"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."

FATTY LIVER REVERSAL WITH OLIGOSACCHARIDE-RICH YACON SYRUP

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 ANCESTRAL CORE-- LEAN, GUT PROTECTIVE MICROBIOTA	uBiome Normal Avg	Adult1 pre low-mod LC paleo RS3-GOS beans daily	Adult1 post 4 TB RUMPS RS3- diet	Child1 pre Starches grains, yogurt semi- paleo	Child1 post 1 TB RUMPS in water + 1 TSP Psyllium husk	Child2 pre	Child2  post 1 TB RUMPS in water
Akkermansia (psyllium, inulin-FOS, GOS, yacon, onions, leeks)	1.2%	16.93	1.45	0.24 5-fold below normal	0.26 psyllium buffered Little change	0.11 11-fold below normal	0.05 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 ANCESTRAL CORE	uBiome Healthy Subject Avg	N=1 TS High Dose 20-40g RS2 potato starch 10-20g RS3 AMGUT	N=1 TS WHOLE FOOD 20-40g RS3 10-20g inulin (no RPS but high doseage for 1.5 years earlier) uBiome
Akkermansia	1.2%	0.07 17-fold below healthy avg	0.12 10-fold below healthy avg
Bifidobacteria (B.animalis) B longum	0.89% (--) 0.4-5%+	11.32 (--)	8.81 (7.90) 0.0021

+estimated

REVERSAL OF LIVER TESTS/FATTY LIVER WITH STOPPING RPS AND TAKING YACON

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!
@Gut_Goddess ALT 50-->26, ALP 101-->66, AST-->23. Getting there.






 CONCLUSION AND ACTIONS

• 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	100g	41g	0
Jerusalem artichoke	100g	18g	0
Dandelion greens	100g	13g	0
Onion (raw)	100g	4g	0
Yacon syrup, 2 TBS	2 TBS	10-14g	0
Garlic (raw)	25g	3g	0
Cowpea, White Lupin	100g	5g	4g
Lentils, Chickpeas, Hummus	100g	4g	2-4g
Pinto Beans (cooked/cooled)	100g	3g	10g
Purple Potato (roasted/cooled)	100g	na	15-19g
Yams (boiled/cooled)	100g	na	6-8g
Potato (boiled/cooled)	100g	na	3-7g
Rice (cooked/cooled)	100g	na	1-2g
Long grain Rice (cooked/cool)	100g	na	2-3g
Sushi Rice (cooked/cool)	100g	na	3-4g

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	Low or none found in babies with allergic colitis; healthy infants are enriched with B longum Only infants of allergic, atopic mothers were colonized with B adolescentis; healthy babies colonized with B. longum. Healthy, disease-free mothers had high amounts of B. longum in breastmilk which was the most frequently detected species in milk B.longum and bifido depleted in chronic liver disease, fatty liver/NASH, obesity, T2D Total bifido and Bifidobacteria longum depleted in celiac patients compared with disease-free healthy subjects	B.longum with FOS improves fatty liver/NASH and elevated liver tests B longum probiotic with other bifido/lacto strains administered to chronic liver patients: GI symptoms improved and SIBO disappeared in 24% v. none in controls	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
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	Interventions to increase Akkermansia muciniphila improve the metabolic parameters in obesity and NAFLD	reductions in Akkermansia -- 2-fold to 17-fold depletions from normal Depleted in ulcerative colitis and resistant starch no benefit in human trial
Christensenella	20-fold depletion in inflammatory bowel disease 5-fold depletion in post-infectious irritable bowel syndrome Christensenellaceae bacteria might be a “keystone” species, “one that wields a disproportionate influence upon the world around it.”'	Tony Federico -- 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