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
IF VIPERS IN SMALL INTESTINES:
E. coli, Other starch eaters
VIPERS IN THE UPPER GUT (SIBO/SIFO)
Early on, very few of the studies on RS2 showed fat loss, weight loss or significant metabolic improvements in any human trials I saw. No improvements in diabetes, insulin resistance, blood pressures, or blood cholesterol panels (triglycerides, HDL or LDL-cholesterols). This deep lack metabolic benefits for humans deviated from decades of studies using other types fiber and prebiotics (eg inulin, FOS, GOS, psyllium, beta glucan, etc). RS2 produced butyrate, but nearly all fiber and prebiotics produce butyrate. Gram for gram GOS, FOS-inulin and (pure) RS3 produce more butyrate than RS2. Beyond butyrate in the lower gut (colon), what benefits were there for RS2? Very few I found. And there is a cost — RS2 at high doses compromises gut diversity and specifically the species that make us human and lean, fat-burning machines: Christensenella, Bifidobacteria longum, and AKKERMANSIA.
If there was fat loss or insulin improvements observed in animal studies with RPS or HAM-RS2, then the authors had poor study design — they had substituted starch (digestible carbs) with RS2. In other words, they ran a VLC or LC (low carb) study, and we all know cutting refined rat chow carbohydrates will produce metabolic improvements, and often dramatic ones.
When bifidobacteria and other guardians in the upper gut are removed by antibiotics, stress, high sugar diets and lack of vertical transmission from mom, the environment in the upper gut becomes vulnerable to opportunistic flora such as the organisms from the lower gut. They crawl up uninhibited. If acid, bile or the stomach’s protein degraders (pepsin, trypsin, chymotrypsin) and pancreatic enzymes become compromised in secretion, they crawl up faster and more furious. If these vipers consume potato starch or RS2 or high amylose maize, they will enjoy ultra fermenting this substrate and can create silent and insidious havoc in the intestines, particularly if the gut guardians are gone (Akk, B longum, lactobacilli, etc).
There is a false ‘myth’, untruth pseudoscience that potato starch granules will ‘carry’ pathogenic bacteria away perpetuated on the internet. Few vipers in the uppergut are ‘carried away’ from what I observe. Potato starch and raw starches ferments furiously and fervently where it lands. Worse, potato starch ‘removes’ the potent guardians of the uppergut, leaving the uppergut vulnerable to infections, E coli, fungi/candida and other potential commensals-turned-vipers and the vipers themselves.
What protects vipers from migrating to the uppergut? How to get rid of the vipers?
[Answer: GUT GUARDIANS (Akkermansia, Bifidobacteria longum, Lactobacillus plantarum, etc), probiotics, soil probiotics, bifido/lacto, weeding with botanicals, inulin/FOS, GOS, psyllium, etc]
Akk — that is today’s topic. Journal club: de Vos et al. It’s one of our best guardians of the upper gut (ileum, small intestines).
Various disease states are connected to microbial fingerprints. At the top is a short list of the vipers that eat raw potato starch and raw starches; they all eat digestible starches too and this is why so many with j*cked up guts do well initially on strict Paleo, SCD, Gottschalks, GAPS and VLC diets. For a short term, limiting starches helps until seeding (weeding) with the right probiotics and weeding of identified vipers occurs. Long term however the root problem is not fixed and may even get worse (low FODMAPS and low fiber diets may lower akkermansia).
The microbial fingerprint for most post-SAD people (and formerly SAD fat/ill/sick):
(1) missing one of ultimate gut guardians: Bifidobacteria longum (recall: the raw potato starch users have nearly none)
(2) missing also another gut guardian: Akkermansia mucinophila (recall: for the family of 4 in their intrepid experiment, raw potato starch lowered everyone’s A. mucinophila except for the one taking psyllium husks)
(3) presence of vipers: alcohol producing yeasts and E coli, Staph, starch eating Prevotella, etc.
|Unique T2 Diabetes Fingerprint:
MISSING MANY (B. longum, and Akkermansia)
EXCESSIVE UPPERGUT PATHOGENS (Bacteroides,
Yeasts/Candida, E coli, Starch Eaters, etc)
If symptoms occur, they often involve joint pain, muscle aches, headaches, rash, challenges with losing body fat, increased blood sugars, or worsening of the respective condition. On stool testing these commensals-turned-opportunistic overgrowths may be evident for those who have the below conditions
obesity (I had this)
- GERD/reflux, heartburn (I had this on high dose potato starch, out of the blue)
- NASH (non-alcoholic steatohepatitis)/fatty liver (Tim Steele had this recently)
skin disorders, acne
IBD, Crohn’s, ulcerative colitis
autism, ADHD, spectrum
and other gut signatures marked by these
HIGH DOSAGE RAW STARCHES INCREASES BODY FAT IN T2 DIABETES SUBJECTS
Bodinham et al 2014. Authors were shocked to find that 40g HAM-RS2 (raw starch, resistant starch type II) failed to improve blood sugars, hyperinsulinemia, or glycemic control. High dosage raw starches actually worsened many parameters including insulin resistance. Several other human studies reflect these results (previous post: sorry, resistant starch type 2 won’t induce fat or weight loss). It appears RS2 can induce changes in metabolism that don’t show up in rodent studies.
Humans aren’t rodents. Our gut flora are vastly different (Moeller et al PNAS 2014). We’re big-brained, long-living furnaces of fatty-acid utilizing carnivores/omnivores. If one eats hamster food, will they develop a lame #HAMSTERGUT?
Raw high-amylose maize RS2 high dosage 40 grams daily for 12 weeks appeared to make subjects with controlled T2 Diabetes fatter………….and higher inflammatory IL6, 30% more fat in the pancreas (‘fatty organs’), higher triglycerides (which corresponds higher insulin and IR, insulin resistance), and higher LDL (dense, atherogenic LDL-particles).
Notable indicators of a healthy microbiome — butyrate and propionate in the stools — were all statistically lower.
So what was raw potato starch feeding, just the bottom feeders? Starving the gut guardians and making extinct Akkermansia and Bifidobacteria longum in the uppergut?
Results Tab 1:
–increased fasting TG (p=.039)
–increased LDL cholesterol
–increased HOMA% (aka nsulin resistance) wtf??!
–~30% increased pancreas fat wtf?
(v control, Body fat depots determined by MRS scanning (n=14).)
–increased fat mass
–increased IL6 (but lower TNFa)
–lower butyrate (p less than 0.001)
–lower propionate (p = 0.021)
MECHANISMS FOR HIGH DOSE RS2 HALTING FAT LOSS?
As you we know antibiotics can cause obesity (Blaser et al 2014). Certain probiotics can cause weight loss (Bifidobacteria longum, Akkermansia mucinophila) and others may induce weight gain (certain Lactobacilli strains). What about prebiotics, fiber and resistant starch?
I think RS2 halts fat loss and for many with susceptible guts, increases subtle fat gain as several studies are showing now.
What I would love to know about these test subjects is their abundance of the insulin sensitizing gut flora and how much % they dropped:
What I’d also love to see is how much fat was gained in the liver and how high the liver tests (AST, ALT) increased. I bet it was a cr*pload since the pancreas increased in fat mass% by about 30%.
After potential losses of B longum and Akkermansia, what vipers/commensals were consequently overgrowing as a result of high dose raw starches, in the uppergut (SIBO/SIFO)?
–alcohol producing E coli?
–alcohol producing Clostridium or Dorea?
–alcohol producing yeasts/candida?
Every gut is unique but the obese, fatty liver/NASH and diabetes one has several overlapping clusters of microbial factors. Namely, the below. These fingerprints are so characteristic they can be predicted now in 80% of cases. A hallmark feature is low diversity. Scientists call this LGC, low gene count. Many gut symbionts are absent. The ones left are opportunistic vipers. Without the gut guardians in the uppergut, only a few vipers can lead to devastating metabolic and disease burdens .
Unique Obesity/ NASH/fatty liver/T2 Diabetes Fingerprint:
- MISSING MANY (B. longum, and Akkermansia mucinophila)
- EXCESSIVE UPPERGUT PATHOGENS (Bacteroides,Yeasts/Candida, E coli, Starch Eaters, etc)
GAME-CHANGER = AKKERMANSIA MUCINOPHILA
When scientists boost Akkermansia in humans with prebiotics (psyllium, inulin-FOS, etc), all the metabolic biomarkers dramatically reverse or improve (fatty liver, elevated liver function tests, circulating LPS, endotoxemia, hyperinsulinemia, elevated blood glucoses, inflammation, etc). Akkermansia is found depleted in every modern illness that it is tested: appendicitis, obesity, T2 diabetes, insulin resistance, high intestinal permeability, fatty liver/NASH, IBD, etc. (However, in severely disrupted guts, Akkermansia will overgrow where the gut barriers are compromised like in severe IBD and colorectal cancer.)
Through the entire animal, bird, fish and reptile kingdoms, Akkermansia is found ubiquitiously. It’s is everywhere, even in deepsea fish that live 5000 meters deep in the ocean. Everyone has it except SAD guts and those on high dosage potato starch.
For healthy guts, it lines the entire GI tract. By scientists’ estimates, our entire microbiome is 3-5% Akkermansia. In stools Akk has an abundance of 1-3% in healthy guts (ubiome avg in healthy subjects = 1.2%). Akk is the game-changer for human disease for many.
“Studies have demonstrated an inverse
correlation between the presence of the closely
adherent mucin-degrading bacterium Akkermansia muciniphila and obesity in humans . Further
studies have confirmed that A. muciniphila is
reduced in obese and type 2 diabetic mice, and
demonstrated that prebiotic feeding enhances the
abundance of this organism with an associated
improvement in the metabolic profile .
Significantly, administration of A. muciniphila to
mice reversed the high-fat-diet-induced conditions
including inflammation, fat mass gain and insulin
resistance via improved control of inflammation
and gut barrier function potentially mediated
by increased intestinal levels of endocannabinoids
 Studies such as these are important in
establishing the causal relationship between
elements of the microbiota and disease states, and
will greatly inform future diagnostic and treatment
protocols for metabolic diseases.” (Joyce, Gahan 2014)
|MOAR CHARLIE HUNNAM BY REQUESTS
Human or Hamster Guts?
What’s his gut guardians (Akk, B longum) and GLP1?
CONCLUSION AND ACTIONS
- Consider the whole spectrum of fiber to feed the flora and amplifying the gut guardian species associated with leanness and longevity: B longum, Akkermansia, and Christensenella by seeding (probiotics), weeding (probiotics, botanicals) and feeding (inulin, acacia, FOS, yacon, onions, leeks, sunchokes, GOS, psyllium, hemicellulose, cellulose, lignins, gums, beta glucan, arabinoxylan, xylans, etc).
- Consider adding in foods and prebiotics that weed out E coli and that raise diversity and B longum and Akkermansia (both Version A and B of bionic fiber) in the 7 Steps.
- Version B is a fat blaster and can help reverse fatty liver/obesity/diabetes (Akkermansia).