The Resistant Starch Challenge: Is It The Key We've Been Looking For?

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia
Yes, in fact I have not taken any B2 or MK4 for ages. I do not need them anymore. It seems that the RS and probiotics are doing their job.
:thumbsup:

Good for you. This would also of course effect MTHFR, which uses a FAD cofactor. This should occur in concert with all the other processes including the heme metabolism, and everything else effected by flavin coenzymes. I bet you wouldn't react to 5-MTHF today like you did in the past. Until people stop having "reactions" to B2, folate, and B12, their GIT has a ways to go.

Slowly but steadily getting better until I do something stupid like take something I am not ready to take yet.
 

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia
Could you elaborate on this a bit, if you have time?
The metabolic changes are rather complex, so I will have to look at my notes, but it clearly relates to, not-surprisingly, the residual composition of the post-AB microbial community. While this is obviously individual, transient reductions in pathogens are eventually replaced by what is viewed as more dysbiotic and less diverse microbial balance and a new metabolic signature. I only have IBD & HE patient populations as a guide, but the end result is not favorable.
 

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
I think it is highly likely that those with ME/CFS are much more susceptible to adversely impacting their individual microbiomes with these substances, although it's hard to predict which whole plant products would be more or less suitable other than by gauging symptoms, which isn't going to be that instructive in the short-term.
I understand. Thank you for your reply.:) If the attention is on the gut, we should take care carefully to everything we consume. The primary focus should always be on our microbiome.

I would think as a general recommendation that patient's with ME/CFS avoid some concentrated, extracted plant compounds and look at the whole plant, and take these things more judiciously. I would argue that just about all of the plants with antimicrobial properties are still better than prescription antibiotics.
Do you have a suggestion for people with such a strong SIBO, who cannot tolerate any RS or fibre? Who react to the tiniest amounts? Kresser suggests as therapy strong GAPS diet for max. 1 month, and herbs like berberine, then start very slowly with RS+fibres and PHD.

It´s not for me, I take RS+fibres, and I am very thankful for this thread and its information and message, to look primarly to the gut to build up immunity slowly.
 

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia
I would be a bit wary of changing the diet too rapidly as GAPS is a radical shift from most diets, especially from what I recall about the induction phase. I can't really offer many comments about these two diets and their appropriateness because I don't remember too much about them. Just bear in mind that one's diet is still going to massively shape the composition of the gut, so changes need to be gradual.

From a general standpoint, I would look at this in the context that the more severe dysbiotic conditions are marked by a severely diminished capacity to degrade many of these carbohydrates and this is purposeful and functional, so in some cases people may need to work from less to more hydrolyzed carbohydrates. Basically more everyday plant fibers versus carbohydrates that one would rarely encounter in their diet as have been described in this thread. It's a fine line to walk though, in that some people are clearly doing better with some of these very selective prebiotics, and they are presumably filling a metabolic and immunomodulary niche. Unfortunately the dynamic is utterly complex and the side effects from these more specialized, uncommon components of "food" are going to be often poorly tolerated. This might mean at first eating more common whole plant materials and slowly increasing the diversity of plant fiber as the initial means of shaping the microbiome.

I would hate to abandon prebiotics altogether, but perhaps there should be avoidance of super concentrated plant extracts, and synthetically hydrolyzed carbohydrate products. Reducing the "dosage" should always diminsh the response, so why not cut back to miniscule quantities. The longer I have done this, the more I see the wisdom in not trying to rapidly force changes, binge, or overdo it. It generally results in set-backs of one sort or another.

There are going to be substances that provoke a much more potent immune response because the only way these carbohydrates become accessible to any significant degree is if you have certain organisms that can chemically sever the bonds that modify the structure of the parent compound. Some of these substances are rather innocuous to those with severe disease simply because the community of organisms to hydrolyze one polymer that is in turn further modified by another, organism is lacking. When we come in with artificially hydrolyzed prebiotics or extraordinary concentrations of these prebiotics, as compared to our usual diet, including some that I am guilty of indirectly advocating, there is more risk of "immune imbalance." There is obviously a reason some of these carbohydrate substances are not found in nature to any significant degree unless biosynthesized or converted by the contributions of microorganisms. The differences in what organisms can break down Beta 1-4 versus Beta 1-3 glycosidic linkages is purposeful. It might be prudent to avoid some of the manufactured products, as in when they use a microbe to hydrolyze a polymeric compound and provide access to something an ill person can't take advantage of and use without excessive immune activation. The degree to which this actually happens in your body is self-regulated and tied to microbial enrichment, so we should proceed cautiously when circumventing nature. The same holds true for vitamin supplementation.

In the future I think we could combine analytic tools with genomic data to analyze one's individual metabolic and microbial signatures to allow predictions about what metabolic pathways need to be supported and microbial fixes need to be made and a very individualized supplemental prebiotic program could be developed. I know my own tinkering has started to narrow down this process to certain kinds of prebiotics. As I have described, I am favoring highly acetylated and sulfated storage polysaccharides and mucopolysaccharides. One commonality is that these are integral to the rebuilding of the intestinal epithelium and the organisms that live there. I also find that he provision of sulfate to facilitate this process is enormously helpful, but I recognize that transdermal magnesium sulfate is not for everyone.

While we have the capacity to gather and analyze metabolic and microbial pathways and compare this to norms, obviously we would need to figure out how to fix this most expeditiously and with the least cost to the host. I believe that these costs can be mitigated first and foremost by not overstimulating the broken immune system. This is where all plant materials have to be considered for what they are.

Things like Berberine are very intriguing, but as I mentioned the whole plant may be better for a number of reasons. One of those reasons is there are myriad ways in which this compound can affect someones microbiome. It possesses properties that will serve to diminish the Toll-like receptor and signalling which triggers an immune response to lipopolysacchride, which is a good thing. It's also a quarternary ammonium so it has antibiotic properties, which can have positive and negative net consequences. The negative meaning that there will be a reactive oxygen consequence to killing off organisms. Accordingly, the plant should facilitate the enrichment of microbes that participate in the differentiation/replication of T-cells. I'm guessing plants containing Berberine are rich in those polysaccharides I discussed above.

Many of these anaerobes in the colon have drug resistance to QA substances, in fact it is often used as an antibacterial agent. For example, Bacillus subtilis is likely largely resistant to the effects of Berberine. The resistance of certain microbes and the susceptibility of others is in large part what shapes the gut. It's that ROS/NS a.k.a. free radical damage that implies that you need the whole plant and the prebiotic contribution it conveys.

There is ample data from studies of inflammatory disease that I believe is on point, and while different inflammatory diseases/conditions clearly have different microbial/metabolic patterns that I have observed, there are some overriding patterns including consistent perturbations in the purine-nitrogen metabolism and TCA-glycolosis-fatty acid metabolism. These have downstream impacts on those processes that have been popularly addressed here chiefly through over-ramping metabolic capacity.

These processes can be dramatically enhanced, at least in vitro, through the provision of some of the key metabolites, principally butyate. I think the same can be achieved via the stimulation of those organisms that produce these, but the metabolic corrections are not so readily achieved. Working backward from butyrate is a good starting point, I think. Looking at some other key metabolites involved in mitigating the effects of endotoxins and modulating the immune response, also seems to be fruitful. I see a place for other things like indole and microbial sphingolipid biosynthesis. I believe these compounds also enjoy very strong evidence for having the capacity to reverse auto-immune processes and cancer, and at the root of this is restoring the energy metabolism and immunocompetence. The fact that these prebiotics substances are perfectly suited to favor the expansion of the known t-regulatory enhancing microbes that are central to synthesis of these same metabolites, and cross-disease microbiomic data tells me these microbes are consistently lacking, suggests we are on the right track. Unfortunately, we have a long ways to go.

I guess my first question is, what is her current diet?

My second question is what prebiotics has she tried, and what effects did these produce? This might be helpful to know.
 
Last edited:

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
Unfortunately, we have a long ways to go.
Yes. But it´s a way, which builds up an immunity that we perhaps never had.

Thanks for your response.:)
I understand, what you write, and it´s very important.
I have one question: why is indol able to reverse auto-immune processes, or why is it a prebiotic? Indol and skatol are both byproducts of the tryptophan metabolism. To much of them are toxic for the liver.
To much Indol is produced with candida overgrowth.
Candida disrupts the tryptophan metabolism by inhibiting the enzym IDO (indoleamine 2,3-dioxygenase), thus increasing 5-hydroxytryptophan and inhibiting IL-17 production. (IL-17 is our host defense against candida). A disrupted tryptophan metabolism produces to much skatol and indol.

The tried prebiotic is RS. Each trial induces strong diarrhoe, bloating or constipation or to much inflammation. A low carb diet stopps this.
 

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
Interesting research concering potatoe starch:
http://www.sciencedaily.com/releases/2014/05/140520093511.htm
The team established gut bacteria cultures in flasks and then 'fed' them two different diets -- either a predigested potato, high-starch diet or a predigested grass, high-fiber diet. Then they tracked changes in the numbers and types of bacteria and measured the metabolites produced by digestion.

Surprisingly, the human cultures on a potato diet produced the highest levels of SCFAs. Even the baboon cultures fed potato produced more SCFAs than the baboon cultures fed grass. When the researchers applied some of these cultures to mouse colon cells in the lab dish, the cells were stimulated to release PYY hormone. Those exposed to human cultures digesting a potato diet released the most PYY, followed by those exposed to baboon cultures on a potato diet.

This evidence argues that the previous view of paleo diets and appetite suppression is flawed and that high-fiber, plant-based diets likely do not lead to increased SCFAs
Starch from potatoes produces much SCFA´s, vegetables did not.
 

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia

Riboflavin
Gelatin I think will help with collagen production, and for this vitamin C is needed too. Besides that, gelatin is a source of glycine, which might set off detox reactions. Also, glycine functions as an inhibitory neurotransmitter in the CNS, which can make people feel more fatigued. Glycine also inhibits cortisol. I get severely fatigued both from pure glycine as well as gelatin.
I've been looking at epithelial cellular kinetics trying to come up with some ways to mitigate the effects of certain chemotherapeutic agents that target these tissues and in doing so I read that expression of MMP-1 has a anabolic effect versus the other matrix metallproteinases, which induce catabolism. MMP-1 degrades interstitial collagens. I think the provision of a large amount of gelatin could inhibit this reaction, which i also see is induced by acetylcholine concentrations.
 

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia
Yes. But it´s a way, which builds up an immunity that we perhaps never had.

Thanks for your response.:)
I understand, what you write, and it´s very important.
I have one question: why is indol able to reverse auto-immune processes, or why is it a prebiotic? Indol and skatol are both byproducts of the tryptophan metabolism. To much of them are toxic for the liver.
To much Indol is produced with candida overgrowth.
Candida disrupts the tryptophan metabolism by inhibiting the enzym IDO (indoleamine 2,3-dioxygenase), thus increasing 5-hydroxytryptophan and inhibiting IL-17 production. (IL-17 is our host defense against candida). A disrupted tryptophan metabolism produces to much skatol and indol.

The tried prebiotic is RS. Each trial induces strong diarrhoe, bloating or constipation or to much inflammation. A low carb diet stopps this.

Indole derivatives stimulate the differentiation of Th-17/T regs and they simultaneously participate in the metabolic mechanism that maintains the structure of the intestinal epithelium where these immune cells are harbored.

Independently the chemicals have efficacy, combined with the microorganisms that metabolize these and you have so much more.

It's virulence depends upon it's chemical modification by microorganisms.

These fungal organisms are filling a void and protecting the host from further harm.
 

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia
Asklipia, this Website is so interesting, that it needs more time to summary the most important Statements. Here is the Website:

http://www.microbialinfluence.com/


If bifidos bind to LPS, this means, it detoxyfies LPS, does this mean, that we can handle Mercury and other heavy metals much more better? As RS and other fibres as LAG and so on create bifidos, it could be important to address first the gut with PHD, RS and fibres, and then we can deal and detoxify heavy metals

Some of the anerobic organisms that I am certain most are missing feature a ridiculous array of heavy metal binding capabilities. I'm guessing the fact that these same organisms also seem to have great redundancy of methyl-accepting chemotaxis proteins has significance. Heavy metals don't "swim", but the bacteria do. There has to be host-bacterial coordination with SH antioxidant status, which our microbes also have their hand in.

For the uninitiated: http://en.wikipedia.org/wiki/Methyl-accepting_chemotaxis_protein
 

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
It's virulence depends upon it's chemical modification by microorganisms.

These fungal organisms are filling a void and protecting the host from further harm.
As Bernard mentioned: "the microbe is nothing the terrain is everything", and we try to treat the milieu.

Very interesting informations, now I have to read and lern. Thank you!

Regards, jepps:balloons:
 

Sidereal

Senior Member
Messages
4,854
Likes
17,243
Paradigm changing probiotic pills on the horizon:

Cambridge, Massachusetts — September 10, 2014 — CAMBRIDGE, Mass., Sept. 8, 2014 /PRNewswire/ -- Seres Health, a clinical-stage therapeutics company developing novel treatments for diseases related to the human microbiome, today announced final data for its single-arm, open-label clinical trial of SER-109, its first-in-field, oral microbiome therapeutic. SER-109, a mixture of bacterial spores, is designed for the treatment of recurrent Clostridium difficile Infection (CDI). The data presented at the 2014 Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) show that in patients with recurrent CDI, SER-109 resulted in clinical cures, with 29 of the trial's 30 patients (97 percent) reaching the 8-week endpoint free of infection.

Analysis of the microbiome using next-generation sequencing technology demonstrated that a single oral dose of SER-109 was capable of generating long-term changes in the microbiome, including the restoration of microbial diversity in the gastrointestinal (GI) tract of patients. Evidence for this was the engraftment of spore forming commensal bacteria from SER-109 in the patient's gut microbiota over the 8-week period. Unexpectedly, it was also determined that SER-109 catalyzed the outgrowth of other healthy non-spore forming organisms in the GI tract. This included critical genera that were missing in patients due to long term exposure to antibiotics.
Source
 

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
Honey as prebiotic:
http://www.honey.com/images/uploads/general/bifidobacteria.pdf
Bifidobacterial Growth
The effect of honey on specific growth rate of both bifidobacteria strains was dependent on the strain of
the bifidobacteria and concentration of honey in the growth medium. Overall, specific growth rate of both
Bf-1 and Bf-6 was enhanced with an increase in the concentration of honey in NDM. Concentrations of 3 percent
and 5 percent were most effective in enhancing growth of either strain compared to the NDM control and other
sweeteners. Five percent honey was the most effective on Bf-1. Sweetener concentration other than
honey did not appear to have an effect on stimulating bifidobacteria growth.
 

Vegas

Senior Member
Messages
577
Likes
766
Location
Virginia
Yes a source of xylo-oligosaccharides, which are really not that common in foods most eat with any regularity. One of the key differences in the various prebiotics is the discrimination between their composition of storage carbohydrates (there is overlap here) versus structural carbohydrates from plants (hemicellulose/lignocellulose). This is the difference between starch and xylan, for example.

These structural polysaccharides are more enriched with pentose sugars versus hexose sugars. The latter common, the former, not so much. The significance of this is extraordinarily important insofar as it stimulates a different set of microbes that utilize a different metabolic pathways.

In looking at inflammatory disease the conclusion that I have reached is that the microbes that utilize pentose sugars are consistently under-represented. The consequence on the human metabolism is unproven, but theoretically results in the accumulation of lactate with the inhibition of acetate and NAD(P)H. This creates a redox imbalance and further impairs the pentose phosphate pathways inhibiting ATP hydrolysis, decarboxylation, and dehydrogenation. This pathway also directly benefits Bifidobacterial organisms.

Honey's enrichment with prebiotics thus provides metabolic benefits assuming the functional microbial correlates are in place. Its metabolic consequence are illustrated by its different impact on blood glucose levels as compared to sugar. I can only imagine similar metabolic consequences would be manifested by eating the whole sugar beet versus simply eating the sucrose extracted from it.
 

adreno

PR activist
Messages
4,841
Likes
10,887
Interesting, @Vegas. We are discussing in a few other threads how to increase NADPH, and from what I can glean from your post above, this would include structural polysaccharides? So xylan would be a good choice here, can you name others? How can I tell which prebiotics would be included in this group, versus the starch based group? Thanks.
 

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
These structural polysaccharides are more enriched with pentose sugars versus hexose sugars. The latter common, the former, not so much. The significance of this is extraordinarily important insofar as it stimulates a different set of microbes that utilize a different metabolic pathways.

In looking at inflammatory disease the conclusion that I have reached is that the microbes that utilize pentose sugars are consistently under-represented. The consequence on the human metabolism is unproven, but theoretically results in the accumulation of lactate with the inhibition of acetate and NAD(P)H. This creates a redox imbalance and further impairs the pentose phosphate pathways inhibiting ATP hydrolysis, decarboxylation, and dehydrogenation. This pathway also directly benefits Bifidobacterial organisms.
Ribose and arabinose (LAG is arabinose+galactose) are pentose sugars. So these sugars are both good sugars for this pathway?

Honey's enrichment with prebiotics thus provides metabolic benefits assuming the functional microbial correlates are in place. Its metabolic consequence are illustrated by its different impact on blood glucose levels as compared to sugar. I can only imagine similar metabolic consequences would be manifested by eating the whole sugar beet versus simply eating the sucrose extracted from it.
Jaminet states not to consume more than 25 g fructose/day, too much is toxic for the liver. As many vegetables and coconut count half fructose/half glucose, and honey has a high fructose content, there is not much place for daily honey. But for me the 1 tsp honey is one of my daily dietary highlights:)
 

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
Chris Kresser´s article about Candida overgrowth:
He suggests to treat Candida only for a short time with antifungicide, but more to support the gut with diet (PHD, with SIBO GAPS onley for a short time), and the restoring of the gut with RS+prebiotics.


http://chriskresser.com/top-4-mistakes-people-make-when-treating-candida-overgrowth
Antifungicides are:

Some of the ones that we use, that have research behind them, and tend to work well would be undecylenic acid; uva ursi; cat’s claw; pau d’arco; lauric acid, which is monolaurin (Lauricidin); high-dose biotin actually is antifungal, like 5 mg per day; Gymnema sylvestre, which is an herb that has been used historically in India for blood sugar issues because it reduces sugar cravings and helps balance blood sugar, has recently been shown to be very effective in terms of inhibiting Candida growth; Saccharomyces boulardii, which is a beneficial strain of yeast, has been shown to inhibit the growth of Candida and also reduce inflammatory cytokine production that is associated with cells that are infected with Candida; soil-based probiotics like Prescript-Assist are I think effective in terms of outcompeting Candida for adhesion sites in the gut.

So resistant starch and non-starch polysaccharides, which are FODMAPs, of course, and also prohibited on a GAPS type of approach, they’re really helpful over the long term for restoring, growing beneficial bacteria in the colon. The reason you want to do that is because that’s what’s going to prevent a recurrence of fungal overgrowth in the future.
Important is to be cautious with antifungicid herbs, because they can disrupt the gut flora, more essential is to focus on RS+prebiotics+probiotics.
Maybe with CFS and compromised gut flora we should better be much more cautios with each kind of antifungicide herbs.

But I´m pleased with "long term restoring" and "prevent fungal overgrowh in future". For me this means, that the longer we take RS+prebiotics+probiotics, the better we will be.:)

Regards, jepps
 
Last edited:

jepps

Senior Member
Messages
514
Likes
677
Location
Austria
Very good post from Tim Steele:
http://chriskresser.com/top-4-mistakes-people-make-when-treating-candida-overgrowth
What a vicious cycle. We are all infected! Normally your yeast would love to keep you free of pathogens and healthy, but when it thinks you are about to die, it will gladly help speed that process, too!

I think the WORST thing anyone can do is the “anti-fungal” medicine route. All you do is make the yeast mad. It shape-shifts and hides. Unless you repair your immune system, you will never win against yeast.

Here’s a scary paper: In vivo imaging of disseminated murine Candida albicans infection reveals unexpected host sites of fungal persistence during antifungal therapy.

In this study, they created a bioluminescent Candida, and infected mice. Then they tried killing the Candida with antifungals.

” We confirmed the kidney as the main target organ but additionally observed the translocation of C. albicans to the urinary bladder. The treatment of infected mice with caspofungin and fluconazole significantly improved the clinical outcome and clearance of C. albicans from the kidneys; however, unexpectedly, viable fungal cells persisted in the gall bladder. Fungi were secreted with bile and detected in the faeces, implicating the gall bladder as a reservoir for colonization by C. albicans after antifungal therapy. Bile extracts significantly decreased the susceptibility of C. albicans to various antifungals in vitro, thereby probably contributing to its persistence.”
There is also a study (afraidly in German) about the connection gall bladder and not only candida, but several fungi+parasites.
http://forums.phoenixrising.me/index.php?threads/pancreas-gallbladder-and-cfs.611/page-2#post-527492

Regards, jepps
 

ahmo

Senior Member
Messages
4,616
Likes
7,075
Location
Northcoast NSW, Australia
@jepps You've got me just 4 days into finally deciding I've no choice but to undertake a major candida cleanse:bang-head: I'm going to be rotating natural anti-fungals, some of which you've mentioned, plus enzymes to disrupt biofilms...Thanks for the post, and Wish me luck!!:eek:;)
 

Asklipia

Senior Member
Messages
994
Likes
1,372
Very good post from Tim Steele:
http://chriskresser.com/top-4-mistakes-people-make-when-treating-candida-overgrowth


There is also a study (afraidly in German) about the connection gall bladder and not only candida, but several fungi+parasites.
http://forums.phoenixrising.me/index.php?threads/pancreas-gallbladder-and-cfs.611/page-2#post-527492

Regards, jepps
Yes, this all connects nicely. Candida would prefer the gallbladder and urinary tract because these are alkaline places, the bile is alkaline and would protect the fungi from acid which they don't like.
This explains why there are such spectacular results with Bifidodacterium longum. A strain that acidifies and helps the gallbladder and brings down blood sugar. If the gallbladder is handicapped by a proportion of candida, then bringing a bacteria that acidifies, like Bifido longum, would clear the gallbladder for a while and bring relief.
I did notice when doing liver flushes a few years ago, some white cotton-like things in the results. Most probably candida or fungi.
One can wonder what is happening in the pancreas then. See departed @Gemma here. It would be anatomically very easy for candida or fungi located in the gallbladder to move into the pancreas.
One wonders if these "diabetes" diseases are not due to some kind of candida infestation. I notice that a lot of the remedies that bring down blood sugar also have an effect of candida. Easy to say that diabetes raises blood sugar and thus feeds candida, but what if it was the way around?

In my own experience, Bifidobacterium longum BB356 cleans the gallbladder, raises morale, improves the gut and decreases fungi.
Good luck!
Asklipia :hug: