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

Discussion in 'The Gut: De Meirleir & Maes; H2S; Leaky Gut' started by Ripley, Dec 11, 2013.

  1. Gestalt

    Gestalt Senior Member

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    There was a really good thread on microglial activation and excitotoxicity on this forum a couple of years ago, but I can't find it. In any case it's integral to understanding the mechanics of brain fog and most other mental issues people w/ CFS experience.

    "Glutamate is a prime example of an excitotoxin in the brain, and it is also the major excitatory neurotransmitter in the mammalian CNS....When the glutamate concentration around the synaptic cleft cannot be decreased or reaches higher levels, the neuron kills itself by a process called apoptosis.

    This pathologic phenomenon can also occur after brain injury and spinal cord injury. Within minutes after spinal cord injury, damaged neural cells within the lesion site spill glutamate into the extracellular space where glutamate can stimulate presynaptic glutamate receptors to enhance the release of additional glutamate." http://en.wikipedia.org/wiki/Excitotoxicity#Pathophysiology
    There is a negative feedback cycle that can be established here where excess glutamate, causes cell death, which causes more glutamate to be released which results in more cell death.

    If neurons really do use lactic acid as a fuel source, and they are dying in large numbers due to excess glutamate activation then it's feasible lactic acid levels may rise as a secondary effect as the neural contents spill out in the Cerebral spinal fluid (CSF). This mechanism would explain the link @Sidereal posted and the one I posted, about lactic acid build up in people w/ CFS and mechanical brain injury.

    Microglial activation relates to this as well as microglia are the CNS's immune system. IIRC they can be triggered by ammonia (produced by yeast in an alkaline gut) as well as LPS. They also get triggered when neurons die from the previous mentioned glutamate issue as a clean up protocol.

    Part of the way they work is that when activated in an inflammation response they release glutamate which can exacerbate the previous noted issue. This is how endtoxin die off could lead to brain fog. In addition they also release NO, nitric oxide; NOO-, peroxynitrite; O2, superoxide; PGE2, prostaglandin E2; TNFalpha and tumour necrosis factor-alpha. All wonderful things that cause all kinds of inflammatory and mental symptoms!

    In the following diagram this process is called "Self-perpetuating neurotoxicity" :eek:


    [​IMG]
    http://www.nature.com/nrn/journal/v8/n1/fig_tab/nrn2038_F1.html

    Again to reiterate, there are well established process's here that explain brain fog perfectly well. There is no need to jump to conclusions and wrongly blame lactic acid itself and that it is somehow magically making peoples brain tissue more acidic thereby explaining their issues. :p

    Lactic acid is pretty important stuff. According to the Lactate shuttle hypothesis: "In addition to its role as a fuel source predominantly in the muscles, heart, brain, and liver, the lactate shuttle hypothesis also relates the role of lactate in redox signalling, gene expression, and lipolytic control."

    It's therefore feasible a lactic acid deficiency due to gut dysbiosis could compromise those organs and aspects of human health. Just like a butyrate deficiency compromises colon health.
     
    Last edited: Jul 11, 2014
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  2. zzz0r

    zzz0r Senior Member

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    I noticed today that I stopped taking LAB that my muscle tension has decreased. There ie defenetly a connecion between LAB, lactic acidosis and muscle tension.
     
  3. Sasha

    Sasha Fine, thank you

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    Took a second dose of 1/4 capsule of L. Plantarum yesterday and spent the day prostrate with a splitting sinus headache, hardly ably to get out of bed, constipation... felt absolutely wretched. Thought it would be one of the easy ones. Giving it a rest today - don't know whether it would be wise to try it again. :aghhh:
     
  4. Sasha

    Sasha Fine, thank you

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    Just started reading "Missing Microbes" by Martin Blaser, the director of the Human Microbiome Program at NYU.

    He says that parents aware of the hygiene hypothesis (being too clean causing children's immune systems not to develop properly) are trying to expose their kids more to pets and farm animals and are allowing them to eat dirt.

    He says: " I beg to differ. To me, such exposures are largely irrelevant to our health. The microbes present in dirt have evolved for soil, not for us."

    I'm aware that the idea in the Paleo community is that our ancestors will have been eating plants straight from the soil without washing them and that we'll have evolved to flourish in the presence of these bugs but presumably Dr. Blaser is aware of that argument too.

    Looking forward to reading the rest of it!
     
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  5. adreno

    adreno 3% neanderthal

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    @Sasha

    So that means no SBOs, according to Blaser?

    I have been wondering about the hygiene hypothesis, too. Should I enforce hand washing on my kids, or just let them be dirty? While strict hygiene will remove some beneficial bacteria, it will also decrease exposure to pathogenic ones, as well as viruses. Seems like we have to chose between everything or nothing; we can't filter the bugs we are exposed to.
     
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  6. Sasha

    Sasha Fine, thank you

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    That's the impression given by that section, but maybe he'll elaborate later (that was only on page 5!).

    Hard to know!
     
  7. Sasha

    Sasha Fine, thank you

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    Still reading Michael Blaser's "Missing Microbes".

    (p. 30): Through their products, your microbes help you maintain stable blood pressure via specialised receptors located in your blood vessels [...]. These sensors detect small molecules created by the microbes that line your intestine. Responding to these molecules affects blood pressure. Thus, after eating, your blood pressure may go down. Could we one day have better treatments for high blood pressure by harnessing these bacteria? Very possibly.​

    I think at least one (@Sushi?) PWME on this thread has had an improvement in their orthostatic intolerance with RS. I had been wondering what the mechanism could have been. I wonder if this could be something to do with it?
     
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  8. Sasha

    Sasha Fine, thank you

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    Been googling a bit on this...wondering if it's possible that PWME are missing some bacteria that would normally help regulate blood pressure, leading to orthostatic intolerance.

    http://www.medicalnewstoday.com/articles/256919.php

    In a new study, US scientists suggest gut bacteria form part of a complex system that maintains the body's blood pressure. They have discovered a specialized odor-sensing receptor normally present in the nose can also be found in blood vessels throughout the body. In the gut, the receptor reacts to small molecules generated by bacteria by raising blood pressure. The study may aid understanding of how antibiotics, probiotics, and changes in diet affect blood pressure.

    The team, led by researchers at The Johns Hopkins University and Yale University, write about their work, which they conducted in mice and lab cultures, in the 11 February online issue of Proceedings of the National Academy of Sciences.

    First author Jennifer Pluznick, assistant professor of physiology at the Johns Hopkins University School of Medicine, says they were surprised to find that gut microbes contribute to blood pressure regulation and health:

    "There is still much to learn about this mechanism, but we now know some of the players and how they interact," she explains in a statement. Olfactory Receptor 78 Present Throughout the Body Receptors are proteins usually found on the surfaces of cells. They bind and react to selective molecules, rather like a lock can only be opened by a specific key. The specific molecules are chemical signals that direct the cell to do something, such as divide, die, or allow specific materials to enter or exit the cell.

    A few years ago, Pluznick found odor-sensing receptors (thought to exist only in the nose) in the kidneys, an event she describes as a "happy coincidence".

    She and her team found one of these, olfactory receptor 78 (Olfr78), was dotted around the major branches of the kidney's artery and also in the small vessels or arterioles that lead into the kidney's filters.

    When they looked further, they found Olfr78 throughout the body, sitting in the walls of small blood vessels, with more of them in the heart, diaphragm, skeletal muscle and skin.

    Short Chain Fatty Acids Produced by Gut Bacteria Influence Blood Pressure
    Intrigued by their find, Pluznick and colleagues set out to determine which molecules bind to Olfr78. They programmed cells to express the receptor on their surfaces, and rigged them so when a molecule bound to it, it triggered the reaction of a light-emitting chemical. So every time the cell "lit up", it meant that particular molecule had bound successfully to Olfr78.

    A series of tests with different molecular cocktails revealed that Olfr78 only bound to acetic acid, more commonly known as vinegar.

    Further tests revealed that propionate also binds to Olfr78.

    Acetic acid, its derivate acetate, and propiniate, are part of a family of molecules called short chain fatty acids (SCFAs). SCFAs are produced in the large bowel as a result of bacterial fermentation of soluble fibre. They are then absorbed into the bloodstream, where they can interact with Olfr78.

    When mice missing the Olfr78 gene were given SCFAs, the scientists observed that their blood pressure went down, suggesting SCFAs usually cause it to go up. But when they gave SCFAs to normal mice that had the Olfr78 gene, they were surprised to find this also caused blood pressure to go down, although not as far as with the other mice.

    Complex, Contradictory Relationships Between SCFAs and Receptors
    The team decided to find out what would happen if they reduced all sources of SCFAs available Olfr78 in the mice, including that produced by the gut bacteria.

    So they wiped out the gut bacteria in the mice by putting them on a three-week course of antibiotics, and monitored their blood pressure. The normal mice showed little change, but blood pressure in the mice lacking Olfr78 went up. This suggested the relationship between Olfr78, SCFAs, and blood pressure was a bit more complicated than it looked at first: were other factors involved?

    The team eventually discovered a non-odor-related receptor, Gpr41, also plays a role. Gpr41 also binds to SCFAs, and when it does, blood pressure goes down.

    So there were two contradictory effects going on: when they bind to Olfr78, SCFAs make blood pressure rise, but when they bind to Gpr41, blood pressure falls. However, the effect of Gpr41 is stronger, so an increase in SCFAs results in an overall decrease in blood pressure.

    Pluznick says there are "many players involved in the maintenance of stable levels of blood pressure", and they've found just some of them.

    "We don't know why it would be beneficial for blood pressure to decrease after eating or why gut microbes would play a part in signaling that change. But our work opens the door for exploring the effects of antibiotic treatments, probiotics and other dietary changes on blood pressure levels in mice, and perhaps eventually people," she adds.

    Grants from the National Institute of Diabetes and Digestive and Kidney Diseases, and the Leducq Foundation, financed the study.

    An animal study published in the Journal of Proteome Research in 2012, suggests that bacteria living in the large bowel may also play a role in obesity by slowing down the activity of energy-burning brown fat.

    Written by Catharine Paddock PhD​
     
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  9. Vegas

    Vegas Senior Member

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    You'd have to give me a bit more information, have you been diagnosed with SPS (Stiff Person Syndrome)? There is an associated CFS co-morbidity that involves the GABA-glutamine cycle. Hypothetically, the right prebiotics could help.

    Do you have food sensitivities/intolerances? Anything that makes this worse, like phenolic compounds?
     
  10. Vegas

    Vegas Senior Member

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    A spoonful a day, not sure of the CFU on this, but it is perhaps in the tens of billions. No, I don't use this for the CFU, but rather for the species and the associated properties that result from this fermentation without oxygen. I can't tolerate much more because of the bacterial displacement it causes, which is noticeably more proximal. By this I mean that I experiences lots of lymphatic soreness in those lymph nodes that communicate with the small intestine, including those along the flanks/lateral ribs. This is distinctly different than the prebiotics that stimulate colonic organisms.
     
  11. Vegas

    Vegas Senior Member

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    Lots to talk about here. I can only touch on some of this today.

    Good stuff on the brain fog, although we would need to add some a number of other contributors to this.

    I do not think that there is evidence of lactic acid deficiency in ME/CFS. We know that many with CFS suffer from metabolic acidosis, as result of mitochondrial dysfunction, and D-lactic acidosis, both require the same infrastructure for metabolism. Commonly in ME/CFS there is what may be considered an overabundance of LAB, but truly there is great variability and it is hard to generalize. I believe with inflammatory disease processes you would find an overabundance of those organisms that rely on homofermentative pathways, which can result in accumulations of lactate at the expense of acetate and butyrate. In reality, the organisms that predominate respond to the combination of all factors that promote their prosperity, pH, fermentable substrates, levels of oxygen, other carbon sources, but you are right that the carboxylic acids are very important.

    Yeast probably does play a role in mitigating the effects on the host in D-lactic acidosis. I think this is a reasonable hypothesis.

    Scand J Gastroenterol. 2005 Oct;40(10):1246-50.
    Yeast mediates lactic acidosis suppression after antibiotic cocktail treatment in short small bowel?
    Bongaerts G1, Severijnen R, Skladal D, Bakkeren J, Sperl W.
    Author information
    Abstract

    During acidotic periods in a girl with a short small bowel, very high D-lactic acid concentrations were measured in blood and urine; the patient's characteristic faecal flora contained mainly lactobacilli, and during antibiotic cocktail treatment also many yeasts. In this case report we sought to understand the beneficial effect of the antibiotic cocktail. Microbiological analysis was performed in faecal samples. Total lactic acid in serum and urine was studied using capillary gas chromatography-mass spectrometry, and D- and L-lactic acid in serum and urine by enzymatic assay. The results were coupled to patient's condition. Antibiotic cocktail therapy reduced the acidosis-associated symptoms, faecal lactobacilli and D-lactic acid production, but simultaneously the antibiotic therapy strongly increased the percentage of yeast in the faecal flora. Four to six weeks after each course of treatment the percentage of yeast decreased, whereas the percentage of intestinal lactobacilli increased; D-lactic acid also simultaneously increased in blood and urine. The patient felt well and showed a high percentage of intestinal yeast, but she often suffered from acidosis owing to a high percentage of lactobacilli. The yeast was identified as the pathogenic Candida glabrata. From the mentioned data together with data from the literature it was concluded that during several weeks the selected pathogenic yeast, C. glabrata, acted as a microbiological and metabolic buffer. Shortly after the course of antibiotic treatment this intestinal yeast strongly competed with the intestinal lactobacilli and thus prevented renewed rapid growth, massive D-lactic acid production from glucose and consequently also D-lactic acid-associated acidosis. The emergence of this yeast led us to consider probiotic lactobacilli or yeast for therapeutic use. The lack of knowledge regarding bile acid-deconjugating activity in both lactobacilli and probiotic yeast means that a final recommendation is not yet possible."

    Those WITHOUT ME/CFS do not suffer from the same energy limitations that undermine the conversion and utilization of lactate. You can efficiently utilize lactate because you have a fully functional PDHC. This changes the equation and prevents one from looking at normal physiology and chemistry, we have fundamentally different energy metabolism and ability to convert lactate back to pyruvate and usable energy.

    D-lactate is a condition that is also found in short bowel syndrome and hepatic encephalopathy and is strongly associated with cognitive dysfunction in all three. This condition can be readily exacerbated by providing glucose, which has a number of consequences, including not just the overgrowth of organisms that produce lactate, but it shifts the metabolic output away from acetate. Lactate precursors have the same effect.

    I have no doubt that aggressive LAB supplementation can benefit many people, but there are quite a few considerations. You spoke of benefits you received when yeast was displaced, I think you might find it interesting that the autolysis of these fungal cell walls will exponentially expand certain LAB populations.

    With regard to the lactate shuttle hypothesis, I think that there is a different model that applies to conditions marked by high oxidative stress. I invite you to look at the newer research that suggests that this lactate has negative effects and is used for the growth of cancer cells.

    Here is a pretty good overview: http://www.jci.org/articles/view/69741
     
    Last edited: Jul 15, 2014
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  12. Vegas

    Vegas Senior Member

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    So can you list the species of LAB in the yogurt and probiotic? L. Plantarum is a heterofermentative organism, I would like to compare this with the yogurt and the specific organisms in the probiotic you took.
     
  13. Ripley

    Ripley Senior Member

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    I don't know what was in the offending yogurts/kefirs and kombucha, as each of them I obtained at a farmer's market.

    But here are the ingredients in Primal Defense Ultra:
    Interestingly, Garden of Life's standard/non-ultra version of Primal Defense appears to be the same thing without the Saccharomyces Boulardii (I think it's cheaper too). I suppose I could buy some and take it to see if it's just the Saccharomyces Boulardii.
     
    Last edited: Jul 15, 2014
  14. Aileen

    Aileen Senior Member

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    @Vegas Which vegetables are you fermenting? What types of probiotics does this give us?

    Does this method produce any kind of odour? I have mcs and would not be able to tolerate fermenting vegetable odours wafting through the kitchen! We can't even cook or heat up food in the house! :(

    If it is odour-free, what method exactly are you using? Is any special equipment required for this? Perhaps you know of a website that clearly explains how it is done?

    Since this is getting off the RS topic, would you please respond on this thread Probiotics: using fermented foods instead of (or in addition to) supplements

    Thanks
     
  15. jepps

    jepps Senior Member

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    If I have In Europe no opportunity to buy raw potatoe starch. What is the best alternative? I take psyllium husks, acazia faser, citrus faser and baobab powder and konjac root.

    I eat paleo with lots of vegetables (carots etc.), berries but no fruits, a little seeds.
     
  16. dmholmes

    dmholmes Senior Member

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    Green banana flour.
     
  17. Sasha

    Sasha Fine, thank you

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    I haven't been able to source this in the UK. If anyone finds a source in Europe, pl
     
  18. jepps

    jepps Senior Member

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    In Germany we have potatoe starch which is produced with temperatures of 30 degrees (68 F). Is this to much for a working RS?

    This thread is so very interesting. Thank you all for your posts, and thank you, Ripley, for the thread and your posts, and Gestalt, for your posts.

    Summary: when I have systemic Candida and other pathogenes, and eat Paleo, and have very low lactos and bifidos in stool: to lower ph in stool and to feed my colon flora, I have to take RS from potatoe starch or green banana starch, up to 4 tb/day. Fibres (f.ex. Oligofructose, acazia, psyllium) alone isnĀ“t much enough. Is this right? Or can I only with prebiotics create an acidic flora?
     
    Last edited: Jul 16, 2014
  19. zzz0r

    zzz0r Senior Member

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    I am following an anticandida diet, and it is mentioned that milk and yoghurt should be restricted. I just do not understand why is that. It is mentioned that lactose must be avoided but why? Also are there any bacteria that will counter the effect of LAB?

    Here is the link of the things that I must avoid eating
    http://www.thecandidadiet.com/foodstoavoid.htm
     
  20. Christopher

    Christopher Senior Member

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    I don't think that diet is based on science.
     
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