Eating papaya with protein rich meals gave me a significant improvement in health

Discussion in 'Diet and Improving Your Gut' started by dejurgen, Jun 16, 2018.

  1. dejurgen

    dejurgen Active Member

    As I try to up NADPH and glutathione recycling by stabilizing blood glucose levels and selectivly using cold treatements I had to look for a reliable source of starch and a low glycemic source of sugar, preferably rich in glucose.

    Apple has low glycemic index, in part due to a high fructose to glucose ratio. But as (I thought) it is reknown for being well digested and healthy (an apple a day keeps the doctor away) I'd try eating some more apples as breakfast.

    I had been eating less fruit apart from papaya for some time. Now my source of papaya was gone I switched to supplements and ate more other fruit again. It went OK-ish until one day I ate two small apples with combined wheight of a big-ish apple as breakfast and nothing but that as breakfast. Within half a day stool was very loose close to dhiarea and abdominal pain peaked high. It was like someone had put a few knitting needles in their entirity in/through my intestines. What a familiar feeling from the period before my papaya try! The next day (very likely) both my adrenals hurt a lot too. Worst of all: significant less energy and a lot lower/more depressed mood.

    Not being truely sure as apples were the cause the next two days I ate a small apple and some oats as breakfast. Problems reduced but did not subside. In a delayed fashion (very likely) my liver started to hurt again. Another familiar sensation before.

    That surprisingly let me to fructan intolerance. Near all of fructans. It fits well with my family history, better then the idea of intolerance to proteins combined with sulphur rich foods. My mother hasn't a strong problem with fructose, but still admits a whole apple on an empty stomach is troublesome and not a good idea. So it's probably the same problem but with a lower treshold. Just as much as her I too feel that apple combined with some other food is better tolerated. It just happens that with fructose malabsorbtion the fructose gets better absorbed when there is a higher amount of glucose going with it. So bread/oats with aplle being less troublesome makes sense, and indicates no dominant gluten intolerance. Good news for a change as it adds at least some foods to the safe(r) list ;-). Wheat and some grains is higher fodmap too however, oat, rice, quinoa are not.

    Other problematic fructan foods in my family are onions, leeks, many sorts of cabbage...

    I had a few remaining mysteries:
    A) what had papaya to do with the improvement; it was more then just eating less apples as I had weeks I didn't ate them before?
    B) some sort of cabage are low fodmap, but in our family they all cause bloating to varying degrees
    C) turnips, celery root and black salsify are supposed to be low fodmap but they are really bad ones; many recommend them as being excellent for diggestive (fodmap) problems but yet a few sites mention them as bad for bloating
    D) how can fodmap problems cause low energy and poor mood so quickly?

    For A) I started with thinking that one intollerance often lowers theshold for other intolerances, so I could have multiple and improving one increased threshold for the other? Or papain breaking down proteins gave enzymes better access to the fodmap contents in cells, increasing effective digestion time? But the answer was unsatisfying.

    For D) I found papain and other protein digesting enzymes can interfere with inflammation (decrease) and immunity (increase), so a change in dose going to supplements might be important; yet this felt inadequate. Maybe it was the bacteria producing hydrogen rather then methane, but would that be poisonous? From there I got to hydrogen sulfide.

    There is a variant of ibs/sibo that passes hydrogen breath test by making hydrogen sulfide rather then hydrogen. And hydrogen sulfide is rather poisonous. In addition the production of hydrogen sulfide decreases sulphur uptake from the diet, and sulpur is needed for producing glutathione (important in numerous things in ME including reducing ROS and protein misfolding) and taurine (important for reducing protein misfolding) and insuline (blood sugar control) amongst others. This is a nice link with a video in it https://drruscio.com/sibo-scenario-breath-test-cant-detect/

    All cabbages are rich in sulphur, so that solves the "why do all cabages cause severe bloating rather then only the high fodmap ones" (question B). As a plus, Onion, leeks, garlic... are both high fodmap and high sulphur food. They are superb at causing bloating in our family.

    Turnips and black salisfy contain inulin, another polysacharide. And Celery root contains pectin-based polysacharides. They're likely less commonly a problem as they're considered low fodmap despite it. But it could answer question C).

    Comming back to A), what has papin to do with it? Sulphur is most often part of proteins. As papain starts very early diggesting proteins in the stomach, protein diggestion likely is a lot more complete when food reaches the large bowel, home of most of the gut microbes. That likely means that plenty of sulphur containing amino acids are already absorbed before reaching it. That's a double plus: more sulphur for the own body and less food for the hydrogen sulphur producing bacteria. That's less bloathing and less toxic hydrogen sulfide to deal with.

    Now why would eating apples, low in sulphur content cause a spike of problems? Well, the basterd buggers probably need both a good source of undiggested carbs (fructose?) and sulphur. I'll work on that one to see how far it gets me and then and only then try probiotics to drive them out. Don't want to mask the effect of changes too much ;-).

    As too supplements: I take a cheap and very local brand containing 50 mg of papain, 50 mg of papaya pulp (probably because it requires less expensive/pure extraction of papain this way) and 10 mg of bromelian. Seems to work somewhat, but I'm not the best placed person to test his now.
     
    Last edited: Sep 6, 2018
  2. Not dead yet!

    Not dead yet! Well-Known Member

    Thank y ou SuzyDee for an in depth discussion on this issue. This quote really resonated with me because

    1. My TG was up above 500 and I was having significant pain that might have been either gut or pancreatic pain

    and

    2. My instinct tells me that I"m in a catch 22. I'm unable to get much exercise, so I'm inactive. My thyroid has only just begun to be properly treated, and therefore, for these and other reasons I'm obese. I carry my weight forward of my trunk, in much the same way that men sometimes get a 'beer belly' except I"m a woman. My hormone imbalances might have a lot to do with that. I 'feel' that my organs are being 'crushed' somehow and I often do backbending exercises, sometimes hanging over the edge of my bed so my organs get more room. It feels wonderful, but the weight is still pressing down on them.

    So my question is, could my centered obesity be causing a similar effect as CMI? I used to say I had some kind of pseudo ileac type of thing.
     
  3. SuzyDee

    SuzyDee Member

    Too much body fat can be an inflammatory thing to alter ion channel function and result in gut ischemia but I would think high triglycerides (and this probably along with high homocysteine levels?) could be a more likely case too in causing plaque stenosis in the mesentery arteries. A Doppler Ultrasound to check your mesentery artery velocities is a simple test to do to check for this.
    Stenosis or any of the abdominal vascular compression syndomes can cause an audible abdominal bruit sound too (but not in all cases) so an even quicker check is just to have have any doctor listen to your abdominal sounds for any evidence of this.
     
  4. Not dead yet!

    Not dead yet! Well-Known Member

    Doppler was done when I had blood clots, but i think they were concerned about my heart so maybe not looking there.

    Every bowel test I've ever had said I was "normal" but with abnormal amounts of gas that were not clearing. I got tired of drinking barium after a while and gave up. I think at this point my gastro is in "wait until I have to operate on you" mode. I think the gastro professions is extremely lazy at providing helpful solutions. I don't blame individual doctors, but there seems to be two modes of operation:

    a. you're fine, just normal bellyache

    and

    b. OMG you need immediate surgery
     
  5. dejurgen

    dejurgen Active Member

    I don't know if American units are the same as European ones. We use mg/100ml IMO. I did find old test results, but they're upstairs now. In 2010 my TG were over 360. Now they're at 75. I'll describe what did that for me:
    • Taking a low amount (half a pill daily, at evening) of the wright statines. I had to try several to get the cardiovascular risk factor down. Some statins reduced the good cholesterol just as much as the bad one and didn't reduce the cardiovascular risk factor. I know statins are under discussion, but that is not the point here. Result: TG went 210-ish
    • Getting away from the low to very low fat diet I followed for years in order to get my cholesterol within normal levels; eating double as much fat and more protein did reduce cholesterol somewhat and reduced TG a lot more. The reduction in cholesterol probably was due to lower TG levels that seem to contribute to bad cholesterol levels. Due to eating more fat my good cholesterol increased somewhat. The total effect did reduce the cardiovascular risk factor a lot. Although I ate very few sugar before and after the change, I before probably ate too much slow carbs still causing blood glucose problems, leading to my liver converting blood glucose to TG. Result: TG went 150-ish (edit, 100+ when checking this one)
    • Starting to eat papaya. Kinda weird, but I believe it may be due to A) having to reduce my caloric intake a bit as my food digested better. B) Eating less fruit and in smaller portions spread over the day, just a side effect of papaya being expensive so I did limit myself to just eat 3 times a day a small piece of fruit. Result: TG 75 now.
    B) sounds kinda weird too: eating less fruit to lower TG? It's supposed to be the opposite IMO due to the healthy fiber. But the body doesn't use fructose directly. It is converted into either glucose, lactic acid, glycogen or TG. If one eats a diet with lots of low GI carbs, glucose and glycogen will be allready plentifull, limiting conversion from fructose to those. Having ME, lactic acid is plenty too. That leaves conversion from fructose to TG as a main pathway IMO. Eating less has an obvious effect. Spreading fruit intake over smaller portions reduces the combined glucose-fructose peaks so a larger portions can be used rather then converted to TG.
     
    Last edited: Sep 16, 2018
  6. dejurgen

    dejurgen Active Member

    The past weeks I looked further into the question "why do fructans and sulphur based vegs cause so much problems and what is the link to eating papaya"?

    This post only describes my line of thinking, the following post probably gets closer to what is actually happening. First let me tell about another important observation I made:

    Together with strong increase in abdominal pain and a sudden onset of near-dhiarea after eating 2 small apples I also had blood loss in stool again. That was very familiar for me for many many years. Together with frequent nose bleedings, those symptoms did disapear when I was at worst of ME. I guess that's due to low blood volumes and blood flow. Getting better, nose bleedings happened a few times again, maybe a sign of better bloodflow. Both forms of bleeding may be increased by low vitamine K that appears to be common with gut problems.

    The blood loss in the stool was more then just a few drops the first time, closer to a small trickle. It wasn't due to the following swinging between dhiarea-ish and constipation-ish after the final onset, as the bleeding started wright at the onset of the first dhiarea fase before constipation happend. So constipation grinding-pressing the gut was not the cause. It's now about two weeks of some blood in my stool every few days even after adjusting diet to my previous one.

    So what could cause apples to cause a very likely larger scale damage to the gut lining up to the point of severe injury? Just some hydrogen production rather then methane by having the wrong gut bacteria fed didn't convince me. Is hydrogen that poisonness? Didn't think so. Was it that more plentyfull than methane production that it caused the gut to burst? Sounds unlikely to me, but plausible. That's why I did think in the direction of H2S producing gut bacteria: poisonness in tiny quantities, producing ischemia like results in the gut lining reducing reparation of the gut lining... and I also did find that H2S decreases production of mucus, thus decreasing production of the gut protecting layer. So H2S does make sense.

    So what is the role of papaya here? Well, the amount of blood loss the first time did indicate sizeable gut damage, leaving options for undigested protein to enter the blood stream. And undigested proteins in the blood stream is a bad thing. Before the apple incident I may well have had smaller scale gut damage allowing undigested proteins to enter the bloodstream. These smaller scale wounds just didn't show up in the stool I guess. So eating papaya reduced undigested proteins entering these micro wounds.

    Still, why was eating 2 small apples so bad? And what has it to do with sulphur rich vegs and proteins? My ideas so far where that the bad bacteria floorished only if they had a good source of carbohydrates, sulphur and nitrogen (protein). I found a paper that saw fermentation in sheep increasing by 100% when adding both S and N to their diet. In sheep that is a good thing, in humans less so.

    Still, many people eat fodmaps and are healthy with it. And most of fodmaps except fructose are not supposed to be diggestable by them neither, so did eating 2 small apples cause SO much more undigested fodmaps to end up in the large intenstine so that the bad bacteria could florish? It sounds unlikely as healthy people on a fiber rich diet feed their gut bacteria more fodmaps then I do.
     
    Last edited: Sep 16, 2018
  7. dejurgen

    dejurgen Active Member

    After reading on fructose intolerance, I do believe fructose malabsorption to be a likely candidate for the specific mechanism. Fructose malabsorption is a rather strange thing:

    People being unable to transfer fructose from the gut to the blood? After all, fructose is very common in nature and is a very simple sugar. I can hardly imagine humans didn't develop a riggid mechanism to absorb fructose after millions of years, while glucose absorption is so unproblematic. Even weirder, fructose seems to absorb so much better if fructose-to-glucose ratio is below 1. That seems to be no fault but deliberate design/evolution to me.

    So I looked further into fructose malabsorbption and did find https://forums.phoenixrising.me/index.php?threads/think-ive-cured-fructose-malabsorption.14749/ and https://www.healthrising.org/forums/threads/fructose-malabsorption.3968/ "According to Dr. De Meirleir 45.8% of his ME/CFS patients has Fructose Malabsorption."

    The first link learned me "blurb says N-A-G combines with mucin secreted from goblet cells to form the glycocalyx, a protective layer of glycoproteins and polysaccharides that lines the digestive tract." That hit me.

    Wikipedia https://en.wikipedia.org/wiki/Glycocalyx#In_the_digestive_tract learned that:
    In the digestive tract

    A glycocalyx can also be found on the apical portion of microvilli within the digestive tract, especially within the small intestine. It creates a meshwork 0.3 μm thick and consists of acidic mucopolysaccharides and glycoproteins that project from the apical plasma membrane of epithelial absorptive cells. It provides additional surface for adsorption and includes enzymes secreted by the absorptive cells that are essential for the final steps of digestion of proteins and sugars.
    Other generalized functions


    • Protection: Cushions the plasma membrane and protects it from chemical injury
    • Immunity to infection: Enables the immune system to recognize and selectively attack foreign organisms
    • Defense against cancer': Changes in the glycocalyx of cancerous cells enable the immune system to recognize and destroy them.
    • Cell adhesion: Binds cells together so that tissues do not fall apart
    • Inflammation regulation: Glycocalyx coating on endothelial walls in blood vessels prevents leukocytes from rolling/binding in healthy states.
    Now That's plenty of things that are important for ME/gut problems! Looking up mucopolysaccharides lead me to it being another name for https://en.wikipedia.org/wiki/Glycosaminoglycan
    "Glycosaminoglycans[1] (GAGs) or mucopolysaccharides[2] are long unbranched polysaccharides consisting of a repeating disaccharide unit."
    "Based on core disaccharide structures, GAGs are classified into four groups.[5] Heparin/heparan sulfate (HSGAGs) and chondroitin sulfate/dermatan sulfate (CSGAGs) are synthesized in the Golgi apparatus..."

    => Disaccharide structures containing sulfur are a vital part of a layer that both protects the small intenstine, boosts enzyme functioning and increases effective gut absorption surface area??? ?!?!?!?!?!?!?BINGO?!?!?!?!?!?!?

    So this gets me following rough hypothesis:
    • Humans have evolved to not absorb fructose well if fructose to glucose ratio is bigger then 1.
    • In near the entire past of human kind, fructose to glucose ratio being bigger then 1 only occured during fall: when fruit was very plentifull.
    • Maybe this (strong) reduction in absorption of fructose to glucose ratio is bigger then 1 evolved to unload the NADPH system needed for recycling glutathione during fall. Winter fat production by eating large amounts of fruit consumes very high amounts of NADPH suppressing glutathione production. If one has the wright gut bacteria, one can pass some fructose to them and let them produce healthy short chain fatty acids from it and offer them to the gut to abbsorb. Nice and efficient. Or this mechanism developped for other reasons; non vital here.
    • Anyway, if too much bad gut bacteria would have developped in the past due to this fall overload of fructose, it would have been wiped clean during late winter till early summer due to the lack of ripe fruit. So development of specific fructose gut bacteria and transmission from mother to child would be strongly reduced by this lack of fructose rich food all year round. A high ratio of fructose to glucose is needed to pass much of fructose to bacteria in the large intestine.
    • Now we have year round ripe fruit, advised to eat a lot because it's healthy. And the food industry drops fructose in nearly every single food as it's cheap and adictive. Worse, soda with sucrose (already bad with a ratio of 1) is replaced with soda with fructose as it's cheaper and sweeter. And it's a liquid! So it passess the small intestine at record speed, providing near zero reduction in fructose before the liquid enters the large intestine.
    • Now why would this fructose be so bad? Many other fodmaps reach the large intestine too. Well, when one has a moderate meal with moderate starch/sugar then glucose is nearly fully uptaken by the small intestine. Larger amounts of fructose or bad ratios may allow more fructose to slip to the large intestine. Having daily high caloric food loads, another recent thing, increase both amounts of fructose and glucose passing through the small intestine and reaching the large intestine. Remains the question: why are fructose/glucose so different from other fodmaps? They are very simple monosaccharides! That means that they are far more easy to use by bacteria then di- or polysaccharides (still a lot of "work" on them needed to transform them into usable components) meaning they very likely allow much much faster bacterial multiplication rates then the di- and poly ones allow.
    • An explosive multiplication rate of ?some? types of bacterias allows for far easier bacterial disbalance then a slower growth where bacteria have to compete far more with each other during a longer time. Result: a few species of bacterias may dominate rather then having a wide range of different bacterias
    • Such fast explosive growth of bacteria may ease back-flow of some of them into the small intestine. If constipation is present that would occur even faster. Some weakness of the "valve" blocking reverse transfer would be a bad thing as well.
    • If some of those bacteria that grew at explosive rate would colonise the small intestine, they would get a further headstart compared to other species, further increasing disbalance.
    • Now, what's all of this to do with severe gut damage? Well, this theorethical mechanisms eases both gut monoculture and SIBO. But bacteria finding "other" food sources in the small gut would further increase their competitive advantage. Bacteria able to "eat" mucopolysaccharides would be able to dominate very well. That may well be bacteria that do well on both simple sugars like fructose/glucose, di- and polysaccharides and sulfur as mucopolysaccharides are rich in sulfur.
    => hence year round consumption of fructose rich food and more calories then strictly needed gives a very fertile ground to a monoculture overgrowing both small and large intestine, and sulfur rich food makes it even a more productive ground for disbacteria IMO. Note that "free" sulfur seems to be worse then "bound" sulfur".
    => Such "fructose aided" SIBO would not only produce bloathing but worse, increase H2S far beyond "normal". Next to being poisionness it also creates iscchemia in the gut amongst others and it decreases mucus regrowth weakening gut lining.
    => Such "fructose saided" SIBO could allow growth of glycocalyx destroying bacteria, further weakening the gut and decreasing food absorbtion a lot; destruction of the glycocalyx alone would be a very bad thing in already weakened ME patients
    => The above would create sufficiently damage to lower the threshold for poorly digested proteins into the bloodstrem a lot, creating all kind of further havoc with imune problems, auto immunity and ER/protein misfolding stress.

    Gluten intolerance would further weaken the already weakened gut. Lactose intolerance would feed another breed of potentially bad bacteria, as it's a disaccharide that is easier to use by bacteria then more complex ones. So it kinda connects many food intollerances and offers some explanation as to why one intollerance lowers the bar for others to join the party.

    The difference in pain in the gut did also deter me from using diaphragma breating after the apple incident as it was unpleasntly painfull, so poor breathing and my unaibility to use diaphragm breathing before may be an indirect result of all of this (unconsionous avoiding it to decrease pain levels).

    I don't know if anything of it is new or not, but I'd love to hear your comments :).

    Dejurgen
     
    Last edited: Sep 16, 2018
  8. dejurgen

    dejurgen Active Member

    Reading further upon Athena's results in https://forums.phoenixrising.me/index.php?threads/think-ive-cured-fructose-malabsorption.14749/ Athena wrote further on page 3:
    "It is such a bummer!
    I have been diagnosed with hypothyroid, and when you have that condition, your body keeps laying down glucosaminoglycans - not just the amount you need, but on and on. It puts them in your intestine (where maybe they don't do any harm?) and also in your joints, where they are essential but haing too much causes terrible pain!
    So I have had to stop taking the glucosamine supplements."

    It relates to kinda question/thoughts I had yesterday: too much glucosaminoglycans resemble a lot of symptoms many of us have: too much deposition of hard too remove deposits in connective tissues, pain, impaired motor function (both resulting from compressed nerves), too high cranial pressure, joint problems, hart problems by deformed hart valves, respiratory infections... see https://en.wikipedia.org/wiki/Mucopolysaccharidosis for the extreme genetic form of it (rather then the form caused by hypothyroid Athena discusses).

    It certainly does not discribe our disease, but there is some commonality. I just wondered how too few glucosaminoglycans in the intestine could relate to this opposite problem of too high production.

    Athena may just have provided the answer: if she would actually produce more of this protective layer (as she believes having hypothyroid), it should be protective rather then causing intestine problems. And using supplements to lay down an extra thick layer should be less necesary then in healthy people IMO.

    So could both at the same time: more production of the body and "adding an additional layer" by taking supplements be benificial if there is already more then in a healthy person who has no fructose intollerance?

    It reinforces my idea that the layer is getting eaten by bacteria. She may produce a thciker layer and that may exactly be the cause of it being eaten by the bacteria: more food for a potential bug that eats the stuff, so more change of developping a potentially harmful monoculture of glucosaminoglycan eating bacteria.

    It reminds me of my boxhedge: since two years caterpillars are doing there best to eat my hedge into destruction. They have very few natural enemies over here so I fight them with a variaty of things. But the point is, being resonably succesful fighting them I still have to (let) trim the hedge every year as it keeps growing. The buggers just could eat the excess and save me the effort of trimming and let the needed core parts of the hedge untouched. But they are not those friendly bugs just eating what needs to be cut. They just eat wholes in it and leave other parts that are too thick untouched.

    Just as much, I guess those supposed nasty glucosaminoglycan eating bacteria don't neatly trim only the excess layer one at a time, taking a nap until there is more excess to eat. They rather will form local colonies eating everything underneed them. So they basicly make the layer resemble Swiss chese.

    Supplementing with N Acetyl Glucosamine 750mg could fill these holes it it attaches better to bare cells rather then to an already thick layer. So indeed after having too much own production of it supplmenting it further *might* be beneficial.

    It doens't need to be a genetical defect. I can imagine it would have been a nice adaption in medival Europe where grains provided the bulk caloric needs. It would have converted part of the excess glucose to glucosaminoglycans, thereby reducing blood sugar spiking, increasing glutathione recycling and improving the thickness of the protective layer against the fairly aggressive effect of wheat/lectines... that were introduced with the farmers diet. Big difference then was: apart from a few nearby fruit trees that provided fructose for a short period of time every year they had nearly no real good source of fructose (nor sucrose as sugar cane was far too expensive for the commoner and sugar beet didn't existed yet).
    As this excessive thick layer is likely gradually moved/slided toward the large intestine, it would provide food for hopefully healthy gut bacteria producing desirable short chain fatty acids. That would convert excess carbs to the very desirable SCFA and increase gut health as long as the microbiome isn't fed fructose/fast sugars/high caloric diets allowing some bacteria to grow at an exponential rate.

    So maybe that'll give me some clues? Worth a try.

    note: Thyroid problems are common in ME. Thyroid problems are also related to NADPH generation and therefore to oxidative stress. Imflamation on the other hand does decrease fructose absorption. So an increase in (temporary) inflamation may decrease fructose absorption. With fructose rich diets that means more fructose is ending up in the large intestine, potentially creating a very fast boom in harmfull bacteria. Once they find there way up in the small intestine, they lock the gut into a state of stronger imflamation and a large general malabsorption of food including fructose further feeding fructose and even more undigested food to the large intestine... ... and the SIBO does require a lot of chronic effort from the imune system. That does increase chances for auto-imunity but it also leaves less part of the imune system available to clean up the other "overproduction" of glucosaminoglycan in the body, potentially increasing joint problems, connective tissue problems, hart problems, respiratory problems... ...it may even make the valves between stomach and small intestine and between small and large intestine malfunction (by deforming it with glucosaminoglycan deposits so it's not a good fit any longer) further entrenching the digestive problems...
     
    Last edited: Sep 17, 2018
  9. Not dead yet!

    Not dead yet! Well-Known Member


    Less fruit to lower TG is not reverse at all. TG is the fat made by the liver from excess carbohydrates. Since many of us suffer from metabolic inefficiency of one kind or another, it makes sense that our TG levels would be high since they're not being used, as they would be in a normal body.

    Lowering carbs lowers TG, that's been my experience, that's also the opinion of my MD. AIP, Paleo, Keto, and a lot of new diets designed to help lower inflammation are also well known to lower TG. Of those, Paleo is the only one where you can eat fruits much, but even there, it's not central.
     
  10. dejurgen

    dejurgen Active Member

    Update. I believe I made a breakthrough regarding the enigma of my strange gut behavior. It feels in fact like it points clearly to a or the dominant driver in my disease. Rather then jumping to the conclusions I'll gradually talk about how I came to this as it's quite easier to understand what I mean if one can follow my reasoning I believe.

    ##########################################
    note: it ain't an easy read for sure; it wasn't easy to produce either and at this time I can't add more structure. I just barely touched the subject by now.

    just read the last section in # to decide if it's worth the effort
    ##########################################

    Let me first start with this however:

    The fruit papaya is better then the current papain supplements I take by a big margin. I can't tell they don't work, but I was stuck in improvement and oscillating around an invisible ceiling for some time until I found a new source of papaya. With changes in season I had difficulties finding fresh fruits. The result: within several weeks after I reverted back to the full fruit I saw a clear line of improvement again and it has stayed that way.

    Now the process of coming to these new ideas:

    For some time I have been wondering if all diet/gut/intolerance related pain is actually gut pain. There was some clear pain in the adrenals I recognized before. But just as one has to learn that pain originates from the adrenals by linking certain stressors together with theory (such stressor does likely trigger adrenal over activation), feeling exactly if it is part of the stomach or part of the bowel that hurts isn't always easy. And sometimes I just assume it is the bowel near the stomach that hurts if it makes no sense whatsoever that a certain action would let the stomach hurt...

    But then I revisited the idea of potentially having helicobacter pylori. In the past I had several experiences that resembled a more typical helicobacter symptom. But as said, how on earth would it make sense that eating 2 small apples causes such strong gut reaction if it were helicobacter doing something in the gut?
     
  11. dejurgen

    dejurgen Active Member

    There is some evidence that there is a correlation/interaction between helicobacter and gut inflammation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047323/, but it ain't very strong. Others proposed that helicobacter pylori interacts with a more typical bad gut bacteria to cause things like SIBO, IBS... in some cases.
    What I learned during this investigation:
    * Bad breath is caused by H2S producing anaerobic bacteria residing between the teeth and on part of the tongue.
    * Helicobacter pylori is an H2S producing anaerobic bacteria that may potentially survive mouth cavity, for sure the stomach and may or may not somewhat survive in the bowels.
    * The above means that, if helicobacter were involved in some way in many cases of ME as evidence suggests, potentially survival of it in the mouth opens a route of infection via saliva and "air born infected micro drops" by burping; this would open a route for non-genetically related people living close together like husband and wife to come both down with ME.
    * Other pathogens may follow a similar route of infection driven susceptibility to ME.
    * The idea of a 2 bacteria "coordinated" infection is a potential reality. If so, it would easier lead to my complex oscillation between constipation and diarrhea when triggering one of many food intolerances.
    * A rather crude and inaccurate idea is for example that helicobacter could survive to some extend in the middle of the "food mass" shortly after leaving the bowel. There the acidity may be for a longer time more favorable for helicobacter sustainment or development. That might trigger an initial bacterial related flushing of the small intestine. Likely wrong, doens't matter, just to show that the idea that helicobacter can't travel from stomach to small intestine is likely not absolute.
    * A 2 bacteria "IBS system" should show greater oscillations in gut and immune reaction, easier leading to instability and inability to resolve the problem quickly.
    * A 2 bacteria "IBS system" should make it a lot harder to study and to observe what triggers it as it would probably require certain foods or food constituents being eaten in combination or require a certain sequence of events.
    * If I had problems with helicobacter, my stomach lining very likely were damaged. Even if it weren't full sized peptic ulcers, there would probably be plenty micro-sized ulcers. Big ulcers just don't pop out of nowhere but likely there are plenty of small injuries that have each a low probability to grow to true peptic ulcers. That's comparable to cancer: it is said all people have micro tumors that appear and disappear but only if one manage to grow out of control it becomes cancer.
    * Anyway, a lot of micro damage would include plenty small open wounds allowing for undigested food to enter the bloodstream. That would be a bad thing. Using papaya, one of very few enzymes able to start digesting protein already in the stomach, could reduce the amount of undigested protein entering the blood stream that way. As undigested protein in the blood stream provokes a strong immune reaction, that is important here.
    * Some people use papaya for wound healing and cleaning. It is unproven, but they claim that the papain enzyme "eats away" dead (or sick) tissue and leaves (most?) of the healthy tissue alone. If so, it could help clean out both stomach and gut micro wounds and thus help them heal.
     
  12. dejurgen

    dejurgen Active Member

    Then I went back to the idea of a "2 bacteria IBS interaction". The idea to find one to clearly explain my situation just was too complex. But it lead me to the idea that one bacteria, like helicobacter, could be found and do some important stuff on places it isn't supposed to be or supposed to be of importance.

    So this is how I came to the following:
    * I was looking for bacteria that can be found at many places and different tissue. Some bacteria like staphylococci or streptococci might fit the bill, but they were to "general" to reason with for now.
    * I felt I had to look more for bacteria that could be present in the gut when they were not supposed to be there. Then I remembered the case of a college who had a lot of acne at age 50+ and then had a bowel surgery with a long revalidation time. Another college at the time explained why he needed it as follows: "you now the man has a lot of acne; appears he has something similar in his bowel and it had to be removed."
    * For me that was no small thing: on fathers side of the family I had inherited vulnerability to adult acne, on mothers side food intolerances are rampant. I know what happens when you "trigger" acne by either mechanical action (friction, pushing...) or even mildly aggressive skin care products: they grow and multiply and can be hard to get rid of once something keeps triggering them like dry skin in the winter.
    * Also I have to be careful when shaving. On my upper neck and under my chin I can have a rash like reaction of all very small mainly reddish pimples just underneath the skin. Hundreds of them pack together. Some of them might form a tiny with doth with pus that can break out if scratched upon just like "regular sized" pimples so I tend to believe it is indeed acne but one showing a patch of plenty of small red dots coloring the skin and making it rough.
    * I know two things about the above: once you have got them, they are hard to get rid of. I have got to shave me (that's why I go with the shaving system that irritates my skin the least) and textile worn close to the neck in the winter irritates it further. It can last for 2 weeks when being careful.
    * The other thing I know about it: it kinda resembles some pictures I've seen about gut inflammation. There seems to be different kind of pictures so different variants I guess.
    * Now imagine such patches of acne like infection on parts of the bowel. Add my many food intolerances (I'm still struggling identifying them all but I now know they really affect me) acting as a daily or more hours lasting irritant to my bowels and their potentially rough inflamed small pimples. Add rough pieces of food from time to time like parts of seeds or hard constipation grinding along these. On the skin, doing all of these inflames the pimples a lot more and might cause them to burst. And so we get another bacteria into the supposedly bacteria free small intestine. It just traveled from the skin pimples through the blood stream to the gut. No need to survive stomach acid.
    * Such infection of the gut wall itself would open up a far better portal to the blood stream and the rest of the body then a simple skin acne infection provides. The gut after all has a very good blood flow towards the body because it needs to provide very good transport of the absorbed food to the rest of the body. That alone would allow for sepsis. ME is often compared to as mild chronic sepsis.
    * If some "gut pimples" were to grow enough to pop then it would not only dump bacteria in the gut, but also allow for undigested gut contends such as other bacteria (in the large bowel for instance), undigested proteins, bacterial toxins... to enter the blood stream. That alone would provide a basis for sepsis too.
    * The gut is very thing. If so may "small pimples" were formed on it it would strongly decrease gut strength, allowing for easy damage and rupture of the gut wall. Result: leaky gut and frequent substantial amounts of blood found in the stool such as I have.
    * One could argue for sure a bacterial gut infection would show up in blood tests. But let reverse the question: have all approximately 45 million USA people with considerable amounts of skin acne an alarming blood test? That would be a hell of a lot false positives!!! Even if acne did give a marker in blood tests it would have been removed as "relevant, indicative" from test long ago because it's such a frequent condition.
    * If acne is so frequent, shouldn't it be unable to cause/trigger such serious conditions as ME? Let me start with saying that eating apples is a very common thing to do, but few have such strong reaction to it as I experienced this summer ;-). Nobody claims "extensive gut acne" is common. And described above there are good reasons to believe it could have far more serious effect in the gut then on the skin (where it is supposed to be if one has it).
     
  13. dejurgen

    dejurgen Active Member

    As these are big claims I had to look into the bacteria likely responsible for acne. There are several that can cause acne or acne like symptoms. Propionibacterium acnes is rather interesting. Main sources https://en.wikipedia.org/wiki/Propionibacterium_acnes and https://www.ncbi.nlm.nih.gov/books/NBK83685/ and https://www.tandfonline.com/doi/abs/10.1586/eri.11.137?journalCode=ierz20. Let's have a look:

    * https://www.ncbi.nlm.nih.gov/books/NBK83685/ has tittle: "Propionibacterium acnes and chronic disease". It's not talking about chronic having pimples ;-).
    * https://www.tandfonline.com/doi/abs/10.1586/eri.11.137?journalCode=ierz20 has tittle: "Propionibacterium acnes: infection beyond the skin"

    * first from wikipedia:
    * "typically aerotolerant anaerobic" -> can survive in the gut
    * "it can also cause chronic blepharitis and endophthalmitis,[6] the latter particularly following intraocular surgery." -> chronic eye infection is fairly different from skin acne so the bacteria is not a one trick pony /// particularly follow surgery? that's a typical ME onset trigger
    * The genome of the bacterium has been sequenced and a study has shown several genes can generate enzymes for degrading skin and proteins that may be immunogenic (activating the immune system). -> producing enzymes degrading skin and proteins? that's ideal for infecting the entire bowel, entering the bowel bloodstream very easy and severely weakening the bowel leading to both rupture and leaky gut syndrome /// activating the immune system? sounds common in ME
    * "It may also be found throughout the gastrointestinal tract.[9]" -> says it all, with reference
    * "C. acnes bacteria secrete many proteins, including several digestive enzymes.[16] ... ... They can also destabilize the layers of cells that form the walls of the follicle." -> A gut has very few layers of cells, so destabilizing them with digestive enzymes sounds a rather aggressive gut treatment
    * "The damage caused by C. acnes and the associated inflammation make the affected tissue more susceptible to colonization by opportunistic bacteria, such as Staphylococcus aureus. Preliminary research shows healthy pores are only colonized by C. acnes, while unhealthy ones universally include the nonpore-resident Staphylococcus epidermidis, amongst other bacterial contaminants." -> While talking about what happens at the skin, the idea can be extended with a bit of imagination to both "gut acne" giving bacteria that don't survive stomach acid a doorway to the gut and to acne creating "mirco caves with access to the gut" sheltering bacteria that wouldn't survive long enough if left wide open in the gut.
    * "Rarely, it infects heart valves leading to endocarditis, and infections of joints (septic arthritis) have been reported.[9" "It is a common contaminant in blood and cerebrospinal fluid cultures." -> quite some links to ME and FM IMO
    * "C. acnes has been found in herniated discs.[23] The propionic acid which it secretes creates micro-fractures of the surrounding bone."
    * "C. acnes can be found in bronchoalveolar lavage of approximately 70% of patients with sarcoidosis and is associated with disease activity, but it can be also found in 23% of controls."
    * "Moderate to severe acne vulgaris appears to be more often associated with virulent strains."
    * "C. acnes is an opportunistic pathogen, causing a range of postoperative and device-related infections e.g., surgery,[28] post-neurosurgical infection,[29] joint prostheses, shunts and prosthetic heart valves. C. acnes may play a role in other conditions, including inflammation of the prostate leading to cancer,[30][31] SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, sarcoidosis and sciatica.[32] It is also suspected a main bacterial source of neuroinflammation in Alzheimer's disease brains." -> nasty list including neurinflammation
    * "The emergence of antibiotic-resistant C. acnes bacteria represents a growing problem worldwide." -> ouch :-(
    * "
    Several naturally occurring molecules and compounds are toxic to C. acnes bacteria. Some essential oils such as rosemary,[48] tea tree oil,[49] clove oil,[50] and citrus oils[51][52] contain antibacterial chemicals.
    The elements silver,[53] sulfur,[54] and copper[55] have also been demonstrated to be toxic towards many bacteria, including C. acnes. Natural honey has also been shown to have some antibacterial properties that may be active against C. acnes.[56]"-> finally some good news ;-)

    From https://www.ncbi.nlm.nih.gov/books/NBK83685/:
    * "P. acnes, previously known by the name Corynebacterium parvum, has been studied extensively by immunologists for its ability to stimulate the reticuloendothelial system"
    -> according to https://medical-dictionary.thefreedictionary.com/reticuloendothelial: "reticuloendothelial system a network of cells and tissues found throughout the body, especially in the blood, general connective tissue, spleen, liver, lungs, bone marrow, and lymph nodes... ...These cells are concerned with blood cell formation and destruction, storage of fatty materials, and metabolism of iron and pigment, and they play a role in inflammation and immunity... ...Some of the cells are motile—that is, capable of spontaneous motion—and phagocytic—they can ingest and destroy unwanted foreign material." -> Note the picture: these cells include microglial cells!!! So this bacteria likely stimulates microglial cells!
    * "In the early eighties, certain bacteria, including BCG and P. acnes, were commonly used to stimulate the innate immune response against cancer in mice and human cells... ...One of the great ironies of this organism is that it is a powerful nonspecific immune stimulant that resides naturally in the skin; its role as an immunostimulant in humans is appreciated when cases of severe acne also develop adjuvant-type arthritis." -> So they were once used as "cures" against cancer /// they are also a powerful nonspecific immune stimulant; now powerful: yes something seems to set are immune system haywire; nonspecific: it sets large parts of the (innate) immune system on fire (and if both innate and specific immune system falters then there remains always a massive CDR reaction I think)
    * "the bacteria are normally present on the skin of a vast majority of individuals, irrespective of the presence of acne lesions.... ...The 4 major recognized pathophysiological features of acne ... ...proliferation of P. acnes, and then inflammation."
    * "In inflammatory acne, comedones rupture and the follicular material becomes dispersed in the dermis rather than on the skin surface." -> means they rather damage and spread through the skin then "above ground"; translated to the very thin bowel: slice and dice the bowel and spread throughout it
    * "A break in the lining of the comedone ... ...attributed to... ...The bacteria secrete many polypeptides, among which are numerous extracellular enzymes such as proteases, hyaluronidases, neuraminidases, and others that could be involved in epithelium permeabilization and inflammatory infiltration (Noble, 1984). P. acnes is also known to produce chemotactic factors (Puhvel and Sakamoto, 1977), proinflammatory cytokine inducing-factors" -> like large scale chemical and imunological warfare in the very thin bowel that is well connected to the main bloodstream; note that bowel has plenty of endothelial cells just like skin
    * "The infiltrate of an early inflamed lesion consists of polymorphonuclear cells that certainly contribute to the lining breakage, but eventually, as time goes by and infection becomes chronic, these cells attract and are replaced by mononuclear cells, predominantly T-cells of the CD4 phenotype" -> I originally came to the idea of using papaya by virtue of having *plenty* of apthous ulcers that are "When early aphthous ulcers are biopsied, the histologic appearance shows a dense inflammatory infiltrate, 80% of which is made up of T cells.[5] Persons with aphthous stomatitis also have circulating lymphocytes which react with peptides 91–105 of heat shock protein 65–60,[2] and the ratio of CD4+ T cells to CD8+ T cells in the peripheral blood of individuals with aphthous stomatitis is decreased.[5]" and "Aphthous stomatitis has been associated with other autoimmune diseases, namely systemic lupus erythematosus and inflammatory bowel diseases." -> so aphtous ulcers are full to the notch with T-cells, located in mucosal and endothelial tissue, cause body wide increased HSP, cause CD4+ types in blood to decrease while they end up / are relocated to lessions caused by this acne bacteria and there is a clear link to IBS and so on... no coincidence IMO. En plus "extent of the ulceration and is worsened by physical contact, especially with certain foods and drinks (e.g., if they are acidic or abrasive)." -> that sounds a lot like what I previously described but only now looked up to stuff this comment; predictive value regarding to interaction with food intolerances ;-)
    * "These studies are important for differentiating bacterial antigens that lead healthy controls to generate a protective immune response and those that might be involved in pathogenesis." -> So disease or health is based on how you react to it, not on how common the bacteria is
    * "Antibody against P. acnes antigenic determinants are found in the blood of most adults, whether they have had acne or not" -> so blood tests must ignore this immune marker as irrelevant
    * "Finally, there have been successful human trials of therapeutic vaccination against P. acnes" -> that could be good news if it also worked once infected (and for youngsters!)
    * "The chronic inflammatory condition of the pilosebaceous follicle caused by P. acnes is generally considered non-pathogenic. However, there is a growing body of evidence that point to the bacterium as being low virulence pathogen in several types of postoperative infections and other chronic conditions."
    * "It has also been recognized as a source of infection in focal intracranial infections"
    * "A recent study from Japan (Ishige et al., 1999) has shown that P. acnes DNA can be detected in lymph nodes of Japanese individuals with sarcoidosis."
    * "have isolated P. acnes from intervertebral disc material of patients with severe sciatica and they hypothesize that low virulent organisms such as P. acnes can gain access to the injured spinal disc and initiate chronic inflammation."
    * "The infected prostheses have been shown to contain bacterial biofilms of P. acnes and/or Staphylococcus epidermidis. The adhesion of P. acnes to the surface of the prostheses has been postulated to be a result of binding of propionibacterial cell surface proteins or adhesion molecules to host plasma or connective tissue proteins such as fibronectin" -> connects to Phils connective tissue angle in FM and Issie's biofilm angl


    Finally https://www.tandfonline.com/doi/abs/10.1586/eri.11.137?journalCode=ierz20, I can only obtain the abstract for free:
    "Propionibacterium acnes is a Gram-positive bacterium that forms part of the normal flora of the skin, oral cavity, large intestine, the conjunctiva and the external ear canal. Although primarily recognized for its role in acne, P. acnes is an opportunistic pathogen, causing a range of postoperative and device-related infections. These include infections of the bones and joints, mouth, eye and brain. Device-related infections include those of joint prostheses, shunts and prosthetic heart valves. P. acnes may play a role in other conditions, including inflammation of the prostate leading to cancer, SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, sarcoidosis and sciatica...."
    -> post operative brain infection?? Who knows it could, if present enough in the blood stream, use it's digestive enzymes to break down the BBB and gain access to it or a least severely weaken the BB
    -> I looked up sciatica and it seems that I live in a line of at least 3 generations that have sciatica-like symptoms...



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    It's a big blob that needs cleaning up. I'll do it later, but if I waited till all things are clearly structured, sorted out and test it'll be 2019 the soonest ;-). I felt I had to post it as it does tell a tale so familiar to me that it fits like a tailor made suit.


    I long thought my disease was dominated by poor blood flow and breathing but the described hypothesis could account for both and far far more of my symptoms. In fact, I don't see any symptoms yet that clearly can't be logically explained by the above hypothesis. It's looks like a common driver driving plenty of the different and distinct disease mechanisms I previously thought and talked about.

    With that I don't claim this is ME. I don't claim it is my variant of ME. But I very strongly feel it might be the one overwhelming thing keeping me into ME.
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