Yes, I think you have some valid points. The accumulation of hydrogen prevents the oxidation of NAD(H) NADP(H) and this has energetic consequences.
My focus on SRB is based upon many factors, and while I do think the dysbiotic conditions in ME/CFS is likely marked by considerable species variance, I would point out to you that this hydrogen competition has definite winners and losers. If we look at kinetic and thermodynamic considerations we can see that SRB can outcompete those other organisms for H2, including acetogens and methanogens. (Acetogens are much, much less capable in this role, but the synthesis of acetate is as much a feature of other environmental /metabolic conditions.) SRB also exist in symbiotic relationships with methanogens that allows them to thrive without sulfate. So a lactate hungry, highly toxic liposaccharide-enriched, acetate oxidizing beast is a force to reckon with. Methanogens definitely carry roles in disease, but I'm looking at SRB as having a leading role, to the extent that one could prioritize these things.
Now, the competition for H2, however, is fought based upon H2 threshold. So the organism that gets the H2 is the one that can utilize the most miniscule quantities with robust growth and preempt H2 oxidation by other organisms.
But I guess the question is, if SRB are so effective as hydrogenotrophs, is there another commensal organism that has superior ability? Based upon what I have read, I believe nitrate reducing bacteria fit this bill. It seems the competition for H2 is based upon redox potential of the terminal electron acceptor. This would imply that microorganisms with denitrification capabilities are important to counteracting the effects of SRB. In fact, I think these species are relatively depleted across many different types of inflammatory diseases, but this is purely based upon metabolic derangements. These organisms are a subset of gram negative, proteobacterial commensals. In fact what we most likely lack are close relatives to SRB without the hydrogen sulfide, which of course inhibits cellular respiration and keeps the inflammatory response in check.
So you see that nitrate availability is what determines if they have access to sulfate. "In all scenarios tested, the SRB were able to initiate strong SO(4)(2-) reduction only when competition for H(2) inside the biofilm was relieved by nearly complete removal of NO(3)(-)." We know from multiple studies that SRB utilize host-derived glycans, mostly mucin, which requires sulfation. So, basically SRB are undermining your intestinal barrier. This is substantially relieved by providing complex carbohydrates, particularly mucopolysaccharides. Sources of inorganic nitrate will similarly be beneficial in curtailing this foraging. This is readily used by denitrifying species.
In fact if you wanted a burgeoning population of SRB you would restrict complex carbohydrates,consume large amounts of protein, and take ABX with wide-activity against gram-negative organisms. I don't recommend this.
Obviously this exists as a very distinct possibility for observed sulfate deficiencies, but these relationships have countless implications when you look at it as a key resource in the soil Nitrate availability enhances the bacterial synthesis of many other nutrients. It is illogical to think that the importance of these nutrients to micororganisms existing in soil or even marine ecosystems does not have similar importance to the same micro-organisms in the gut. Unfortunately many of these metabolic factories are broken.
Environ Sci Technol. 2012 Oct 16;46(20):11289-98. doi: 10.1021/es302370t. Epub 2012 Oct 5.
Interactions between nitrate-reducing and sulfate-reducing bacteria coexisting in a hydrogen-fed biofilm.
Ontiveros-Valencia A1, Ziv-El M, Zhao HP, Feng L, Rittmann BE, Krajmalnik-Brown R.
Author information
Abstract
To explore the relationships between denitrifying bacteria (DB) and sulfate-reducing bacteria (SRB) in H(2)-fed biofilms, we used two H(2)-based membrane biofilm reactors (MBfRs) with or without restrictions on H(2) availability. DB and SRB compete for H(2) and space in the biofilm, and sulfate (SO(4)(2-)) reduction should be out-competed when H(2) is limiting inside the biofilm. With H(2) availability restricted, nitrate (NO(3)(-)) reduction was proportional to the H(2) pressure and was complete at a H(2) pressure of 3 atm; SO(4)(2-) reduction began at H(2) ≥ 3.4 atm. Without restriction on H(2) availability, NO(3)(-) was the preferred electron acceptor, and SO(4)(2-) was reduced only when the NO(3)(-) surface loading was ≤ 0.13 g N/m(2)-day. We assayed DB and SRB by quantitative polymerase chain reaction targeting the nitrite reductases and dissimilatory sulfite reductase, respectively. Whereas DB and SRB increased with higher H(2) pressures when H(2) availability was limiting, SRB did not decline with higher NO(3)(-) removal flux when H(2) availability was not limiting, even when SO(4)(2-) reduction was absent. The SRB trend reflects that the SRB's metabolic diversity allowed them to remain in the biofilm whether or not they were reducing SO(4)(2-). In all scenarios tested, the SRB were able to initiate strong SO(4)(2-) reduction only when competition for H(2) inside the biofilm was relieved by nearly complete removal of NO(3)(-).
It might have been due to a misunderstanding on my behalf then. Here's one of the actual quotes and source...
I took warfarin for 1.5 years. Plus my mother had calcium oxalate kidney stones, my father too just passed s kidney stone a few days ago, plus both my parents have high uric acid, so the thing is compounded genetic+environmental for meI wouldn't worry about taking K2 right now, since it causes pain. ( I wonder if it's mobilizing calcium from tissues,ouch.)
I've read that calcium can be precipitated into tissues in an acidic environment.
Yeah, I couldn't really grasp the table myself so it's good to hear that it's not just me.The problem doesn't lay with you! Setting aside the fact that the table itself is rather bizarre, it doesn't show what they conclude. Several genera in the table are shown to be at least an order of magnitude more abundant than Bifidobacterium - it couldn't possibly constitute 90% even on the figures shown.
This is an amazing problem. Could you be one of a kind? It sounds like a HPA axis + vagus nerve issue, and so does your husband's, but with some opposite symptoms. I think it would be a good topic for a new thread.
Do you remember your husband and you simultaneously having a flu or possibly an exposure to a pesticide? Maybe moving into a new house or getting a new carpet?
Do you have any symptoms of vagus nerve innervation (I don't know how else to say it) such as gastroparesis?
@Basilico, ever seen an autonomic specialist? It sounds like the sympathetic branch of your ANS is underfunctioning.
I am wrestling with this question right now. Since constipation is a major problem, I am afraid to add any pre or probiotic in case it feeds/colonizes something in or too close to the small intestine. I also would rather avoid antibiotics if possible.The garden metaphor hits the nail on the head! Thank you Basilico and South, for bringing this up. IMHO, this is central to creating a personal road map in healing gut disbyosis. This crucial step defines what treatment approach to take. And there are many different camps here as to the approach and in what order.
IMHO, if there is an overgrowth of weeds, fertilizing OR planting new seeds will do little. Think about it. How much grass will grow in your yard if you attempt to seed it in it's present state of dense dandelions? There is no space for the grass to grow. And even if some blades of grass grew and found a way to survive, they will do nothing for reducing the dandelion spread. Eventually they will have no room to grow and die due to the over abundance of dandelions. Same if you added fertilizer, which at this point will only strengthen and make the dandelions grow faster. At least that has been my experience, based on experimenting with herbals, prebiotics and probitics. So, I've come to the conclusion on this new approach: Make space for the good bacteria by initially eliminate or at least reduce the bad bacteria numbers. Then re-seed (probiotics), then fertilize (prebiotics) in that order. This is key.
The question then becomes how to create space for new microbiome?
So, I've come to the conclusion on this new approach: Make space for the good bacteria by initially eliminate or at least reduce the bad bacteria numbers. Then re-seed (probiotics), then fertilize (prebiotics) in that order. This is key.
Fortunately there is some good momentum on increasing knowledge on these bugs. Elsewhere, I received excellent information from the Great Plains Lab OAT test. Perhaps limiting since this test cannot check for the thousands of possible pathogenic bacteria species, it's still helpful for more common pathogenic bacteria. Here, I was identified with an overgrowth of bad clostridia (not to be confused with CB in same family), along with fungal indications, which is been the focus of my therapy. It gave me something to work with, factual data. The recommended antibiotic flagyl has been nothing short of godsend. Many of my GI bloating issues, IBS has been eliminated. And I say this under resentment of taking antibiotics due to the damage they have caused in my past history.
I am wrestling with this question right now. Since constipation is a major problem, I am afraid to add any pre or probiotic in case it feeds/colonizes something in or too close to the small intestine. I also would rather avoid antibiotics if possible.
I am wondering if using magnesium citrate (those nasty colonoscopy prep drinks) for a short while to flush out the whole system. I am hoping that in addition to a good clean out, perhaps it would wash out some of the gut flora -- enough so that the good stuff I put in and feed will actually become established.
Any opinions on this idea? Anyone tried this approach? I need to take the "next step" but I can't figure out what that is. Really getting confused and overwhelmed.
CB is purported to be able to kill pathogens such as Candida...Have developed a chest infection off and on ever since staring this. Have been rereading bits of the thread and it seems that others have had something similar. Might be something to do with the drainage from the sinuses that I'm getting.
Candida Die Off Symptoms
Common Symptoms
The symptoms indicate a large number of yeast are dying, thereby, increasing the toxic overload in the body. If you are already suffering from yeast infection or candidiasis, the symptoms may get more worse. These dying yeast secrete toxins, which get mixed with the toxins released by the live Candida. As a result, due to population of yeast in your bloodstream increasing, there are more health problems. It becomes difficult for the body to overcome the toxin production. If the symptoms are too severe, it is advisable to decrease your dose of antifungal drug. Following are a list of symptoms:
- Headache, tiredness, and fatigue
- Gastrointestinal problems such as diarrhea, nausea, constipation, and bloating
- Fever, chills, sore throat, sweating, and hypotension
- Feeling sleepy, anxiety, depression, blurred vision, and sudden anger reactions
- Chest pain, sinusitis, and heart palpitations
- Muscle cramps, joint soreness, body itching with pain
- Rashes on the body, due to allergic reaction
- Eagerness to eat sweet foods that contain carbohydrates
But you had a worsening even though you were taking it?So I did notice that Mutaflor worked to alleviate my constipation.