Microbiome - Butyrate - Inflammation

[LINE]

I will keep posting on this thread with updates on my experiments. I hope this helps.

NAG experiment:
@Mary and @Hip have commented on NAG in that it helps with sleep and anxiety, it is also attributed to joint and muscles. However, I found that the gastrointestinal environment uses NAG mainly in Mucin production. I bought a $15 bottle (Source Naturals).

The first 2 days, I experienced loose stools, at first, I thought it was a negative reaction. Muscle testing proved otherwise, and I continued on the experiment. The loose stools vanished, and I have having normalized stools. The IBS stopped. I have experimented with its cousin, glucosamine in the past.

There is growing evidence in medical journals that the gut/brain axis is closely associated. Anxiety comes from high glutamate production which impairs GABA (calming neurotransmitter), that is well established. Glutamate production spools up from stress and I am thinking immune stress. So possibly what is happening is that NAG is calming the intestinal immune reactions down by helping the mucin layer.

If you want to read more about mucins > https://pmc.ncbi.nlm.nih.gov/articles/PMC8442341/

 

[LINE]

Akkermansia (UpNourish): no problems to report. IBS is better.

Cranberry Extract (AZO): No problems to report, IBS is better.

Other items included during this time are
1/ Beef stock (for the collagen, peptides and glycine) mixed with spice mix. Also rich in carnitine and carnosine.
2/ Vitamin A (support gastro immunity as does Vitamin D and colostrum (SiGA).
3/ Ginger and peppermint (has anti-inflammatory action in the gut)
4/ Tazo Passion for the proanthocyanins found in hibiscus.
5/ Benfotiamine (B1)
6/ My general vitamin/mineral supplement which contains basic b vitamins, minerals, antioxidants. I use Life Force from Source Naturals. Many people have responded to the supplement in a favorable way.
7/ Other things not listed.

 

[Violeta]

think you might be onto something with the high ROS btw, but I think it might just be due to viruses in the gut that cause the ROS in the first place, or bacteria of course. It's just a theory sadly but I experienced 90% for the first time in 8 years start of 2023, assume it was low to no viral load briefly in the GIT which meant no ROS, which meant very high butyrate production. I felt amazingly well compared to how I feel now.

@godlovesatrier , what happened in between when you felt good at the start of 2023 and now? Do you know what caused you to go downhill?

 

[Violeta]

This is a tangent, but have you seen that Akkermansia levels are high in people with Parkinson's.
However, levels of Prausnitzii are low in people with Parkinson's.

(People with allergic conditions and autoimmune diseases have shown reduced levels of F. prausnitzii. By promoting the balance between pro-inflammatory and anti-inflammatory immune pathways, F. prausnitzii can help prevent the development and progression of these immune-mediated disorders.)

Oxidative stress?

Low levels of Faecalibacterium prausnitzii can be caused by a number of factors, including: Physicochemical factors, Host-related factors, Microbiome-related factors, and Oxidative stress


Anyone have a thought about this?

 

[LINE]

@Violeta Thanks for posting that information, do you have a link to the article?

The article that came out about CFS and the gut, indicated low levels of f. prausnitzii and another that the name escapes me. The issue is that prausnitzii is very sensitive to oxygen levels and when high levels come out, then the prausnitzii cannot thrive. It was my understanding that the oxygen that killed them off was due to high oxidization from the immune response.

One of the questions was/is why is the immune system booting up, is it due to a bad bacteria that the immune system is trying to rid of, 2/ is it due to some environmental toxin 3/ genetic 4/ out of line nutrient needs 5/ hormonal dysfunction?

Bacteria are very individualistic meaning that one species needs may be completely different than another species. For example, maybe one species does well with copper while another likes more zinc than copper. That list could extend for some time. They have found specific environmental toxins that inhibit certain species which may explain the increase in GI problems.

My first suspicion is that a bad bacteria entered the gastrointestinal system and is evoking an immune response.

One thing that pops up in journal articles is that good bacteria like polyphenols. Cranberry is one but there are many more such as green tea. These provide the substrate for good bacteria growth. Polyphenols can also inhibit bad bacteria which is important.

Update: I found an article that stated there were several species higher in PD patients which includes Akkermansia but also bifidobacteria and another. They indicated that medicines given for Parkinson's may be influencing higher bifidobacteria while Akkermansia becomes higher with aging (their suspicion).

I think this article mentioned Klebsiella population being higher. Klebsiella is not necessarily a good bug to have living in the gut and since it is a gram negative, they are a little more ferocious. It could be the Klebsiella is the culprit. It would evoke a strong immune reaction which could bring down the prausnitzii. Best guess.

 

[Violeta]

High levels of akkermansia in Parkinson's article:

https://pmc.ncbi.nlm.nih.gov/articles/PMC8881719/

Depleted F Prausnitzii in PD

depletion of bacteria belonging to the Lachnospiraceae family and the Faecalibacterium genus, both important short-chain fatty acids producers, emerged as the most consistent PD gut microbiome alterations.
https://pmc.ncbi.nlm.nih.gov/articles/PMC7946946/

Reduced Prausnitzii in ME/CFS
https://www.nih.gov/news-events/news-releases/studies-find-microbiome-changes-may-be-signature-mecfs
Dr. Williams and his colleagues found that people with ME/CFS had abnormally low levels of several bacterial species compared to healthy controls, including Faecalibacterium prausnitzii (F. prausnitzii) and Eubacterium rectale.

Thanks for the clues, I'll look around more after breakfast. Especially interesing is the zinc/copper idea.

Yes, I saw that green tea is good for akkermansia, too. I bought some of the Tazo Passion tea you mentioned earlier and am adding some green tea and cranberry juice to it. I see Prausnitzii does well with inulin, so I will add some inulin to it.

I am actually worried about having Klebsiella because when I eat starches I get pain in my low back. I have been experiencing it since I quit the HFLC diet a week or two ago when I realized it is bad for akkermansia and probably having tried low carb high fat off and on so many times I probably have made my problem much worse.

I never stuck with the HFLC diet because it helped for a short time but them problems would pop up, I would lose too much weight, turn yellow, and so many other problems.

The day before yesterday I actually took some aloe ferox for the back pain, which I am sure is caused by something in my gut, but then read it may not be good for mucin generation, so I stopped taking it. I don't know if I will go back to it or not.

 

[Violeta]

Bacteria are very individualistic meaning that one species needs may be completely different than another species. For example, maybe one species does well with copper while another likes more zinc than copper. That list could extend for some time. They have found specific environmental toxins that inhibit certain species which may explain the increase in GI problems.

First mineral I looked up was manganese due to reports of manganese toxicity in Parkinson's, and found this.
I don't specifically see akkermansia or prausnitzii mentioned, but this does make me think along the lines of metals with respect to prausnitzii and akkermansia.

Quitting high purine foods (due to ammonia concerns) definitely affects the amount of copper and zinc in the diet: I will have to make sure I get enough zinc.

Gut Microbiota as a Potential Player in Mn-Induced Neurotoxicity​

https://pmc.ncbi.nlm.nih.gov/articles/PMC8469589/

 

[Violeta]

Zinc also has an effect on microbiome.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8567254/

I don't understand why Akkermansia levels rose with high-zinc diet but also increased under low-zinc conditions.

The high-Zn diet was associated with enrichment of Akkermansia, Faecalibaculum, Helicobacter, and Ileibacterium compared to other diets. Mice fed the 600 mg/kg Zn diet showed a higher abundance of Dubosiella, Caulobacter, and Bradyrhizobium and a lower proportion of Romboutsia, Bacteroides, Lactobacillus, and Bifidobacterium.

Long-term Zn alteration reversed the distribution of some bacterial genera compared with short-term Zn intervention (Fig. S1B). Under low-Zn conditions, an increase in the relative abundance of Akkermansia, Blautia, Alloprevotella, and Ruminiclostridium and a decrease in Thermovirga were found in cecum of mice

 

[Wishful]

One thing that concerns me about microbe-based theories: lateral transfer. Microbes are continuously swapping genetic information, so isn't it possible that the theoretically "good" bacteria can start producing whatever some "bad" bacteria does? Clinical tests might show healthy levels of Goodforyou, but it's pumping out enterocyte-harming enzymes because it swapped in some genes from NastyEvil, even if you don't have measurable amounts of that strain anymore.

 

[vision blue]

My population of butyrate producing bscteria was decimated by a bad gi infection in may.
Eating lots of foods with inulin has done nothing

Before this had high leveks of the FP bacteria. Have not measured now but probablyvwiped out

Interesting on klebesla pnomenae or howver its spelled. When i had an abcess cultures last year, that grew.

The usual commercially available probiotics have the wrong type of bacteria for me i think. Already have plenty of acetate apparently and sll those lactobaccilus and bifido strains just lead to that. Its my butyrate (and valprouc acid) that have been decimated. I have the befire and after numbers

 

[Violeta]

My population of butyrate producing bscteria was decimated by a bad gi infection in may.
Eating lots of foods with inulin has done nothing

Before this had high leveks of the FP bacteria. Have not measured now but probablyvwiped out

Interesting on klebesla pnomenae or howver its spelled. When i had an abcess cultures last year, that grew.

The usual commercially available probiotics have the wrong type of bacteria for me i think. Already have plenty of acetate apparently and sll those lactobaccilus and bifido strains just lead to that. Its my butyrate (and valprouc acid) that have been decimated. I have the befire and after numbers

If you have had klebsiella overgrowth, you may be interested in this, even if you aren't taking cranberry extract. I found this after I started drinking cranberry juice for raising akkermansia levels.

From this study about cranberry extract:

Supplementation with a cranberry extract favors the establishment of butyrogenic guilds in the human fermentation SHIME system​

https://pmc.ncbi.nlm.nih.gov/articles/PMC11480733/

Strong enrichment (> 4 log2FC, P < 0.05, Wald test) of genera belonging to Proteobacteria (Shigella, Escherichia-Shigella, and Klebsiella) (6/6 donors)

What a bummer.

The study did contain some good news, though.

"The overall bacterial metabolism shifted from acetate to propionate and, notably, butyrate production following PAC (proanthrocyanidins) supplementation. "

 

[vision blue]

Thanks for the reference. One thing i wonder though is if iit changes balance by feeding preexisting bacteria, like all probiotics do. its possible i am at zero of the stuff i needin which case giving them food they like wont help.

I also seem to have pkenty of proprianate- that percent went up along with acerate after the infection.

Interesting feeds proteobacteria - im assuming theyre not all bad tho just because the nasty ones in there? Havent read the article, just the abstract

Is that substance also in pomegranates? I can look it up.

Thing in the abstract i liked the most was the different effects on different parts of the colon I hadn’t really thought about that before adds a whole new layer of depth and complexity and interest to thinking about it all

 

[Violeta]

Yes, it's in pomegranates, too.

If I read anything else about prorianate going up but not butyrate I'll bring it here. Brain dead now, it's quarter to 9, it was a long day.

Boy, cranberries are really acidic, though. I don't know if my body can handle it. I have never tried pomegranate, is it sour?

Just remembered something, F. Praunitzii...

Introduction. Faecalibacterium prausnitzii has been consistently reported as one of the main butyrate producers found in the intestine (Barcenilla et al., 2000; Duncan et al., 2002).

And I think it feeds off the akkermansia metabolites. But I also read inulin helps it, but inulin isn't helping to raise your butyrate. I don't know, maybe LINE will have a clue.

 

[vision blue]

Pomegranates are wonderful! One of my faves. Sweet with jan edge of tart but not over the top, berry flavors. If its not sweet means ita a bad or unripe one and woulldnt eat it. And they shoukd be bright red or vivid maroon but never gray or muddy or whitish/transparent. But i dont eat the seeds and i dont know if thats the part with benefecial stuff.

Cranberries are too a idic for me. Id have to mix it with stuff including sugar

Right inulin not helping- asparagus, zuchinni, shallots, pomegrwnates. I know not sll my have inulin. Cant remember off too of head. As i was mentioning there has to be something ready there for it to grow

Yes that good bacteria- i used to have tons - tho am skeptical how was measured since thought was an anaerobe. My understanding id this and other natural butyrate producing
Bacteria are not in probiotics because tgey are aneribes so not going to live long on the shelf. Not sure dies immediately but for profit supplements are all about the shelf life

Conmercially butyrate producing strains are being called “next generation probiotics”. Read some research paper reporting on the saftey (in rats) of a butyrate producing bacteria that had a long shelf life. But really an unnatural bacteria.

Im curious to see what my next test shows on whether theres been any increase. Sometimes tho there are confounds. So the loiser the stools, the higher level of SCFA measured. I think with rapid trabsit time more for becteria to eat and therefore higher SCFA but am not sure. Also forgetting what the seperate roles are of protein, fat and carb

@Violeta - if you can spare the time and energy, can you have a look at my new thread i atarted yesterday (friday) on exposure to an illness im now hoping to head off before i get it! I woukd greatly appreciate your input.

 

[Wishful]

They should be able to coat anaerobic bacteria granules in something that keeps oxygen out but breaks down in the colon. Since they can make white bread last 3 months on the counter without going bad, bacteria should be easy.

 

[LINE]

One thing that concerns me about microbe-based theories: lateral transfer. Microbes are continuously swapping genetic information, so isn't it possible that the theoretically "good" bacteria can start producing whatever some "bad" bacteria does? Clinical tests might show healthy levels of Goodforyou, but it's pumping out enterocyte-harming enzymes because it swapped in some genes from NastyEvil, even if you don't have measurable amounts of that strain anymore.

That is a valid point - I realize from reading many journal articles that there is more going on than thought. The idea that taking a probiotic will cure my ills are archaic compared to new information. Your point is well taken btw but the inverse can also occur. DNA corruption does happen (bad influencing good) but I suspect that the inverse could be true (though I don't have enough evidence to support that at the moment .

Thinking a little more about your point, I do believe that there are homeostatic principles involved in the gut environment that are able to balance the equation, much like the other self-regulating mechanisms that are present in many other systems. The question is what helps reset the equation. Certainly, if there are pathogens that are aggressive, then homeostasis is definitely more difficult. One class is gram negative bacteria (ESKAPE pathogens). Gram negative bacteria are well documented in medical literature as being disruptive due to their two-tiered membrane which makes them more resistant. (I should not leave out the gram positives that are disruptive).
It seems to me that there are more questions than answers.

Yes, it's in pomegranates, too.

If I read anything else about prorianate going up but not butyrate I'll bring it here. Brain dead now, it's quarter to 9, it was a long day.

Boy, cranberries are really acidic, though. I don't know if my body can handle it. I have never tried pomegranate, is it sour?

Just remembered something, F. Praunitzii...

Introduction. Faecalibacterium prausnitzii has been consistently reported as one of the main butyrate producers found in the intestine (Barcenilla et al., 2000; Duncan et al., 2002).

And I think it feeds off the akkermansia metabolites. But I also read inulin helps it, but inulin isn't helping to raise your butyrate. I don't know, maybe LINE will have a clue.

That is a good question, thanks for asking. I did a quick search and found this article (did not do deep research but may be helpful). - https://pmc.ncbi.nlm.nih.gov/articles/PMC6137959/

 

[LINE]

@Violeta Something I found that is leading to more answers (I think - Akkermansia feeds off the mucins in the gut, so it gets its energy from available mucins.

I am still hazy about the role of mucins, how they are formed etc., so bear with me. Please add any knowledge.

Mucins line the gut, they are also known as mucous. Mucins are made of glycoproteins and I think that oligosaccharides are involved with the glycoproteins. Oligosaccharides are diverse, inulin is an oligosaccharide.

What I found important is that mucins interact with the tight junction proteins. Which leads me to the question that perhaps supporting the tight junction proteins (start of the thread) would be more helpful if the mucins are supported. Hope that makes sense.

The mucous layer in the gut helps protect from invasion of pathogenic bacteria and acts as a protection from inflammatory cytokines.

 

[LINE]

Question for readers: Do any of you have a dry mouth? Reason for the question is that mine has been pasty dry since the gastro issue. I am connecting the dry mouth to low mucous which is sensible but thinking that it might indicate low mucous in the gastro tract.

 

[Violeta]

@Violeta Something I found that is leading to more answers (I think - Akkermansia feeds off the mucins in the gut, so it gets its energy from available mucins.

I am still hazy about the role of mucins, how they are formed etc., so bear with me. Please add any knowledge.

Mucins line the gut, they are also known as mucous. Mucins are made of glycoproteins and I think that oligosaccharides are involved with the glycoproteins. Oligosaccharides are diverse, inulin is an oligosaccharide.

What I found important is that mucins interact with the tight junction proteins. Which leads me to the question that perhaps supporting the tight junction proteins (start of the thread) would be more helpful if the mucins are supported. Hope that makes sense.

The mucous layer in the gut helps protect from invasion of pathogenic bacteria and acts as a protection from inflammatory cytokines.

Yes, that was probably my most important reason for trying it.

Are you thinking that the building mucin is more the issue? That does make sense.

The relationship of Akkermansia with the mucin lining seems like a connundrum. How it helps the lining but at the same time degrades it is difficult for me to understand.

I have seen that overcolonization can be damaging.

I found this, but haven't read the study yet.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10018180/#:~:text=Akkermansia muciniphila normally colonizes the,et al., 2017).

"Akkermansia muciniphila normally colonizes the outer layer of loose mucus and upregulates the synthesis of MUC2 by goblet cells through metabolites (Meng et al., 2020). Although A. muciniphila degrades the mucus layer, it does not change its thickness, which reaches a dynamic equilibrium (Derrien et al., 2017)."

However, A. muciniphila cultivated in the absence of mucin can lead to αSyn aggregation in cholecystokinin (CCK)-positive EECs. However, buffering mitochondrial Ca2+ can reverse the damaging effects.
(They found this when doing research about Parkinson's)

 

[Violeta]

Question for readers: Do any of you have a dry mouth? Reason for the question is that mine has been pasty dry since the gastro issue. I am connecting the dry mouth to low mucous which is sensible but thinking that it might indicate low mucous in the gastro tract.

I have read that dry mouth and dry eye can somehow have something to do with acetylcholine deficiency.


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Choline can help with dry mouth because it can help regenerate salivary glands. Acetylcholine, a neurotransmitter that triggers the release of saliva, can be blocked by anticholinergic drugs, which can lead to dry mouth. "

I don't know how a gastro issue would affect acetylcholine levels, though, so maybe there are other reasons.

But look at this:

"Phosphatidylcholine (PC)
A PC molecule contains choline, and PCs are a key component of intestinal mucus. The choline head of a PC molecule binds to the negatively charged mucins in mucus. The fatty acid chains in PCs attract other PC molecules to form a hydrophobic bilayer that seals the mucus and prevents bacteria from entering."