Clostridium Butyricum - A Game Changer?

[JPV]

I will be interested in this, too. I have high IL-10. I started Miyarisan recently & lately, my sleep has been erratic & I wake up feeling unrefreshed. I didn't realized it could be possibly correlated. I am only taking 1/2 tab 3x/week. That's what i can tolerate at this time. It will be good to know what has worked to lower IL-10 for others.

Yeah, I have a harder time getting to sleep using CB and was having infrequent nightmares, which is very rare for me. I wake up easier and more refreshed while taking it though. Go figure.

I can't say for sure if IL-10 is the problem. Several people on the forum have speculated that it could be due to an increase in Acetylcholine which is purported to be created by CB.

I'm just throwing out the idea about IL-10 to encourage discussion as a possible alternative explanation for the sleep disrupting properties of CB that some of us seem to be experiencing. This came to my attention because Kenny De Meirleir made comments about seeing elevated IL-10 in his patients and feels that it's a major contributor for their disrupted sleep symptoms.

 

[Avengers26]

@JPV I just did a quick search on google but didn't find anything non-prescription which specifically lowers IL-10. But, at same time, my TNF a is high. So, I wonder if high IL-10 is a good (protective in a compensatory way) or bad thing?

High ACh Symptoms have been my achille's heel for a long time. I have never found a satisfactory answer to the question Why. Is it in response to something or some imbalance or the body's self-protective mechanism at work against some insult?

 

[JPV]

I just did a quick search on google but didn't find anything non-prescription which specifically lowers IL-10.

Here's an excerpt from an article that was quoted by @heapsreal on another thread from a few years back...

DHEA and Immune Function

A study published in the Journal of Clinical Endocrine Metabolism showed that when old female mice were treated with DHEA, melatonin, or DHEA and melatonin, splenocytes (macrophages) were significantly higher as compared to young mice. B-cell proliferation in young and in old mice significantly increased. DHEA, melatonin, and DHEA and melatonin helped to regulate immune function in aged female mice by significantly increasing the cytokines interleukin-2 and interferon-gamma and significantly decreasing the cytokines interleukin-6 and interleukin-10, thus regulating cytokine production (Inserra et al. 1998).

 

[Avengers26]

Thanks @JPV
Unfortunately, My IL-2 is high, my DHEA is high & my Cortisol is low. So, both melatonin & DHEA are no go. LOL, I feel like the guy from the movie "the maze runner",which came out last year.

 

[JPV]

Unfortunately, My IL-2 is high, my DHEA is high & my Cortisol is low. So, both melatonin & DHEA are no go. LOL, I feel like the guy from the movie "the maze runner",which came out last year.

I hear you. This disease is nothing but a horrible game of Whac-A-Mole most of the time.

 

[adreno]

@adreno, I don't recall you mentioning that you experienced any sleep disruptions with CB. Are you by any chance taking anything that might help with regulating IL-10 production? Or perhaps IL-10 isn't an issue with your condition.

I don't remember any particular sleep disruption, but this, as you say, may pertain to my particular condition. IL-10 and Tregs are reportedly low in autoimmune conditions. IL-10 is basically an allergy cure, so I definitely want mine higher, not lower.

 

[Sidereal]

I don't remember any particular sleep disruption, but this, as you say, may pertain to my particular condition. IL-10 and Tregs are reportedly low in autoimmune conditions. IL-10 is basically an allergy cure, so I definitely want mine higher, not lower.

When I was on CB, I experienced a marked reduction in seasonal allergies to pollen etc. but my weird MCAS reactions to food etc. made a comeback. I had gotten rid of that stuff last year with RS so to have it come back was disturbing but reassuring at the same time that I had been right all along about it being caused by dysbiosis in the gut. It's a complicated situation I don't understand but I concluded a few months ago that CB is not for me at this time. I need to work on some other things first.

 

[adreno]

When I was on CB, I experienced a marked reduction in seasonal allergies to pollen etc. but my weird MCAS reactions to food etc. made a comeback

That is weird, as butyrate is known to inhibit mast cell activation.

 

[Sidereal]

That is weird, as butyrate is known to inhibit mast cell activation.

Yes, I was very surprised by what had happened so to make sure I wasn't misinterpreting the situation I stopped and reintroduced CB several times and each time the same thing happened. What was also interesting is that I experienced a massive reduction in normal IgE mediated allergies at the same time as the weird MCAS stuff flaring up which just goes to show you how that stuff isn't allergy in the traditional sense.

 

[nandixon]

@Avengers26 and @JPV

Cimetidine, available OTC as Tagamet in the U.S., is an immunomodulator - mostly an immunostimulant - that decreases regulatory T cell (Treg) activity and in the process lowers IL-10 (and also TGF-beta).

So cimetidine might be good for a subset of us who may be immunosuppressed and/or who have high IL-10 levels. I've not had my IL-10 levels measured but cimetidine is helping me (and not via a general H2 blocker effect, since neither ranitidine nor femotidine help).

For its effect on IL-10, see for example:
Cimetidine enhances immune response of HBV DNA vaccination via impairment of the regulatory function of regulatory T cells

On the other hand, decreasing Treg activity would generally be the opposite of what you'd want to help improve things in an autoimmune disease situation, I think. So cimetidine seemingly wouldn't be so great there, in theory.

 

[JPV]

So cimetidine might be good for a subset of us who may be immunosuppressed and/or who have high IL-10 levels.

Thanks for the advice.

On the other hand, decreasing Treg activity would generally be the opposite of what you'd want to help improve things in an autoimmune disease situation, I think. So cimetidine seemingly wouldn't be so great there, in theory.

I'm just going on what De Meirleir say in regards to elevated IL-10 levels causing sleep disruption. What he talks about really resonates with me but I haven't taken any test to confirm that I have issues with IL-10. That's next on the list as soon as my cash flow improves.

I'm guessing the issue isn't about completely knocking out IL-10 production but just balancing out possible overproduction.

 

[adreno]

Yes, I was very surprised by what had happened so to make sure I wasn't misinterpreting the situation I stopped and reintroduced CB several times and each time the same thing happened. What was also interesting is that I experienced a massive reduction in normal IgE mediated allergies at the same time as the weird MCAS stuff flaring up which just goes to show you how that stuff isn't allergy in the traditional sense.

It might be LPS from die-off that aggravates the MCAS. LPS enhances mast cell activation.

 

[Sidereal]

It might be LPS from die-off that aggravates the MCAS. LPS enhances mast cell activation.

Yes but there's more to it than that. Other probiotics and prebiotics that caused (sometimes fairly massive) bacterial die-off didn't trigger mast cell activation for me.

 

[Avengers26]

Thanks @nandixon I will try out cimetidine. For now, I slept poorly another night. Thus, I have decided to take a break from CB for 1-2 weeks & will make a few more changes.
Low & Slow is the way to go for my hypersensitive body.

Also, I recently came across the thread here about Dr. Goldstein. Cimetidine was one of the meds he used.

 

[nandixon]

@Avengers26, speaking of "low and slow," the dose of cimetidine that works best for me is 50mg (1/4 tablet) taken twice a day about an hour after breakfast and maybe 2 hours after dinner (trying to minimize its acid-reducing effect on digestion). So a total of just 100mg/day.

 

[Avengers26]

@nandixon , Thank You.

 

[Hutan]

I don't remember any particular sleep disruption, but this, as you say, may pertain to my particular condition. IL-10 and Tregs are reportedly low in autoimmune conditions. IL-10 is basically an allergy cure, so I definitely want mine higher, not lower.

The Light et al paper 'Gene expression at baseline and following moderate exercise in patients with CFS and FM' suggested that the expression of the IL10 gene was elevated after exercise (compared to normal people) for people with CFS and elevated all the time for people with fibromyalgia. (There was one subset of CFS patients for which this was not true - a minority but a significant minority).

The authors note that 'the findings of enhanced post-exercise anti-inflammatory cytokines response in at least a subset of CFS patients has been reported previously using serum levels which are more definitive measures'.

Adreno, do you have an autoimmune condition as well as ME? Have you had your IL10 measured? If the Light study is correct and you are like their majority CFS subset, it seems all you have to do to increase your IL10 for a few days is to jog around the block...

IL-10 and Tregs are reportedly low in autoimmune conditions.

Is IL-10 reportedly low in all autoimmune conditions?

 

[adreno]

Adreno, do you have an autoimmune condition as well as ME? Have you had your IL10 measured? If the Light study is correct and you are like their majority CFS subset, it seems all you have to do to increase your IL10 for a few days is to jog around the block...

I believe Lipkin found lower IL-10, so the question is still open.

As I have said before, I have allergies, which is normally characterized by low IL-10. Also, my OI/POTS fit an autoimmune (antibody) pattern. I'm going more on gut feeling, since I don't have any tests.

 

[Hutan]

IL-10 and Tregs are reportedly low in autoimmune conditions.

I'm floundering around here with little knowledge, so bear with me. One general reference (below) suggests high IL-10 is associated with autoimmune diseases, perhaps causally.

http://www.ncbi.nlm.nih.gov/books/NBK6234/

The Role of IL-10 in Autoimmune Pathology
Andrew W. Gibson, Jeffrey C. Edberg, Jianming Wu, and Robert P. Kimberly.
The association of high levels of IL-10 with autoimmune diseases suggests that this cytokine plays an important role in the disease pathogenesis.​

Yes, there seems to be evidence that OI/POTS has an autoimmune component. And now perhaps for ME.

I believe Lipkin found lower IL-10, so the question is still open.

Interesting if Lipkin et al found lower IL-10 (when Light et al found even before exercise that mean IL-10 was higher in CFS patients as compared to control - although the Light Il-10 confidence intervals overlap greatly so there may not be a real difference). However, it was during and after exercise that the IL-10 really increased in most CFS patients. And the Lipkin study didn't specifically measure after exercise.

Also the Light study reportedly found a subset of CFS patients that did not show the across the board upregulation of genes including IL10, so averaging their results with the others would muddy the waters.

So cimetidine might be good for a subset of us who may be immunosuppressed and/or who have high IL-10 levels. I've not had my IL-10 levels measured but cimetidine is helping me (and not via a general H2 blocker effect, since neither ranitidine nor femotidine help).

So perhaps the subset of CFS patients with high IL-10 levels (at least after exertion) is large.

 

[adreno]

@Hutan,

I'm no expert on immunology, but that article you quote is 15 years old. I think we've learned a thing or two since then:

Interleukin 10 (IL-10) is a potent anti-inflammatory cytokine that plays a crucial, and often essential, role in preventing inflammatory and autoimmune pathologies.3,4 Deficiency or aberrant expression of IL-10 can enhance inflammatory response to microbial challenge but also lead to development of inflammatory bowel disease and a number of autoimmune diseases.5–7 Thus impaired IL-10 expression or signaling can enhance clearance of pathogens during an acute infection, but also exaggerate inflammatory response, resulting in exacerbated immunopathology and tissue damage.8–10,11Conversely, some pathogens can harness the immunosuppressive capacity of IL-10 to limit host immune response, leading to persistent infection.12,13 All in all, Il-10 plays a largely nonredundant role in mediating host anti-inflammatory response and, therefore, identifying the cellular sources of IL-10 as well as the molecular mechanisms that regulate IL-10 expression are critical to developing therapeutic strategies directed against pathology-associated impaired IL-10 production.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410706/

Whether IL-10 is high or low in ME, I don't know. Perhaps it's a matter of subsets. High IL-10 would fit with the "persistent pathogen" hypothesis, while low IL-10 would fit with an autoimmune hypothesis. Personally, I'm leaning towards the autoimmune hypothesis of ME.