hows it going so far with this? you said histamine receptor, does it help you with digestion? brain fog?
has anyone else tried?
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I wish I could tell you something definitive. I really can’t yet, but based on what i’ve seen I’m compelled to go at this until I can realize this myself.
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Is BioGaia Osfortis pretty readily available, like could I buy it in Walgreen’s or CVS or something, or is Amazon my best bet?
I’ve used BioGaia Protectis for the past 4-5 months after reading about it on another thread here. The first few 2-3 days I took it there was a noticeable surge in libido and erection quality. That tapered off after a few days but my overall digestion has been much better while on it. Curious what the extra strains in the Osfortis will do.
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It’s the same strain titled here just 100x more potent. 10 billion daily dose as opposed to 100 million is it? Quite strange they offer both products now.
I’ve actually upped my dose to 20 billion a day for the time being.
They used 10 billion every day for a year in a trial for womens Bone health, that’s where this supplement comes from.
Just throwing down some notes here. Ironically Baylor has been doing some studies on this bacteria.
L. reuteri-Mediated Immunomodulation
novel strains of probiotics that can be safely administered to effectively prevent or even treat gastrointestinal inflammation in the near future.
1.Targeted approach: rsiR
• RsiR may modulate TNF-inhibitory histamine production through regulation of hdc cluster gene expression
2.Global approach: eriC
• Inactivation of eriC resulted in loss of TNF suppressive activity, decreased expression of genes in the hdc gene cluster and diminished amounts of TNF-inhibitory histamine
• EriC may play a role in relieving the inside-negative membrane potential that accumulates during histidine decarboxylation.
Separate study, but could be related
Histamine induces MUC5AC expression via a hCLCA1 pathway.
Histamine upregulated MUC5AC gene expression and mucin protein production in a dose-dependent and time-related fashion.
and finally, cant remember if I posted this already? Again from Baylor.
Microbial-based treatment reverses social deficits in mouse models of autism
Lactobacillus reuteri leads to specific changes in the brain that restore social behaviors through a mechanism that involves the vagus nerve and the oxytocin-dopamine reward system.
We and others have previously shown that Lactobacillus reuteri increases oxytocin levels in the brain, but we didn’t know the channel of communication by which this microbe affects the brain. In this research, we determined that the vagus nerve and the oxytocin-dopamine reward system were both necessary for the social behaviors to be restored. When we cut the vagus nerve, the treatment with the bacteria had no effect. When we prevented the oxytocin to bind to its receptors in the specific brain area involved in social reward, the bacteria was not able to have an effect either. So L. reuteri needed both the vagus nerve and the oxytocin receptors to restore the behavior.
this probiotic looks interesting.
want to try it to see if it helps with digestion at the very least. but so many people report other benefits its very intriguing.
I try to take any mental aspect out of this thought and look for something real.
I was at the dentist the other day and the hygienist said my gum tissue looked really healthy and hardly bled on probing. This normally isnt the case for me, I might post something on this soon.I believe my vision has become a little less sensitive to light.
Thats it for now.
There’s also what some might perceive as negative effect, but I push through things maybe more then some in an effort to learn more.
I plan on to keep going with this for now. its been a little over 2 months.
To put things in perspective even a hard core drug like Accutane is normally a 16 to 30 week course.
Hi @guitarman01, any updates? How has the L. Reuteri doses you’ve been taking affected you? Anything worthy to report? Still trying to find the link to buy the 10billion dose that you’ve mentioned, I’m in the US. Which should I buy?
As someone whose main symptom is insomnia, the 100 million CFU version i.e. Gastrus already gives me horrible hellish insomnia and some hives but YMMV.
I am using BioGaia Protectis which contains the other strain of L. Reuteri at 100 million CFU. I got it for my serious constipation but I am almost done with it and I think it was a waste of money.
So maybe you could barely tolerate the histamine producing strain, but the non histamine producing strain you barely noticed?
Your gi issues are a big deal to me too I’ll get back to you on some thoughts on that. BTW have you ever tried a h2 blocker?
I am fairly sure I read once that l.reuteri does not survive in a retinol deficient environment, maybe I’m mistaken, but makes you start to wonder what’s happening now.
Have you read this as well? I’m not sure if it need retinol or retinoic acid to survive.
No, I can’t tolerate the histamine producing strain at all, unfortunately. I felt effects like increased libido, increased penile sensitivity, mental calmness with it so it’s a real shame.
The non-histamine producing strain though I still have yet to notice it making any difference. It sure didn’t do anything for my constipation.
I haven’t tried any H2 blockers, luckily. I’ve used PPIs in the past for mild acid reflux which hadn’t come back.
I do look forward your thoughts regarding my GI issues.
I had a ct scan of my abdominal area from a gi doc and the only thing they found was alot of reason to recommend Miralax.
Id also keep this test in mind, ive tested positive for this antibody.
acetylcholine ganglionic neuronal antibody
Autoimmune GI dysmotility: A new direction
“if the immune system can cause inflammation of the optic nerve, spinal cord or cerebral cortex, then why can’t it cause a problem with the gut? After all, the gut contains 100 million neurons — more than the spinal cord or the peripheral nervous system.”
Immunotherapy trial as diagnostic test in evaluating patients with presumed autoimmune gastrointestinal dysmotility
Ganglionic AChR antibodies are proven to cause AGID in active and passive immunization animal models
Autoimmune Dysautonomia Evaluation, Serum
https://www.mayocliniclabs.com/test-catalog/Clinical+and+Interpretive/92121
The most commonly encountered autoantibody marker of autoimmune dysautonomia is the neuronal ganglionic alpha-3-acetylcholine receptor (AChR) autoantibody. This autoantibody to date is the only proven effector of autoimmune dysautonomia
Regarding 6475, it activates h1 and h2 receptors, but supposedly blocks inflammatory h1 effects by a metabolite the bacteria produces.
HISTAMINE PRODUCTION
BioGaia’s L. reuteri strains have anti-inflammatory effects
Production of histamine is the prerequisite for one mode of action
L. reuteri ATCC PTA 6475, 5289 and 4659 can produce histamine
L. reuteri DSM 17938 can’t produce histamine
Histamine production and anti-inflammatory effects
L. reuteri ATCC PTA 6475 (6475) can produce histamine in the intestine
In the cell membrane of epithelial cells you find 4 different histamine receptors,
of which the first two are key receptors in inflammation
When histamine binds to H1R, inflammation is induced
When histamine binds to H2R, inflammation is reduced
6475 can also produce the enzyme diacyl-glycerol kinase, DagK
DagK degrades diacyl-glycerol in the cell wall of the epithelial cells and thereby blocks the pro-inflammatory pathway connected to the H1R
The histamine that binds to H2R, results in a reduced inflammation
^This is immunosuppression. I have thought more of this being a bad thing in our case initially though, so im still careful about this.
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Welp, either way that info gives me little recourse seeing as how I respond to histamine producing strains.
Here’s a wet blanket on probiotics’ therapeutic potential for constipation :
Ha. We could go back and forth all day, months, years with conflicting studies. Lets take the word probiotic out of the equation. Bacteria (our microbiome) affects intestinal transit time and motility. This could be related to whats been termed “poo pellets” on here or no longer having man/massive sized shits. Im also showing you some other things to consider. If you feel you have such a great reaction to histamine produced in the gut, why not test the opposite route with a h2 blocker?
Histamine could affect gastric emptying as well. Just like inflammation could also in this next study,
APRIL 5, 2019
Researchers find probiotics may increase intestinal motility in mouse model
Emory researchers have found that adding good bacteria into the intestines can guide the development of the enteric nervous system, also called “the gut brain,” while increasing intestinal motility, or movement of the digestive tract, in a mouse model. The results are good news for medical conditions such as irritable bowel syndrome, Parkinson’s disease, autism and others, where activity in the digestive tract is slowed. The findings were published in the journal Gastroenterology on March 28, 2019.
I am not sure if we can put a rat study and a meta-analysis of RCTs on equal footing. Rat studies of the psychobiotic l. rhamnosus JB-1 didn’t translate to human results.
I mean, aside from the recent scare concerning ranitidine and other H2 blockers and unsafe NDMA levels, shouldn’t H2 induction help diarrhea rather than constipation as it triggers smooth muscle relaxation? Either way, as someone who doesn’t have GERD, messing with the H2 receptor seems excessively invasive.
Oh, and I think the tribulus was worsening my constipation. It’s bizarre in that I was losing the urge during higher doses of it i.e. 2-3 pills/day of Mediherb Tribulus.
I have a feeling this will get a little tedious. That study was a quick example of conflicting studies, even being released the same month nonetheless.
I could give about 50 more on the topic, but I dont see a point in that.
Regarding the h2 receptor i’ve spent some time on here recently showing its involved in alot more then acid secretion.
Speaking of gastric acid secretion, this could play a role in normal digestion and whats termed gi compartmentalization, or preventing bacterial translocation. This along with mucus production could make solid food more easy to pass.
I mainly brought up the thought of trying a h2 blocker because you seemed highly sensitive to a histamine producing bacteria. (I believe this also depends on protein consumption containing histidine)
Gi bacterial production of histamine could either play a pathological or protective role, and if you’ve seen all my postings on histamine, thats something to keep in mind.
I also look at the h2 receptor possibly playing a major role in immunity. One example that might apply, (you want balance here though or regulation). Same with the histamine and exercise study I just posted, how it could relate to Ed. Too much in either direction… loss of blood pressure/ loss of force.
Inducible histamine protects mice from P. acnes-primed and LPS-induced hepatitis through H2-receptor stimulation.
Inducible histamine and histamine H2-receptors have been suggested to be involved in innate immune response.
skip to the conclusion,
These findings as a whole indicated that endogenously produced histamine in Kupffer cells/macrophages plays a very important role in preventing excessive innate immune response in endotoxin-induced fulminant hepatitis through the stimulation of H2-receptors.
im losing my edits again. oh well.
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Excellent.
I could probably plop this into one of the histamine threads, but here’s another example looking at MS. What they are talking about here could possibly be manipulated by bacteria as well.
Potential immunological consequences of pharmacological suppression of gastric acid production in patients with multiple sclerosis
Interventions for gastric disturbances can influence the activation state of the immune system, a principal mediator of pathology in multiple sclerosis. Although histamine release promotes inflammation, activation of the histamine receptor-2 can suppress a proinflammatory immune response, and blocking histamine receptor-2 with an antagonist could shift the balance more towards immune stimulation. Studies utilizing an animal model of multiple sclerosis indicate that histamine receptor-2 antagonists potentially augment disease activity in patients with multiple sclerosis.
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