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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Thanks for the informative posts bro.
I’ve been experimenting with L. Reuteri ATCC (BioGaia Gastrus) and just like @Mercked it gave me all the typical histamine intolerance symptoms (e.g. Itchiness; flushing; stuffed nose; nausea; lower BP; headache; eczema… etc.) after supplementing for a while. Interestingly, I’ve also noticed that morning erections disappear along the process. I’ve read about similar experiences on Reddit and elsewhere. It appears there’re a subset of people who are very, very sensitive to histamine spikes. Taking other strains known to degrade histamine helped to balance things but I eventually had to stop L. Reuteri ATCC altogether.
I learned that you’ve been taking 10B CFU a day for a while, how are you feeling?
This became more of a problem then a solution. I wouldnt recommend it. I did trial this for months on end non-stop at a10 billion per day dosage. I talked about stopping this on a couple different threads. I suppose it would be good to place that here as well.
I had plenty of reasons to look at this based on the research and studies, but we all know this more than likely does not translate as a real solution. I always think I might find some things out one way or another as to how Im affected outside of a placebo effect.
Talking about microbes that degrade histamine though, if you want to fully look into this, one quick study comes to mind. Then go check my Viome results for Bifidobacteria.
I would also like to seperate “histamine intolerance” from the 1000s of holistic websites.
This is still a controversial thought.
Microbial patterns in patients with histamine intolerance.
Histamine intolerance represents a controversially discussed disorder. Besides an impaired degradation of orally supplied histamine due to diamine oxidase (DAO) deficiency, a deranged gut flora may also contribute to elevated histamine levels. Our aim was to determine the intestinal bacterial composition in patients with proven histamine intolerance in comparison to other food intolerances and healthy controls. A total of 64 participants were included in the study, encompassing 8 patients with histamine intolerance (HIT), 25 with food hypersensitivity (FH), 21 with food allergy and 10 healthy controls (HC). All participants underwent blood testing for total and food-specific immunoglobulin E, plasma histamine and DAO serum activity. Stool samples were used to analyze stool histamine and zonulin levels and bacterial composition by 16s rRNA sequencing. No significant differences in stool histamine levels were observed, but HIT patients showed elevated levels of stool zonulin. Microbiota analysis revealed increased levels of Proteobacteria (5.4%) and a significantly reduced alpha-diversity in the HIT group (P = 0.019). On family level, HC showed a significantly higher abundance of Bifidobacteriaceae compared to other study groups (P = 0.005), with lowest levels in the HIT group (P = 0.036). Also significantly reduced abundances of the genera Butyricimonas (P = 0.026) and Hespellia (P = 0.025) were observed in the HIT patients, whereas Roseburia were significantly elevated (P = 0.021). We concluded that the altered occurrence of Proteobacteria and Bifidobacteriaceae, reduced alpha-diversity as well as elevated stool zonulin levels suggest a dysbiosis and intestinal barrier dysfunction in histamine intolerant patients, which in turn may play an important role in driving disease pathogenesis.