You know what? I’m starting Align right away 
Id look at the higher dose if your in the States, id also maybe double the dosage to possibly notice effect sooner. 10 billion seems to be a ballpark for alot of probiotics for a daily dosage. I only tell you this because I know you have some previous knowledge and interest.
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Im looking at thoughts as I mentioned above for other then just IBS and c.diff.
A high-dose transplant and/or repeated FMT increase the response rate and the intensity of the effects of FMT.
Increasing the Dose and/or Repeating Faecal Microbiota Transplantation (FMT) Increases the Response in Patients with Irritable Bowel Syndrome (IBS)
When fecal transplants for C. diff. fail, try, try again
Indeed. I’m back on Align + Pro4-50 combo and will do them for two more weeks or longer. I’m super interested in B. Infantis 35624 blocking (or at least lowering) TNF-a and IL-6 while also inducing Tregs.
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Honestly if it was me I might not be mixing all those different strains, especially if trialing Align again. Certain bacteria even probiotics can compete with one another. If you look on the packaging of Align you can see its already somewhat unstable to begin with. Id also want to know whats doing what, thats a little hard to tell when taking multiple supplements.
I’ve been mostly experimenting with single strain products (e.g Mutaflor; Align; Culturelle; BioGaia; etc.). Pro4-50 comprises of 4 strains, however. I’m specifically on it to deal with suspected D-Lactate as mentioned but yes you make a good point.
Care to elaborate on
"you look on the packaging of Align you can see its already somewhat unstable to begin with."
If you check the labeling, they claim 5 billion cfu’s at time of manufacture but only guarantee 50 million by the best by date.
So theres a pretty large fluctuation there, even with (im guessing) one of the highest levels of quality control for any probiotic. It could be more so the nature of the strain. For example, if you check bb-12 also sold by Align, its much more stable.
Also 35624 is of human origin, bb-12 is not.
50 million! Holy moly! I’ve been facing similar issue with several other probiotics. Refrigerated ones are super challenging with regards to shipping. Bacterial viability is a real concern even though some studies state that heat-killed bacteria can still exert effect. This is my 3rd day on Align and I can feel some gastrointestinal changes already. I’m looking forward to its effect in reducing systemic circulation of pro-inflammatory biomarkers TNF-α and IL-6 and increasing Tregs. I’ll keep you posted.
This is something ive mentioned a few times, stool samples do not tell the whole story.
“The murine & human gut mucosal microbiome only partially correlates with stool”
In this work, we profiled the homeostatic mucosal, luminal, and fecal microbiome along the entirety of the gastrointestinal tract of mice and humans. We demonstrated that solely relying on stool sampling as a proxy of mucosal GI composition and function may yield limited conclusions.
Personalized Gut Mucosal Colonization Resistance to Empiric Probiotics Is Associated with Unique Host and Microbiome Features
https://www.sciencedirect.com/science/article/pii/S0092867418311024
Our results highlight several important concepts. First, we expand the scope of description of the human microbiome bio-geographical compositional and functional landscape (Donaldson et al., 2016, Mowat and Agace, 2014), and indicate that extrapolation from stool microbiome communities to those of specific GI mucosal and luminal niches may lead, in some cases, to inaccurate conclusions.
I think that could be an important study I just posted.
Still looking at Vitamin As possible involvement. ’
Impact of Retinoic Acid on Immune Cells and Inflammatory Diseases
Vitamin A metabolite retinoic acid (RA) plays important roles in cell growth, differentiation, organogenesis, and reproduction and a key role in mucosal immune responses. RA promotes dendritic cells to express CD103 and to produce RA, enhances the differentiation of Foxp3+ inducible regulatory T cells, and induces gut-homing specificity in T cells. Although vitamin A is crucial for maintaining homeostasis at the intestinal barrier and equilibrating immunity and tolerance, including gut dysbiosis, retinoids perform a wide variety of functions in many settings, such as the central nervous system, skin aging, allergic airway diseases, cancer prevention and therapy, and metabolic diseases. The mechanism of RA is interesting to explore as both a mucosal adjuvant and a combination therapy with other effective agents. Here, we review the effect of RA on innate and adaptive immunity with a special emphasis on inflammatory status.
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Just like with Accutane, imagine never needing an SSRI to begin with.
Still looking at this same strain here.
First of all,
Tryptophan is an essential amino acid necessary for the synthesis of serotonin, melatonin, and niacin. Low plasma concentrations of tryptophan have been associated with clinical observations of insomnia, anxiety, and depression.
The plasma tryptophan ratio predicts brain tryptophan uptake and serotonin production. If this ratio is low, serotonin function may also be low.
The microbiota could contribute to the pathophysiology
of IBS through a number of mechanisms
; similarly, numerous hypotheses have been invoked to explain probiotic benefits in IBS. These include anti-inflammatory effects, modulation of intestinal transit,
motility and sensation, as well as alterations in the intraluminal milieu via deconjugation of bile acids, generation of
short chain fatty acids and gases.
It should also be noted, in addition, that bacteria can produce
neuroactive compounds. Of these, serotonin may be of particular interest, given biopsy evidence of defects in serotonin
signalling in the gut among IBS patients, as well as evidence that B. infantis 35624 can increase plasma concentrations of tryptophan, the precursor of serotonin. Although
meta-analyses suggest that selective serotonin reuptake
inhibitors do not significantly improve IBS symptoms, serotonin delivered locally by bacteria could be more effective.
solely relying on stool sampling as a proxy of mucosal GI composition and function may yield limited conclusions .
^Going back to this, Im not sure if there is another commercially available probiotic that was isolated directly from the GI tract, not the stool.
Bifidobacterium longum subspecies infantis 35624 (B infantis) is a commensal microbe originally isolated from the human gastrointestinal mucosa.
Bifidobacterium longum subsp infantis 35624 (B. infantis) was originally isolated from resected human healthy gastrointestinal tissue about 15 years ago.
It could be a matter of duration and dosage.
You would also possibly zero in on Bifido species because of its possible importance and selectivity from birth.
Populations of bifido decrease over the age of 60.
Problem isn’t just the dosage but the diversity of bacteria that can only be obtained through fmt. Delivery method is also likely a player.
Actually I could post a rebutile to these statements, its why I posted the studies.
So when you see this what could it also say about fecal transplants?
Solely relying on stool sampling as a proxy of mucosal GI composition and function may yield limited conclusions
What is in the stool does not necessarily correlate with mucosal gi composition, hence FMT may yield limited results, or the use of bacteria mostly found in the stool, after all this is waste.
Also, another study I posted the example being c.diff.
Among adults with RCDI, FMT via oral capsules was not inferior to delivery by colonoscopy for preventing recurrent infection over 12 weeks. Treatment with oral capsules may be an effective approach to treating RCDI.
This is still just looking at a single strain. This single strain has quite a bit going for it.
They talk about “keystone” bacteria when it comes to success of fmt.
Bifidobacterium infantis 35624 has been shown to normalize noradrenaline levels in the brainstem region that regulates mood but also alters other neurotransmitters, such as gamma-aminobutyric acid and serotonin.
I dont feel bad about wanting to know others experience with this probiotic.
Meaning im pretty sure its not going to make you worse.
I would be looking at a minimum dosage of 10 billion per day.
Some more thoughts looking at the 10 billion or more per day dosage.
You can also see they can recover this strain from tissue biopsies, not just the feces.
They’re basically saying 1 billion per day at 8 weeks might not be enough for effect.
Fecal excretion of Bifidobacterium infantis 35624 and changes in fecal microbiota after eight weeks of oral supplementation with encapsulated probiotic
using B. infantis 35624 transformed with a rifampicin resistance gene as a marker for enumeration, the investigators demonstrated that the strain had established itself in the colon of these patients, reaching levels of 105–108 cfu, depending on the individual; the strain could be recovered from fecal samples and colon biopsies.
Consequently, our study does not allow firm conclusions about the impact of B. infantis 35624 supplementation on the GI tract microbiota. However, exploratory studies from our laboratory, which characterized fecal microbiota using terminal restriction fragment polymorphism (t-RFLP) analysis of microbial DNA, showed that controlled daily administration of 1010 cfu B. infantis 35624 in milk for three weeks helped normalize the intestinal microbiota. The analysis of fecal samples from 24 subjects (13 with IBS and 11 controls) revealed 3 DNA fragments associated exclusively with IBS, 29 fragments that differed in proportion between IBS patients and healthy controls prior to treatment and a probiotic-associated shift to equivalent proportions of 16 of these 29 fragments in the microbiota of both groups (unpublished data). Hence, more robust and comprehensive surveys (and, possibly, longer interventions) may be needed to detect potential changes in GI tract microbiota associated with B . infantis 35624 supplementation
We conclude that further fecal microbiota studies with more comprehensive microbial surveys and additional doses of B. infantis 35624 administered for longer durations are needed to further explore the role of the intestinal microbiota composition and metabolic processes
I think ive posted this one before,
Suppression of gut dysbiosis by Bifidobacterium longum alleviates cognitive decline in 5XFAD transgenic and aged mice
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best thing to do is take inulin (prebiotics), lots of fibre and cut out sugar. The bacteria is already there, it just needs the right environment. No need to spend hundreds of dollars on supplements
The thought is missing or lost bacteria.
The goal would be to reestablish select bacteria.
Inulin could be non-selective as it could be a growth factor for numerous species both beneficial and not. If some have decreased intestinal motility, inulin would not be recommended.
Most prebiotics are not recommended in the case of SIBO for example.
One thought on inulin and some other prebiotics is it could act as a decoy or binder for some types of pathogenic bacteria to literally flush out or act as a clearance pathway.
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Here’s another example of differing stool and mucosal microbiomes in a disease state, so to just look at the stool (or treat with fmt) might not be enough.
Colonic mucosal microbiome differs from stool microbiome in cirrhosis and hepatic encephalopathy and is linked to cognition and inflammation
@guitarman01 just opening up this topic out of interest. What is your opinion on the topics discussed in this thread today? 
Did you or anyone else try a treatment with the certain bacterias / pro-biotics discussed here? If so, what have been their results?