Why don’t I bother reporting microbiome studies as the next great cure and why not report all the supportive (scientifically interesting) animal studies which give us “Cure of the week”.
Simple…the data seems to be something that is produced via the intestine and the effects are simply not good or consistent enough….for it to be ready for prime time.
This week Lactobacillus (gut bacteria) hit the news and in this weeks PeeNas we have
Interactions between host genetics and gut microbiota determine susceptibility to CNS autoimmunity. Montgomery et al. PNAS 2020; https://doi.org/10.1073/pnas.2002817117
Significance “Our results demonstrate a complex interplay between host genotype and gut microbiota in autoimmune disease, and identify a single species capable of modifying disease susceptibility in a genetically susceptible host. Our studies underscore the need to consider host genetics and baseline gut microbiota composition in autoimmunity”.
“We identified specific gut bacteria and their metabolic functions associated with EAE susceptibility, implicating short-chain fatty acid metabolism as a key element.
“Manipulation of the gut microbiome by transplantation and cohousing demonstrated that transfer of these microbiomes into genetically identical hosts was sufficient to modulate EAE susceptibility and systemic metabolite profiles. Parallel bioinformatic approaches identified Lactobacillus reuteri as a commensal species unexpectedly associated with exacerbation of EAE in a genetically susceptible host, which was functionally confirmed by bacterial isolation and commensal colonization studies”.
These results reveal complex interactions between host genetics and gut microbiota modulating susceptibility to CNS autoimmunity, providing insights into microbiome-directed strategies aimed at lowering the risk for autoimmune disease and underscoring the need to consider host genetics and baseline gut microbiome composition.
Therefore you start to ask, is it a practical approach?.
What does Lactobacillus reuteri do in other peoples hands? Well it makes it worst (Miyauchi et al. 2020)… no I mean better (He et al. 2019)…Hence a potential problem
Miyauchi et al. (2020) Gut microorganisms act together to exacerbate inflammation in spinal cords.Nature. doi: 10.1038/s41586-020-2634-9
It says “No statistical methods were used to predetermine sample size. The experiments were not randomized and investigators were not blinded to allocation during experiments and outcome assessment”
So maybe a bias experiments but it says the bacteria make T cells reactive to myelin
“Here we show that two distinct signals from gut microorganisms coordinately activate autoreactive T cells in the small intestine that respond specifically to myelin oligodendrocyte glycoprotein (MOG). After induction of experimental autoimmune encephalomyelitis in mice, MOG-specific CD4+ T cells are observed in the small intestine. Experiments using germ-free mice that were monocolonized with microorganisms from the small intestine demonstrated that a newly isolated strain in the family Erysipelotrichaceae acts similarly to an adjuvant to enhance the responses of T helper 17 cells. Shotgun sequencing of the contents of the small intestine revealed a strain of Lactobacillus reuteri that possesses peptides that potentially mimic MOG”.
Lactobacillus is bad news, but other studies says Lactobacillus is good news
He B, Hoang TK, Tian X, Taylor CM, Blanchard E, Luo M, Bhattacharjee MB, Freeborn J, Park S, Couturier J, Lindsey JW, Tran DQ, Rhoads JM, Liu Y. Lactobacillus reuteri Reduces the Severity of Experimental Autoimmune Encephalomyelitis in Mice by Modulating Gut Microbiota. Front Immunol. 2019 Mar 7;10:385.
“The gut microbiome plays an important role in immune function and has been implicated in multiple sclerosis (MS). However, how and if the modulation of microbiota can prevent or treat MS remain largely unknown. In this study, we showed that probiotic Lactobacillus reuteri DSM 17938 (L. reuteri) ameliorated the development of murine experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS, a model which is primarily mediated by TH17 and TH1 cells. We discovered that L. reuteri treatment reduced TH1/TH17 cells and their associated cytokines IFN-γ/IL-17 in EAE mice. We also showed that the loss of diversity of gut microbiota induced by EAE was largely restored by L. reuteri treatment. Taxonomy-based analysis of gut microbiota showed that three “beneficial” genera Bifidobacterium, Prevotella, and Lactobacillus were negatively correlated with EAE clinical severity, whereas the genera Anaeroplasma, Rikenellaceae, and Clostridium were positively correlated with disease severity. Notably, L. reuteri treatment coordinately altered the relative abundance of these EAE-associated taxa. In conclusion, probiotic L. reuteri changed gut microbiota to modulate immune responses in EAE, making it a novel candidate in future studies to modify the severity of MS.”
So look at the data. Ask “Is it a “Cure of the Week”? The simple answer is No.
The effect on the disease is marginal, so don’t expect the disease to go away.
If you want to take probiotics, take pro biotics but don’t expect earth-shattering changes. The work is too early to be prime time…yet clinical trials are already full steam ahead and as you can imagine I think if we are lucky we will see a small influence….Enough for a platform presentation at ECTRIMS 202X, but not challenging pharma for the top spot in disease control.
I could be wrong and you may get
So when you pop down to the local health spa or pop-up one-stop-shop to get your faecal transplant for a few thousand…just see it as a bit of pampering and RnR…that you are paying for. Then you won’t be disappointed if the results don’t go the way you are led to believe by dubious docs, the media and scientific hype.
When it is ready for prime time, I will be there chocolate shake in hand.