Random, interesting studies
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@Mauritio Yeah I was thinking of your post and looked into it a but
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Apple polyphenols protect from aspirin induced stomach damage.
https://pubmed.ncbi.nlm.nih.gov/25069887/
https://pubmed.ncbi.nlm.nih.gov/18482463/Honey and propolis help as well.
https://www.mdpi.com/2072-6643/13/9/3169
https://www.sciencedirect.com/science/article/abs/pii/S2214785321029254The protection always seems to stem from the polyphenol content of those foods. So I suspect that eating anything that has alot of polyphenols with the aspirin should work. Berries, fruits, or a glass of Orange juice.
Dare to think.
My X:
x.com/Metabolicmonstr -
@Mauritio said in Random, interesting studies:
anything that has alot of polyphenols with the aspirin should work.
Yes, to counteract excess oxidation and then inflammation. But we need to optimize mucin thickness with glutamine (and taurine to counteract the excitotoxcity in the brain).
I take half a teaspoon of taurine and the same with glutamine powder, one hour before bedtime, when I feel a stomach acidity. No glutamine if you suffer from dysbiosis (suspicion of candidiasis: it feeds the bacteria).
When it's nervous, L-theanine 225 mg and 1 tsp collagen do the job (cramp). Never take SSRS as a usual med... -
"The effect of vitamin A supplementation on plasma estrogen and progesterone were studied in pregnant women. While there was no change in the estrogen concentration, the mean increment in plasma progesterone in the supplemented group was significant when compared to the unsupplemented group. It is suggested that vitamin A supplementation to undernourished pregnant women may have beneficial effect on feto-placental function."
https://pubmed.ncbi.nlm.nih.gov/1856040/ -
Now here's something controversial and interesting from Cell:
To take probiotics post-antibiotic treatmentcanwill inhibit restoration of one's microbiome in contrast to simply letting things run its course without any post-antibiotic intervention (if one's lucky enough to not get a CDI, of course. Yet the course for that may have been set already during Abx treatment, we don't really know if probiotics after Abx can rescue that).
A much more effective method could be "autologous fecal matter transplant". No foreign donor required.
Collecting, filtering, liquefying and freezing one's pre-antibiotic healthy microbiome and using this once on day 0 after antibiotic treatment.
Like in hamsters: Eating your own shit. This enriches the (mostly preserved) endogenous microbiome reserves and puts them back from the end to the more proximal parts of the digestive system.Compared to spontaneous post-antibiotic recovery, probiotics induced a markedly delayed and persistently incomplete indigenous stool/mucosal microbiome reconstitution and host transcriptome recovery toward homeostatic configuration, while aFMT induced a rapid and near-complete recovery within days of administration.
In rodent experiments, the degree of mucosal colonization and shedding of human-specific probiotics even after antibiotic pretreatment was small. Pointing yet again to a huge importance of specificity between host species and strain.
I.e. rodent studies for testing probiotic benefits in humans ought to be quite garbage.
The study went on to human volunteers with the same and apparently very reasonable 11-strain Lactobacillus + Bifidobacterium probiotic blend ("Supherb Bio-25", 25 billion CFU twice daily):Following antibiotic treatment, seven participants were followed by watchful waiting for spontaneous microbiome reconstitution, six participants received aFMT (STAR Methods), and eight participants received the aforementioned 11-strain probiotics preparation administered bi-daily for a period of 4 weeks (Figure 3A).
participants from the aFMT arm received an intrajejunal infusion of 150 ml of processed and liquefied stool (on day 0), which had been obtained from the participant prior to the antibiotics therapy
In the spontaneous recovery group, significant differences in stool composition compared to baseline abated within 21 days of antibiotics cessation (Figure 4B). In contrast, probiotics-consuming individuals did not return to their baseline stool microbiome configuration by the end of the intervention period (day 28), and dysbiosis was maintained even 5 months after probiotics cessation, with all stool samples collected through day 180 remaining significantly different from baseline
dun- dun dun dun.
And here's another interesting find from nature microbiology, where they blasted volunteers with the three "last-resort" antibiotics meropenem, gentamicin and vancomycin:
Recovery of gut microbiota of healthy adults following antibiotic exposure, 2018
The gut microbiota of the subjects recovered to near-baseline composition within 1.5 months, although 9 common species, which were present in all subjects before the treatment, remained undetectable in most of the subjects after 180 days.
That latter part sort of negates the first statement, doesn't it?
Finally, some species detected at D0 were not detected again within the study time frame.
These included: (1) members of genus Bifidobacterium that are considered pathogen-protective and immunostimulatory;
2) butyrate producers such as Coprococcus eutactus and Eubacterium ventriosum and
(3) methane-producing Methanobrevibacter smithii associated with the efficient digestion of polysaccharides.Remarkably, only two F. prausnitzii strains were able to recover by D180, another six could not recover through the study period (Supplementary Fig. 3), reflecting the different recovery capacities between conspecific strains.
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" F prausnitzii EXL01 strain did not induce pro-inflammatory pathways compared with LPS, but up-regulated Oxidative Phosphorylation while down-regulating Glycolysis and Apoptosis pathways (Figure 5D and E)."
"Interestingly, increasing doses of F prausnitzii EXL01 strain blocked LPS-induced glycolysis activation and OXPHOS inhibition (Figure 6B and C)."
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@CrumblingCookie just saw you also posted about f. Prausnitzii. Nice synchronicity.
For the purpose you mentioned above kestose might be beneficial. Since it increases butyrate and F. Prausnitzii. -
Interesting study showing endogenous metabolite of C15 fatty acid is a potent endocannabinoid, anti-inflammatory, agonist on 5HT1A + B, and Antagonist on histamine receptors.
C15 is part of idealabs LipOdd.Dare to think.
My X:
x.com/Metabolicmonstr -
@Mauritio pea?
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@lobotomize full sentences?
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