Random, interesting studies
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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?
Dare to think.
My X:
x.com/Metabolicmonstr -
@Mauritio Palmitoylethanolamide similar effects
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Activating the dopamine receptor D2 enhances life span. Using known longevity pathways like AMPK (in C. elegans).
https://pubmed.ncbi.nlm.nih.gov/35317792/D2 is the gift the keeps on giving.
I made a thread about D2 years ago:
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Clary Sage
shown to activate several dopamine receptors d2 as well
https://pubmed.ncbi.nlm.nih.gov/20441789/did not significantly increase estrogen when inhaled, increased prgesterone more than estrogen
https://www.mdpi.com/2076-3417/16/7/3234increases Ca:ph ratio
https://pdfs.semanticscholar.org/215c/5e47d31c14f3842b4bb095bf36de43d18723.pdfincreased testosterone and especially progesterone in vitro
"A significant (P<0.05) stimulation of testosterone secretion was recorded at 250 μg/ml for 24 h, while the prolonged cultivation time significantly (P<0.05) increased the testosterone and progesterone production at 150, 200, 250 and 300 μg/ml. "
https://pmc.ncbi.nlm.nih.gov/articles/PMC8549893/it helps with reproductive health damaged by cadmium
https://pmc.ncbi.nlm.nih.gov/articles/PMC10682483/ -
Why haven't y'all started superdosing melatonin yet instead of wasting lifetime and effort on quinones and saturating cardiolipins etc.?
Melatonin precedes the importance of quinones as it binds to and activates quinone reductase type 2 (NOQ2) to degrade oxidized, i.e. toxic quinones. Thus, clearly of top priority before adding any K2 (Mk-4) etc.
Melatonin reverses the Warburg-type (glycolytic) metabolism of cells.
This effect is self-enhancing, as reinstated OXPHOS enables intracellular melatonin synthesis.
Just as, without such exogenous intervention, the opposite development is a self-sustaining vicious cycle.Pathological neurons often exhibit Warburg type metabolism and redirect pyruvate into the mitochondria restores mitochondrial redox homeostasis; examples of diseases where this aberrant metabolism occurs include Alzheimer’s, Parkinsonism, amyotrophic lateral sclerosis and others (Reiter et al., 2021b). The ability of melatonin to interfere with Warburg type metabolism presumably relates to its inhibitory action of hypoxia inducible factor 1α (HIF1α), which suppresses the activity of pyruvate dehydrogenase kinase (PDK) which disinhibits PDC allowing pyruvate to enter the mitochondria followed by its conversion to acetyl CoA such that the limited availability of acetyl CoA no longer is a factor in the amount of melatonin synthesized in the mitochondria (Fig. 3) (Mota et al., 2019). These actions of melatonin are reminiscent of those using dichloroacetate, a pharmacological agent that also reverses Warburg type metabolism, perhaps by the same signaling pathway as melatonin and has generated interest as a useful pharmaceutical drug to treat several diseases (Chen et al., 2024b, Kakafika et al., 2024). It has limitations regarding its side effects, actions that do not accompany melatonin use (Bianchi et al., 2024).
Here you get a picture to go along with this:
https://journals.physiology.org/doi/full/10.1152/physiol.00034.2019And here's a table with clinical observations on melatonin relevance in metabolic syndrome (humans):
https://pmc.ncbi.nlm.nih.gov/articles/PMC11107716/table/Tab2/
And a table with experimentally shown effects of melatonin in animal models of metabolic syndrome:
https://pmc.ncbi.nlm.nih.gov/articles/PMC11107716/table/Tab1/Even better: Postmitotic cells aren't doomed to be left by themselves with their inherited pool of malfunctioning mitochondria because melatonin stimulates the transfer of mitochondria from healthy cells to damaged cells via tunneling nanotubes (TNTs)!
If you're now wondering what are tunneling nanotubes, here are pictures of them. They can form between mitochondria of the same cell as a precursor step to fusion and they can form between cells:
Disturbingly and one the downside of this spectacular mechanism, even cancerous cells may use nanotubes to steal mitochondria from T-cells:
t-cell-nanotube-cancer
(I reckon those cancer types can't be running Warburg metabolism - or do they just steal the mitos and their ATP from the immune cells only to then crush them?) -
@CrumblingCookie Yeah you cooking us here ngl
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Yeah you cooking us here ngl
No cap fr fr?
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Yeah you cooking us here ngl
No cap fr fr?
Peat was generally suspicious of melatonin, especially as a darkness/stress-associated hormone. In one article, he grouped melatonin with “nocturnal/stress hormones” and argued it could make the retina more vulnerable under certain conditions
Peat cited A.V. Sirotkin’s porcine ovary work, saying melatonin inhibited progesterone and stimulated estradiol. He then interpreted that pattern as similar to low thyroid: higher estrogen, lower progesterone, lower resistance to stres
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@lobotomize Lol you are proving the crumbling cookie right. Muh darkness hormone.
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