Random, interesting studies
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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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