Random, interesting studies
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@Mauritio wild study which makes an argument that those taking cold showers are actually using it as instinctual self medication
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@lobotomize yes but i think you'd have to be in somewhat decent shape to reap the benefits of cold showers. There is such a thing is cold resistance when it comes to thermogenesis and uncoupling.
IIRC there was a study showing that grains of paradise were able to reverse that state in humans. -
I have posted about the hypermetabolic übermice before.
I'm trying to understand the mechanism. From what I can tell increasing PEPCK-C in the muscle, mainly inhibits anaerobic glycolisis (fermentation metabolism) and increases OxPhos. I think that is the fundamental mechanism. The fact that tjsr doubles life span and increases reproductive health so much, corroborates what Peat said for decades."...we identified a progressive decrease in cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C), a longevity-associated metabolic enzyme, and a reciprocal increase in glycolytic pyruvate kinase (PK) that were necessary and sufficient to limit lifespan. Decline in PEPCK-C with age also led to loss of cellular function and integrity including muscle activity, and cellular senescence. Genetic and pharmacologic interventions of PEPCK-C, muscle activity, and AMPK signaling demonstrate that declines in PEPCK-C and muscle function with age interacted to limit reproductive life and lifespan via disrupted energy homeostasis. Quantifications of metabolic flux show that reciprocal changes in PEPCK-C and PK with age shunted energy metabolism toward glycolysis, reducing mitochondrial bioenergetics. Last, calorie restriction countered changes in PEPCK-C and PK with age to elicit anti-aging effects via TOR inhibition. Thus, a programmed metabolic event involving PEPCK-C and PK is a determinant of aging that can be modified to modulate aging."
https://pubmed.ncbi.nlm.nih.gov/26631730/
"...overexpression of the central gluconeogenic gene pck-2 (encoding PEPCK) increases health measures via a mechanism that requires DAF-16 to promote pck-2 expression in specific intestinal cells. Dietary restriction also features DAF-16-dependent pck-2 expression in the intestine, and the healthspan benefits conferred by dietary restriction require pck-2. Together, our results a new paradigm in which nutritional signals engage gluconeogenesis to influence aging quality via DAF-16."
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008982"Finally, a synergistic induction of PEPCK gene transcription by T3 and cAMP is described. "
https://pubmed.ncbi.nlm.nih.gov/1657985/ -
It has been wondered how Helicobacter pylori actually spreads from human to human.
Beside the fecal-oral transmission in low hygienic standards, some few people have it in notable amounts even freely in their saliva, from where it can spread by aerosols, kissing or sharing drinks.Another transmission vector and reservoir, however, appears to be through oral, vaginal, food-borne and environmental spread of H.pylori-infected yeasts, which provide greatly enhanced protection to these bacteria, as shown by these Iranian researchers:
Vacuoles of Candida yeast as a specialized niche for Helicobacter pylori, 2014
The internalized H.pylori also reproduces inside yeast vacuoles and when the yeast divide, H.pylori is imparted to the daughter generation.
Helicobacter pylori (H. pylori ) have been observed within yeast vacuoles by light and fluorescence microscopy, and their presence has been confirmed by the detection of H. pylori -specific genes and proteins in yeast extracts, such as VacA subunits, UreA, peroxiredoxin and thiol peroxidase.
Moreover, non-culturable H. pylori cells have been found in subsequent generations
of yeasts, indicating the generational transmission of the bacteria is part of the transfer of vacuolar content.
H. pylori are therefore well-equipped to establish in the vacuoles of yeast, which provide them with essential nutrients such as ergosterol for multiplication, as a pre-adaptation for invasion of human cells.Indeed, H. pylori-specific genes ureAB and babAB were detected in Candida yeasts from Iranian traditional breads (Sangak, Taftoon and Barbary), yogurt, banana skin, grape juice and quince jam, which carried vacuolar fast-moving and non-culturable BLBs (Figure 2)[87].
Thus, foodborne yeasts originating from the environment, which were once considered as harmless microorganisms when ingested through fermented foods such as dairy products[38,89], including kefir and kumis[94,95], could now be pinpointed as a public health problem source. In this regard, occurrence of yeast in food and environment can be considered as an important indicator of contamination with H. pylori and other pathogenic bacteria. Therefore, a key approach for the control of H. pylori infection may be to reduce the yeast content of foods through proper hygienic practice, especially by food handlers and during food processing[87]Would be interesting to know about the contamination in foods from "Western" sources and if H.pylori also infects saccharomyces boulardii/cerevisiae (baking yeast) and amoeba (water sources). And whether when we go buy goods which have not been baked like beer, (pasteurized) fermented foods or baking yeast (supplements?) they are free from intracellular bacteria?
There's a criticism of the study above which strongly questions the ability of bacteria to enter yeast cells. They do bring up amoeba and water supply, however:Interestingly, several articles in the literature have shown similarity in prevalence of Acanthamoeba in drinking water sampled from different geographical locations and the prevalence of H. pylori in patients[8-19]. While we cannot observe such overlap between yeast and H. pylori incidences, it is more logical to believe that yeast cannot be a reservoir of H. pylori but that Acanthamoeba can play such a role.
Indeed, in an earlier publication, the same Iranian researchers also showed commensalism in a co-culture of amoeba and H.pylori.
And they also found H.pylori in saccharomyces cerevisiae (baking + beer yeast) which was meant as a negative control - although in a less virulent, CagA-toxin free variation. Which could be coincidence or not. No testing for VacA-toxin was done in this context. -
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SOD3 Overexpression completely reveres weight gain on a high fat diet.
It also improves insulin sensitivity, triglycerides, fatty liver and increases PGC1a and UCP2.Interesting that a simple enzyme that reduces oxidative stress is so impactful.
Even though antioxidants don't get the best rap in the peat world. This study is similar to the ones using selegiline, ergothioneine or catalase overexpession, in the sense that their main mechanism of action is protection from oxidative stress. -
"Platelet COX inhibition was nearly complete already at 37.5 mg aspirin daily, as evidenced by >98% suppression of serum thromboxane B2 ..."
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@Mauritio Bro this is insane.
https://pubmed.ncbi.nlm.nih.gov/18505478/
If the mice were drinking 3.2ml of water a day, that is 0.032mg of DNP.
They weighed around 0.0475kg
So 0.67mg / kgHED is 0.0536mg per kg
80kg man: 4mg
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@alfredoolivas yes lve posted this and similar studies on X and maybe also on here.
Microdose DNP is very beneficial. Its also being researched to treat Ms.Dare to think.
My X:
x.com/Metabolicmonstr -
@Mauritio Yeah I was thinking of your post and looked into it a but
