This picture of VDR knockout mice being "lean" and "obesity resistant" is taking some of the trees for the forest and claiming it's the whole forest. If you are insulin resistant, generally force-feeding a lot of carbohydrate substrate without any other measures is probably not a good idea. Are carbohydrates bad? No. Vitamin D has been skewed, I am sure intentionally, as a general calcified public is also "paradoxically" calcium deficient, or more aptly on a very low calcium:phosphate ratio, focusing on inflammatory, active D (1,25) paints the perfect, evil picture of vitamin D overall and is frankly wrong. Hydroxylases tightly regulate local conversions to 1,25 from 25. What interrupts this regulation? Calcium deficiency, estrogens, PUFA. In other words pre-inflammatory state. Knockout mice, barring all other factors of health - which is usually the game here in these worthless studies - will not experience this inflammatory, dysregulated system. And looking only at this narrowly through a lens, you derive your conclusion you are looking for: manipulating the meaning and function of things. In reality, in the real world, the better method in avoiding these inflammatory responses is, you guessed it, sufficient calcium, low PUFA, in turn keeping estrogen in check, and being careful of other inflammatory things. Much like the knockout mice scenario, removing some apparatus to prove something is bad, when that something itself is hijacked and fed into a detrimental cycle is a sleight of hand, not proof. Vitamin D is not the problem, and VDR knockout doesn't prove it is, only in that if 25 is converted via inflammation. Lipopolysaccharide derived MKP-1, inhibition by inactive D already shows vitamin D is an anti-inflammatory, but not 1,25. And 1,25 is one of the resident experts of inflammation, when conditions of health are not met. Get tho9se conditions met and D does what it does that is good for us. By the way, progesterone and methylene blue also help Also, "constant milk intake" is an absurd, hyperbolic suggestion. I am certain nobody here has an IV of milk coursing through their veins 24-7. You have some milk throughout the day, then we all fast whether we know or not: it's called sleep.

does the free acetyl also have this interactions with CAII?

I have been taking 10mg boron for a couple months and I'm wondering if it's triggering aromatase due to low SHBG and high total T. Any thoughts on if this could actually be the case?

https://youtube.com/watch?v=2KPTiSYuzwg

Probably because the cells utilize more sugar as a concerted effort to recover from infection. If we picture a U curve, with the state of infection being one extreme side, more sugar would perhaps satiate the need to recover from infection with the surplus leveling out for glycogen formation.

Acute first aid treatment after brain injury Case Report: Buccal administration of hydrogen-producing blend after a mild traumatic brain injury in a professional athlete https://pubmed.ncbi.nlm.nih.gov/32595937/

@sphagnum I wouldn't worry about the ratio, just consume enough Calcium and Magnesium foods/supplements to your well-being and tolerance. Also in the cited study above, the ratio is 2.3, not 2:3, so it's more than two times elemental calcium than magnesium. 2:1 seems to be the recommended ratio in health institutions. Calcium to Magnesium Ratio Higher Than Optimal Across Age Groups Objectives The ratio of calcium to magnesium (Ca: Mg) intake has gained immense attention in recent years, since a ratio above 2:1 has been associated with increased risk of metabolic, inflammatory and cardiovascular disorders. The objective of this study was to assess Ca: Mg ratios across age groups and to determine the relationship between Ca: Mg ratios and markers of inflammation. https://pmc.ncbi.nlm.nih.gov/articles/PMC6574898 Calcium: magnesium intake ratio and colorectal carcinogenesis, results from the prostate, lung, colorectal, and ovarian cancer screening trial Conclusion Higher calcium intake may be related to reduced risks of incident advanced and/or synchronous adenoma and incident distal CRC among subjects with Ca:Mg intake ratios between 1.7 and 2.5. https://pmc.ncbi.nlm.nih.gov/articles/PMC6889387 Dietary calcium and magnesium intake and risk for incident dementia: The Shanghai Aging Study Our findings suggest that high dietary intake of Mg is associated with an increased risk of dementia mainly among older adults with low Ca:Mg intake ratios. Proper balance of Ca to Mg in the diet may be critical to the relationship between Mg intake and risk of dementia. https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/trc2.12362

I noticed the reprint of Nutrition for Women says "100 short articles by Ray Peat, PHD," where the old one said "92...". What did they add to it? Also, note that From PMS to Menopause is for sale on Peat's website but not Amazon, and Peat's website doesn't have Generative Energy. Weird. I wonder if Katherine gets more of the money if you order from Peat's site. I'd imagine so.

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/

@cs3000 any update on your electrical symptoms from sunlight and vitamin D?

@LunaticRed said in Fatty acid oxidation drives senescence: I recommend you to use Claude-opus-4-6-search instead of Gemini3, it's more powerful and better at searching information Thanks for the info. I appreciate. Here is a link for my first try / search on Vit k2 MK4 (in French): AI Conversation No. 3: HD Vit. K2 MK4 to target vascular, cerebral and hormonal aspects. https://mirzoune-ciboulette.forumactif.org/t2185-conversation-avec-lia-n3-hd-vit-k2-mk4-pour-cibler-les-aspects-vasculaire-cerebral-et-hormonal#30719 Need [image: 1775046783689-aa.emoticon-coffee.gif]

@user73636 what AI did you use for this? Grok 4.20 Expert is not suggesting that this is happening.

@lobotomize said in WARNING Alkaline environments hyper-accelerate the Maillard: aspirin also does the blocky thing Yes, very useful but we have to manage the impact on platelet renewal, whatever the dose is. 10-12 days to recover a functional system. I can give a link if interested.

Not sure about this type of cancer, but there are good case studies for cyproheptadine. There was a thread on the old forum that cyproheptadine completely cured liver cancer in one case. All I could find on leukemia is this: https://pubmed.ncbi.nlm.nih.gov/18502826/. Keep in mind that it makes people groggy and tired a lot. So if the goal is to make your uncle feel better, it might not be the best option, even if it helps a bit. Good luck!

Fat loss has absolutely nothing to do with metabolic efficiency. When the body has enough nutrients it will spend some of that nutrients on building new fat cells. This can only be stopped by inhibiting mTOR activation, usually through APMK, which naturally happens during fasting and during heavy exercise. The threshold is high, passively burning more energy will not suddenly spike APMK.

Guess: it's a subconscious/evolutionary defense mechanism to "increase energy" by simply doing more activity. Clearly, it doesn't work anymore.