MCT for Health

I’ve written about the effects of vinegar/sodium acetate many times here — usually in a positive light. I’ve also frequently noted that adding HIF-1α  to search queries often leads to very interesting studies. In my previous post, I explored the idea that combining vinegar, for instance, with overeating might lead to obesity — perhaps a healthier or less dangerous form than without vinegar. Acetate, produced by gut bacteria in the presence of excess polyunsaturated oils, facilitates the creation of new fats from acetate, glucose and amino acids by increasing insulin secretion. Today, we’ll look at a study that goes even further. It shows that, under oxygen-deprived conditions, cancer cells readily use acetate molecules as a carbon source to produce fats and promote growth. This occurs through histone acetylation — activating fat-production-related genes. Interestingly, acetate concentrations don’t even need to be high. This aligns strongly with my earlier hypothesis: cells absorb a...

Let me start with some reasoning because there’s still a lot of confusion surrounding the metabolism of seed-based vegetable oils, which primarily contain the omega-6 fatty acid linoleic acid (LA). Studies show very mixed results, which is why irreconcilable camps of supporters and opponents of seed oils have formed among different dietary preference groups. You already know my stance, but I always try to remain as unbiased as possible first. This post is meant as a hard blow to researchers because everything might be completely different from what we’ve thought so far. The reason is that our researchers often forget to measure some basic metabolic parameters, which then secretly skew the results in one direction or another far more than the observed variables. But more on that later. A while back, I explained that when linoleic acid is burned in the mitochondria, there’s an increased consumption of NADPH molecules because the enzyme 2,4-dienoyl-CoA reductase (DECR) is activated. I ne...

The circle is now closing. The cellular senescence of stem cells appears to be the root of the problems in our nearly perfect self-repairing organism. If we lose our functional stem cells, the repair mechanisms will be severely limited. To prevent this, we need to understand how it works in detail. Which molecules are degraded, and which processes are disrupted? Adding extracellular vesicles produced by senescent cells (P5 EVsG93A or P5 EVsWT) increases DNA damage (β-Gal+ cells). This is due to the effect of misfolded, oxidized superoxide dismutase (SOD1). Research on Alzheimer's disease may help. I’ve mentioned the issue of cognitive impairment related to this serious disease several times before. The most interesting was a study on a mouse model, tracking metabolic changes linked to enzyme acetylation and the availability of acetyl-CoA molecules in the cytoplasm . Back then, I didn’t realize that cellular pseudohypoxia is a manifestation of cellular senescence — cellular aging. T...

If you’re still unaware of what cellular senescence (cellular aging) is, check out older posts . In short, cellular senescence is emerging as a major trigger for chronic, hard-to-treat metabolic and health problems. The only difference lies in where senescent cells accumulate and stop obeying central commands — for example, to multiply or, conversely, to break down. These cells interfere with healthy ones, sending them misleading signals (SASP), but overall, it still appears that everything is functioning almost as before. A typical trigger for cellular senescence is when the antioxidant system fails to break down hydrogen peroxide, leading to the release of signaling molecules from mitochondrial membranes. Depending on the state of the membranes, corresponding defense mechanisms are activated — for instance, oxidative metabolism (OxPhos) is halted and replaced by fermentation, which produces less hydrogen peroxide and doesn’t require oxygen. All this happens in an environment where ox...