MCT for Health

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...

In my previous post , I pointed out a study in which scientists extended the lifespan of mice by up to five months, about 17%, through mechanical stress induced by ultrasound. I also mentioned that it would be beneficial to combine the therapy with the supplementation of sodium acetate or vinegar, as these activate the same pathways, namely SIRT1 and AMPK . Immediately afterward, I came across a study showing the successful suppression of cellular senescence using sodium acetate in vascular endothelial cell cultures — the inner lining of blood vessels. Almost as if on cue, the study was published just a few days ago, on May 12th of this year. This is a fascinating study that combines the investigation of substances produced by gut bacteria that damage our blood vessels and accelerate the aging of the inner vascular lining. Researchers identified the compounds phenylacetic acid (PAA) and phenylacetylglutamine (PAGln), which are primarily produced by bacteria of the genus Clostridium. T...

In my previous post , I discussed aging and how it can be influenced. We saw that aging is closely linked to the aging of individual cells, with their undamaged DNA, and the activity of repair mechanisms. To ensure proper DNA repair, the cellular energy production system — specifically, ATP synthesis — must function correctly. This requires a well-working antioxidant system based on glutathione, which must not be disrupted by products of auto-oxidation of omega-6 linoleic acid. These oxylipins (e.g., HNE) bind to enzymes and impair their function. If they block DNA repair, they trigger cellular senescence. As we age, senescent cells accumulate . This is the body’s defense mechanism — cells reduce energy production via oxidative phosphorylation and switch to fermentation, keeping auto-oxidation within tolerable limits. While senescent cells remain partially functional, they cannot replicate when needed, nor can they be cleared when in excess. They also ignore external signals. Is it pos...

Aging affects everyone, whether they care or not. We might not pay much attention to it, but it’s a fascinating phenomenon. Right now, it’s still unclear how to slow it down, stop it, or even reverse it. Some animal experiments suggest possible directions, but first, we should clarify what aging actually is and how to measure it. That’s not a simple problem. The easiest way is to count the time from birth until now—but that’s probably not what interests us. What we really want to know is how we compare to others in a similar population. Are we more worn out or less? Is there a chance we’ll live longer than others, or not? Let’s explore this using studies and logical reasoning.   First, we need to define how we measure aging. Health might be a good metric. We don’t just want to live long if it means being bedridden, unaware of our surroundings, with a failing body and mind. That’s not a good vision of longevity. We want to stay active and healthy. We want all our organs fully f...