MCT for Health

The amino acid glycine is a commonly available dietary supplement for athletes. I have been using it for quite a long time. I do not know whether it really works, but I do know that as a person ages, the level of glycine in the body decreases and decreases. I have already written about this in older posts. Recently, a conversation with Dr. Joel Brind about the effects of glycine popped up for me on YouTube . A very interesting interview in which he mentions the problem of excess methionine and a lack of glycine in our diet. Glycine is considered a non-essential amino acid, but the pathways producing glycine have limited capacity tied to other processes, and therefore they can never fully satisfy demand. Poor availability of glycine can thus lead to metabolic problems. These problems can be easily addressed by adding glycine as a sweetener, for example to coffee or other beverages. Yes, glycine, an amino acid, is actually slightly sweet, easy to use. The amount he recommends is about 8 ...

That sugar isn’t healthy is something almost everyone knows today, even if they don’t really care or restrict themselves. But that sugar could be harmful even without sugar in food? That sounds strange, doesn’t it? Do we have evidence, studies, results? Yes, I think we do. I found a nice PhD dissertation that tries to answer exactly this question. And the results are very interesting. I’ll try to summarize them briefly here. In discussions on X, I came across a great experimenter in the field of nutrition. He runs his blog at exfatloss.com . Recently, he raised an interesting point about the low-carb keto diet . For some people, it simply doesn’t work, and no one knows why. He observed this himself and shares his findings with others on his blog. The idea came to him while listening to lectures by Rick Johnson, M.D., on fructose research. Specifically, that the body produces fructose on its own, for example, with too much salty food and a lack of water, or when consuming food containin...

We continue with the effects of hydrogen sulfide on enzyme activity. We have already seen that H₂S affects the S-sulfhydration of sirtuins, i.e., the activity of deacetylases that change the activity of many enzymes by preventing their “decoration” with an acetyl group . In the case of sirtuin modification, for example, this facilitates the “decoration” of some enzymes with ubiquitin, which leads to their removal. Or it increases their activity after the removal of acetyl “decoration,” if that decoration interferes with the enzyme’s function. Even at this level, things are already quite complicated. But that’s not all. S-sulfhydration of certain sites can occur on many proteins, not just on sirtuins! Research shows that H₂S also sulfhydrates the enzyme pyruvate carboxylase (PC) and also the key metabolic switch, the enzyme AMPK. That would explain further phenomena observed both in vitro (in the test tube) and in vivo (in whole organisms) related to changes in hydrogen sulfide levels. ...

This is a loose continuation of the previous post about the effects of hydrogen sulfide (H₂S) on cellular metabolism . This time, we will look at a study related to diabetes, focused on the protection of insulin-producing cells—meaning the protection of pancreatic beta cells from high blood glucose levels. We will see that hydrogen sulfide activates the deacetylase SIRT2, improves antioxidant protection via GSH, reduces the level of aldehydes formed by oxidation of polyunsaturated fats in a high-glucose environment through activation of the enzyme ALDH2, and thus acts in a way that makes beta cells more resilient and able to survive even in unfavorable conditions. In the figure, we can actually see everything we need to know. If I were to follow up on the post where I showed that amino acid deficiency activates the enzyme SIRT2 and suppresses the formation of new fats , here we can see the mechanism more precisely. ALDA1  is an activator of the enzyme ALDH2, which removes toxic ald...

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...

As I wrote elsewhere, when I add the transcription factor HIF-1α to the search, activator of (pseudo)hypoxia, activator of metabolism without the use of oxygen, something interesting always appears in the results. So this time it's quite the bomb. Fat cells spread cancer by spreading the message of lack of oxygen. The study does not say it directly, but if we consider that the activation of the transcription factor HIF-1α is behind the hypertrophy of fat cells , i.e. their constant enlargement to enormous dimensions, then it is not surprising that these cells spread many problematic signals around the body. One such little-known signal is small extracellular vesicles called exosomes. Extracellular vesicles containing regulatory signals sent by fat cells. I have already shown several times here that the activation of (pseudo)hypoxia, i.e. the transcription factor HIF-1α in adipose tissue, is at the beginning of subsequent changes in the entire organism. Studies in mice show that if ...