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 ...

In the past, fatty liver with subsequent liver cirrhosis was associated exclusively with alcohol consumption. But that is the past. The term non-alcoholic fatty liver disease (NAFLD, MASLD) emerged, where alcohol clearly could not be the cause. So what is the cause of liver damage? A post by Chris Masterjohn on X clearly identifies choline deficiency as the main cause . The fat that is formed in the form of triglycerides simply must be packaged into VLDL particles and sent out into the body. For that, sufficient choline must be available. The production of choline requires the amino acid methionine. But what does this have to do with alcohol or other foods? When I look at my older posts, I think we can find a number of answers there. Let’s take a look . For example, in this post it is clearly shown that choline deficiency can be significantly promoted by a deficiency of hydrogen sulfide , produced via the enzyme CSE from sulfur-containing amino acids (CSE-KO). Even choline deficiency a...

So here I have another quite provocative headline. Don’t you think? The fact that omega-6 polyunsaturated fats, specifically linoleic acid contained in vegetable seed oils, promote the development of chronic inflammatory processes is generally well known. There is nothing provocative about that. But that this process could take place through the polyol pathway? Or even through endogenous fructose production? That, I think, is not generally known. Is it really so? To demonstrate this, we must first accept that the linoleic acid peroxidation product 4-hydroxy-2-nonenal (HNE) is capable of activating the production of an enzyme called aldose reductase (AR). This enzyme is able to degrade HNE, preventing its further accumulation. If we suppress AR activity, for example with sorbinil, HNE accumulates, as a study has shown . The whole mechanism works as follows: if there is a reduction in antioxidant protection within the cell (for example due to fructose via the shutdown of SIRT2), the prod...

Some time ago I wrote about how, in one study, scientists found that when cells are exposed to glutamate/glutamine, oxidative metabolism in the cell is suppressed and replaced by a fermentative one . This one does not require oxygen. It does not use it even when oxygen is available, at its normal concentration. This is related to the release of ammonia molecules during deamination of excess glutamine for entry into the TCA cycle, that is, for its conversion into energy ATP. In another post I wrote about how ammonia activates NMDA receptors, i.e., glutamate receptors . Turning them off using the substance MK-801 protects superoxide dismutase from damage, and excessive activation of NMDA receptors by glutamate and ammonia thus probably leads to cellular senescence . The main function of NMDA receptors, as I understand it, is to allow calcium ions to enter the cell and activate the cell to act. Typically, ROS production increases. The main role in this is played by NOS enzymes, which prod...