MCT for Health

So I was going through some older studies I had saved, and this one caught my attention. I don't remember seeing it at all, but it illustrates beautifully how deceptive things can be. What is it about? Essentially, it is a study of how adding fiber (fructo-oligosaccharide, FOS) to the diet favorably affects metabolism. Perfect. Opinions on fiber vary widely. My view is that fiber in the large intestine triggers signaling similar to overeating. The presence of undigested food in the large intestine signals that we have eaten more food than would have been necessary, and so the intestinal bacteria feed on it as well. What comes out of this is quite a lottery, because each of us has a different composition of bacteria in our gut, so we don't know what those bacteria will actually produce. If things turn out well, the bacteria produce acetate (and other short-chain fatty acids, SCFAs), and this signals to the body that there is indeed enough fuel, and the body adjusts accordingly. ...

Today it will be more of a summary, a more general reflection. In one of my recent posts, I commented on a study that quite clearly showed that if we remove the regulatory processes limiting the rate of fat burning, then the rate of burning is suppressed only after mitochondrial damage, loss of cardiolipin, loss of the necessary phospholipids , simply through oxidative stress . It is not a good idea to switch off regulatory mechanisms and think that things will be better without regulation—they will not. If researchers try to switch mice or rats to a high-fat diet, they almost always damage their mitochondria. We now know that they will probably deprive them of sufficient cardiolipin, a phospholipid necessary for the proper functioning of the enzymes that produce cellular energy in the form of ATP molecules. We also know that this can be prevented by a different composition of fats, for example if the diet contains fish oil , or if it contains MCT oils, or if it contains vinegar/aceta...

The effort to lower blood glucose levels seems obvious, the reason is simple. High glucose levels cause oxidative stress and damage to body organs (eyes, blood vessels, kidneys, etc.). This leads many people to promote and apply low-carb and ketogenic diets. But is it really glucose that causes it? After all, it is the most common fuel for obtaining energy so that cells can function at all. Isn't that strange? Moreover, the cell can easily defend itself against overload by means of insulin resistance. So why doesn't it work? Is it really glucose that is harmful to the body? So let's take a closer look. If you are reading this blog, I think you already know where the core of the problem is. Yes, it is the activation of an enzyme that is supposed to serve only in emergency situations, otherwise it should be deactivated. It is the enzyme aldose reductase (AR, AKR1B1). It is present in the liver, vascular endothelium, cornea, etc. It is the first enzyme of the so-called polyol ...

Overweight and obesity are fairly common nowadays, much more common than they were, say, fifty or a hundred years ago. There are many opinions on the causes, but to me it currently appears to be the result of poisoning from food, drink, or the environment—whether the air we breathe or contamination by foreign electromagnetic signals. I assume that the environment and food simply play a role. Let’s review the most important processes that influence fat storage and obesity. First of all, rapid and easy storage into adipose tissue does not cause a problem and quickly removes fats from the blood. To achieve this, it is necessary to maintain metabolically healthy adipose tissue protected by the glutathione antioxidant system. How much fat will be stored is determined by excess—some fat is constantly being burned, and excess is stored. So it is determined by the ratio at which fats and glucose are burned. With any change in the ratio of fats and carbohydrates in the diet, suppression of fat...

What is AR? It is the enzyme aldose reductase. An enzyme that processes excessive cytosolic glucose into sorbitol. Before we look at a study involving AR , let us first look at what is required for fat formation in the liver. Also see an older post on the same topic. In the first study, we see that activation of the enzyme SCD1 is required for fat storage in the liver. Without it, this cannot occur. This enzyme desaturates longer saturated fats, namely palmitic acid and stearic acid, into monounsaturated fatty acids. Since palmitic acid C16:0 is formed mainly by de novo lipogenesis from acetyl-CoA molecules, it is at the same time rapidly elongated to stearic acid C18:0 and further desaturated by the enzyme SCD1 to oleic acid C18:1. Perhaps it is not so much about the desaturating enzyme SCD1 itself, but rather about the presence of oleic acid C18:1. This fatty acid is absolutely essential for fat storage in triglycerides. So essential that shutting down desaturation prevents fat stor...

It is strange. Mechanistically, it is clear that dietary linoleic acid is associated with increased oxidative stress and odd auto-oxidation products such as 4-HNE, which is a molecule that binds to enzymes in a way that prevents them from functioning properly . It even prevents its own removal, so its concentration increases, and it should be easy to arrange a simple experiment: give one group of people more linoleic acid in the diet than the control group receives, and the result should be a clear difference. But that is not how it works. Thus, for example, when Tucker Goodrich, a well-known blogger and proponent of the theory about the harmfulness of linoleic acid, is asked on the X network to support with a human study that linoleic acid causes inflammation, he presents a study with this conclusion : "Our meta-analysis suggested that increasing dietary LA intake does not have a significant effect on the blood concentrations of inflammatory markers. However, the extent of chang...