MCT for Health

The headline always has to be a little provocative, but it is possible that this is indeed the case. Quite recently, I pointed out the historical work of Dr. Bates , who considered the main cause of vision problems to be excessive tension in opposing eye muscles, which shape the eyeball, affect the axial length of the eye, and thus focus or defocus the image on the retina. This strain is caused by stress in the brain.  If the brain cannot recognize what it is looking at, this causes stress and increases the tension in the muscles around the eye, including the tension in those muscles that are supposed to remain relaxed. How does modern science view refractive errors? It seems that studies are already emerging that consider feedback systems, in which the eye is exposed to various influences and therefore has to constantly "fine-tune" itself. They call them the GO signal and the STOP signal. The GO signal lengthens the eyeball, while the STOP signal stops this lengthening. Noth...

Something strange happened this summer...  During the pandemic, I looked at the death statistics published on the EuroMOMO portal. Occasionally even now. I remember them and take a look. I am usually interested in whether those strange humps from the COVID era are still there and whether the epidemic is already over or is still ongoing. You may object that the epidemic ended a long time ago. Well, I think it is not that simple. You only need to take a quick look at the graphs.  Where is the epidemic? Do you really see it there? I don't, at least not much—or it hasn't ended. There is a certain wave there, but it seems that epidemics recur almost every year, practically up to the present day. But they were there before that as well; it is just no longer visible because the older data is not there. Isn't that strange? After all, we are told that the effective mRNA vaccine dealt with the epidemic, as all the mouthpieces controlled by the World Health Organization (WHO) say. But...

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...

Could an excess of the omega-6 fatty acid linoleic acid in the diet and in adipose tissue create the paradoxical situation in which linoleic acid (LA) is lacking in the phospholipids needed to form mitochondrial cardiolipin? That would mean reduced mitochondrial function and increased oxidative stress, which we observe in animal models fed very high-fat diets. We have already encountered a similar situation with omega-3 fats. Take a look. The percentage of omega-3 phospholipids in cell membranes initially increases sharply but then declines as the consumption of more plant-derived omega-3 and omega-6 fats increases. This phenomenon is explained by changes in the activity of the enzymes that elongate and desaturate plant fats into the long-chain fatty acids EPA and DHA, which are found primarily in fish oil. The same enzymes also elongate and desaturate linoleic acid (LA) into arachidonic acid (ARA), whose concentration is maintained relatively stable. Thus, a higher intake of LA mean...

Recently, Georgi Dinkov commented on an interesting study on his blog, which shows that uncontrolled fat burning could damage mitochondria. Let's take a closer look at this study, considering all the facts known so far. Should we be afraid of fats or not? We must first show the position of the study authors. Quote "Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction" "Collectively, these results indicate that although FAO is essential for cardiac energy production, therapeutic strategies aimed at stimulating cardiac FAO may be detrimental rather than beneficial in heart failure." Unquote So, can promoting fat burning really be harmful? Well, we already know that promoting fat burning without overeating extends the life of mice . Cells need fat burning to improve resilience . So the scientists' statement about the dangers of promoting fat burning is contradictory to these findings,  so something...