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. ...

Why are there so many light sensors in adipose tissue? Until today, I have always considered the influence of light only in terms of its direct effect on the functioning of enzymes in mitochondria . It is time to change that.  A strange question occurred to me, the one you see in the headline. Could modern LED displays on computers and mobile phones, with their limited emission spectrum, be causing not only the epidemic of myopia , but also metabolic problems and obesity? So I started investigating.  First, I asked artificial intelligence whether it happened to know anything about it:  AI quote  “Yes — OPN5 (opsin 5, neuropsin) has a demonstrable connection to the regulation of metabolism and thermogenesis, but so far mainly from experiments in mice. And interestingly, the connection with the thyroid gland was not directly confirmed in the key study.  What is known so far  OPN5 is a light-sensitive receptor. In the brain, specifically in the preoptic area o...

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...

We have already discussed conjugated linoleic acids (CLA) here several times. Unlike ordinary linoleic acid (C18:2n-6), CLA are also C18:2 fatty acids, but they differ in the spacing of the double bonds along the carbon chain—they are closer together. They can also have different combinations of trans and cis double bonds. What they have in common is that they are less stable than linoleic acid and are more susceptible to peroxidation . They are therefore better sensors of oxidative stress. They more accurately reflect the state of metabolism and respond more sensitively to metabolic disturbances, breaking down more readily into various signaling molecules,  but they probably do not produce the aldehyde HNE. The most common source of CLA in our diet is milk fat. However, our bodies can also produce CLA from trans-vaccenic acid (TVA) , which is also present in milk. There are animal studies showing that as little as 1% of calories from CLA in mice completely eliminates arterial pla...

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 ...

In the previous post, I showed how the omega-6 linoleic acid peroxidation product 4-hydroxy-2-nonenal (HNE) suppresses signaling of cellular energy deficiency, i.e., a shortage of ATP molecules . This forces the cell to switch into an energy-conserving metabolic mode, activate glucose fermentation or cellular senescence, or ultimately undergo apoptosis—programmed cell death. Today, we will look at another older study  (from 2014) in which researchers investigated whether fatty liver disease could be alleviated by suppressing the function of the AR enzyme, i.e., by inhibiting aldose reductase. If you have not yet heard of aldose reductase (AR, also known as aldo-keto reductase AKR1B1), I have published a large number of posts on this blog presenting studies showing that AR activation is the basis of virtually all modern chronic diseases, whether it is obesity , liver damage , or vascular endothelial damage . Today, the main activators of AR are not only elevated blood glucose l...