MCT for Health

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...

While exploring the positive effects of various conjugated linoleic acids (CLA), I also found studies on the effect of CLA on the development of cancer and tumors . Results from animal experiments make therapies based on supplementing several percent of CLA appear very interesting. For example, this study of artificially induced cancer (DMBA) in rats shows the effect of adding 0% (A3), 1% (B3), and 2% CLA (C3) to the diet. The results are very interesting, approximately a 10-fold reduction in both the number and size of tumors. For such a small dietary change, this is quite a large effect. What could be causing it? The same study also reports that dietary CLA reduces the activity of certain enzymes involved in processing polyunsaturated fats (D6D, delta-6-desaturase). This reduces the conversion of linoleic acid into arachidonic acid and its concentration in membranes. But it also reduces the conversion of the plant omega-3 ALA into the long-chain omega-3s EPA and DHA.  As we will...

Today we will look at how the composition of fats in a low-fat diet affects metabolism in mice, for example how it affects fatty liver development. The low-fat diet is an important factor here; the researchers did not overload the mice’s bodies, so in my opinion we are getting fairly relevant results. So what does the study tell us ? We’ll take it slowly. There are six diets here: lard (L1, L2), soybean oil (S1, S2), and a mixture of lard and soybean oil (LS1, LS2), each with either 10% or 15% fat in the diet. For example, this is the difference in blood free fatty acid levels between diets containing 10% and 15% lard. Isn’t that interesting? Such an ordinary low-fat diet. And if it contains 10% fat in the form of lard, it still works reasonably well. But if we increase the lard content by 50%, to 15%, the level of free fatty acids in the blood rises by about 75%. Clearly, something is not right here. What happens if instead of pure lard we provide a mixture of lard and soybean oil in ...

By chance, I looked at an older study from 2004 , which shows that oxidative stress affects the export of fats from the liver in the form of VLDL particles. Imagine that each lipoprotein particle VLDL/LDL contains exactly one molecule of the ApoB100 protein, so they are absolutely essential for the export of fats from the liver. So we already have three essential products needed for successful fat export from the liver, i.e. oleic acid, H2O2 , and ApoB100. We obtain oleic acid from food or from saturated fats through the slow process of DNL. With a relatively low-fat diet, this is not a problem. Saturated fats, when in excess, also produce enough H2O2 to activate the enzymes synthesizing VLDL. What about ApoB100? It is also easily produced. But the study tells us that there is a system that controls the quality of exported fats in VLDL particles. If peroxidized polyunsaturated fats are present, the enzymatic system PERPP degrades ApoB100 molecules and no VLDL particles can be exported,...

Do not expect me to answer the question in the title with certainty. You probably understand that the body is very complex and nothing is that simple; moreover, each of us is different, and when something works for one person it may not work for someone else. So let’s get back to reality, we will look at two studies and I will try to comment on the observed results in my own way. Take it as you wish—believe it or not, that is up to you. The answer to the basic question “What is good and what is bad?” may not be easy at all. Is easy and rapid fat storage good or bad? Recently it has become increasingly clear that easy and rapid storage of fat in adipose tissue is a sign of good metabolism and does not lead to obesity . Obesity is determined by overeating, the easy availability of overly tasty and overly digestible food, and insufficient satiety signaling. The ability to quickly store these surpluses without damaging metabolism determines the health of adipose tissue; unhealthy adipose t...