MCT for Health

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 ...

I would like to loosely follow up on the previous post about conjugated linoleic acid (CLA) as a potential treatment for atherosclerosis. We saw that a 1% CLA mixture in the diet was able to almost completely heal blood vessels in mice within eight weeks; the previously formed atherosclerotic plaque in the aorta almost disappeared. This was not a slowing of plaque deposition processes, but its removal! What could the mechanism be? Could this work in humans as well? In one older post , I showed how the number of unsaturated bonds in polyunsaturated fatty acids determines the degradation rate of apoB100 molecules, and therefore also the liver production of VLDL/LDL particles. The greater the susceptibility to peroxidation, the faster the degradation of apoB100 and the lower the export of fats and cholesterol from the liver. Take a look at the following findings. Unlike the previous study, linoleic acid and palmitic acid behave the same way here. Human liver cells were used, which could ...

If you think that vegetable (seed) oils protect your blood vessels, that is probably not true . This is suggested by studies examining their effects in older age or looking at lifespan. Vegetable oils may lower cholesterol, but low cholesterol levels are associated with shorter lifespan. But what would you say to the information that simply adding 1% of a special mixture of polyunsaturated oils—specifically processed linoleic acid—to the diet causes vascular plaque to disappear in an animal model within a few weeks! However, the processing of these vegetable oils was not carried out by any industrial food company. No—the processing was performed by bacteria in the cow’s stomach! The resulting product is called CLA, conjugated linoleic acid. There are several types, but the most interesting is rumenic acid, c9,t11-CLA. Another is t10,c12-CLA, but the first one is found in butter at ten to twenty times higher levels than the second. Could it be, then, that full-fat dairy products—especia...

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...

You probably already know this. Oxidative stress of any kind triggers the activity of enzymes called phospholipases, especially iPLA2γ, which releases oxidized polyunsaturated fats from the mitochondrial membrane . This is how cells monitor their condition and oxidative stress, and the released oxidized products derived from omega-6 linoleic acid (LA/ARA, e.g., 4-HNE) serve as signals for many processes. For example, they can also trigger chronic inflammation by activating aldose reductase (AR) and the polyol pathway . Elevated glucose levels (HG), when the enzyme ALDH2 functions insufficiently and 4-HNE molecules are attached to it, become problematic and instead of correcting oxidative stress they deepen it further. The missing ALDH2 activity can be restored using H2S (NaHS was used here) or by activating the CSE enzyme (e.g., by restricting methionine and cysteine in the diet ). I have many posts about this here; most of them concern liver cells or pancreatic cells, and therefore a...