MCT for Health

Once again, I deliberately chose a provocative question for the title. It concerns the harmfulness of alcohol—specifically, ethanol itself. Do not understand this as me defending excessive or habitual alcohol consumption. No, alcohol consumption is addictive. But research conducted some time ago suggested that alcohol in small amounts might actually be beneficial, whereas now it is claimed that any amount of alcohol is harmful, even very small amounts. And that does not seem very likely to me, if I consider that alcohol can help activate the enzyme ALDH2, which appears to be very important for the detoxification of aldehydes derived from polyunsaturated oils, such as 4-HNE. Why am I asking this question? Think about it! What if there existed some dietary component that could suppress or even repair liver damage during alcohol consumption. Wouldn’t that imply that the liver is being damaged by some other substance? It could not be alcohol itself! With this, I loosely follow up on a prev...

A slightly provocative question, right? But why not try to look for answers even to questions like this. We will look at two studies on aging and lifespan related to glycine. The first study directly shows in mice that administering glycine (8% by weight) in the diet starting at 9 months of age extends lifespan in male mice by approximately 6%, and in females slightly less, by 4%. The study was conducted at three different sites using specially crossbred genetically heterogeneous mice. Lifespan extension was consistent and statistically significant at all sites. Alongside the glycine test, other interventions were also tested at one site (aspirin at two concentrations, inulin, TM5441), but these did not demonstrate lifespan extension. The credibility of the results therefore appears to be high. The diet used was 5LG6 with 12% fat and 22% protein. Another important finding of this study is that supplementation does not worsen health status and is safe. Causes of death in the glycine gr...

Many readers already of course suspect which amino acid it might be, but I’ll leave that for later. It is becoming increasingly clear that the main problem of modern civilization diseases could be one relatively little-known, but in our time overly active enzyme. You already know it from previous posts: aldose reductase AR, the beginning of the polyol pathway. Yes, it is the enzyme that converts glucose into sorbitol and subsequently the enzyme SORD breaks it down by converting it into fructose. It is also the enzyme that processes 4-HNE, an aldehyde derived from the omega-6 linoleic acid, into active inflammatory signaling molecules. I have already shown here how sorbinil, an AR inhibitor, completely suppresses inflammation signaling caused by LPS, i.e., bacterial endotoxins. Switching off AR interrupts signaling to other cells; no chronic tissue inflammation then takes place. This may be good in the case of inflammation activation by dead material such as LPS. It may not be so good d...

It occurred to me to start looking for a relationship between glycine supplementation and the polyol pathway, specifically whether glycine might have some relationship to the activity of aldose reductase (AR). This enzyme (together with fructokinase KHK) appears to be at the center of events related to obesity, oxidative stress, chronic inflammation, etc. Turning it off interrupts inflammatory signaling and the response to endotoxins, but it also disrupts the breakdown of certain toxins. Its inhibition therefore may not always be desirable. And it seems to me that I have found a certain connection between glycine and AR. It is a rather innocent-looking cataract study in diabetic rats from 2019. The authors apparently had the same idea: what if glycine interacts with aldose reductase? And they tested it in diabetic rats. And it worked! The study was conducted in such a way that at a certain point the rats’ pancreas was chemically damaged, so insulin production stopped. This leads to an...

Aging of the organism appears to depend on food intake. I have previously pointed out that prolonging life can probably be achieved by preventing any overeating, even short-term . During a discussion on the X network, the well-known blogger Peter ( @Peter_InNorfolk ) shared a study examining the lifespan of rats on three diets: a standard diet (16% of calories from fat), a moderately high-fat diet (35% of calories from fat) without quantity restriction, and the same diet but restricted to the same caloric intake as the standard diet. He mainly commented on the shortening of lifespan on the unrestricted high-fat diet, which he attributes to the relatively high content of omega-6 linoleic acid in the fat, i.e., in lard. Control – low-fat pellets, IHF – high-fat diet with isocaloric restriction, FHF – high-fat diet without restriction, experiment performed on male rats. The high-fat diet without restriction (FHF) slows metabolism and reduces heat production. However, from the previous pos...

Yes, we have already discussed this here, take a look at an older post . But this time we will look at a study that has this question directly in its title. Really! This graph might remind you of something, right? It is a typical graph of food intake in the first days after a sudden switch to a high-fat diet. It manifests itself as incredible overeating. The authors do not provide a reasonable explanation; my explanation can be found here . Such a procedure provides clear results, such as the experiment in the next image. It does not matter whether it is lard or vegetable oils. So obesity is caused by fat in the diet, period. Really? Let us continue with another test from the same study. This one is much more sophisticated. In this case, it is a gradual transition to a high-fat diet, modified so that the mice first received a precisely defined amount of fats and, in addition, could consume standard low-fat pellets ad libitum. The first week 0%, the second week 25%, then 50%, then 90% o...