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Can glycine help extend lifespan or make you younger?

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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...
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Which amino acid suppresses chronic inflammation?

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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...
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Does glycine function as an AR inhibitor? Does it suppress endogenous fructose production?

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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...
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Does fatty food increase longevity?

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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...
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Why do animals overeat on a high-fat diet?

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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...
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Glycine as a fighter against lipid peroxidation?

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The amino acid glycine is a commonly available dietary supplement for athletes. I have been using it for quite a long time. I do not know whether it really works, but I do know that as a person ages, the level of glycine in the body decreases and decreases. I have already written about this in older posts. Recently, a conversation with Dr. Joel Brind about the effects of glycine popped up for me on YouTube . A very interesting interview in which he mentions the problem of excess methionine and a lack of glycine in our diet. Glycine is considered a non-essential amino acid, but the pathways producing glycine have limited capacity tied to other processes, and therefore they can never fully satisfy demand. Poor availability of glycine can thus lead to metabolic problems. These problems can be easily addressed by adding glycine as a sweetener, for example to coffee or other beverages. Yes, glycine, an amino acid, is actually slightly sweet, easy to use. The amount he recommends is about 8 ...
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How does fatty liver develop?

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In the past, fatty liver with subsequent liver cirrhosis was associated exclusively with alcohol consumption. But that is the past. The term non-alcoholic fatty liver disease (NAFLD, MASLD) emerged, where alcohol clearly could not be the cause. So what is the cause of liver damage? A post by Chris Masterjohn on X clearly identifies choline deficiency as the main cause . The fat that is formed in the form of triglycerides simply must be packaged into VLDL particles and sent out into the body. For that, sufficient choline must be available. The production of choline requires the amino acid methionine. But what does this have to do with alcohol or other foods? When I look at my older posts, I think we can find a number of answers there. Let’s take a look . For example, in this post it is clearly shown that choline deficiency can be significantly promoted by a deficiency of hydrogen sulfide , produced via the enzyme CSE from sulfur-containing amino acids (CSE-KO). Even choline deficiency a...
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Do omega-6 fats cause inflammation via aldose reductase and fructose?

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So here I have another quite provocative headline. Don’t you think? The fact that omega-6 polyunsaturated fats, specifically linoleic acid contained in vegetable seed oils, promote the development of chronic inflammatory processes is generally well known. There is nothing provocative about that. But that this process could take place through the polyol pathway? Or even through endogenous fructose production? That, I think, is not generally known. Is it really so? To demonstrate this, we must first accept that the linoleic acid peroxidation product 4-hydroxy-2-nonenal (HNE) is capable of activating the production of an enzyme called aldose reductase (AR). This enzyme is able to degrade HNE, preventing its further accumulation. If we suppress AR activity, for example with sorbinil, HNE accumulates, as a study has shown . The whole mechanism works as follows: if there is a reduction in antioxidant protection within the cell (for example due to fructose via the shutdown of SIRT2), the prod...
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Protein restriction, FGF21, oxidative metabolism, and gluconeogenesis — is it related?

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Some time ago I wrote about how, in one study, scientists found that when cells are exposed to glutamate/glutamine, oxidative metabolism in the cell is suppressed and replaced by a fermentative one . This one does not require oxygen. It does not use it even when oxygen is available, at its normal concentration. This is related to the release of ammonia molecules during deamination of excess glutamine for entry into the TCA cycle, that is, for its conversion into energy ATP. In another post I wrote about how ammonia activates NMDA receptors, i.e., glutamate receptors . Turning them off using the substance MK-801 protects superoxide dismutase from damage, and excessive activation of NMDA receptors by glutamate and ammonia thus probably leads to cellular senescence . The main function of NMDA receptors, as I understand it, is to allow calcium ions to enter the cell and activate the cell to act. Typically, ROS production increases. The main role in this is played by NOS enzymes, which prod...
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