MCT for Health

I enjoy controversial topics, and fructose is unique in this regard. Some experts completely condemn it, but as I’ve mentioned before , we have consumed fructose in fruit throughout our existence. To my knowledge, it has never been an issue until the last century. What are we doing wrong?    I’ll let you guess — what do you think? You see results from a study involving three low-fat diets (13% fat): mice on standard chow feed, starch-enriched feed, and sugar/sucrose-enriched feed (39%). For now, guess which curve corresponds to which diet. . I will attempt here to formulate a way to avoid overeating based on presumed mechanisms. The way we eat, especially the rate of food intake, is crucial. We must not overload the biological systems available to us. Every overload causes lasting changes.  First method:  Higher protein intake improves satiety signaling because excess amino acids are converted to liver glycogen via gluconeogenesis, which precisely signals when...

I have mentioned the positive effects of acetic acid and sodium acetate on metabolism many times here . Studies show that if the negative consequences of a high-fat diet are caused by fructose, i.e., the fructose contained in sucrose or produced in the liver from glucose (practically always), then sodium acetate often manages to reverse this effect in rodents, resulting in positive effects such as fat burning and weight loss. Mice, therefore, lose weight, normalize blood sugar and insulin levels, etc. We have also shown that the negative effects of fructose in combination with fats are caused by acetylation , specifically by the suppression of deacetylation by the enzyme SIRT2. This, among other things, causes the loss of CPT1 carnitine transporter molecules for the transport of long-chain fatty acids into mitochondria, so the fats must be stored. Fructose activates the enzyme KHK-C, and its increased presence (KHK-C OE) suppresses the enzyme deacetylase SIRT2. Thus, fructose prevents ...

I have a free continuation of my thoughts on how food intake is controlled in animals, and I assume that the same mechanism will work similarly in humans. If you haven't read it yet, I recommend it here and here . I have a feeling that we have not yet fully exploited the possibilities offered by the use of glucose as a dietary supplement. This is probably because it is glucose that increases insulin in the blood, and therefore, it is the main culprit that we must avoid. Really? Well, that is, of course, true if we undergo, for example, an oral glucose tolerance test ( OGTT ). Then yes, the culprit will be fully manifested here. But that is not what I mean. We already know that the main negative factor is the rate of intake. We know this from Dr. Richard Johnson and others. It is enough to finely grind or dissolve carbohydrates and mice will start to gain weight on their standard diet, just as they do on a human high-fat diet . So the speed of flooding the liver is decisive. How n...

A deficiency of amino acids (proteins) in the cell activates the enzyme SIRT2 . Activation of the enzyme KHK-C, i.e. the mere presence of fructose, which needs this enzyme for its activation, turns off the enzyme SIRT2 . Therefore, fructose controls the acetylation of many enzymes and reprograms metabolism. After reading many studies on fructose, I must conclude that sugar could really be behind the epidemic of obesity, diabetes, high blood pressure, etc., although I still think that the long-term effects of fructose are linked to the consumption of plant polyunsaturated oils, their peroxidation into aldehydes, and the initiation of cellular senescence . This is especially supported by the increase in their consumption in the 20th and 21st centuries. We have been consuming fructose in fruit and honey since time immemorial. SIRT2, as an indicator of the deficiency of amino acids, deacetylates ACSS2 and suppresses the formation of new fat droplets. Diabetics have their artificial sweeten...

I'm following up on the previous post, read it if you haven't already. I have to go back to fructose and its interaction with fat burning. If we want to come to any substantiated statement about the harmfulness of fructose and oils, it won't be easy. Both have their clearly negative but also positive effects, as I already wrote, it depends on the situation and criteria. But when it comes to long-chain polyunsaturated fatty acids, I can't help  I feel that they come in second place. At the beginning of the metabolic degradation process, fructose, probably in combination with any long-chain fat, is the culprit. We can even trigger the same negative service by combining glucose with any long-chain fat because flooding the liver with glucose can trigger the production of fructose from glucose, the so-called polyol pathway . So even if you avoid fructose and regular sugar, any fast carbohydrates can trigger the production of fructose. This is probably related to the need to...

And again, fructose! Sugar! White poison! Well, wait, maybe it depends on the situation. Let's look at an interesting study that examined the effects of fructose on the metabolism of mice. Animal models have the advantage that you have everything under control, so you can easily observe the mechanisms of how things happen. We already know about fructose , it activates the processes of glycolysis of glucose to lactate to obtain energy without the need for oxygen . This is not always bad, sometimes it can be useful, sometimes not. With simple reasoning, we can directly deduce that fructose does not promote the oxidation of fats to ATP energy, because only glucose or some amino acids can be fermented. On the contrary, when there is an excess of glucose, fermentation to lactate can be useful because it relieves the mitochondria and helps reduce the level of glucose in the blood. I mentioned the mechanism of increased lactate production in another post, see for yourself . What is intere...