MCT for Health

I can't help myself, I have to theorize. In the previous post , we saw how easy it is to get fat, i.e. in the rat model. We also saw how to achieve weight loss again, feel free to take a look. It all follows from the fact that if we frequently change the macrobiotic ratios of the diet, i.e. the ratio of long-chain fats in relation to carbohydrates plus proteins together, the body cannot respond to the changes and derives the feeling of satiety from how quickly it fills the liver's glycogen reserves.  During the entire period of adaptation to the new food composition, the body will overeat.  The speed of adaptation of the metabolism to the new composition of the diet depends on the amount of short and medium fats in the food. The more of them the consumed fat contains, the faster the adaptation will take place. The lower will be the risk of overloading fat cells  (or rather their poisoning with endotoxin LPS from the digestive system )  and their probability of switching to pseu

How is food consumption controlled? You may think that our will decides this. Perhaps, sometimes. But animals probably have no such will and yet know when they have had enough and how much to eat. They know better than we do! That's a surprise. So how do they know when they've had enough to eat or not yet?   I haven't delved too much into this issue yet , so it might not be as well thought out as it should be. But it doesn't matter, it has to start somehow. What led me to this problem is this picture from a study on laboratory rats and also an excellent blog written by Peter . We are seeing several step changes in their diet. First, at the very beginning, a change from a standard rat diet to a high-fat, human-like western diet. We first see an interesting transitional event there, when fats are not a food for rats, which would relieve them of hunger. They cannot oxidize them for energy. Only over time will they learn to process them and can therefore gradually reduce e

The strengthening and hardening of soft tissues by calcification is a very interesting phenomenon. The same process takes place in the strengthening of bones, but is usually undesirable in the case of soft tissues. Actually, it is not calcium as such at all, but calcium phosphate ( hydroxyapatite, HA, Ca10(PO4)6(OH)2 ), which strengthens soft tissues. It is the very same material that is missing from the bones in osteoporosis, while it builds up and damages the soft tissues. The driving force of calcification is therefore not calcium at all, but phosphorus, or inorganic phosphate (Pi). And to make it not so simple, it depends on its form. Inorganic phosphate (Pi) accelerates calcification, inorganic pyrophosphate (PPi) protects against calcification. The difference or ratio between the levels of these two forms of inorganic phosphorus is stabilized and balanced by a group of enzymes called alkaline phosphatases (ALP/TNAP). These break down the pyrophosphate into two phosphate molecules

In several older posts, I have shown that about 5% sodium acetate in the diet of laboratory mice or rats can suppress or even correct metabolic changes caused by a high-fat diet . Could vinegar/acetate also counteract the negative changes in metabolism caused by fructose, i.e. sugar? Given that the essence of both metabolic changes is identical, namely the initiation of de novo lipogenesis (DNL), i.e. the activation of the ACC1 enzyme and the reversal of the direction of mitochondrial isocitrate dehydrogenase, accompanied by the production of ammonia and urea and the slowing down of metabolism . So it can be assumed that vinegar/acetate will also work against fructose. First, let's review what we already know about what fructose causes. The results of studies are not always unequivocally negative. Fructose alone manifests itself differently than when combined with glucose, such as in regular sugar. Fructose, specifically fructose-1-phosphate (F1P), affects glycolysis without being