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What causes atherosclerosis?

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I have already discussed here several times that the main actor in the formation of narrowed blood vessels and plaque is not cholesterol, as official medicine still tells us, but oxidative stress. I showed that oxalic acid (oxalate) and its neutralization by calcium in food play a big role here . In this post, I will continue following the trail of the AMPK enzyme, which controls the phosphorylation of very important enzymes related to some civilization diseases. For example, it phosphorylates the enzyme ACC and thus suppresses the formation of new fats and thus solves obesity. AMPK suppresses hepatic glucose production and gluconeogenesis and thus resolves diabetes . And in this post we will see how activation (phosphorylation) of AMPK reduces oxidative stress on the inner surface of blood vessels (endothelium) and thus suppresses atherosclerosis. So I am continuing the serie that monitors the effects of acetate on the metabolism of liver and fat cells, brain cells and now also vascu
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Are carbohydrates toxic?

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In an older post, I focused on what to eat , what is probably harmful to us and, above all, in what quantity. I used the information here from Paul Jaminet's book  Perfect Health Diet . In the section on carbohydrates, it states that the recommended maximum amount of carbohydrates is 150 g (600 kcal). Why? What happens in the body when the daily intake of carbohydrates is higher? So let's investigate. First, let's look at this image from a study examining changes in metabolism in humans with varying amounts of carbohydrates and fat consumed , which I've added a little. The picture shows the dependence of DNL on energy intake, CH=carbohydrates, P=proteins, fat intake does not affect this process. Empty bars show continuous process, full bars when eating. What do we see here? The process of de-novo lipogenesis (DNL), i.e. the formation of fats from glucose, is a natural protection against high carbohydrate intake. The total amount of fat thus produced in the liver or adip
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Can Vinegar Be the Solution to Alzheimer's and Senile Dementia?

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Vinegar or acetate is a very interesting substance, a food supplement. If you would like to know more and in detail about it and its metabolism in the body, read this two-part article . It is devoted to acetate only and has two parts, a total of 49 densely annotated pages in two columns. All this about a molecule that contains only two carbons. Incredible. It apparently affects all processes in the body. Acetate acts not only by activating AMPK during its conversion to acetyl-CoA, but also directly on the FFAR2 receptor, thus, for example, it supports vasodilation, i.e. better blood and oxygen supply to tissues. First, let's review the basic mechanism by which acetate in the body acts against obesity. It is the result of the processes associated with the activation of acetate in the cell, i.e. the connection with the CoA molecule to form acetyl-CoA. This reaction consumes energy (ATP) and creates a signal of shortage, activates the enzyme AMPK, which limits the ACC enzyme by phosp
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The mystery of the missing Acetyl-CoA molecule, acetate as a solution?

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What is cytosolic acetyl-CoA? We all know vinegar, it is an acid containing two carbons, the shortest fatty acid. We have already met MCT oils here , which contain medium fatty acids with eight or ten carbons, coconut oil contains lauric acid with twelve carbons. So if we go in the direction of fewer carbons, we get to butyrate in butter, a fatty acid with four carbons, and acetic acid with two carbons. If the acid is dissolved in water, hydrogen is separated as a proton and we are talking more often about the molecule of acetate, butyrate, oleate, etc., not about the acid as such. That's just an introduction. But what is acetyl-CoA? Acetate is a small molecule, so that the cell can control the flow of these small molecules, it attaches a part called Coenzyme A abbreviated CoA to them. The process of attaching acetate to CoA requires energy (ATP) and it's actually the activation of the acetate molecule for use in the cell. This  process sends out a signal (AMP) to support ener
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Beware of hypoxic fat cells, they spread cancer!

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As I wrote elsewhere, when I add the transcription factor HIF-1α to the search, activator of (pseudo)hypoxia, activator of metabolism without the use of oxygen, something interesting always appears in the results. So this time it's quite the bomb. Fat cells spread cancer by spreading the message of lack of oxygen. The study does not say it directly, but if we consider that the activation of the transcription factor HIF-1α is behind the hypertrophy of fat cells , i.e. their constant enlargement to enormous dimensions, then it is not surprising that these cells spread many problematic signals around the body. One such little-known signal is small extracellular vesicles called exosomes. Extracellular vesicles containing regulatory signals sent by fat cells. I have already shown several times here that the activation of (pseudo)hypoxia, i.e. the transcription factor HIF-1α in adipose tissue, is at the beginning of subsequent changes in the entire organism. Studies in mice show that if
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Is increased cholesterol production a rescue mechanism for electron export?

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A provocative study was recently published showing that elevated cholesterol is better managed by twelve Oreo cookies a day than by traditional statin treatment. Of course, only in a special situation, but that's how it is. That situation is a very low-carbohydrate diet combined with low body fat. This led me to think that increased cholesterol is probably a way to solve some metabolic problem, specifically a lack of intermediate products of the TCA cycle. These are necessary for the export of energetic electrons through membranes, i.e. for the transfer of beta oxidation products (NADH) from peroxisomes to the cytosol and further to the mitochondria. In the case of a low-carbohydrate keto diet, electrons obtained by beta oxidation of fats in perixosomes can't be exported via the normal pathway via lactate or malate, but cholesterol synthesis  as rescue mechanism can be used.  And I even found a study that pretty much confirms it . Cholesterol synthesis is a relatively complex
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Is photobiomodulation better with red, green, blue or white light?

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We have already seen the healing power of red light . Let's review what it can do. According to the latest research, red light passes through the skin into the tissues, even through the bones. It acts through nitric oxide (NO), probably by producing NO from nitrites by the enzyme CcO, which limits oxidation on the fourth mitochondrial complex CcO. This leads to a better distribution of oxygen throughout the tissue, resting oxidation improves, i.e. obtaining energy from food in the most efficient way through oxidative phosphorylation. But it's not a cure-all. This is because oxidation will not increase under load. Nitric oxide conserves oxygen and promotes the fermentation of glucose to lactate. Thus, energy in the form of ATP molecules is increased, but their origin is largely from glycolysis, not from oxidative phosphorylation. Let's try to find an even better solution, for example, we can look at what other colors of light or combinations of several colors do. Different w
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