What is worse, sugar or sunflower oil?
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 quickly convert glucose into fat to get glucose out of the bloodstream. The protective effect of glucose, such as the one I showed in the study example in the previous post, can easily be reversed. So be careful with the rate of carbohydrate intake!
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| Sugar (fructose) is harmful mainly in the relatively high-fat diet common to humans by limiting fat burning and increasing its storage, e.g. in the liver. |
So where do we have the evidence that fructose is the primary cause? Analysis of results and measurements from studies of high-fat diets in rodents. If we analyze the composition of the best diets that cause obesity, they always contain some sugar. It is very interesting; quite often, the authors do not even mention that there is any sugar in it and simply call this diet HFD (high-fat diet). If sugar is absent from the diet, then the results are not clear, and for example, oils with omega-6 linoleic acid may not cause obesity at all if the study is only short-term.
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| Even a small amount (3.5%) of fructose in the diet of mice suppresses the enzyme CPT1a for the transport of long-chain fatty acids into the mitochondria, fructose reduces fat burning. There is also a protective effect of glucose (HFD+G), which was not seen in another study. |
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| Another study had slightly different results. Glucose does not protect here, fructose does not increase fat storage... |
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| ...but shows that fructose activates fat-making enzymes (ACC1, FASN, SCD1), even glucose with fat does it as well... |
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| ...and it is caused by the elevating presence of the KHK-C enzyme. |
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| Fructose, along with fat, also changes the size of mitochondria towards greater fragmentation and a much higher proportion of the smallest mitochondria. |
Oils have long-term effects, but in the short term, they seem fine and healthy. This is very misleading and the proponents of these oils have arguments to support them. Sugar is different. Even a small amount of fructose works immediately, activating the enzyme ketohexokinase (KHK-C), also known as fructokinase, and suppressing the transfer of fats into the mitochondria. It prevents fat burning and activates new fat formation from glucose or amino acids. It does this by suppressing the function of the deacetylase SIRT2, i.e. causing acetylation of a wide range of enzymes, which thus reduce their activity or are marked for elimination.
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| Fructose activates the enzyme KHK-C. The increased presence of this enzyme (KHK-C OE) itself strongly suppresses the deacetylase SIRT2. |
First, even a small amount of fructose will cause the disappearance of the CPT1a enzyme, so the transfer of long-chain fats to the mitochondria for burning is impaired. It will also cause the suppression of the IDH2 enzyme in the TCA cycle, which is extremely important for maintaining the level of NADPH during fat burning, and the lack of which will disable antioxidant protection. Without this protection, fats cannot be burned. These changes occur after the activation of the enzyme for fructose processing. The increased presence of the KHK-C enzyme itself turns off the SIRT2 deacetylase, and thus the acetylation of CPT1a and IDH2 significantly increases, which has the effect described above. Fructose also redirects the flow of glycolysis towards the formation of lactate and sets the cell to produce ATP without the presence of oxygen, it easily reaches the state of activation of the transcription factor HIF1 and, therefore, pseudohypoxia.
Disabling antioxidant protection (IDH2) leads to excess ROS and activation of the PLA2 enzyme, which releases free fatty acids from the cell membranes, that accumulated during previous life. If it is mainly oleic acid, nothing happens; UCP enzymes are activated, i.e. mitochondrial uncoupling, and more heat is produced.
HIF1 activation strongly correlates with the emergence of senescent cells. Lactate from glycolysis supports HIF1 activation. The mechanism is again dependent on the elimination of antioxidant protection (IDH2), activation of the PLA2 enzyme, and the composition of cell membranes. Senescence is triggered when peroxidized omega-6 fats are released from the membranes, and the aldehydes formed from them cause damage to DNA. Here we have the effect of vegetable oils, which promote cell senescence. They stop cell development. However, without the initial restriction of fat burning by fructose, this could not happen. Polyunsaturated fats would be burned quickly. They would not be able to get into the membranes. They would not be able to be stored for a long time. Fructose and, therefore, sugar is a necessary condition at the very beginning of the process, it prevents the preferential burning of polyunsaturated fats.
This whole process begins with damage to the intestinal wall and its permeability. And here, short-chain fatty acids, vinegar, and butyric acid enter this process. These nourish the cells on the surface of the intestines, where there is a lack of blood supply. A diet that contains these substances can provide enough energy for the surface cells and the intestinal wall will remain intact. It will only let through what it is supposed to let through. Even soluble fiber in food, which feeds intestinal bacteria, will not save us here. These bacteria are only in the large intestine, not in the small intestine. The nutrition of the epithelium of the small intestine must be provided by food, short-chain fatty acids, and perhaps, glucose. If the food does not contain at least a certain percentage of short-chain fatty acids, vinegar, or butyric acid, then the small intestine may have a problem with a lack of nutrition. And here we are again with the issue of oils that do not contain any short-chain fatty acids. It may, therefore, be very appropriate to combine them with vinegar.
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Processes suppressed by increased presence of the enzyme KHK-C, by fructose. Fat burning (Fatty Acid Oxidation) is most suppressed. Alcohol processing is also greatly suppressed. |
If we do not have a healthy small intestine, fructose easily enters the liver, where it activates KHK-C and creates a barrier against fat burning through enzyme acetylation. Only short and medium fatty acids pass through this barrier. We know that medium-chain fatty acids (MCTs) have a preventive effect. Therefore, if medium-chain fatty acids are present at the same time as fructose, nothing happens, fat burning does not stop, and pseudohypoxia or senescence does not activate. However, if the cell is already senescent, then even MCT fats cannot repair it.
However, there is one possibility. If acetate is also delivered to the liver along with fructose, AMPK is activated and APMD2 is deactivated, uric acid production is reduced, the formation of new fat stops, and the cells suddenly start functioning normally. Perhaps the repair of damaged genes is also triggered, and thus, the disappearance of cellular senescence. Perhaps the combination of fructose with acetate is needed for this, as acetate itself provides ambiguous results in studies and can also become a substrate for the formation of fats. Fructose may help activate AMPK and UCP here.
But there is another way to suppress the effect of fructose. This procedure is used by, for example, fruit. It is a combination of fructose and flavonols. It is not as effective as the combination of fructose with short fatty acids, but at a high concentration of flavonols, it works very well as a prevention. We have studies on mice. Flavonols are apparently able to eliminate changes in gene expression by stopping the penetration of transcription factors into the cell nucleus. They probably reduce the acetylation of enzymes and prevent the stabilization of the HIF1 factor, thus preventing pseudohypoxia and cell senescence. How exactly they do this is a question. In any case, fruit that is not too sweet and also contains flavonols is safe for us. If it is sweeter, it will allow us to prepare for the winter and gain fat, but probably much safer than without flavonols.
In conclusion, I would recommend trying to avoid fructose (sucrose/sugar) completely or combining it with butter or vinegar. Some diets completely avoid sugar. It would probably be enough to use dextrose (glucose) instead of sugar to satisfy the desire for a sweet taste. There are other sugar variants, but dextrose seems to be the least problematic and affordable. It is ideal to sweeten just before eating, you will get the most sweet taste with the smallest amount.
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| Different oxidation rates of SCFA. This is why, under normal conditions, bacteria produce acetate/propionate/butyrate in a ratio of 3/1/1. High concentrations of butyrate lead to the formation of reactive ROS, cause epithelial cell senescence, and lead to cancer. Butyrate in butter is in the right concentration. |
I also recommend frequently adding vinegar or butter to food, to provide food for the epithelial cells of the small intestine. In the more distant colon, intestinal bacteria produce these substances for the epithelial cells of the intestinal tract, but in the small intestine, no bacteria produce them. Therefore, they must be part of the food, especially if you want to consume fats and, therefore, the vitamins stored in them. I do not think that giving up the consumption of animal fats is a reasonable choice. You see, the composition of butter is such that it supports the health of the intestinal wall of the small intestine. Butyrate (butyric acid) in the colon may not be so beneficial, as this study shows. It probably increases the risk of colorectal cancer. Nature has everything figured out optimally, our interventions often disrupt this balance. So we cannot be surprised that the body reacts to these imbalances in its own way, even with chronic diseases.
References:
Gut bacteria identified in colorectal cancer patients promote tumourigenesis via butyrate secretion
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