What is so special about MCT oil?

MCT oil is a fat (triglyceride) composed of three medium-length saturated fatty acids linked by glycerol. In particular, Caprylic acid C8:0 and Capric acid C10:0 are valued. We find them mainly in the most historically common animal and some vegetable fats, butter, goat and cow's milk and in coconut oil and palm kernel oil (but not in palm oil), I don't know the content in lard, but beware, it is not contained in margarines, sunflower, rapeseed or olive oil. Butter, for example, contains up to 13% short or medium chain fats, ie four to ten carbons. They can also be bought separately as a dietary supplement, I recommend select by the composition so that they should contain mainly C8:0 and C10:0.

From twelve carbons upwards, fats are characterized as long, although there is no complete agreement on this. Sometimes twelve-carbon fats are referred to as medium, which only encourages the confusion surrounding fats. Unlike shorter acids, lauric acid C12:0 can cause insulin resistance of the liver in rodents, although it is unclear in humans. Since the removal of fat from liver and pancreas is our main goal, which will improve our metabolic syndrome, we will also try to avoid lauric acid and we do not have to wait until we lose weight all over the body to see an improvement in the OGTT test. It will only take a few weeks.


 Butter contains 10 to 13% of short and medium fats. 

The main difference between short and medium vs long fatty acids is in the completely different processing in the body when swallowed. Short and medium are led directly into the blood of the portal vein, which leads to the liver. They are intended for burning because they are not suitable for storage in adipose tissue.

Long ones, on the other hand, are very suitable for storing energy and are difficult to process in the digestive system. First, digestive enzymes must brake them down into individual fatty acids that can enter the cells of the digestive tract. There they wait for the right moment to be assembled back into triglycerides and stored in so-called chylomicrons containing these triglycerides and also containing a label with the identification protein. In this way, they are then safely released through the lymphatic system into the blood, where the fat cells safely take them over.

As you can see, the body considers free long-chain fatty acids to be a dangerous material, so it handles them very carefully. Free long-chain fatty acids are normally found in the blood only after the changes associated with food consumption have disappeared, after the increased insulin and glucose have disappeared.

However, another situation occurs when our metabolic system is already disturbed, for whatever reason. There is no purification of the blood from free long fatty acids at the beginning of the meal. This causes them to experience elevated levels of insulin and glucose. This elevated level is to some extent normal during and after a meal. However, the presence of long-chain fatty acids causes the formation of triglycerides in places where it is not good, in the glands, liver, pancreas. It doesn't matter for a while, but if it happens repeatedly and for a long time, the situation will gradually get worse. It manifests itself in various diseases, the cause is marked as unknown.

In the table of the composition of vegetable oils, notice the first two lines, these are the MCT components, ND means that there are no MCT oils at all, so they create a deficit in humans. The last column is coconut oil. 

If these long-chain fatty acids are poly-unsaturated (PUFAs), which are mainly omega-6 from vegetable oils, then extra glucose, and fructose even faster, degrades these fats into toxic metabolites that damage mitochondria, the power plants of our cells, suppress fat burning and cause poison you, damage the liver, pancreas, blood vessels, heart, etc. Therefore, completely avoid consuming rapeseed or sunflower oil, heated or cold, they will always be harmful. It is stored in your adipose tissue and cell membranes. In the time between meals, it suddenly appears preferentially in the blood and is harmful even after many days, months and years. They will still circulate in your blood in an endless cycle of re-deposition into adipose tissue and new release. They will have enough time to peroxidize or convert to toxins. It will not allow you to burn other stored fats, you will be dependent on glucose, ie on carbohydrate consumption. In the absence of MCT, energy from saturated fats will be unavailable to you.

If you are worried that you will not have enough intake of essential polyunsaturated fatty acids, then these are unnecessary worries. These fats are a building material, you don't need a lot of them. You always have enough Omega-6 and if you eat fish occasionally, you will also have Omega-3. Other sources of Omega-3 are not recommended, oils degrade very quickly and plant flaxseed provides only ALA and you need DHA and EPA. Only about 1% of ALA is converted to DHA and EPA.


Demonstration of mitochondrial complex activity depending on the type of food in laboratory mice - LF = low fat, MCFA = medium  chain fatty acids, LCFA = long chain fatty acids  The darker, the more active

As for the mechanism by which short and medium fats promote fat burning so strongly, it could be a special form of fatty acid reaction known as omega-oxidation of fats. The fatty acid thus gains symmetry and subsequent beta-oxidation forms succinic acid. It significantly increases metabolic activity and energy expenditure through heat. This acid can increase mitochondrial complex II activity by 57% as shown above. On the contrary, the lack of medium and short fats with an excess of long ones reduces the activity of mitochondrial complex II by 7%. It is therefore not a question of whether, but rather how much short and medium fatty acids to eat.


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References:

Milk fat

Fatty Acid Composition, Oxidative Stability, and Radical Scavenging Activity of Vegetable Oil Blends with Coconut Oil

Medium chain triglycerides dose-dependently prevent liver pathology in a rat model of non-alcoholic fatty liver disease

Enhancement of muscle mitochondrial oxidative capacity and alterations in insulin action are lipid species dependent: potent tissue-specific effects of medium-chain fatty acids

Dietary intakes of polyunsaturated fatty acids and indices of oxidative stress in human volunteers

Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease

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