Is coconut oil safe? What about soy or olive?

How does coconut oil compare to other vegetable oils? Someone recently argued on the X network a study comparing coconut, olive, and soybean oil in a mouse model of obesity. The conclusions of the study are that one would not take coconut oil by mouth. It is true that I also point out here that coconut oil contains mainly lauric acid C12:0, which can cause fatty liver because it strongly suppresses lipolysis and allows, unlike shorter fatty acids, fat storage in the liver. But it is also a way to clean the blood from free fatty acids, which modify the metabolism of the entire organism.

Let's analyze the data from this study preprint a little while knowing the IR 2.0 model and you will see that things can be a little different than the way the authors present them. In addition, they provide us with further arguments by giving fat in two amounts, such as 7% or 21% of the food. In addition, they performed this on two types of mice, mice with active and disabled peroxisomes (using PPARα KO genetic modification).

Let's repeat what my proposed model of insulin resistance IR 2.0 says:

We have two types of insulin resistance.

1. Metabolic insulin resistance arises as fuel competition

- some fuels have priority over others, they process NAD+ to NADH faster and thus create a lack of NAD+ in the cytosol for other fuels, especially for the breakdown of glucose. In this way, the reluctance of the cell to receive additional glucose will arise when there is a demand for increased activity by the insulin or H2O2 signal.

2. Epigenetic insulin resistance in adipose tissue

- fat cells that cannot deal with excess fuel, using succinate as a product of the enzyme SDH running in the opposite direction, activate the transcription factor HIF-1α. They switch to anaerobic metabolism and obtain energy by fermenting glucose to lactate and beta-oxidizing fat followed by lipogenesis (DNL), so they do not produce any CO2 and thus promote oxygen deficiency in adipose tissue. These cells do not respond to the insulin level and permanently release DNL products (mainly saturated fat C16:0 - palmitic acid) into the body and negatively affect the overall metabolism.

3. Epigenetic insulin resistance is triggered by insufficient metabolic insulin resistance with fuel mixture, oxygen deficiency and H2O2 excess. Metabolic insulin resistance prevents excess ROS and has a protective effect.

4. Metabolism of polyunsaturated fats with an unsaturated bond in the even position supplies enough NAD+ to the cytosol for glycolysis. In addition, it produces enough H2O2 for glucose to enter the cell. An excess of glucose in the cytosol activates DNL and the ACLY enzyme and allows further NAD+ formation in the conversion of oxaloacetate to malate. Both processes can cause and maintain excessive insulin sensitivity, which overrides the protection of metabolic insulin resistance in the event of excessive ROS production. This will accelerate the switch to epigenetic insulin resistance induced by HIF-1α activation.

And now we are equipped with the tools to analyze the above study.

The authors prepared for us a nice model with high insulin sensitivity (PPARα KO). Look, especially at 7% dietary fat, preferably in the form of omega-6 soybean oil. Switched off peroxisomes lead to the fact that all fats are processed in the mitochondria, and it seems that they do not fundamentally affect the processing of glucose in the cytosol, there is always enough NAD+. Great. Really?

SO soybean, OO olive, CO coconut oil, Wild type control, PPARα KO with disabled peroxisomes

The highest insulin sensitivity is shown by the blue curve, oops, the most obese. Why? According to IR 2.0, high insulin sensitivity will cause excess fuel, many ROS, which will start to switch fat cells to anaerobic metabolism, glucose will be metabolized to lactate and fat. Why is the red curve of coconut oil 21% the best? We see this in graph G and H, the curves of the drop in glucose level after insulin injection. After all, after 60 minutes, NAD+ in the cytosol is exhausted and glucose stops being loaded into fat cells, there is not so much material for fat formation.

And what happens if we leave the peroxisomes functional?

The situation has changed a lot. From the 7% graph, one might judge that soybean oil is the best. But on closer inspection, the 21% graph shows us that it's only a matter of time before something changes and soybean oil becomes the worst oil. I marked it with purple arrows. What will happen? As you can guess, according to the IR 2.0 theory, HIF-1α was activated in some fat cells. But what does coconut oil do for us here? Whether a little or a lot, a lot of fat is always stored. We'll have to speculate to clarify. MCT oils effectively suppress lipolysis, the release of free fatty acids from fat droplets. It can be seen that they also effectively prevent glucose from entering the cells, so there is a lack of NAD+ in the cytosol. HIF-1α activation should not occur, coconut oil protects oxidative metabolism. Interestingly, there is a significant increase in the level of LPS toxins passing through the intestinal wall, i.e. poisoning. But the effect on obesity is still minimal, so apparently they have a protective effect against LPS. An increase in endotoxin in the blood is not a good thing. So I must warn, coconut oil as well as shorter MCT oils C10:0 and C8:0 should not be used alone, but after mixing with butter or olive oil.

SO soybean, OO olive, CO coconut oil, WT wild type, PPARα KO with disabled peroxisomes
TLR4 receptors of LPS, NF-kB inflammation transkription factor

From this study, olive oil comes out the best. It can be seen that it almost does not activate peroxisomes and thus does not cause obesity. This is surprising because other studies show weight gain caused by monounsaturated oleic acid. It is possible that the quality of the olive oil matters a lot, especially the content of polyphenols will play a big role.

The study further deals with the intestinal microbiome and intestinal permeability to LPS endotoxin. From this point of view, olive oil is perfect, and soybean oil seems to be too, but as we already know, it causes other serious problems.

Addendum, what is the relationship between adipose tissue composition and insulin resistance measured by glucose and insulin infusion in humans:

The main component of coconut oil C12:0 as protection against insulin resistance, the main component of olive oil C18:1n-9 is neutral but metabolic products of omega-6 linoleic acid from other vegetable oils (C20:3n-6, C20:4n-6, C22:4n-6) definitely do not help. Even long omega-3 fats do not help.


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References:

Consumption of soybean or olive oil at recommended concentrations increased the intestinal microbiota diversity and insulin sensitivity and prevented fatty liver compared to the effects of coconut oil 

Acetylation stabilizes ATP-citrate lyase to promote lipid biosynthesis and tumor growth 

Adipose tissue fatty acids and insulin sensitivity in elderly men  


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