Andrew Huberman· PhD
That's because, as I mentioned before, fat oxidation, this conversion of fatty acids into ATP and the mitochondria, is inhibited by insulin. If you keep insulin low, you're going to increase that process.
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The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
That's because, as I mentioned before, fat oxidation, this conversion of fatty acids into ATP and the mitochondria, is inhibited by insulin. If you keep insulin low, you're going to increase that process.
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High insulin does one more thing. It basically tells your body, take this sugar, get rid of it from the blood and store it as fat. How does it do that? It pushes our liver to turn it into triglyceride. The triglycerides can a go into our blood as a form of VLDL and go and attach themselves to the heart. And that's why PCOS patients, you have to screen them their lipid panel because of their cholesterol, risk of cardiovascular disease, risk of diabetes, all of that.
But if insulin's elevated, it can't burn it. Normally, the liver would take those fatty acids and just say, "Well, I'm going to burn it into ketones." But if insulin's elevated, it can't happen. The liver has to store it. The pancreas starts to store it. But as I mentioned earlier, the triglycerides are not the cause of insulin resistance. But now we have the high insulin, which is an acute cause of insulin resistance. and a lot of free fatty acids.