It might be hard to believe but eating healthy fats is actually good for you. By removing carbs from their diets, researchers from Saint Louis University found that entering a keto state could completely prevent, or even reverse heart failure caused by a metabolic process.
The findings were published in the journal Nature Metabolism. The research team, led by Kyle S. McCommis, Ph.D., assistant professor in Biochemistry and Molecular Biology at SLU, looked at a metabolic process that seems to be turned down in failing human hearts.
In an animal model, drastic heart failure in mice could be avoided by switching to high fat or “ketogenic” diets, which could completely prevent, or even reverse the heart failure.
“Thus, these studies suggest that consumption of higher fat and lower carbohydrate diets may be a nutritional therapeutic intervention to treat heart failure,” McCommis said.
Ketosis is a metabolic state in the body where fat is used for energy instead of carbohydrates. It takes the average person approximately two days to a week, while eating less than 50 net carbs to enter ketosis.
How Does Ketosis Protect The Heart?
Your heart muscles require large amounts of chemical energy stored in nutrients to fuel cardiac contraction. To maintain this highly energy demanding process, the heart is flexible and can adapt to altered fuel supplies when required.
The mitochondrial pyruvate carrier (MPC) complex, composed of MPC1 and MPC2, is required for pyruvate import into the mitochondria. This study demonstrates that MPC expression is decreased in failing human and mouse hearts, and that genetic deletion of the MPC in mice leads to cardiac dysfunction.
“Interestingly, this heart failure can be prevented or even reversed by providing a high-fat, low carbohydrate “ketogenic” diet,” McCommis said. “A 24-hour fast in mice, which is also “ketogenic” also provided significant improvement in heart remodeling.”
Diets with higher fat content, but enough carbohydrates to limit ketosis also significantly improved heart failure in mice lacking cardiac MPC expression.
“Our study reveals a critical role for mitochondrial pyruvate utilization in cardiac function, and highlights the potential of dietary interventions to enhance cardiac fat metabolism to prevent or reverse cardiac dysfunction and remodeling in the setting of MPC-deficiency,” McCommis said.
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