 Hey, until we all have arc reactor hearts that can be replaced by anyone with small enough hands to reach inside the socket. Is it safe? Yeah. Heart transplants are the last thing we want. I'm not getting my chest ripped open. I don't care if your 3D printed me a perfect replica of Usain Bolt's heart. I'm good. DCM is a disease that is a leading reason people need heart transplants, and it's because their hearts literally run out of energy. Scientists already knew that increasing NAD in mice with DCM had restorative effects on the heart, which led them to ask why. A new study figured out how one enzyme controls the creation of energy in heart muscle cells. It's like a little nanobot arc reactor inside each cell, and now that we know what it does, the future could have a lot less need for 3D printed hearts. So yeah, sorry if you were working on that. Welcome to Lifespan News, I'm Emmett Short. Today we're talking about heart energy. Dilated cardiac myopathy, DCM, basically sabotages the mitochondria of heart muscle cells, and mitochondria are the cells powerhouse, so DCM essentially robs your heart of power. This new study published in Nature Cardiovascular Research focuses on lysine dimethylase-8, known as KDM-8. We need KDM-8. Without it, mouse embryos die of heart failure before they are even born, so yeah, kind of important. This study wanted to know the impact of KDM-8 on living animals, so the researchers mutated up some mouse crossbreeds genetically designed to produce less KDM-8 specifically in the heart, and what they found could explain why NAD works so well against DCM. For some background, NAD or nicotinamide adenine dinocleotide is a key coenzyme that is found in all cells and is essential for life. Many in the longevity community supplement with NAD or its precursors NMN or NR and niacin in hopes of combating the aging process, but the science is still being debated. You can learn more about NAD on the Lifespan IO website at the link here or in the video description. We also have an entire Lifespan news playlist dedicated to the science surrounding NAD, which you can find here. These KDM-8 deficient mice had normal hearts up until about four to six months of age, and then they developed DCM and lived on average nine months. Mice with two copies of the mutation lived even shorter lives, about seven months, and all of them died of heart failure. As opposed to the non-genetically modified mice, the non-mutants lived for 27 months on out. When they looked at the heart muscle cells, the gene methylation showed that the KDM-8 heart cells had widespread malfunction, and specifically their NAD metabolism was all out of whack. Basically, reduced KDM-8 activity meant that the cells couldn't synthesize or consume NAD as efficiently, and the creation of the NAD precursor NAMP-T was also reduced, meaning there was way less energy to go around, also missing several sirtuins associated with longevity. All this meant that, at six months of age, these mice had half the ATP, half the energy normal mice hearts have. The results suggest KDM-8 is critical to mitochondrial energy use in heart cells, and is critical to aging, and backs up a previous study showing KDM-8 mutant mice suffering from DCM saw improvements from NAD treatment. Questions remain, would stimulating the creation of more KDM-8 in the human body create super hearts? Can we develop treatments that enhance KDM-8 activity or bypass its function altogether? How are sirtuins involved? Will Usain Bolt be able to copyright his heart's genetic blueprint? Lots more to discover, and when it's discovered, you can find out about it right here, so make sure you subscribe and hit the bell so you don't miss out. And if you want to learn more about NAD, check out Lifespan IO, where there's an entire page dedicated to everything you need to know. I'm Emmett Short, and we'll see you next time on Lifespan News.