by matznerd | 2025-05-21 17:00:07+00:00
There is a reason that longevists, longevity researchers, and biohackers focus on mitochondrial enhancement through various means, supplementing NAD/NR, Ubiquinol, PQQ, ALCAR, photobiomodulation, etc

"Your eyes transform light into electrical impulses that coalesce into an image in your visual field, and your ears transform air-pressure waves into electrical pulses that you eventually perceive as sounds. Likewise, mitochondria transform dozens of hormonal, metabolic, chemical, and other information streams into their electrical membrane potential. This “bioenergetic” state then leads to the production of secondary messenger molecules that are intelligible to the nucleus. So in the same way you read messages on your phone, which receives signals, transforms them and projects decipherable information onto its screen, the nucleus of your cells can “read” the environment through the MIPS that surrounds it. Rather than having supplementary roles like those of battery chargers, mitochondria are more like the motherboard of the cell. Genes sit inert in the nucleus until energy and the right message come along to turn some of them on and some others off. Mitochondria provide these messages, speaking the language of the epigenome—the malleable layer of regulation that sits on top of the genome to regulate its expression.

My colleague Timothy Shutt of the University of Calgary likes to call mitochondria the “CEO of the cell”: the chief executive organelle. This metaphor captures how mitochondria not only are involved in integrating information but also give orders. They dictate whether the cell divides, differentiates or dies. Indeed, mitochondria have a veto on cell life or death. If the MIPS deems it necessary, it triggers programmed cell death, or apoptosis—a form of self-sacrifice for the greater good of the organism.

So vital are mitochondria that in difficult times cells may donate entire mitochondria to other cells. “In cellular emergencies, newly arrived mitochondria might kick-start tissue repair, fire up the immune system or rescue distressed cells from death,” journalist Gemma Conroy noted in a Nature news story last April. Inside tumors, cancer cells and immune cells appear to compete for mitochondria, using them as a kind of bioweapon. An international effort I participated in, led by Jonathan R. Brestoff of the Washington University School of Medicine in St. Louis, recently created an entirely new lexicon to guide the emerging field of mitochondria transfer and transplantation. All well and good, you may think. What does all this mean for my health or how long I’m going to live?

The short answer is that it may have everything to do with human health. Diabetes, neurodegenerative conditions, cancer and even mental health illnesses are all emerging as metabolic disorders involving malfunctioning mitochondria. And these findings are indicating new routes for intervention.

Mitochondria drive health—or disease—in several ways. One route derives from their role as energy processors. In an electrical circuit, if we crank up the input voltage too much, we can blow it out. Similarly, if our cells are exposed to too much glucose or fat—or, worse, both together, causing what doctors refer to as glucolipotoxicity—the mitochondria undergo fission and fragment into little bits, accumulate mtDNA defects, and produce signals that end up prematurely aging or killing the cell. Experiments in cells and in mice have shown that pharmacologically or genetically preventing mitochondrial fission induced by excessive glucose and fats may protect against insulin resistance. Cancer, too, may be a disorder of cellular metabolism. Cancer cells can burn glucose without oxygen, which suggests either that something is wrong with their mitochondria or that they prefer to reserve mitochondria for use in cell division—and proliferation.

A second pathway is through mitochondria’s influence on gene expression. Mitochondrial signals alter the expression of more than 66 percent of genes in the nuclear chromosomes. By changing which genes are expressed and to what extent, mutations in mtDNA may completely alter the nature, behavior and stress resilience of cells and ultimately of the whole organism."