Your Longevity and the Composition of Your Mitochondria

Research in recent years has made it clear that the composition of the membranes in your cells - the relative proportions of proteins and amino acids that make up their structure - has a lot to do with how long you live. When comparing longevity between species, at least. This is the membrane pacemaker theory of longevity:

The membrane pacemaker hypothesis predicts that long-living species will have more peroxidation-resistant membrane lipids than shorter living species.

Mitochondria, the power plants of your cells, generate damaging reactive oxygen species (ROS) in the course of their operation: ROS will race off to damage the first thing they can find by reacting with it, such as a cell membrane. Mitochondria themselves have membranes, and are first in line to be damaged by the ROS they generate. Eventually damage accumulates and cascades to change the surrounding cellular environment very much for the worse. This process is an important root cause of degenerative aging.

This is why those species more resistant to the damaging effects of reactive oxygen species live longer than their peers. A good example is the naked mole rat, which lives eight times longer than similarly sized rodent species.

With this theme in mind, I noticed an open access paper today that looks at membrane composition differences a little closer to home: in the mitochondria of primates:

The mitochondrial (mt) gene tree of placental mammals reveals a very strong acceleration of the amino acid (AA) replacement rate and a change in AA compositional bias


the rate acceleration in the simian lineage is accompanied by a marked increase in threonine (Thr) ... his Thr increase involved the replacement of hydrophobic AAs in the membrane interior [and] analysis reveals a statistical significant positive correlation between Thr composition and longevity in primates.

Even in primates, the composition differences are important - no doubt altering the process of ROS damage and mitochondrial dysfunction that contributes to aging. It reinforces just how central our mitochondria are to aging and longevity, and how vital it is to speed research into repairing damaged mitochondria in humans.