Cover photo by Kate Trifo

⚡️Mitochondria, power, energy and sex have evolved together for billions of years 

Around 2 billion years ago the single-celled microorganisms archaea — similar to bacteria but evolutionarily distinct from bacteria — were invaded by the bacteria alpha-proteobacterium. After tolerating the bacteria for a while, however, the invaded archaea evolved (became smarter) and took advantage of the bacteria, ending up integrating them for good. As a consequence, the bacteria became the mitochondria (mt), namely the powerhouses (power stations) of their hosts.

Then, thanks to these new powerhouses the archaea had plenty of energy ready for use and so they afforded to build a kind of new control center, like a new government —the cell nucleus. By doing so, they evolved from archaebacteria (organisms made of one cell with no nucleus) into eukaryotesorganisms made of one or more cells with a nucleus. 

In the end, what started as an arrogant invasion by the bacteria, allowed to the archaea to start a new “civilization” on earth, that is the famous and well known “eukaryotic mega-kingdom (actually a domain)” that conquered the earth eventually, and created the four kingdoms of Protista, Fungi, Plantae and Animalia (namely us).

Fast forward that very important prehistoric event and today we know that the main function of our mt is to produce adenosine triphosphate (ATP)—a chemical that cells use as fuel — and heat from digested food with the help of the 02 we inhale. Accordingly, they dump several waste products during this process: 

  • C02 (that we exhale),  
  • H20 (that we pee out) and 
  • free radicals, mostly coming from oxygen atoms and called Reactive Oxygen Species (ROS). And this is a big problem for our mitochondria! Let’s see why.

Even though most of our DNA sits in the nucleus of each of our cells, outside the nucleus, however, our mt have retained some DNA of their own: a circular genome known as the mitochondrial DNA (mtDNA), characterized by the absence of protective histones (proteins that package the DNA in the nucleus into chromosomes and play essential regulatory role in turning genes on and off).

Therefore, due to the continuous exposure to ROS (of very high concentration) the mtDNA has a higher mutation rate than the nuclear DNA. And this creates in the end a level of somatic mosaicism (mitochondrial heteroplasmy) during development and aging. And this is bad!

For example, by quantifying the prevalence of mitochondrial heteroplasmy and its pathogenic effect in healthy individuals, a total of 1,085 human individuals from 14 global populations have been sequenced and at least 20% of these individuals harbor heteroplasmies reported to be implicated in a disease such as classic mitochondrial diseases, premature aging, type 2 diabetes mellitus, cancer and neurodegenerative diseases. 

However, in contrast to the original theory favoring ROS as a cause for mtDNA mutations, there are now strong data arguing that most mammalian mtDNA mutations originate as replication errors made by the mtDNA polymerase. In fact, in this study researchers suggested that the ROS-induced high mutation frequency on mtDNA could be indirectly caused by oxidation of the mtDNA polymerase (a polymerase is a protein used to assemble DNA by copying a DNA template). 

But, even though most of our mtDNA tends to accumulate mutations (causing mitochondrial dysfunction), hopefully these mitochondria and modified genes do not pass to the next generation. In fact, thanks to maternal inheritance of mt, you take only brand new mt from your mother, simply because female gametes start to use their mt only after they have been fertilized. 

Surprisingly, many agree that the evolution of sex is likely to have a lot to do with your mt! In particular, Nick Lane, a British biochemist and writer, suggested in his book (Life ascending: the ten great inventions of evolution) that the early mitochondrion would provide an unending source of foreign DNA that would have contaminated the nuclear genome, and this contamination of foreign DNA would have imposed selection for recombination (namely sex) between host genotypes to preserve nuclear chromosomes with beneficial mutations, while purging deleterious ones. 

Simply put, think of the mtDNA as an ancient and transient “transfer station” for novel genetic material to eventually reach the nucleus (the final destination), and sex as the quality control process of this transfer. Yes, sex is power after all, mitochondrial power apparently!

But now, let’s leave behind us “science for adults” and let’s talk about “science of aging” and mitochondrial dysfunction.

These tiny guys of our mt— that have essentially remained the same for the last ~2 billion years—they have evolved to regulate other cell functions (apart ATP production) like apoptosis and β-oxidation of fatty acids that contribute to the aging process, inflammation, senescence and apoptosis. 

In general, biological aging is characterized by buildup of intracellular debris (e.g., oxidative damage, protein aggregates, and lipofuscin/ residues of lysosomal digestion), which fuels a ‘vicious cycle’ of cell/DNA danger response activation, chronic inflammation (‘inflammaging‘) and progressive cell deterioration. 

In other words, as we age several factors such as ROS leaked while ATP is produced, accumulated oxidative damage to mtDNA, genomic susceptibility, toxic metals, persistent organic pollutants, some prescription drugs and alcohol, are all associated with increased mitochondrial damage, linked with cancer, diabetes and neurodegenerative disorders. 

So, how can you protect these little guys? 

The answer is simple. 

You should use mitochondrial supportive nutrients like:  

Thanks for reading

PS: If you want to monitor your mitochondria just buy AgeCurve’s test 🚀📲📱 that provides deep age profiles by sequencing and quantifying thousands of human proteins (wet biomarkers) implicated in the Nine Hallmarks of Aging

AgeCurve’s test, based on non-invasive saliva collection, has been designed to help you monitor your aging process by giving you a score for seven out of nine hallmarks of aging, in this case for mitochondrial dysfunction and therefore your cell’s energy ⚡️ levels. 

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