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Mitochondria and Aging 

Aging is a complicated process that isn’t attributed to just one determining factor.  

However, researchers today have been looking for answers on the molecular level to understand the aging process more clearly. And scientists have gravitated towards the mitochondria, a powerful organelle within the cell, as the subject of study.  

 

What are mitochondria? 

The mitochondria are the “powerhouse of the cell.” They generate 90% of your cell’s energy, operating like miniature power plants. Without them, your cells would cease to function.  

How do mitochondria generate energy? 

Your mitochondria generate their energy by turning the macronutrients from your food, carbohydrates and fatty acids, into an energy storage molecule called ATP (adenosine triphosphate).  

ATP molecules are like supercharged batteries, waiting to release their bountiful energy at a moment’s notice. But why do your mitochondria create stored energy in these molecules instead of straight “pipelining” power to all the necessary parts of the cell? 

Portability.  

These ATP molecules can travel to all the essential parts of the cell. Once they arrive at their destination, they break apart, creating a surge of energy for use by their nearby neighbors.   

 

What role do mitochondria have in aging? 

There are many functions in the cell that require the energy created by our mitochondria. If that energy source were to be interrupted in some way, our cells would be in trouble. Much like a rolling blackout in a bustling city, a lack of power could impede several vital operations in your cells.  

When your mitochondria don’t behave the way that they should, it’s called mitochondrial dysfunction. And mitochondrial dysfunction has been proposed as one of the nine hallmarks of aging.  

 

Let’s talk about the mitochondrial free radical theory of aging. 

Mitochondria research has been such a strong topic of aging research that a prevailing theory resides in the scientific community: the mitochondrial free radical theory of aging. 

The theory proposes that the free radicals produced by your mitochondria are the culprits of mitochondrial dysfunction.  

During the process of turning your food into energy, your mitochondria produce unfortunate byproducts. Like a gasoline engine releasing carbon emission, your mitochondria emit free radicals.  

Free radicals are unstable molecules that can wreak havoc in your cells, damaging your DNA and other important cell functions. Typically, your body has enough antioxidants to combat these free radicals, achieving a balance in your system. However, there may be certain lifestyle factors that can place your mitochondria into overdrive. 

Poor diet, drinking, sleep disruption, overtraining, sun exposure are just a few ways your mitochondria undergo this imbalance between your free radicals and antioxidants, also known as oxidative stress. 

Your mitochondria have their own DNA. 

Unique to some of your other organelles, mitochondria have their own DNA known as mtDNA. 

The popular belief is that the mitochondria used to exist entirely separate from  cells, operating as single-celled organisms on their own.  

Sound familiar?  

Yes, they may have looked and behaved a lot like bacteria. But instead of attacking your cells, like some bacteria, they decided to live symbiotically. Without your mitochondria, we would have never become the complex organisms we are today.   

Adding more to their intrigue, mtDNA can only be passed down from mother to child, making you more genetically similar to your mother than your father. Popular ancestry DNA kits lean on mtDNA to make their deductions.  

MtDNA mutations may be a factor of aging. 

Traditionally, the causal link between DNA damage and aging has primarily looked at your DNA housed in the nucleus. MtDNA has now been a popular subject of aging research in the most recent years. Studies suggest aging is correlated to the damage caused by free radicals to your mtDNA as well.   

A review published in The Journal of Clinical Investigation states, 

There is solid evidence that the amount of mtDNA mutations increases with age in humans; for example, deletions in mtDNA have been observed in the aged human central nervous system, skeletal muscle, and hepatocytes…In general, mutations of mtDNA may arise as a consequence of unrepaired DNA damage, for example, damage caused by ROS, or by replication errors during normal mtDNA synthesis.” 

Mutations to your mtDNA cause a proliferation of errors in the replication process, further disrupting your normal mitochondria function. And the less efficient your mitochondria become, a domino effect of issues occur to other cell functions that rely on mitochondrial energy. 

 

Your mitochondria are too close to the problem. 

Free radicals created by mitochondria are linked to all sorts of problems in the cell, and you can find them to be a culprit amongst the other hallmarks of aging. However, since your mitochondria are the primary source of free radicals, they may be getting the brunt of the damage. 

A review published in Cell argues that the mitochondria’s proximity to the problem could be accelerating its own decline.  

The review states, 

“In postmitotic tissue such as brain, the levels of oxo8dG are significantly higher in mitochondrial compared to nuclear DNA. Reasons for these differences are thought to include the proximity of mitochondrial DNA to the source of oxidants and the lack of any protective histone covering.”  

The free radicals produced from your mitochondria can create an immediate vicious cycle. Like a factory that poisons nearby villages with toxic runoff, the problem meets full circle when you realize the factory workers live in the nearby villages.  

 

Your mitochondria count changes with age. 

Mitochondria is the plural form of a mitochondrion. But hardly anyone refers to mitochondria in their singular form. Why? Because your cells, depending on their location, may have thousands of them in just one cell.  

For example, energy-demanding organs like the heart require loads of energy, primarily fueled by these tiny powerhouses. According to the British Society for Cell Biology, 40% of the cytoplasmic space in heart cells consist of mitochondria.  

Your mitochondria find their strength in numbers. The more mitochondria we have, the less burden one mitochondrion has to sustain your energy.  

However, researchers from the School of Kinesiology and Health Scientists at York University show we make fewer mitochondria as we age.   

A lower mitochondria count can overload the system, burdening your tiny powerhouses with the same energy demand but with fewer hands to divide the work.  

 

You need to stay active as you age. 

A comparative study published in the Journal of Gerontology shows that exercise can help promote mitochondrial biogenesis, a process where your body creates more mitochondria. 

Your mitochondria are very responsive organelles. If they detect an increase in energy demand, they can replicate themselves to provide more help for the new workload.  

However, the inverse is also true. If you have a more sedentary lifestyle, your mitochondria see that your day-to-day energy needs are minimal. And supporting multiple mitochondria is an expensive process. In response, your mitochondria will reduce their numbers to maintain efficiency.  

It's important to incorporate an active lifestyle, especially as you age, so that your mitochondria know to supply ample amounts of energy. In turn, your mitochondria will multiply and help stave off mitochondrial dysfunction. 

 

NAD+ boosting supplements can help. 

The unsung heroes of your mitochondria are their collaborators, NAD+ (nicotinamide adenine dinucleotide).  

NAD+ are tiny helper molecules that essentially keep the wheels turning within the engines of the mitochondria. Without them, the mitochondria would sit dormant. 

Studies suggest that increasing NAD+ can support mitochondrial function. A preclinical study published in EMBO Molecular Medicine shows supplementation with nicotinamide riboside (NR), a novel form of vitamin B3 that increases NAD+, resulted in mitochondrial biogenesis in mice. 

 

You don’t have to “feel” old if you take care of your mitochondria. 

If “feeling old” was tied to our propensity for fatigue, mitochondrial dysfunction could be the cause. 

An article published in Integrative Medicine highlights that the loss of function in your mitochondria can result in excess fatigue, a common symptom of aging. And supporting your mitochondria may be one of the best ways to fight it.  

Health advocates may focus their attention on big-picture health advice, like participating in routine exercise and maintaining a healthy diet. But you might not realize that these steady steps are actually making real molecular changes in your body. And taking care of your mitochondria is just one of the numerous ways that can help you improve the way you age. 

 

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