Quick overview of what you’ll learn from this blog post:
- What mitochondrial dysfunction is
- Why it happens
- The consequences of mitochondrial dysfunction
The Hallmarks of Aging describes mitochondrial dysfunction as the decline of the mitochondria and their ability to produce energy for the cell.
The powerhouses of the cell
The mitochondria are frequently referred to as the powerhouses of the cell. They act by turning the food we eat into a form of universal cellular energy currency called adenosine triphosphate (ATP). Our cells use ATP to fuel the many different cellular processes they perform from producing proteins, dividing to make new cells, repairing or recycling cellular components, and their many interactions with other cells.
Without the mitochondria to power our cells life would be impossible. These miniature energy factories are highly efficient but unfortunately, as we age, they start to deteriorate and things break down.
What causes mitochondrial dysfunction?
- Reactive oxygen species
Reactive oxygen species describes a number of reactive molecules and free radicals derived from molecular oxygen. These species are a byproduct of energy production, like how smoke is a byproduct of burning wood.
Reactive oxygen species produced by the mitochondria bounce around the inside of the cell and can strike the mitochondrial DNA which can cause a mutation. Normally, this isn’t a problem: the amounts produced are relatively low and manageable due to our cells having a number of ways to neutralize it. However, the amount of reactive oxygen species produced rises significantly as we age, making our cellular defenses become less effective.
Over time, these mutations build up, causing a decline of energy production, risk of cancer, and loss of proteostasis. - Decline of mitophagy
Our cells have a variety of quality control and repair systems, including mitophagy—the selective degradation of mitochondria by autophagy. But as we age, these begin to break down.
When we’re young, mitophagy maintains the quality of mitochondria. This disposes and replaces defective or damaged mitochondria. But as we get older, mitophagy becomes increasingly less effective, allowing damaged mitochondria to evade destruction. The problem comes when mitochondria has mutations that provide an improved survival rate. Over time, the mutated mitochondria outcompetes the healthy ones until the cell fills with inefficient and dysfunctional mitochondria. - Loss of NAD+
Nicotinamide adenine dinucleotide (NAD+) is a coenzyme central to metabolism found in all living cells. As we age, NAD+ levels decline, leading to shortages. While our ability to create NAD+ doesn’t decline, the consumption of that limited pool increases. This then leads to a breakdown in the communication between the cell nucleus and the mitochondria.
What can we do about mitochondrial dysfunction?
Researchers are working on ways to solve the problem of mitochondrial dysfunction and there is also some evidence that fasting might help clear out damaged mitochondria.
- Boosting NAD+ with self-injections, patches, or nose sprays
- Reducing the level of inflammaging
- Transferring the mitochondrial DNA to the cell nucleus
- Replacing dysfunctional mitochondria
- Inducing mitophagy (a sub division of autophagy) via drugs or fasting
If scientists can find ways to keep our mitochondria protected and healthy, it could help slow down how fast we age and protect us from a variety of age-related diseases.
Note: The above statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.