“Perhaps no other structure is so intimately and simultaneously connected to both the energy of youth and the decline of the old.” – Nuo Sun¹

The science on aging has now shown the pivotal role mitochondria play in healthy cellular function and identified this “powerhouse” of the cell as a central factor controlling how we age. A single cell can have hundreds or even thousands of mitochondria. Working inside individual cells throughout the body, mitochondria produce the life-sustaining energy powering everything we do daily, from moving to breathing to thinking.

An essential function of mitochondria is to convert nutrients from the food we eat and oxygen from the air we breathe into ATP (adenosine triphosphate) — what naturally fuels our cells day and night.² Each cell needs a sufficient number of healthy and fully functioning mitochondria so it can work at full capacity to meet ever-changing energy demands.

Once known only as energy producers, scientific insight into complex mechanisms within the mitochondria have transformed aging research. Our understanding of the pivotal role mitochondria play in the health of our cells after middle age has grown significantly. And, this has focused our attention on mitochondrial dysfunction as a key driver of accelerated cellular aging and Age Associated Cellular Decline (AACD).³

Mitochondria are found in greater numbers in tissues and organs where energy needs are the highest such as your muscles, heart, brain, liver and kidneys.⁴ This is also why these organs are at greater risk of dysfunction and disease in older age as mitochondrial function declines.

The impact of mitochondrial dysfunction can be far-reaching, as mitochondria play an important role in nearly every aspect of cellular function. This includes those vital to providing efficient energy production, and influencing the pool of reactive oxygen species (ROS), toxic byproducts, and debris within cells.⁵

During the natural process of producing cellular energy, toxic byproducts and ROS are created and can begin to build up, especially if mitochondria are functioning with less efficiency. This accumulation results in mitochondrial damage and cellular damage when levels of protective glutathione and other antioxidant defenses are insufficient.

After middle age, declines in levels of glutathione and NAD+ (nicotinamide adenine dinucleotide) are likely and can impair healthy cellular functioning. NAD+ is a coenzyme essential to turn nutrients into energy and vital for mitochondrial energy production. The age-related decline of this helper molecule leads mitochondria to lose efficiency. This results in decreased cellular energy production and increased ROS.⁶

Once cellular levels of glutathione and NAD+ are no longer enough and the extent of mitochondrial dysfunction becomes too high, cellular functioning becomes impaired. The impairment of cellular functioning is slow and progressive. The impact on the body may only be noticed when it begins to affect our tissues and organs. This progressive deterioration can lead to a variety of dysfunction such as:^7-9

• Lack of motivation
• Decline in daily energy levels
• Poor exercise tolerance
• Muscular cellular strength and stamina decline

Over time, a noticeable loss of muscle strength and function and other signs of accelerated aging may happen. If these declines in functioning are not controlled, conditions such as sarcopenia (muscle loss) or cognitive diseases may develop.

In order to maintain efficient cellular energy production and healthy functioning, mitochondria are equipped with quality control mechanisms.¹⁰ Natural processes called mitophagy (removal of damaged mitochondria) and mitochondrial biogenesis (growth and division to create new ones) help to protect the mitochondria and cell from dysfunction.¹¹

However, these natural processes tend to decrease in older age and are weakened by oxidative stress and inflammation.¹² As these quality control mechanisms become less and less effective, errors begin to slip through. Because of this, poorly functioning mitochondria are able to survive and accumulate. The result is mitochondrial dysfunction and AACD.

As our understanding has grown of how mitochondrial dysfunction is a key driver of accelerated cellular aging, this insight has been transformed into research and innovative therapies targeting the mitochondria to support healthy cell function and improve AACD.1