Ask anybody what they remember about the mitochondria, and they’ll probably say: “it’s the powerhouse of the cell.” That simple phrase has evolved from a biology class memory trick, to a meme expressing a general malaise or indifference. Because despite the necessity of these little energy-making machines, most of us still don’t know what the mitochondria are. And those of us who do remember that phrase, see it as the end of the story, rather than the beginning of one. 

But our mitochondria are the reason food gives us energy. They’re the reason we feel a sugar rush, and a sugar crash. They’re why we eat, drink, and ultimately how we survive. 

After over 40 years of research, scientists are turning to these powerhouses with one simple question: How do we keep these powerhouses full of power? 

An Energy Takeover

Before the mitochondria became invaluable to human cells, they existed completely outside of them as bacteria. They were simple single-celled organisms, lacking even the typical membrane structure of the bacteria we know today. Until they merged with another simple cell to become a more complex organism that makes us human beings. 

At first the plan wasn’t just to merge. The mitochondria, as bacteria, only wanted to rob the host cells of their energy and then leave them to die. But the bacteria soon realized they were better off working together with those cells rather than against them. This process eventually led to the more complex, structured organisms known as eukaryotic cells.

Today eukaryotic cells make up everything from mushrooms, apple trees, and dust mites to you. Human cells are eukaryotic which is why they have membranes, nuclei, and a bunch of other structural terms we probably learned in biology class but no longer remember. And the mitochondria’s initial energy takeover is now the very reason why we exist at all. 

The fact that mitochondria existed independently of the cell gave them their shape and purpose within the human body. It explains not only why the mitochondria look like bacteria, but also why they’re so uniquely vital to generating the energy we need to survive. 

A Powerful Purpose

Once they’d taken over, the mitochondria had a primary purpose: to generate energy. It sounds simple, and in some ways, it is. Even though there are several complicated processes taking place inside our cells, they all have the joint mission of creating a much-needed molecule known as ATP (adenosine triphosphate). ATP is energy.

Creating ATP is essentially a highly advanced game of microscopic hot potato. Whatever we eat or drink is broken down into pieces, and our cells toss those pieces (specifically electrons) over to oxygen molecules. Which allows the rest of the cellular respiration process to produce ATP. 

Research over the last few decades has shown we make less mitochondria as we age. It’s also shown that what mitochondria we do have left, aren’t very effective. Some scientists theorize this is a result of an imbalance of free radicals and our cells’ ability to get rid of them. Others found evidence pointing to the leftover DNA in mitochondria as what led to their future potential for dysfunction. But most of their studies agreed on one thing: mitochondria grow less effective over time because of their decreased ability to make ATP.

In some ways, you could say this makes the mitochondria somewhat human-like. They too, need a purpose. But as they age, they grow less effective at their purpose of creating energy. They become dysfunctional, diseased, and die. As a result, the less ATP we create, the less energy we have to get through the day. And we all know what “not enough energy” feels like.

Only You Can Prevent Energy Loss

Although we make less mitochondria as we age, the number of mitochondria we do create is almost completely dependent on how much energy we need. The more active we are, the more energy our cells require, the more mitochondria are created to match our needs. 

That closely knit relationship also means that whenever we change our lifestyle or habits, our mitochondria adjust their number to that change. Some scientists have caught onto this and believe there is a connection between exercise routines and a process called mitochondrial biogenesis. They’ve found that exercise initiates a series of complex chemical reactions within the body that signal the need for more ATP and therefore more mitochondria. 

But the opposite is also true. A sedentary lifestyle can signal to the body that we don’t need as much ATP and inhibit the mitochondria from creating more of themselves. This reduces cellular energy, which can be felt all over the body, and is connected to more general metabolic dysfunction. 

Thankfully, there are a few different ways to control the number of mitochondria in our cells. They can be made from scratch (mitochondrial biogenesis), divided, donated, or selectively removed from a cell altogether. All of these methods help the mitochondria directly match their supply to our need. Ultimately, our lifestyle and habits are important indicators of how much ATP we need and therefore how many mitochondria exist to meet that need. 

The Not-So Mighty Mitochondria

As crucial as mitochondria are for creating energy, it’s not as simple as one organelle. A bunch of different chemical reactions are at play, with the help of various chemicals, coenzymes, and one critical molecule known as NAD (nicotinamide adenine dinucleotide).

NAD is how the mitochondria turn food into energy. It’s how they make ATP, and how they play that energy-generating game of hot potato (a part of cellular respiration). Without NAD, the mitochondria could not generate energy. It’s safe to say that without NAD, the mitochondria would stop functioning, and so would we. 

The amount of NAD we produce declines with age, and like ATP, is heavily dependent on our lifestyle and habits. Things like working out can naturally increase NAD levels, but a bunch of other things like age, stress, staying in the sun for too long, drinking, or eating too much can all deplete NAD. Leaving our mitochondria to fight over a diminishing supply of their most powerful energy-generating resource.

Scientists at universities around the world are researching the effects varying NAD levels can have on overall human health as we age. So far, the results are more than promising. Recent human clinical trials show increased NAD does everything from help maintain muscle mass, to support heart health in older adults. With so many age-related health problems being linked to mitochondrial dysfunction, it only makes sense researchers would want to examine the very molecule that keeps mitochondria functioning in the first place. 

Knowledge Is Power To Your Cells

It’s okay if the only thing we remember from biology class is the “mitochondria are the powerhouse of the cell,” because they truly are. The mitochondria are why we evolved from single-cell organisms to the complex human beings we are today.  

Would we still be here today if the mitochondria had never joined forces to overtake and eventually bond with eukaryotic cells? Possibly. There’s no way to know for sure. But that’s not the point. Because they did merge. We are alive because of the mitochondria. We can read long blog posts like this one because of the mitochondria. They need us, just like we need them. Without the other, we are nothing. But together, we are the stuff of life.

When we look in the mirror, it can be hard to imagine how our cells have anything to do with the image staring back at us. How can something so small, something we can’t even see, influence what we look like or how we feel?

A new study published last month provides an intriguing answer to this question. Lead author Bhupendra Singh and colleagues at the University of Alabama at Birmingham uncovered a direct link between the health of our mitochondria and two common and highly visible signs of aging: hair loss and wrinkles.

Which Came First, the Mitochondrial Dysfunction or the Age?

Mitochondria aren’t called the “powerhouses of the cell” for nothing. It’s estimated that these islands of power generate 90% of our cellular energy. With lots of help from NAD (nicotinamide adenine dinucleotide), mitochondria keep our cells operating at their best.

Scientists have noticed that our mitochondria become less efficient as we get older, leading to decreased cellular energy and a host of related problems.

Declining mitochondrial health is now widely considered a hallmark of aging. But does aging cause mitochondrial dysfunction or does declining mitochondrial health lead to the physiological changes we associate with aging? Or is the truth somewhere in between?

This chicken-and-egg conundrum inspired Singh and colleagues to dive deeper into this complicated relationship between mitochondrial health and aging.

Gene On, Gene Off

The researchers engineered a special mouse to study the effects of mitochondrial dysfunction independently of other age-related processes. By turning a single gene on or off they could directly control the mitochondrial health in young, 8-week-old mice (that’s about 20 years old in people years).

When they turned this gene “on” mitochondria became dysfunctional. When they turned the gene “off” mitochondrial function could be restored.

A few weeks after making mitochondria dysfunctional, the researchers started noticing some striking changes. Visible skin wrinkles appeared. Hair fell out. Males and females even showed different patterns of hair loss, with males showing patchier hair loss than females.

Now here’s where things get really interesting. When the researchers made mitochondria functional again, these changes disappeared.

In just one month, previously wrinkled skin became smoother and thinned out hair regrew. The changes caused by mitochondrial dysfunction could be reversed by simply restoring mitochondrial health.

One Step Closer to Understanding the Aging Process

While this study doesn’t mean we suddenly have a solution for male pattern baldness or sun-weathered skin, it does provide interesting new insights about how we age.

First, it establishes a stronger causative link between mitochondrial health and some of the changes we associate with aging. By manipulating mitochondrial health independently of age, this mouse study shows that inducing—and reversing—mitochondrial dysfunction can directly affect visible signs of aging.

Second, this study suggests that supporting the health of our cellular powerhouses may not only prevent outward signs of aging but also has the potential to reverse changes that have already occurred.

We’ll need to see more research, particularly in humans, to be able to put this into practice. But these preliminary results show promise for supporting our health, inside and out, as we age.

Where The Research Goes From Here

Dr. Keshav Singh, a professor of genetics in the University of Alabama at Birmingham School of Medicine, led the team of scientists working on this study. “To our knowledge, this observation is unprecedented,” he said in a press release.

“Further experiments are required to determine whether phenotypic changes in other organs can also be reversed to wildtype level by restoration of mitochondrial DNA,” Singh said. Meaning that keeping mitochondria healthy could mean good things for the rest of our bodies, too.

Healthy Mitochondria = Healthy You

While we not-so-patiently wait for scientists to figure out the secrets of healthy aging, this study serves as an excellent reminder that, while invisible, our cells—and the mitochondria they contain—are an integral part of our overall health.

Whatever approach we may take, it’s clear that keeping our cells healthy can keep us at our best.