The Biology of Aging: What Actually Changes and What Can We Control?

Join Dr. James Odell for Season 2 of the Science of Self-Healing Podcast! He's the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years, and he's here to share with you his extensive knowledge of medicine from a different perspective.

The Bioregulatory Medicine Institute

The Science of Self-Healing Podcast

What if aging isn’t simply a matter of getting older—but a complex biological process that we may have more influence over than we once thought? 

In this episode of The Science of Self-Healing, Dr. James Odell explores what actually happens inside the body as we age, from changes in our cells, mitochondria, hormones, immune system, microbiome, and epigenetics to the gradual shifts that occur in our muscles, bones, cardiovascular system, and brain. 

You’ll discover why people can age at remarkably different rates, how everyday factors such as movement, nutrition, sleep, stress, and social connection can influence the aging process, and why many age-related changes are not as inevitable as they may seem. 

Rather than searching for a mythical fountain of youth, this episode takes a fascinating look at the science of healthier aging—and the practical choices that may help us remain stronger, more resilient, and more capable throughout life.

Transcript: The Biology of Aging: What Actually Changes and What Can We Control?

Today I want to talk about something that happens to every one of us: aging. What actually changes inside our cells and tissues as the years pass? Why do some people stay remarkably healthy and resilient well into later life, while others decline much earlier? And how much of the way we age is actually within our control?

We'll look at the biology behind aging — DNA, mitochondria, inflammation, muscle, metabolism, hormones, the brain, and the gut microbiome — and then at what we can do to protect our health and function as we get older.

What We See in the Mirror Is Only Half the Story

So, let's get started. We tend to think of aging in terms of what we can see. Our hair turns gray. Wrinkles appear. We lose some muscle. We don't recover from a strenuous day quite as quickly as we once did. But those are really just the outward signs of something much more interesting happening beneath the surface.

Biological aging is not simply the passage of time. It is a gradual change in the body's ability to regulate itself—to repair damage, produce energy, respond to stress, maintain balance, and recover. And that distinction is important, because while we cannot stop chronological aging, we may have considerably more influence over biological aging than we once thought.

Two People, Both 65, and Completely Different Bodies

So, let's begin with an important distinction: chronological age versus biological age. Chronological age is easy. It is simply how many years you have been alive. Biological age is more complicated. It attempts to describe how well your body is functioning relative to those years.

Think about two people who are both 65 years old. One may have excellent cardiovascular fitness, good muscle strength, normal glucose regulation, sharp cognition, and very few medications. The other may already have significant metabolic disease, poor mobility, loss of muscle, and declining cardiovascular health. They have the same chronological age, but biologically, they may be quite different.

Genetics certainly contribute to those differences. But so do decades of nutrition, physical activity, sleep, stress, environmental exposures, smoking, alcohol consumption, illness, and many other factors.

There Is No Single Clock Ticking Inside Us

So perhaps the more useful question isn't simply, "Why do we age?" It's this: Which parts of aging are unavoidable, and which parts can we influence? To answer that question, we have to begin at the cellular level. Every organ in your body is made of cells that are constantly maintaining themselves.

Cells produce energy. They manufacture proteins. They repair DNA. They remove damaged components. They communicate with neighboring cells and respond to hormones, nutrients, immune signals, and environmental conditions. And aging gradually affects nearly all of these processes.

Researchers sometimes describe these changes as the "hallmarks of aging." They include DNA damage, telomere changes, epigenetic alterations, mitochondrial dysfunction, impaired cellular recycling, cellular senescence, stem-cell exhaustion, chronic inflammation, changes in nutrient sensing, and altered communication between cells. But these aren't isolated problems. They interact.

A dysfunctional mitochondrion can increase cellular stress. That stress can contribute to DNA damage and inflammation. Inflammation can interfere with cellular signaling and tissue repair. Poor tissue repair can then further impair the function of an organ. So aging isn't one clock ticking away somewhere inside us. It is better understood as a network of biological systems gradually becoming less efficient at maintaining balance.

And this is one reason I am skeptical whenever someone claims that a particular supplement, drug, food, or biohack can "stop aging." There isn't just one aging mechanism to stop.

Our DNA: Stable, but Not Indestructible

Now, let's look a little more closely at what happens to our DNA as we age. DNA contains the biological instructions that cells use to function. It is remarkably stable, but it isn't indestructible. Normal metabolism can damage DNA. So can ultraviolet radiation, inflammation, toxins, environmental exposures, and many other forms of cellular stress.

Fortunately, our cells have sophisticated DNA-repair systems. When we're young, these systems are generally quite efficient. Damage occurs, repairs are made, and cellular function continues. Over time, however, some damage accumulates, and the repair systems themselves may become less efficient. Some cells acquire mutations. Others begin functioning differently or stop dividing altogether.

Why "Long Telomeres Equal Long Life" Is Too Good to Be True

Then there are telomeres. Telomeres are protective structures at the ends of chromosomes. You can think of them as helping protect the integrity of genetic material during cell division. Telomeres tend to shorten during many forms of cellular replication. Extremely short or dysfunctional telomeres can cause cells to stop dividing.

But the popular idea that "long telomeres equal long life" is much too simplistic. Telomere biology is complicated, and simply making telomeres longer would not automatically make someone younger or guarantee a longer life.

The Switches That Decide Which Genes Get Used

Aging also affects something called epigenetics, which is essentially the system that helps control how our genes are used. The DNA itself doesn't have to change for a cell to start behaving differently. Instead, small chemical markers on DNA and the proteins around it can act like switches, helping determine which genes are turned on and which are turned off. As we age, these patterns of gene activity gradually change, which can affect how well our cells function.

Researchers have even developed what are called "epigenetic clocks," which use patterns of DNA methylation to estimate biological aging. These tools are scientifically fascinating, but they're still evolving. They should not be viewed as crystal balls that can precisely predict how long someone will live.

The important point is that aging involves changes not only in our genetic material, but also in how our cells read and use that genetic information.

Mitochondria: The Powerhouses That Need Housekeeping

Moving along, another major piece of the aging puzzle involves our mitochondria. Most people know mitochondria as the "powerhouses of the cell" because they help convert nutrients into ATP, the usable energy that powers cellular activity. But mitochondria do much more than produce energy. They're involved in metabolism, cellular signaling, stress responses, and even programmed cell death. As we age, mitochondrial function can decline. Some mitochondria become damaged or less efficient. Fortunately, the body has a housekeeping system for dealing with this.

One of those processes is called autophagy. During autophagy, cells break down and recycle damaged proteins and other cellular components.

A more specialized process called mitophagy removes damaged mitochondria. This is incredibly important. A cell cannot simply continue accumulating defective machinery forever and expect to function normally. It has to identify damaged components, remove them, recycle what it can, and replace what is needed. When these cellular housekeeping systems become less efficient, dysfunctional components can accumulate.

Older Tissue Is Not Passive Tissue

But here we encounter one of the most encouraging themes in aging biology: Older cells and tissues still retain the capacity to adapt.

Exercise is a wonderful example. Physical activity can stimulate mitochondrial adaptations in skeletal muscle. In effect, you're sending a biological message to the body saying, "I still need this system. Maintain it." That doesn't make exercise an anti-aging cure. It demonstrates something much more important: aging tissue is not necessarily passive tissue. It can still respond to appropriate biological signals.

The Cells That Retire but Never Leave

Next, I'd like to talk about a fascinating feature of aging involving cells that essentially retire—but don't leave. These are called senescent cells. A senescent cell remains alive, but permanently stops dividing. This can happen because of DNA damage, telomere dysfunction, or other cellular threats. And cellular senescence isn't inherently bad.

If a severely damaged cell is at risk of becoming cancerous, preventing that cell from continuing to divide can be protective. Senescent cells can also play useful roles in processes such as wound healing. The problem occurs when too many of these cells accumulate.

Some senescent cells begin releasing inflammatory molecules and other signaling compounds known collectively as the senescence-associated secretory phenotype, or SASP. When enough of these cells accumulate, they can contribute to chronic inflammation and alter the behavior of surrounding tissues.

Inflammaging: When the Fire Never Goes Out

And that leads us naturally to another important feature of aging: something researchers call "inflammaging." Acute inflammation is essential to survival.

If you cut yourself or develop an infection, your immune system generates inflammation to deal with the threat and begin repairing the damage. The problem isn't inflammation itself. The problem is inflammation that doesn't resolve appropriately.

As we age, many people develop persistent, low-grade inflammatory activity. Senescent cells may contribute, but so can metabolic dysfunction, accumulated cellular damage, changes in immune regulation, alterations in the gut microbiome, and chronic disease.

At the same time, parts of the immune system become less effective. So we can develop this strange combination: too much background inflammation while simultaneously becoming less capable of mounting a precise immune response when one is actually needed.

The goal, therefore, isn't to eliminate inflammation. It is to restore appropriate regulation—an immune system that can generate inflammation when necessary and then turn it off when the job is done. That's a very important distinction from a bioregulatory perspective.

Muscle: The Most Modifiable Part of Aging

So far, we've been looking at aging largely at the cellular level. Now let's move outward and look at how these changes begin to affect the body as a whole.

And one of the most important places we see this is skeletal muscle. Loss of skeletal muscle is one of the most consequential physiological changes associated with aging. Beginning in adulthood and accelerating later in life, we can gradually lose muscle mass, strength, and power. When this becomes significant, it can contribute to sarcopenia.

But here's the important part: Muscle loss is not entirely predetermined. Inactivity can dramatically accelerate it. And skeletal muscle remains remarkably responsive to resistance training even at advanced ages. When you challenge a muscle, you're providing a biological signal that says, "This tissue is still needed."

And maintaining muscle isn't simply about looking fit. Skeletal muscle is metabolically active tissue. It helps regulate glucose, supports joints, protects bones, enables mobility, and provides a metabolic reserve during illness or injury.

Protein also becomes increasingly important because aging muscle may become less responsive to small amounts of dietary protein—a phenomenon known as anabolic resistance. So adequate nutrition and resistance exercise work together.

Can You Get Off the Floor?

But strength alone isn't enough. Balance, coordination, and power also matter tremendously. Can you get out of a chair easily? Climb stairs? Carry groceries? Catch yourself if you stumble? Get down onto the floor and back up again? Those abilities may tell us far more about healthy aging than the number on a bathroom scale.

This is one of the clearest examples of the difference between aging and disuse. Some decline occurs biologically. But inactivity can magnify it enormously.

Does Metabolism Really Just "Slow Down"?

Next, let's talk about metabolism, because we constantly hear that metabolism simply "slows down" as we get older. The reality is more nuanced. Energy expenditure depends on body size, body composition, muscle mass, activity, and the amount of energy required to maintain tissues. As people become less active and lose muscle, their energy requirements can change. Aging can also affect insulin sensitivity and glucose regulation.

And this brings us back to muscle. Skeletal muscle is one of the body's major destinations for glucose after we eat. Maintaining active muscle tissue can therefore have profound effects on metabolic health.

Visceral fat is another important consideration. This is the fat stored around abdominal organs, and higher levels are associated with insulin resistance, inflammation, and cardiovascular risk.

Why the Scale Doesn't Tell the Whole Story

Importantly, body-fat distribution can change with age even when body weight doesn't change dramatically. So the scale doesn't tell the whole story. Healthy aging is not necessarily about becoming progressively thinner. Maintaining metabolically active tissue and physical capacity may be much more important.

Muscle mass, waist circumference, cardiovascular fitness, blood pressure, blood lipids, glucose regulation, sleep, and physical function can tell us much more about metabolic aging.

The Aging Brain Doesn't Move in One Direction

Moving along, we can't talk about aging without talking about the brain. The brain does change as we get older, but those changes don't necessarily mean a steady decline in our mental abilities. We may process information a little more slowly, and certain types of memory may not be as sharp as they once were. The brain itself also undergoes physical changes as we age.

But at the same time, many mental abilities can remain remarkably strong. Vocabulary and accumulated knowledge may be well preserved, and years of experience can actually improve our ability to recognize patterns, solve familiar problems, and manage our emotions.

And perhaps most encouraging is that the brain never completely loses its ability to change. It retains what scientists call neuroplasticity—the ability to adapt, reorganize, and form new connections in response to learning and experience.

What Actually Protects the Brain

Cardiovascular health is especially important for the brain because it relies on a steady supply of oxygen and nutrients. Exercise helps maintain healthy blood flow to the brain and also stimulates biological processes that support brain cells and the brain's ability to adapt and form new connections.

Sleep is equally important. During sleep, the brain consolidates memories, regulates hormones, and performs essential maintenance functions. Chronic sleep disruption has metabolic, cardiovascular, and cognitive consequences.

Social engagement and mentally challenging activities may also contribute to what researchers call cognitive reserve—the brain's ability to tolerate age-related changes or disease while maintaining function. But, no crossword puzzle, supplement, or brain-training program can guarantee that someone will never develop dementia.

But maintaining cardiovascular health, remaining physically active, sleeping adequately, continuing to learn, and staying socially connected are all reasonable ways of supporting brain health throughout life.

Hormones: Where We Need to Be Careful

Another area that changes considerably as we age is hormonal signaling. Sex hormones change substantially during menopause and more gradually in aging males. Growth hormone signaling, melatonin rhythms, insulin regulation, thyroid function, and stress-hormone patterns can also change. These shifts can influence bone density, muscle mass, body composition, sleep, temperature regulation, reproduction, and metabolism.

But here's where we need to be careful. A hormone level that tends to decline with age isn't automatically a deficiency that needs to be corrected. Hormones operate through tightly regulated feedback systems. Simply increasing a hormone because younger people tend to have more of it doesn't necessarily restore youth—and it can introduce significant risks.

Treating a diagnosed hormonal disorder is one thing. Using hormones in an attempt to reverse normal aging is something quite different. From a bioregulatory perspective, the goal isn't to maximize every biological marker associated with youth. The goal is appropriate signaling and regulation.

The Trillions of Microbes We Age Alongside

Next, let's turn to another biological system that we're only beginning to fully appreciate: the gut microbiome. The human intestinal tract contains trillions of bacteria, fungi, and other microorganisms that influence digestion, nutrient absorption, immune function, metabolism, and the integrity of the gut barrier. Each person's microbiome is unique.

Our gut microbiome does change as we age, but age is only part of it. What we eat, the medications we take, our health, physical activity, stress levels, where we live, and even our surroundings can all influence which microbes thrive in our gut.

Dietary fiber is particularly important because certain intestinal bacteria ferment fiber and produce short-chain fatty acids. These compounds interact with intestinal cells, immune signaling, and metabolism.

One of the best ways to support microbial diversity may therefore be dietary diversity. Vegetables, fruits, legumes, whole grains, nuts, seeds, herbs, and other minimally processed plant foods provide different fibers and phytochemicals that interact with the gut ecosystem. The microbiome gives us another important lesson about aging: We do not age in isolation from our environment. Our physiology develops through constant interaction with food, microbes, movement, stress, toxins, sleep, relationships, and our surroundings.

What We Cannot Control

Now, after hearing about all of these different biological processes, it would be tempting to conclude that if we simply do everything correctly, we can prevent aging. Unfortunately, biology doesn't work that way. Genetics influence longevity and disease susceptibility. Random cellular events occur. We cannot completely avoid environmental exposures. Cells accumulate damage. Tissue regeneration changes. Hormonal transitions occur. Immune function shifts. Recovery often becomes slower. And people can do everything "right" and still develop serious disease.

That's why claims that perfect nutrition, supplements, fasting, cold exposure, or other biohacks can completely prevent aging are misleading. Lifestyle changes probabilities. It doesn't provide guarantees. But that's very different from saying lifestyle doesn't matter.

What We Can Control

So, let's turn to the part of this discussion that is probably most useful: what can we actually control? Although we cannot stop aging, many of the factors that determine how well we age are modifiable.

Physical activity is probably one of the most powerful. Ideally, that includes aerobic exercise, resistance training, balance work, and simply moving regularly throughout the day. And what's remarkable about exercise is how many parts of the body benefit from it at the same time. It strengthens the heart and muscles, improves blood-sugar regulation, supports mitochondrial function and bone health, and even benefits our mood and brain function.

Nutrition matters too—but primarily as a long-term pattern rather than a collection of superfoods. A diet emphasizing vegetables, fruits, legumes, whole grains, nuts, seeds, healthy unsaturated fats, and adequate protein provides a strong foundation for metabolic and cardiovascular health.

Sleep is another fundamental biological regulator. Sleep influences metabolism, immune function, cognition, hormone signaling, appetite, and recovery. Chronic sleep deprivation shouldn't be dismissed simply because someone has learned to function while tired.

The Unglamorous Interventions That Matter Most

And then there are the less glamorous interventions. Don't smoke. Know your blood pressure. Pay attention to cholesterol and glucose regulation. Maintain cardiovascular fitness.

These things may not sound nearly as exciting as the latest longevity molecule, but preventing a heart attack, stroke, diabetes, or severe frailty can add years of functional life.

Psychological and social health matter as well. Chronic stress can influence sleep, cardiovascular function, eating behavior, glucose regulation, and hormonal signaling. Social isolation is also associated with poorer health outcomes. Human biology does not operate independently of our emotional and social environment.

What I Personally Take, and Why

And, of course, no discussion of healthy aging would be complete without addressing something that generates enormous interest in longevity medicine: supplements.

There are nutrients and compounds that may influence oxidative stress, mitochondrial function, inflammatory pathways, and other processes involved in aging. One of my personal favorite antioxidants is vitamin C. Coenzyme Q10 and alpha-lipoic acid are also interesting because of their roles in cellular energy metabolism and antioxidant systems.

For mitochondrial support, I personally use nicotinamide mononucleotide, or NMN. NMN is a precursor that the body can use to synthesize NAD+, or nicotinamide adenine dinucleotide. NAD+ is involved in energy metabolism, DNA repair, cellular signaling, and many other biological processes. NAD+ metabolism has therefore become an active area of aging research.

It's important, however, to remember that understanding how a supplement may benefit the body is not the same as proving that it can slow aging or extend human lifespan. That requires much more research.

Another compound I use is Urolithin A. Urolithin A has attracted interest because of its relationship with mitophagy—the mitochondrial housekeeping process we discussed earlier. It appears to influence signaling involved in identifying and clearing dysfunctional mitochondria. Again, the biological mechanism is fascinating, but research into its long-term effects on human aging is still developing.

For inflammatory support, I also use curcumin and algae oil.

And when it comes to the microbiome, interventions may include probiotics, prebiotics, and, depending upon the individual situation, nutrients or compounds intended to support the intestinal barrier.

Supplements Supplement. They Don't Replace.

But I want to emphasize the words "individual situation." Supplements should supplement a healthy biological foundation. They cannot compensate for severe sleep deprivation, inactivity, smoking, poor metabolic health, or an unhealthy diet.

And hormone support should be particularly individualized and based upon appropriate clinical evaluation and testing rather than simply attempting to recreate the hormone levels of a 25-year-old. The objective is not to push every marker toward "younger." The objective is to support appropriate biological function.

Healthspan May Matter More Than Lifespan

And that brings me to something I think we often overlook when we talk about longevity: perhaps lifespan isn't actually the most important measurement. We spend enormous amounts of time asking how long humans can live. Can we live to 100? 110? 120? But perhaps the more important question is: How many of those years can we remain healthy, capable, mentally engaged, and independent? That's healthspan. Living longer has limited appeal if the additional years are dominated by severe disability and chronic disease.

So perhaps the goal of aging research shouldn't simply be to extend life at any cost. It should be to compress disease and disability into as small a portion of life as possible while maintaining physical and cognitive function for as long as we can.

A resistance-training program may never make you live to 120. But if it helps you remain strong enough to live independently at 85, that is an extraordinary anti-aging intervention in a very practical sense.

Treating high blood pressure may not sound like cutting-edge longevity medicine. But preventing a stroke can preserve decades of function.

Improving sleep may not "reverse your biological age," but it can improve cognition, metabolic regulation, immune function, and quality of life.

Aging as a Gradual Loss of Resilience

The interventions with the greatest value may not be those promising immortality. They may be the ones that preserve resilience. And that brings us back to the idea I introduced at the beginning of this podcast.

Perhaps one of the most useful ways to understand aging is as a gradual loss of physiological resilience and adaptive reserve. When we're young, the body is remarkably good at bouncing back. We get sick, lose sleep, overdo it physically, or encounter another stress, and our systems usually find their way back toward normal.

As we age, the same stressor may hit harder. Recovery may take longer. Eventually, some systems may not return completely to their previous baseline.

The Body Becomes Resilient by Being Challenged

But healthy aging doesn't mean eliminating all stress. In fact, biological systems often require appropriate challenges in order to remain adaptive.

Exercise itself is a physiological stressor. When properly dosed and followed by recovery, that temporary stress stimulates repair and adaptation. Muscle becomes stronger. Mitochondria adapt. Cardiovascular capacity improves. The system becomes better prepared for the next challenge. This concept is sometimes referred to as hormesis.

The distinction is between manageable, intermittent challenges followed by adequate recovery—and chronic stress that continually exceeds the body's ability to repair itself. That distinction may be enormously important to how we age.

Aging Is Inevitable. The Trajectory Is Not.

So, as we bring everything together, aging isn't one biological clock slowly winding down. It is a gradual change across many interconnected systems—and some of those changes are simply part of being human.

Genetics matter. Time matters. And no lifestyle, supplement, or medical intervention can make us biologically immortal. But that doesn't mean the way we age is entirely predetermined.

Throughout this episode, we've seen that even older tissues retain an extraordinary ability to respond and adapt. Muscle can become stronger. Mitochondria can adapt. Metabolic health can improve. The brain can continue forming new connections. And many of the systems that support repair and resilience remain responsive to how we live.

So perhaps the goal isn't really to fight aging at all. The goal is to support the body's ability to regulate, repair, respond, and recover for as long as possible.

Aging is inevitable. But the trajectory of aging is not entirely fixed. And that may be one of the most encouraging insights modern aging biology has given us.

That's all for today's podcast. Please tune in again in two weeks for another episode of The Science of Self Healing. Until then, be well.

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