The biggest myth about aging, according to science | Morgan Levine: Full Interview

Most of us measure our lives by the candles on a birthday cake. We assume that the number on our driver’s license dictates how we feel, how we move, and what diseases we might face. However, emerging science suggests that this chronological number is merely a placeholder. The metric that truly matters is your biological age—the rate at which your cells and tissues are actually declining.

Dr. Morgan Levine, a leading researcher in the science of aging and author of True Age, argues that aging is not a fixed, inevitable slide into decline. Instead, it is a malleable biological process that can be measured, managed, and potentially decelerated. By understanding the cellular mechanisms behind aging, specifically epigenetics, we gain the power to influence our health span and delay the onset of chronic disease.

Key Takeaways

• Biological age is distinct from chronological age: Two people of the same age can have vastly different risk profiles and physical capabilities based on how fast their bodies are biologically degrading.
• Epigenetics is the operating system of aging: Chemical tags on your DNA (methylation) determine cell function, and these patterns become "messy" as we age, leading to dysfunction.
• Aging is malleable: Lifestyle factors like diet, exercise, and stress management can decelerate the aging process and potentially reverse biological age markers.
• Caloric restriction and hormesis: Mild biological stressors, such as fasting or caloric deficits, stimulate resilience pathways that may extend healthy life.
• The goal is compression of morbidity: The objective of longevity science is not immortality, but shrinking the window of time spent in poor health at the end of life.

The Distinction Between Chronological and Biological Age

We have become fixated on chronological time—months, days, and years since birth—because it has historically been our only metric for aging. However, chronological age is simply a correlate, not a cause. The biological aging process refers to the systemic degradation of function over time, where cells perform worse than they did previously.

This process is highly variable. Just as a 10-year-old dog has aged significantly more than a 10-year-old human, variation exists within our own species. You can observe two 50-year-olds standing side by side; one may exhibit the vitality of a younger person, while the other shows advanced signs of decline. This divergence is what scientists term "biological age."

Quantifying the Aging Process

To manage aging, we must first measure it. Dr. Levine’s lab focuses on quantifying biological age to predict future health outcomes. By analyzing biomarkers—such as liver function, kidney function, metabolic health, and inflammation levels—scientists can calculate a "phenotypic age."

We all age, but we don't all age at the same rate. So my lab is really interested in can we actually put a number to that? Can we measure how fast or slow a given person might be aging?

In a standard population, most people fall within five years of their chronological age. However, outliers exist. Some individuals possess a biological age 10 or 20 years younger (or older) than their birth certificate suggests. Tracking this data is critical because it moves medicine from a reactive state—treating disease once it appears—to a proactive state where we treat the underlying decline before it manifests as pathology.

Epigenetics: The Cellular Operating System

To understand why we age, we must look deeper than our organs, down to the molecular level. A primary hallmark of aging is epigenetic alteration. While genetics involves the DNA sequence you are born with, epigenetics is the "operating system" that tells your cells how to read that DNA.

Every cell in your body contains the exact same DNA. The reason a skin cell behaves differently than a brain cell is due to the epigenome, which uses chemical tags (specifically DNA methylation) to turn certain genes on or off. This system dictates cell identity.

The Epigenetic Clock

As we age, this operating system accumulates errors. The precise patterns of methylation become remodeled due to stress, random errors, or environmental factors. Cells begin to lose their identity and forget their specific functions. When enough cells become dysfunctional, tissues degrade, organs fail, and systemic disease emerges.

Scientists use "epigenetic clocks" to measure these changes. These clocks analyze methylation patterns to estimate biological age with high precision. Notably, accelerated epigenetic aging is linked to a higher risk of nearly every major age-related disease, including cancer, Alzheimer's, and diabetes.

Can We Reverse the Aging Process?

The discovery that the epigenome is malleable has revolutionized our understanding of aging. It implies that aging is not a one-way street caused solely by the accumulation of wear and tear. Instead, it is a process that can, at least in theory, be reversed.

This was demonstrated famously by Shinya Yamanaka, who won a Nobel Prize for discovering four specific factors that can reprogram an old, specialized cell back into an embryonic, age-zero state. When applied to cells in a dish, these factors erase the epigenetic errors accumulated over a lifespan.

From Petri Dishes to People

While we can reverse the age of individual cells, applying this to a whole human body remains complex. We cannot simply reset an adult human to an embryonic state. However, current research is exploring "partial reprogramming"—reversing the epigenetic age of cells just enough to restore youthful function without causing them to lose their identity.

Our risks of disease are not written in our genes. Yes, we will probably all age, and we're not going to essentially stop that, but the rate at which that happens... really comes down to a lot of what you do in your everyday life.

While pharmaceutical interventions and cell reprogramming are on the horizon, lifestyle remains our most potent current tool for reversal. Dr. Levine warns against "biohacking" for the sake of a single number, but notes that consistent improvements in diet, sleep, and stress management are reflected in improved biological age scores.

Nutrition, Hormesis, and Longevity

Diet is perhaps the most studied lever for influencing longevity. Historically, the most robust intervention for extending life in animal models has been caloric restriction (CR)—reducing calorie intake by roughly 20% without malnutrition.

The mechanism behind this is likely hormesis. Hormesis refers to a mild biological stress that triggers adaptive responses, making the organism more resilient. Just as exercise stresses muscles to make them stronger, a slight caloric deficit or fasting window stresses the body enough to activate repair pathways and improve survival.

Practical Nutritional Strategies

Dr. Levine suggests that for humans, extreme caloric restriction is difficult to maintain and may not be necessary to reap the benefits. Instead, we can apply the principles of CR through more sustainable methods:

• Avoid Overconsumption: Simply moving away from the modern tendency to overeat aligns the body with its actual energy needs.
• Intermittent Fasting: Compressing your eating window mimics the hormetic stress of caloric restriction, potentially offering similar cellular benefits.
• Plant-Forward Diets: Evidence suggests that diets lower in animal proteins and high in whole plant foods correlate with slower aging.
• Personalization is Key: Nutritional needs change with age. For example, while low protein might benefit a younger adult, an elderly person at risk of sarcopenia (muscle wasting) may require higher protein intake to maintain function.

Redefining the Goal: Health Span Over Lifespan

A common misconception is that longevity science aims for immortality. The true objective is increasing health span—the number of years we spend in good health, free from disability and disease.

Currently, there is often a disconnect between how long we live and how well we live. This is evident in the "health-survival paradox," where women tend to live longer than men but spend a significant portion of those extra years suffering from age-related disabilities like arthritis or dementia.

Compression of Morbidity

The ultimate metric of success in aging science is the "compression of morbidity." This concept envisions a life where a person remains high-functioning and disease-free until the very end, squeezing the period of decline into a very short window before death. This pattern is often seen in centenarians, who live vibrantly for 100 years and then decline rapidly, rather than suffering a slow, decades-long deterioration.

By shifting our focus from treating individual diseases (like cancer or heart disease) to treating the aging process itself, we have the potential to delay all these conditions simultaneously. As Dr. Levine notes, we have more power over this process than we realize. Through monitoring our biological age and adapting our lifestyles, we can dictate not just how long we live, but how well we live.

Conclusion

Aging is the single biggest risk factor for the diseases that plague modern society, yet it is rarely treated as a condition we can manage. The science of "True Age" shifts the paradigm from passive acceptance to active intervention. Whether through future epigenetic therapies or today’s lifestyle choices, the ability to modulate our biological clock offers a path toward a future where we don't just survive longer, but thrive longer.