Longevity Genes: Myth or Science? What Really Determines How We Age
We all know at least one person about whom we say, “He’s just lucky when it comes to his genes.” We use this explanation for people who look younger than their age, rarely get sick, or seem to maintain their energy regardless of their age. And vice versa. When there’s a family history of chronic or cardiovascular diseases, we often assume that our future is predetermined and already written somewhere in the helix of our DNA.
It sounds logical. Except that modern biology is gradually beginning to challenge precisely this notion. More and more scientists believe that the question has never been whether “longevity genes” exist. The more important question is what causes the same genes to function differently in different people. This is where one of the most fascinating scientific stories of the past two decades begins.
For a long time, genetics was viewed as a fixed script. We receive our DNA at birth and simply follow what is written in it throughout our lives. Today we know that the picture is far more complex. The DNA sequence itself hardly changes at all, but the way our bodies use the information encoded in it is constantly changing. Some genes are “turned on,” others are temporarily “silenced,” and still others begin to function at varying intensities depending on the state of the cells. It is precisely this mechanism that epigenetics studies.
Among the most interesting tools to emerge in aging research are the so-called epigenetic clocks. One of the best-known is the model developed by Prof. Steve Horvath, which uses specific patterns of DNA methylation to estimate the age of tissues and cells. Today, epigenetic clocks are widely used in research on biological aging, although scientists continue to refine the methods and the way their results should be interpreted.
Prof. Milena Georgieva, a molecular biologist and leading researcher in the field of epigenetics, is investigating precisely this connection between epigenetic regulation, chromatin organization, and the processes of cellular aging. Her scientific publications demonstrate how important it is not only the DNA sequence itself, but also the way in which genetic information is organized and utilized by the cell.
That is why modern science has gradually abandoned the idea of a single “longevity gene” and now speaks of complex biological networks. These networks involve hundreds of genes that coordinate DNA repair, cellular energy production, inflammatory processes, immune system function, and cellular self-cleaning mechanisms.
And yet, are there specific markers in the DNA code of centenarians? The answer is yes. Science has indeed identified genes that are much more common in people who have passed the 100-year mark. One of the best-studied examples is FOXO3. Certain variants of this gene have been linked to a higher likelihood of exceptional longevity in various human studies. FOXO3 is involved in biological pathways related to the cellular response to stress and the maintenance of cellular resilience, but it cannot, on its own, explain the complex phenomenon of human longevity.
But how much does our genetic heritage really influence us? For decades, it was believed that about a quarter (25%) of our lifespan was predetermined by the cards our parents dealt us. More recent scientific publications, however, suggest that this figure may be much higher and likely depends heavily on how it is measured, so it remains the subject of active scientific debate.
This means that genetics matter, but they do not, on their own, determine how we will age. Lifestyle, environment, and the condition of our cells constantly interact with our genetic program. Genes outline the possibilities, and our daily choices influence how much of that potential will be realized.
In scientific circles, there is increasing discussion of yet another key indicator that is changing the way we view aging. This is biological age. Unlike chronological age, which simply counts the years that have passed, biological age indicates the functional state of the body. That is why biological age is becoming an increasingly interesting tool for studying individual differences in the aging process.
Viewing aging as a dynamic biological process has also changed the way scientists study it. Today, there are tools that allow us to track the molecular characteristics of aging and study how they change in response to various interventions. Epigenetic clocks are one example of this development.
In their research, Prof. Milena Georgieva and her colleagues examine aging as a process in which genetic information, chromatin organization, and cellular responses to stress are closely interrelated. Their research, for example, examines how cellular stress affects DNA damage, redox processes, and gene expression, as well as how changes in chromatin organization are linked to cellular aging.
This is precisely where modern epigenetics and the science of longevity intersect. Healthy aging is not determined by a single gene, nor by some mythical “magical” molecule. It is the result of the ability of numerous biological systems to maintain their perfect balance. DNA repair, cellular energy conservation, effective autophagy, control of chronic inflammation, and optimal mitochondrial function are not isolated events. They function as a finely coordinated network in which each element directly influences the others.
Just how rapidly this field is advancing is also demonstrated by experiments with the so-called Yamanaka factors—a combination of four factors used for cellular reprogramming. In experiments with mice, partial reprogramming is associated with younger epigenetic profiles and changes in a number of molecular characteristics of aging. These results are particularly interesting because they show that certain characteristics of cellular aging can be influenced; however, the approach remains experimental and is not a clinical therapy for humans.
This shift is clearly evident in the way the World Health Organization defines the concept of “healthy aging.” The focus is no longer on the number of years, but on maintaining physical, mental, and social abilities for as long as possible. In other words, the real goal is not simply a longer life, but more years spent in good health and with a high quality of life.
Alpha Life Sciences follows a similar philosophy . The company views healthy longevity as a process that begins long before the first symptoms or visible signs of aging appear. Instead of seeking one-size-fits-all solutions, it monitors developments in the fields of cell biology, epigenetics, and preventive medicine. It is precisely in these areas that new insights emerge on how we can support the body over the long term.
Perhaps this is the greatest change that science has brought us in recent years. Genes are no longer viewed as a final verdict, but as a starting point. They determine our potential, but not our inevitable fate. The story of our longevity is written every day through billions of small decisions that leave a mark on every cell. And perhaps that is precisely why the conversation about the future no longer begins with the question of what genes we have inherited, but rather what we do with them today.
Sources and Further Reading
- Miloshev, G., Ivanov, P., Vasileva, B., Georgieva, M. (2025). Linker Histones Maintain Genome Stability and Drive the Process of Cellular Aging. Frontiers in Bioscience (Landmark Edition), 30(4), 26823. DOI: 10.31083/FBL26823.
https://www.imrpress.com/journal/fbl/30/4/10.31083/FBL26823
- BTA (2026). Longevity Panel Explores Work, Aging, and AI. May 30, 2026. Article on Prof. Milena Georgieva’s participation in the discussion “Longevity: Who Wants to Work Forever.”
https://www.bta.bg/en/bg-world/1137062-longevity-panel-explores-work-ageing-and-ai
