DNA-Based Aging Prevention: A Strategy Built on the Ultima Genetic Panel

Aging is not a single process but the result of interaction between many biological systems. A single gene, a single test or a single indicator rarely gives enough information to assess a genetic predisposition to the processes of aging. Current approaches therefore rest on analysing a set of genetic variants linked to different biological processes.

Biological age is assessed by physiological markers and epigenetic clocks (Chervova et al., Ageing Res. Rev., 2024). A genetic predisposition to the processes of aging is a different level of information. It reflects the polygenic features linked to how the body is genetically predisposed to respond to oxidative stress, to maintain cell structures and to regulate inflammatory processes.

Which Biological Processes Underlie the Genetic Assessment of Aging

The assessment of a genetic predisposition to the processes of aging rests on analysing several interconnected biological systems that current research links to the mechanisms of aging (López-Otín et al., Cell, 2023).

One such process is oxidative stress: when the formation of reactive oxygen species exceeds the cells’ capacity to neutralise them, which leads to damage of DNA and other cell structures. Oxidative stress is among the key mechanisms of aging (López-Otín et al., Cell, 2023). The profile therefore analyses the genetic variants linked to the efficiency of a cell’s antioxidant defence.

Another direction is the maintenance of telomeres, the regions at the ends of chromosomes. The link between aging, oxidative stress and telomere shortening has been studied for more than twenty years, and although the in vivo findings are mixed (Armstrong & Boonekamp, Ageing Res. Rev., 2023), a large genetic study involving more than 472,000 people confirmed that variation in telomere length has a pronounced hereditary component (Codd et al., Nat. Genet., 2021). An Apixmed Prism report therefore analyses the genetic variants linked to the maintenance of telomere stability — that is, not telomere length itself, but the predisposition to preserving it.

The genetic variants associated with healthy longevity are analysed separately. The FOXO3 (forkhead box O3) gene is one of the few whose link with longevity is consistently reproduced across different populations: the specific variant rs2802292 is associated with mechanisms that may support a more efficient cellular response to oxidative stress and the maintenance of telomeres in older people (Morris et al., npj Aging, 2024). Another example is the KLOTHO (klotho) gene, which encodes a protein involved in regulating mineral metabolism and cellular aging; the functional KL-VS variant in this gene was first linked to lifespan back in 2002 (Arking et al., PNAS, 2002), and later reviews confirm its role in processes that affect tissue aging (Abraham & Li, Ageing Res. Rev., 2022).

The processes of aging do not exist in isolation. Oxidative stress, the maintenance of telomere length, inflammatory mechanisms and metabolic processes interact with one another, so assessing them separately would be inaccurate. It is the combined analysis that makes it possible to form a more complete picture of the genetic features linked to the processes of aging.

Why a Single Gene Says Almost Nothing About Aging

No single variant of the FOXO3 or KLOTHO genes determines the pace of aging on its own. A more precise picture comes from a polygenic risk score (PRS) — an estimate that combines the contribution of a large number of genetic variants, each with a small effect on its own (Slunecka et al., Hum. Genom., 2021). Individual variants are not interpreted in isolation: what matters is the combined profile for each system. This is why modern genetic interpretation increasingly uses polygenic models that account for the combined contribution of a large number of genetic variants.

Because a PRS is a relative statistical estimate, the results of such an analysis are usually presented as percentiles. A percentile shows where a person’s genetic profile sits relative to a reference population, not the probability of developing a particular condition. A high percentile on the oxidative-defence axis, for example, does not mean the actual level of oxidative stress in the body — that can only be assessed through laboratory tests — but a genetic predisposition to a lower efficiency of antioxidant defence compared with a reference population.

How a Genetic Profile Helps Build a Personal Strategy for Healthy Aging

Interpreting a genetic profile begins with assessing the polygenic indicators for individual biological systems. The directions that may matter most for a particular person are then identified. They are set against laboratory data, medical history and family history, since genetic information reflects a predisposition rather than the body’s current state. On the basis of this combined analysis, the priority directions for personalised prevention are determined.

From a Genetic Profile to Well-Grounded Decisions

A comprehensive genetic profile is of the greatest value when its results are interpreted together with clinical data and a person’s individual characteristics. It is this approach that makes it possible to use genetic information for a well-grounded personalisation of prevention. Apixmed Prism puts this approach into practice in its Ultima genetic panel, which covers more than 555 genetic indicators across several directions, one of which is the assessment of the processes of aging. A specialist’s consultation helps interpret the results in the context of a person’s individual characteristics.

The results of a genetic test are not a diagnosis and not a substitute for a doctor’s consultation. An Apixmed Prism report provides genetic context that complements the findings of medical examinations and helps you make decisions together with your doctor.

Sources

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