Measuring Aging Is Not the Same as Preventing It

Why resilience needs a framework of stress adaptation—not just biological clocks

A recent editorial in Clinical and Translational Medicine by Hernandez and Ibanez makes an important and timely proposal: aging research should move beyond vulnerability and disease risk, and begin to study resilience—why some individuals age well despite adversity.

To do this, the authors introduce the idea of expotype–phenotype resilience and propose using multimodal aging clocks (epigenetic, brain, biobehavioural, and multi-omic clocks) to identify people whose biological aging is delayed relative to their exposures. These “unexpectedly healthy agers,” they argue, can teach us as much—or more—than those who age rapidly.

This shift in focus is welcome. But it also exposes a widespread misconception in the longevity space that deserves careful correction.

The widespread misconception

“If we just measure biological age, we can prevent disease.”

This idea is now everywhere—in marketing, clinics, apps, and even research discourse.

And it is fundamentally flawed.

Biological age measurements can be informative, but they are not preventive. They tell us where someone appears to be on an aging trajectory, not why they are there, nor whether that trajectory is reversible, compensated, or nearing exhaustion.

In other words: measurement is not mechanism.

What the editorial gets right

The editorial makes several key contributions:

• Aging trajectories vary widely, even under similar exposures

• The exposome (social, environmental, political, behavioural stressors) strongly shapes biological aging

• Resilience is multimodal, emerging from interactions across biology, psychology, behaviour, and environment

• Some individuals show delayed aging despite adversity, suggesting protective or compensatory mechanisms

• Studying these individuals can refine precision medicine and prevention strategies

Most importantly, the authors emphasize that resilience is not a single trait, but a configuration—a pattern.

This is exactly where the real opportunity lies.

The missing link: how exposures become biology

What the editorial does not fully resolve is the process layer between expotype and phenotype.

• How do chronic exposures translate into biological states?

• Why does the same expotype produce different phenotypes in different people?

• Why can aging appear “delayed” while functional capacity is quietly eroding?

The answer lies in the framework of stress adaptation.

Stress adaptation: the invisible middle layer

Stress adaptation describes how organisms respond to repeated or sustained challenges—metabolic, psychological, inflammatory, social, or environmental.

Adaptation allows survival and function under pressure.

But adaptation is not free.

It requires:

• Energy

• Substrates

• Time

• Recovery capacity

When stress is persistent and recovery is incomplete, the body adapts by reallocating resources, prioritizing short-term function over long-term maintenance.

This is where resilience can become deceptive.

ERM: when adaptation quietly becomes costly

The Exposure-Related Malnutrition (ERM) framework helps explain this paradox.

ERM does not describe starvation or deficiency in the classic sense. Instead, it describes a state in which bioenergetic availability becomes constrained due to chronic stress adaptation. The body may appear stable—or even resilient—while repair, renewal, and reserve are progressively compromised.

From this perspective:

• A “favourable” biological age score may reflect successful compensation, not restored health

• Delayed aging clocks may coexist with reduced recovery capacity

• Resilience is conditional, not unlimited

ERM reframes resilience as the ability to keep going—not necessarily the ability to fully recover.

Bridging expotype and phenotype properly

Seen together, the pieces align:

• Expotype defines the cumulative load (exposures across life)

• Stress adaptation defines how that load is handled biologically

• ERM defines the energetic cost and limits of sustaining adaptation

• Phenotype / aging clocks reflect the net outcome of this process

Without stress adaptation and ERM, aging clocks risk being interpreted as targets to optimize, rather than signals to understand.

What prevention actually requires

True prevention does not come from tracking a number.

It comes from restoring the conditions that allow recovery:

• Adequate bioenergetic availability

• Rhythms of stress and rest

• Resolution of chronic metabolic and inflammatory load

• Social, psychological, and environmental support for recovery

Biological age metrics may help describe risk—but prevention depends on addressing why adaptation has become costly in the first place.

A more grounded takeaway

The editorial is right to call for a resilience-centered aging science.

But resilience should not be defined solely by delayed clocks.

A more complete framing would be this:

Biological age reflects the outcome of long-term stress adaptation.Prevention depends not on measuring aging, but on restoring the biological capacity to recover.

That is where stress adaptation and ERM fill the critical gap—turning descriptive aging metrics into meaningful, mechanistic insight.

Hernandez, H., & Ibanez, A. (2026). Expotype–phenotype resilience and multimodal aging clocks. Clinical and Translational Medicine, 16, e70558. https://doi.org/10.1002/ctm2.70558