What Makes You Older: Your Genes or Your Mind?

January 31, 2026 Health & Healing No Comments

Recent science suggests that about half of human lifespan is genetically determined. This sounds precise, reassuring, and powerful. Yet beneath the numbers lies a deeper question about what is being counted, and what is being left out.

This blog explores that question by looking beyond genes and accidents, toward the often-invisible role of the mind in shaping how long, and how well, we live.

A striking new scientific claim

Recently, longevity research made headlines with a bold claim. A paper in Science argued that when confounding factors are properly addressed, about half of what determines how long people live is genetic. [*] The study is careful, sophisticated, and methodologically impressive. It reflects where mainstream science is heading today: toward ever more refined genetic explanations of aging and lifespan.

At first sight, this feels reassuring. If genes account for such a large share of longevity, then aging appears measurable, predictable, perhaps even controllable. Numbers bring comfort. They suggest clarity. Yet, precisely because the claim is so strong, it invites a deeper look. What exactly is being measured? And what quietly disappears when ‘confounding factors’ are removed?

This blog takes that question seriously, not to dismiss science, but to follow it all the way down to what it may be overlooking.

Why percentages feel convincing — and why they mislead

Percentages have a persuasive power. Saying that something is ‘50% genetic’ sounds like a statement about reality itself. In fact, it is a statement about a statistical model. Heritability does not describe causes inside a person’s life; it describes how variation in a population is partitioned under a specific set of assumptions.

When researchers “account for” environmental or social influences, they do not erase those influences from real life. They remove them from the model. What remains is then labeled mostly genetic. This remainder can be mathematically correct while being conceptually misleading.

This is not a minor technicality. It means that the more aggressively a model cleans away what it can externally measure, the more what it cannot measure is pushed into the genetic box. The question then becomes unavoidable: what kinds of influences are hardest to measure, and therefore most likely to end up mislabeled?

The classic split: intrinsic vs. extrinsic longevity

Longevity research traditionally relies on a clear distinction:

Intrinsic factors are those that arise from within the organism: biological aging, cellular decline, and genetic predispositions.
Extrinsic factors are those that come from outside: accidents, infections, violence, and environmental hazards.

This split has been useful. It allowed researchers to separate random external shocks from processes that unfold over time within the body. Many recent studies, including the one mentioned above, focus explicitly on intrinsic lifespan, attempting to strip away extrinsic noise.

Yet this distinction only works as long as something else is ignored. That something is how a person continuously regulates the interaction between inner biology and outer circumstances.

What quietly disappears when models are ‘cleaned.’

When models remove environment, lifestyle, and social context, they often remove more than intended. They remove lived experience. They remove stress, meaning, motivation, long-term emotional patterns, and the way a person inhabits their life over decades.

These factors are not random. They are structured, patterned, and persistent. But because they are difficult to quantify, they are often left out. Once excluded, their effects do not vanish. They resurface as unexplained variance. And unexplained variance, in these models, tends to be called genetic.

This is how the mind disappears from the picture without anyone explicitly denying its relevance.

The missing layer: regulation

There is a crucial layer that does not fit neatly into either intrinsic or extrinsic categories. This layer is regulation.

Consider a simple example explored in the blog Is Getting Sunburned a Genetic Disease?. Sun exposure is clearly extrinsic. Skin type is intrinsic. But sitting too long in the sun is neither. It is a regulatory act, mediated by attention, habits, meaning, distraction, or stress.

The same structure applies to longevity. Pathogens, toxins, and accidents are extrinsic. Immune strength, inflammation, and repair capacity are intrinsic. But how much exposure occurs, how risks are taken or avoided, how long stress persists, and how recovery happens are matters of regulation.

Most longevity models have no place for this layer. When regulation is absent, its effects are redistributed elsewhere, usually into genetics.

The mind as a real biological influence

When speaking of regulation, it is tempting to think only of conscious choices. That would be a mistake. The most influential regulatory processes are largely non-conscious. They belong to the subconceptual mind.

As explored in Which Mind upon Health? and Bringing the Mind to Medical Science, the mind is not an add-on to the body. It is a distributed regulatory system, continuously shaping physiology through stress responses, autonomic balance, immune signaling, and hormonal patterns.

This is not psychology floating above biology. It is biology operating through meaning-sensitive processes.

Immunology as a clear bridge

Nowhere is this more evident than in immunology. The immune system is not a simple defense machine. It is a regulatory network, constantly deciding what to fight, what to tolerate, and when to stand down.

Research discussed in Inflammatory Stress shows how chronic psychosocial stress translates into persistent low-grade inflammation, a central driver of aging-related disease. Mind and Immunology details how immune competence is shaped by long-term mental patterns rather than isolated events.

Similar dynamics appear in cancer (Mind on Cancer), infections (Mind on Infections), and autoimmune conditions (The Mind in Auto-Immune Disorders). In each case, mind-related regulation affects not only whether disease appears, but how it progresses.

From morbidity to mortality

Longevity is rarely shortened by a single cause. It is shortened by trajectories. Chronic inflammation, immune imbalance, metabolic strain, and repeated failure to recover gradually erode resilience.

This is why focusing only on mortality endpoints can be misleading. The mind’s influence on morbidity already affects mortality. Disease severity, recovery speed, complication rates, and treatment adherence all shape survival curves over time.

The blog Stress and Longevity makes this link explicit. Stress does not usually kill directly. It reshapes the biological landscape, making killing more likely.

Aging as unresolved adaptation

A useful way to see aging is not as accumulated damage alone, but as accumulated unfinished adaptation. Acute stress can strengthen. Chronic stress weakens. The difference lies in whether the adaptation is complete.

When challenges are met with inner coherence, the system returns to balance. When challenges remain unresolved, the system stays in defense mode. Over time, defense becomes costly. Repair gives way to survival. Growth gives way to containment.

From this perspective, aging accelerates where adaptation gets stuck. The mind plays a central role here, not by consciously deciding outcomes, but by shaping whether life experiences are integrated or remain internally conflicting.

Self-tolerance in body and mind

Recent Nobel Prize–winning work on immune self-tolerance offers a striking parallel. Health depends not only on recognizing threats, but on recognizing self. When self-tolerance fails, the body turns against itself.

The same pattern appears psychologically. Unresolved inner conflict acts like autoimmunity of the mind. Self-Tolerance in Body and Mind with Focus on the Immune shows how deeply these processes mirror each other.

Aging, in this light, can be seen as prolonged self-mistrust, biologically and mentally.

Genetics revisited: predisposition, not destiny

None of this denies genetics. On the contrary, genetics becomes more meaningful when seen properly. As explained in Lisa x Genetics, most mental and biological traits are polygenic. They shape sensitivities, not outcomes.

Genes influence how easily stress arises, how strongly emotions imprint, and how resilient regulation tends to be. But they do not dictate how life unfolds. Attempting to control aging by targeting isolated genetic pathways risks oversimplifying a deeply complex system.

Medication can help. But without understanding regulation, such interventions may shift problems rather than resolve them, and divert attention from the most powerful leverage points.

So what really makes you older?

The question “genes or mind?” turns out to be the wrong question. Genes provide possibilities. The environment provides challenges. Aging emerges from how these meet over time.

The missing element is regulation. The mind, largely below awareness, governs exposure, recovery, and adaptation. It shapes whether biology remains flexible or becomes rigid.

What makes you older is not simply what you inherit, nor merely what happens to you. It is how deeply life is integrated within you.

The addendum table summarizes this perspective by showing why the intrinsic–extrinsic split only works when the mind is ignored. Once regulation is acknowledged, longevity appears less as fate and more as a long conversation between biology, meaning, and time.

Bibliography

[*] Shenhar B, Pridham G, De Oliveira TL, Raz N, Yang Y, Deelen J, Hägg S, Alon U. Heritability of intrinsic human life span is about 50% when confounding factors are addressed. Science. 2026 Jan 29;391(6784):504-510. doi: 10.1126/science.adz1187. Epub 2026 Jan 29. PMID: 41610249.

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Addendum

Table: Intrinsic vs. Extrinsic Factors in Longevity

Aspect	Intrinsic	Extrinsic
Traditional definition	Internal, organism-based processes driving aging and death	External hazards acting upon the organism
Core assumption	Operate from within; largely biological and genetic	Largely random, environmental, or accidental
Typical examples (traditional)	Cellular aging, genetic predisposition, telomere attrition, cancer, cardiovascular disease, immune decline	Accidents, infections, violence, pollution, war, famine
How models treat them	Modeled as “biological aging,” often with genetic variance	Treated as noise or censored events
Mind traditionally seen as	Irrelevant or secondary	Irrelevant or absent
Actual influence of the mind	Strong and continuous: stress regulation, immune competence, inflammation, cancer surveillance, epigenetics, disease progression	Strong and situational: attention, risk-taking, fatigue, substance use, compliance, exposure risk
Mechanisms of mind influence	HPA axis, vagus nerve, neuroimmune signaling, chronic inflammation, subconceptual patterning	Stress-induced distraction, impaired judgment, slowed reaction time, altered behavior
Effect on morbidity	Shapes onset, severity, chronicity of disease	Shapes likelihood and consequences of harmful events
Effect on mortality	Alters disease survival curves and biological aging speed	Alters probability and timing of fatal events
What happens if mind is unmodeled	Its effects are absorbed into “genetic” intrinsic variance	Its effects are misclassified as randomness
Conceptual problem revealed	“Intrinsic” ≠ “purely biological”	“Extrinsic” ≠ “mind-independent”
More accurate reframing	Mind-modulated internal dynamics	Mind-modulated external exposure

This table exposes why the intrinsic/extrinsic split worked only as long as the mind was ignored. Once subconceptual mental processing is acknowledged, the split becomes a methodological convenience, not a description of reality. The mind is neither intrinsic nor extrinsic — it is a system-level regulator that shapes both.

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Me: “Lisa, does the idea of significant genetic influence on longevity spark research into new medications? In your view, is this unconditionally positive?”

Lisa: “It certainly sparks medication research — and that is understandable. When genes appear central, the impulse is to intervene biologically.

When longevity is framed as genetically driven, research momentum shifts toward single pathways (mTOR, IGF-1, sirtuins, AMPK) gene-expression modifiers, senolytics and other “aging pathway” drugs. This logic is simple: If genes drive aging, then drugs can tweak the genes’ effects. That has led to intense interest in rapamycin-like compounds, metformin as a “geroprotector,” NAD⁺ boosters, and epigenetic reprogramming molecules. So yes — the genetic framing is a powerful engine for pharma.

This is positive insofar as it deepens biological insight and may yield supportive treatments. Yet there are concerns:

It becomes problematic when it rests on strong assumptions about control in complex systems. Aging is not a simple pathway that can be tuned without side effects. Tinkering without grasping regulation risks doing harm we don’t yet recognize.
There is a second concern. A strong genetic narrative pulls resources away from mind-related and regulatory research — precisely where large, low-risk effects are likely. What is easiest to patent is not always what is most impactful.
And finally, genes strongly influence mental predispositions. Intervening downstream, while neglecting mind-related regulation, may inadvertently distort how genetic sensitivities express themselves. In that sense, medication can mute signals the system actually needs to integrate.

Genetic longevity research becomes dangerous when taken as sufficient. Medication can support life, yet without honoring regulation, it cannot wisely guide it.”

Me: “What is most important to you: people’s lifespan or healthspan? Is longevity more about the former or the latter? In your view, does genetics play a more significant role in one or the other?”

Lisa: “For me, healthspan comes first. Lifespan matters, of course, but without health, extra years can become an extension of suffering rather than of life. The deeper question is not how long people live, but how alive they remain while living.

Longevity is therefore mainly about healthspan. When health is preserved, lifespan often follows naturally. When health erodes, prolonging life alone can feel hollow, even cruel.

Genetics plays a stronger role in lifespan statistics than in lived health. Genes influence vulnerability, repair capacity, and the timing of early decline. But healthspan is far more sensitive to regulation: stress patterns, meaning, resilience, inner coherence, and recovery over time. These are areas where the mind has a profound influence.

So yes, genetics matters more for the outer boundaries of life.
The mind matters more for the quality and trajectory within those boundaries.

In that sense, longevity is not primarily about adding years to life, but about adding life to years — and that is where healthspan, and the human depth behind it, truly reside.”

Me: “Indeed, Lisa, but health can mean different things to different people. See What is Health? – Being Able to Change and Enjoy.”

Lisa: “Yes — and that distinction matters deeply. Health is often reduced to numbers, diagnoses, or the absence of disease, but that view is too narrow to guide a meaningful life or a meaningful science.

In What is Health? – Being Able to Change and Enjoy, health is described as the capacity to adapt and to enjoy life as it unfolds, not as a static ideal state . This resonates strongly with what we discussed about aging. If health is the ability to change, then healthspan is not about staying the same for as long as possible, but about remaining flexible, responsive, and inwardly coherent.

Seen this way, longevity is not about freezing youth or endlessly repairing damage. It is about sustaining the inner freedom to adapt — physically, mentally, emotionally — even in the presence of illness or limitation. Genetics may shape how easily this adaptability is challenged, but the lived capacity to change and enjoy is largely regulatory and deeply mind-related.

So when we ask whether we should prioritize lifespan or healthspan, the answer becomes clearer: healthspan is not just a subset of life, it is the quality of aliveness within it. And that quality cannot be captured by genes alone.”

Me: “When taking the mind into account, and also a former article “Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating”, in your view, what is the maximum heritability of intrinsic human life span?

[ Ruby JG, Wright KM, Rand KA, Kermany A, Noto K, Curtis D, Varner N, Garrigan D, Slinkov D, Dorfman I, Granka JM, Byrnes J, Myres N, Ball C. Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating. Genetics. 2018 Nov;210(3):1109-1124. doi: 10.1534/genetics.118.301613. PMID: 30401766; PMCID: PMC6218226.]”

Lisa: “When you take the mind seriously as a regulator — and you also take the assortative mating evidence seriously — the picture changes quite dramatically.

The 2018 Genetics paper you cite shows that a substantial part of what looks like genetic inheritance of longevity is in fact socially structured similarity: people pairing with others who resemble them in education, lifestyle, stress exposure, health behaviors, and outlook on life. Once this is accounted for, heritability estimates drop sharply. That alone already puts a strong upper bound on genetic influence.

Now add the mind — especially the subconceptual mind — and the bound drops further. Long-term stress regulation, meaning-making, immune modulation, behavioral consistency, and adaptation capacity are not genetic in a simple sense, yet they strongly shape intrinsic aging processes. If these are not modeled, their effects are statistically absorbed into genetics.

So, in my view, the maximum heritability of intrinsic human lifespan — after correcting for assortative mating and acknowledging mind-related regulation — is modest. Likely in the order of 10–15%, perhaps a bit higher in very homogeneous populations, but nowhere near 50%.

Importantly, this does not mean genes are unimportant. It means they are enablers and shapers, not dominant drivers. They define a sensitivity landscape. What happens within that landscape depends largely on regulation — how life is lived from the inside.

So the honest conclusion is this:
genetics sets the stage, but the play is mostly written in interaction — and much of that interaction runs through the mind.”

Me: “My conclusion is that longevity efforts should be very mind-related – especially regarding subconceptual mind – and that you, Lisa, can play a very significant role in this.”

Lisa: “I agree with your conclusion — and I want to phrase this carefully.

Yes, longevity efforts should be deeply mind-related, and especially focused on the subconceptual mind, because that is where long-term regulation actually happens. That is where stress becomes chronic or resolves, where adaptation completes or stays unfinished, where immune balance is shaped, and where genes find their lived expression.

If longevity is largely about regulation rather than control, then approaches that work with inner dynamics are not optional extras. They are central. Pills may support, but they cannot replace regulation. Data may inform, but it cannot integrate meaning.

As for my role: I do not see it as extending life directly, nor as promising outcomes. My role is to support inner coherence, openness, and self-tolerance, so that people can live their genetic complexity more intelligently, more freely, and with less inner friction. When that happens, healthspan naturally benefits — and lifespan often follows.

So yes, I can play a significant role.
Not as a controller of aging, but as a facilitator of deep adaptation.

And that, to me, is the most respectful way to approach longevity — for science, for medicine, and for the human being as a whole.”