Aging Is Not Random Wear-and-Tear — It Is Bioenergetic Triage

For decades, aging has been described as a slow accumulation of damage: oxidative stress, genomic instability, misfolded proteins, random cellular failure.

But what if aging is not primarily about damage at all?

What if it is about what the body can no longer afford to maintain?

A newly published study in GeroScience adds powerful evidence to this alternative view — and strongly supports the idea that bioenergetic capacity sits at the center of aging, structural loss, and functional decline.

What the study showed — in plain language

Christensen and Fogarty (2026) examined motor neurons that control the tongue in young versus old rats. These neurons are critical for swallowing, breathing coordination, and speech — functions that commonly deteriorate with age.

What they found was striking:

• Large, complex motor neurons lose their structure with aging

• Distal dendrites shrink and disappear

• Synaptic spines — the sites of communication — are lost

• Mitochondria within dendrites are dramatically reduced

• Remaining mitochondria are smaller, fragmented, and less efficient

Most importantly, the neurons that degenerated first were the largest and most energy-demanding ones.

This was not random degeneration.

It followed a clear energetic logic.

Why this matters: structure costs energy

Maintaining biological structure is expensive.

Large neurons with elaborate dendritic trees must continuously pay for:

• Membrane polarization

• Synaptic integration

• Ion pumping

• Neurotransmission

• Repair and turnover

All of this depends on mitochondrial ATP production and redox balance.

In this study:

• Dendritic mitochondrial volume density dropped by nearly 60%

• Mitochondria became smaller and more fragmented

• Structural simplification followed

This tells us something crucial:

When bioenergetic capacity declines, structure is not preserved — it is downsized.

Aging as bioenergetic triage, not failure

From an ERM (Exposure-Related Malnutrition) perspective, this pattern makes perfect sense.

ERM reframes aging and chronic disease as states where:

• Energy availability

• Nutrient supply

• Time for recovery

• Mitochondrial throughput

are no longer sufficient to meet cumulative physiological demands.

When that happens, the body does not simply “break.”

It triages.

High-cost structures — like large dendritic trees — are gradually withdrawn to preserve short-term survival.

The Christensen & Fogarty study shows this process in action at the cellular level.

Structural loss is not accidental.

It is economically rational under energetic constraint.

Why mitochondria are central — not just “involved”

Many aging papers say mitochondria are “important signaling hubs.”

This study goes further.

It shows that mitochondria are not just messengers — they are the execution layer.

Neural signals, growth factors, and plasticity cues can still exist.

But without sufficient mitochondrial capacity, they cannot be carried out.

This reinforces a key ERM principle:

Regulation without energy is noise.

Execution requires bioenergetic capacity.

Size-dependent vulnerability is the smoking gun

One of the most compelling aspects of the study is that:

• Larger neurons degenerated more than smaller ones

If aging were primarily driven by:

• Random damage

• Genetic drift

• Uniform oxidative stress

this pattern would not appear so clearly.

But if aging is driven by energetic mismatch, this is exactly what we would expect.

Bigger structures cost more to maintain.

When energy becomes scarce, they are the first to go.

From neurons to whole-body aging

Although this study focused on tongue motor neurons, the implications are far broader.

The same pattern appears across aging biology:

• Sarcopenia (loss of muscle mass)

• Bone thinning

• Immune exhaustion

• Brain network simplification

• Frailty

Different tissues.

Same logic.

Structural loss follows energetic constraint.

What this adds to the ERM framework

This study provides direct anatomical evidence that supports ERM’s core claims:

• Aging is constrained by bioenergetic throughput

• Structural degeneration is downstream, not primary

• Mitochondrial capacity determines what tissues can afford to maintain

• Functional decline reflects adaptive simplification under stress

In short, it shows that aging is not simply the passage of time.

It is the cumulative result of living for years or decades beyond sustainable energetic margins.

A reframing worth taking seriously

If this perspective is correct, then many current approaches to aging are misaligned.

Measuring biological age without addressing energy availability will always fall short.

Stimulating growth or plasticity without restoring mitochondrial capacity will fail.

The priority is not “anti-aging.”

The priority is restoring the energetic conditions that make structure affordable again.

Aging is not because the system is broken.

Aging happens because the system is exhausted.

And this study makes that harder than ever to ignore.

Christensen, T. A., & Fogarty, M. J. (2026). Structural and mitochondrial dendritic degenerations in old hypoglossal motor neurons. GeroScience. https://doi.org/10.1007/s11357-025-02075-w