Rapamycin and the Future of Longevity: A Disease-Oriented Approach to Aging

Based on Dr. Mikhail V. Blagosklonny’s paper published in Aging (Albany NY), 2023.

Does Aging Really Exist—or Just Age-Related Diseases?

In his thought-provoking 2023 paper, Dr. Mikhail V. Blagosklonny of Roswell Park Comprehensive Cancer Center challenges one of biology’s most fundamental questions:
Does aging exist as an independent process, or is it merely the accumulation of age-related diseases?

According to Blagosklonny, aging is not a single disease but rather a collection of pathological processes — each linked to hyperfunctional cellular activity that continues long after its developmental purpose has ended.
In other words, the same biological programs that drive growth in youth eventually contribute to disease in later life.

The “Hyperfunction Theory” and the Role of Rapamycin

Blagosklonny’s well-known Hyperfunction Theory of Aging suggests that aging is caused by the continued overactivation of growth-promoting pathways, particularly mTOR (mechanistic target of rapamycin).
This overactivity leads to conditions like atherosclerosis, diabetes, cancer, and neurodegeneration — the so-called age-related diseases.

Here, rapamycin emerges as a unique intervention:
it works not by targeting one disease, but by modulating the central aging pathway itself.
By inhibiting mTOR, rapamycin may slow or delay multiple disorders simultaneously, essentially treating aging as if it were a treatable syndrome.

Why “Disease-Oriented Dosing” Matters

Blagosklonny argues that the key to using rapamycin for longevity lies not in one universal dose but in “disease-oriented dosing.”
Each person ages differently — some are more vulnerable to cancer, others to cardiovascular or metabolic decline.
Therefore, rapamycin dosing should ideally be personalized according to an individual’s disease risks, biology, and overall health profile.

He emphasizes that rapamycin is not a miracle pill — its effects depend on careful balance.
Too little may be ineffective; too much may suppress essential immune functions.
The optimal approach, he suggests, is long-term, low-dose, intermittent use designed to prevent rather than treat disease.

Aging as a Preventable Phenomenon

Blagosklonny’s argument reframes how we understand aging altogether:
if all age-related diseases are manifestations of the same underlying hyperfunction, then controlling that hyperfunction may prevent aging itself.

In this view, “aging” ceases to be a mysterious, unstoppable force — and becomes a biological imbalance that can be regulated.
The concept unites longevity research and medicine: treating one age-related disease may inevitably slow others, since they share a common mechanistic root in mTOR-driven hyperactivity.

From Theory to Practice: The Path Forward

Although the idea of disease-oriented dosing remains theoretical, it aligns with the growing trend of precision medicine — tailoring interventions to individual biology rather than applying a single protocol to all.
Future studies may identify distinct dosing patterns for different “aging phenotypes,” such as metabolic, cardiovascular, or neurodegenerative profiles.

Blagosklonny envisions a future where longevity therapy becomes personalized healthcare:
Rapamycin and related drugs (rapalogs) might be administered the way we now prescribe preventive statins or low-dose aspirin — but with broader impact on aging as a whole.

Conclusion: Rethinking Aging Through the Lens of Disease

Blagosklonny’s work doesn’t deny aging — it redefines it.
By proposing that aging is the sum of its diseases, he shifts the focus from “treating old age” to managing the biological causes behind it.
In this framework, rapamycin becomes not just a longevity compound but a tool to align medicine with the biology of aging itself.

His central message is clear:

“To extend life, we must treat the diseases of aging before they appear.”