Hyperfunction Theory (Blagosklonny)

What it proposes

Aging is not (primarily) the accumulation of damage. It is the continuation of developmental growth programs — especially mTOR signalling — past the point where they were useful. The same signalling that built the body now drives hypertrophy, hyperplasia, lipid accumulation, and immune dysregulation that manifest as age-related disease.

Blagosklonny calls this “quasi-programmed aging”: not an evolved program to age, but the unintentional continuation of growth programs because evolution had no reason to switch them off in post-reproductive life.

Why it fits the data

• mTOR inhibition (rapamycin, caloric restriction) reliably extends lifespan across species — consistent with “turning down the growth program” extending healthspan.
• Many age-related diseases are essentially “over-doing” physiology: benign prostatic hyperplasia, hypertension, insulin resistance, atherosclerosis — all involve persistent activation of pathways that served a developmental or stress purpose.
• Damage-only theories struggle to explain why mTOR inhibition by drugs with no antioxidant or repair activity extends lifespan.

Practical implications

If hyperfunction is the right frame, then the strategy is suppressing overactive signalling in adulthood, not (only) repairing damage. This aligns with the empirical success of mTOR inhibition, caloric restriction, and pharmacological attenuation of growth-axis signalling.

Related entries

mTOR, Rapamycin, Antagonistic pleiotropy.