Press Release

Aging-US: From causes of aging to death from COVID-19


Aging-US recently published "From Causes of Aging to Death from COVID-19" by Blagosklonny et al. which reported that COVID-19 is not deadly early in life, but mortality increases exponentially with age - which is the strongest predictor of mortality.

The Review covers:

  1. Age
  2. Age-related diseases
  3. Male Gender
  4. Mortality from aging compared with COVID-19 mortality
  5. Age-related diseases
  6. Cytokine storm as a hyperfunction
  7. Hyperfunction theory of quasi-programmed aging
  8. Covid-19 vulnerability as an age-related syndrome
  9. Inflamm-aging and immunosenescence
  10. Cellular senescence as a continuation of growth
  11. Figuratively, rapamycin rejuvenates immunity
  12. Anti-aging medicine
  13. Rapamycin and everolimus as anti-aging drugs and,
  14. Potential applications of rapamycin/everolimus to COVID-19

The author contends that at its deepest level, aging is driven by inappropriately high cellular functioning. The hyperfunction theory of quasi-programmed aging explains why COVID-19 vulnerability is an age-dependent syndrome, linking it to other age-related diseases.

These conditions are typical age-related diseases: hypertension, diabetes, obesity, ischemic heart disease, chronic obstructive pulmonary disease, and other diseases.

This is because pre-existing conditions are manifestations of biological age, ultimately meaning that A. aging and B. diseases are two sides of the same coin.

The Blagosklonny Research Team goes on to highlight that an anti-aging intervention, such as rapamycin, may slow aging and age-related diseases, potentially decreasing COVID-19 vulnerability.

The Aging-US Review also reported that as soon as the COVID-19 epidemic started, it became clear that COVID-19 vulnerability is an aging-dependent condition, and the use of rapamycin was immediately suggested by independent researchers.

Figure 5. Prevention of COVID-19 vulnerability by staying young. Hypothetical graph in the absence of COVID-19. COVID-19 vulnerability (log scale) increases exponentially with age (blue line). The line ends at age 120, a maximum recorded age for humans. In theory, a continuous rapamycin treatment would slow down an increase of the vulnerability with age (red line). The increase is still logarithmic but at a different slope, because rapamycin slows the aging process. The maximum lifespan, in the absence of COVID-19, is extended because the 100% natural death threshold is achieved later.

By decreasing biological age and preventing age-related diseases, long-term rapamycin therapy may, in theory, decrease the COVID-19 mortality rate in the elderly.

As specifically discussed in the Review section titled “Figuratively, rapamycin rejuvenates immunity”, mTOR inhibitors can improve immunity to viral infections, improve immunization and vaccination to some viruses such as the flu.

The hypothetical graph in the absence of COVID-19. COVID-19 vulnerability increases exponentially with age.

Then as discussed in the section “Cytokine storm is a hyperfunction”, cytokine storm and hyper-inflammation is the main cause of death in COVID-19 pneumonia Rapamycin, an anti-inflammatory agent, inhibits hyper-functions, cellular senescence and decrease secretion of cytokines.


Full Text -

Correspondence to: Mikhail V. Blagosklonny email: or

Keywords: aging, mTOR, transcription, rapalogs, senolytics SARS-CoV-2 COVID-19 coronavirus

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

To learn more about Aging-US, please visit or connect with @AgingJrnl

Aging-US is published by Impact Journals, LLC please visit or connect with @ImpactJrnls

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