Dr. Mikhail Blagosklonny, MD PhD

COVID-19 is not deadly early in life, but mortality increases exponentially with age, which is the strongest predictor of mortality. Mortality is higher in men than in women, because men age faster, and it is especially high in patients with age-related diseases, such as diabetes and hypertension, because these diseases are manifestations of aging and a measure of biological age. At its deepest level, aging (a program-like continuation of developmental growth) is driven by inappropriately high cellular functioning. The hyperfunction theory of quasi-programmed aging explains why COVID-19 vulnerability (lethality) is an age-dependent syndrome, linking it to other age-related diseases. It also explains inflammaging and immunosenescence, hyperinflammation, hyperthrombosis, and cytokine storms, all of which are associated with COVID-19 vulnerability. Anti-aging interventions, such as rapamycin, may slow aging and age-related diseases, potentially decreasing COVID-19 vulnerability. PLUS My theory on why men are effected by disease states and die younger than woman. And it’s so simple you’ll dismiss it immediately. Dr. Blagosklonny is editor-in-chief of the journals Aging, Cell Cycle, and Oncotarget. In addition, he is associate editor of the journals Cancer Biology & Therapy and a member of the editorial board of Cell Death & Differentiation. http://mikhailblagosklonny.com PLUS My theory on why men are effected by disease states and die younger than woman. And it’s so simple you’ll dismiss it immediately.

From causes of aging to death from COVID-19

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346074/

mTOR and Testosterone

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529800/#!po=1.78571

[3:30] The story behind Dr. Blagosklonny’s work with rapamycin.

• Originally studied for its effect or cellular senescence.
• No established LD50

[12:15] the Dr.s newly published paper.

• Death from covid seems to be age dependent.
• You don’t die because of the # of your age. You die from the accumulation of disease that comes with aging.

[21:40] Thoughts on hyper functional senescent cell’s contribution to the cytokine storm.

• Few cells are “classically” senescent.
• Rapamycin can inhibit excessive cytokine production.
• It is adaptogenic in nature.
• It can potentially be utilized for it prophylactic effect on viruses.

[37:00] the way forward to treatment should include intermittent rapamycin to reduce senescent load.

• Its effects on MTOR suggest treatment potential and prevention of several different diseases, including cancer.
• One model has shown 90% reduction in cancer cells in mice exposed to smake.

[42:11] Rapamycin stimulates mitophagy.

[47:55] Dog aging project.

• Blagosklonny has heard of it but is not involved.

[51:00] Will high protein intake blunt the effect of rapamycin?

• Rapamycin doesn’t decrease muscle size.

[58:03] Clarification of what is meant by the term “anti-aging”.

• Reduction in allostatic load from accumulation of diseases can prevent you from dying soon than you should.

[1:00:00] Is Dr. Blagosklony planning on opening clinics in the states?

[1:14:27] Why do men die faster than women?

• Senescent cell load from higher iron levels.
• Testosterone also increases the uptake of iron.
• Testosterone also affects MTOR.