Removing Senescent Cells: A Revolution in Longevity

"Removing senescent cells"—is it just a futuristic fantasy? No! It's a reality that can dramatically transform human lifespan and health! There are numerous strategies for longevity: activating sirtuins through fasting, inactivating mTOR by restricting carbohydrates and amino acids, stimulating brown fat cells with cold to activate sirtuins again, and increasing NAD+ with NR or NMN. So many ways to defy time! MUDA MUDA MUDA MUDA MUDA MUDA MUDA!

Strategies for Longevity

For those who train, some of these strategies may seem unfavorable due to their effects on muscles, such as fasting or mTOR inactivation. However, cold stimulation and NAD+ increase are more viable as they not only benefit longevity but can also help increase muscle mass.

The Hayflick Limit

Human cells can divide about 50 times before the telomeres shorten so much that they can no longer divide. This is the Hayflick Limit. Although the enzyme telomerase can prevent this shortening, it also increases the risk of cancer. When telomeres shorten, chromosome ends are exposed, and cells interpret this as DNA damage, triggering a repair attempt that can incorrectly join different chromosome ends, destabilizing the genome and leading to cell death.

To remove these damaged cells, autophagy can be effective, though it doesn't always have only positive aspects. Another method is to stop cell proliferation, resulting in senescent cells.

Senescent Cells: The Double-Edged Sword of Stress

When cells are damaged or stressed, their proliferation stops, activating tumor suppressor proteins like p53 and pRB. p53 induces the expression of the CDK inhibitor protein p21, activating pRB, which in turn represses the transcription factor E2F, stopping the cell cycle in the G1 phase. Senescent cells are usually cleared by the innate immune system, but this function declines with age, allowing senescent cells to accumulate and release inflammatory cytokines, triggering inflammation. GOGOGOGOGOGO...

Removing Senescent Cells: The Future of Longevity

The accumulation of senescent cells might be an evolutionary strategy to prevent cancer in youth, at the expense of health in old age. However, removing these cells could reduce inflammation and extend lifespan. Enter senolytics—drugs that remove senescent cells. Studies show that removing them reduces the incidence of arteriosclerosis, cataracts, and improves lung function, even extending the maximum lifespan in mice. ROAD ROLLER DA!

Senolytics: The Drugs of the Future

The GLS-1 inhibitor has generated excitement as a potential "aging vaccine," though practical use may take time. In the meantime, quercetin and fisetin are available. Quercetin, combined with the tyrosine kinase inhibitor dasatinib, has been shown to remove senescent cells and improve function in progeroid mice. Quercetin also benefits trainers by reducing post-training inflammation and increasing IGF-1 and IGF-2.

Fisetin, similarly powerful in removing senescent cells, is more affordable than quercetin. It's a type of flavonol that can activate sirtuins, has antioxidant properties, and anti-inflammatory effects via Nrf2 induction. ZA WARUDO!

---

The Future of Anti-Aging Medicine

Once, considering aging as a treatable disease was deemed madness. Today, many scientists are seriously working on anti-aging therapies. In a few decades, human lifespan could be dramatically extended.