The Science of Cellular Senescence

Cellular senescence leads to the gradual degradation of tissue function. As we age, we accumulate a higher proportion of senescent cells to healthy cells, leading to fragility and the beginning of age-related chronic disease.

The Rise of Zombie Cells

A cell can go into a state where it is not allowed to replicate or continue to grow. When cell growth and replication are arrested, it is considered to be a senescent cell. The cell isn't dead, but it's not healthy, either. It's a zombie cell.

Senescent cells are particularly dangerous because they can recruit healthy cells into becoming senescent cells—building up the zombie army. Over time the underlying tissue that the senescent cells make up loses its original function, which makes us more fragile and prone to age-related disease.

A Witch's Brew of of Pro-inflammatory Molecules

The defining characteristic of a senescent cell is the inflammatory distress signal that it emits. Because a senescent cell is in a damaged state, it signals out to other cells that it is under duress by emitting a witch's brew of inflammatory molecules that we call the SASP (senescence-associated secretory phenotype). This inflammatory response damages the tissue and causes cells adjacent to the senescent cells to become senescent as well.

Across most age-related chronic diseases, we see these inflammatory phenomena wreaking havoc as we get older.

Attacking Scenesent Cells from The Inside Out


Autophagy is the cell's process to clean out and recycle cellular debris. In terms of senescence, autophagy reduces SASP inflammatory molecules created by senescent cells. In doing so, it reduces the ability of a senescent to make its neighbor cells into being senescent as well.

Autophagy is one of the great levers we have to increase our healthspan. We can induce autophagy in a cell through three well-known healthspan interventions: fasting, the supplemental usage of molecules like Metformin and Rapamycin, and exercise.


Senolytics are molecules that bind to a special receptor on a senescent cell and detonate the senescent cell's programmed cell death instructions. Senolytics offer precision targetingof these dysfunctional cells, while not causing damage to neighboring healthy cells.


In aging, all roads lead to senescent cells. Through the advent of senolytic and senomorphic therapies, we can target the growth and progression of senescent cells—protecting overall tissue integrity, improve our overall well-being, and prolonging our healthspan.

Topical Rapamycin (with EGCG)

Topical rapamycin skin cream is a powerful and effective solution to reduce the accumulation of damaged senescent cells and maintain healthy skin. Infused with EGCG to enhance skin absorption, it provides targeted treatment for aging skin, improving its appearance and health.

Strength of Research Rating
Rating is based strength of the research from human studies. However, we'd like to see more published studies.


Rapamycin is considered to be the most promising healthspan-promoting interventions for its role in slowing down the formation of senescent cells through its inhibition of the mTOR complex 1 pathway.

Strength of Research Rating
Rating is based on a small amount of research studies, primarily focused on mouse models.


Metformin is one of the most promising and well-researched interventions to slow down the accumulation of senescent cells by inducing autophagy. Metformin's benefits extend beyond the induction of autophagy and include optimizing metabolic pathways and upregulating the molecules that maintain the epigenome.

Strength of Research Rating
Rating is based on extensive research into the safety and efficacy of Metformin, and its many modes of action to curtail age related disease.

Your Longevity Care Team

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Healthspan offers a personalized approach to healthcare that goes beyond your normal doctor's visit. Our team of experienced researchers and clinician specializes in innovative interventions targeting cellular senescence to help you achieve optimal health and wellness.

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