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.
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.
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 witches brew of inflammatory molecules that we call the SASP (senescence-associated secretory phenotype). This inflammatory response damages the tissue and cause 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.
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 targetting of these dysfunctional cells, while not causing damage to neighboring healthy cells.
In aging, all roads lead to senescent cells. Through the advent of senolytic therapies, we can eradicate senescent cells—protecting overall tissue integrity, improve our overall wellbeing, and prolonging our healthspan.
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.
We've put together a health kit that targets the three major longevity intervention pathways: senescence, autophagy, and metabolic health.
The Healthkit Includes
Fisetin is a naturally occurring molecule that has been shown to target certain subtypes of senescent cells. There is preliminary research to show that intermittent use of Fisetin clears certain senescent cells, without being toxic to healthy cells.
The Pillars of Aging
Dr. David Sinclair
David Sinclair is a professor in the Department of Genetics and co-director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School, where he and his colleagues study sirtuins—protein-modifying enzymes that respond to changing NAD+ levels and to caloric restriction—as well as chromatin, energy metabolism, mitochondria, learning and memory, neurodegeneration, cancer, and cellular reprogramming.
* Dr. David Sinclair is not involved with Healthspan and does not sell Metformin.
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