Stopping your cells from quiet quitting

April 16, 2023

Welcome to Issue 43 of Science Says! Our weekly newsletter where you’ll learn the latest healthy aging and C15:0 research news that our team of doctors, scientists, and experts are most excited about—without having to go search for it.

Eric and Steph
Co-Founders, Doctors, Nerds

What Dr. Stephanie Venn-Watson, our co-founder and author of The Longevity Nutrient and over 80 peer-reviewed scientific publications, is reading.

Healthy Aging

Senescent cells can be toxic

The ability to reverse aging is no longer science fiction. Sounds too good to be true? In this series, we will talk about the latest peer-reviewed science on how slowing, and even reversing aging is becoming a reality.

This week, let’s talk about a hot age-reversing target: cellular senescence.

Great! Wait – what is cellular senescence?

Our cells quit early for the same reason we might quit a job – stress. As described by Campisi et al. in Nature Reviews, when cells are too stressed, they will simply shut down. In science terms, this is called premature senescence. A cooler term for early cell quitting is M0 (for mortality phase 0).

When good cells turn bad.

Normally, when cells stop working, they are recycled out, leaving behind healthy cells – and healthy organs, too. Sometimes, however, our cells stop replicating… but they don’t die. The result? Zombie senescent cells that don’t just quiet-quit – they interfere with our normal tissue function.

Campisi et al. show how, in our tissues, these zombie cells trigger a chronic inflammatory state called a senescence-associated secretory phenotype, or SASP. In turn, this toxic SASP environment can exacerbate age-related diseases.

Neutralizing zombie cells.

Leading scientists are now on the hunt for ways to clear our bodies of senescent, zombie cells.

As covered by Benhamu et al., potential anti-aging treatments in this space involve senolytics, which aim to kill zombie cells, and senomorphics, which neutralize damage caused by zombie cells. Here are a few of the molecules that have been most extensively tested:

Senolytics (clearing zombie cells)

Dasatinib + Quercitin (D+Q). D+Q has been shown to effectively lower the number of senescent cells. The ability for this senolytic duo to demonstrate clinically relevant benefits, however, has been hit and miss.
Fisetin. Fisetin can help to put senescent zombie cells to rest – for good. Clinical trials are ongoing.
UBX0101 and UBX1325. Based on encouraging mouse studies, these compounds were ramping up to be the holy grail of senolytics. Human studies, however, have been less promising.

Senomorphics (neutralizing zombie cells)

Rapamycin. By inhibiting mTOR, this leading anti-aging candidate supports an anti-inflammatory (and anti-SASP) environment. Rapamycin also has many other anti-aging benefits, too.
Metformin. Another longevity leaderboard candidate, metformin activates AMPK to provide many longevity-supporting benefits, including lowering inflammation and stopping senescent cell damage. It is also the world’s leading treatment for type 2 diabetes.
BIRB796. You know, BIRB796. Okay, this was a new one for us, too. This senomorphic candidate goes after a key inflammatory target, called MAPK.

In summary, while there has been a bunch of anti-aging fervor around senolytics (which aim to clear our bodies of rampant zombie cells), the most promising studies seem to be coming from molecules that are senomorphics – which aim to neutralize the negative effects of zombie cells.

C15:0 keeps our cells healthy… and neutralizes zombie cells, too.

Here’s the thing. Instead of just cleaning up zombie cells to slow aging, wouldn’t it be better to keep our cells healthy in the first place?

That’s where C15:0 comes in. C15:0 has been shown in peer-reviewed studies to lower cellular stress, improve cellular resilience, and neutralize toxic environments that can be caused by zombie cells. Here’s how:

C15:0 strengthens our cells. In our cell membranes, polyunsaturated fatty acids are easily oxidized, which make our cells stressed and weak, especially as we age. C15:0 is a stable fatty acid that is resistant to oxidation, effectively armoring cells against cellular stress. Studies have shown that C15:0 can improve cellular stability by 80%, and as demonstrated by Soboleva et al., people with higher C15:0 levels have more resilient cells – and lower measurements of cellular stress.
C15:0 lowers pro-inflammatory cytokines. Chronic inflammation creates a toxic environment for our cells. C15:0 has been demonstrated to have significant immune calming effects on over 24 pro-inflammatory cytokines. Kurotani et al. showed that people with higher C15:0 levels had calmer, healthier immunity.
C15:0 lowers reactive oxygen species (ROS). When we get older, our mitochondria can stop producing good energy and start producing damaging reactive oxygen species. C15:0 has been shown to directly repair our mitochondrial function by up to 45%, enabling our cells to have the energy they need – while also reducing the stress of ROS.

In addition, by activating AMPK and having downstream mTOR-inhibiting effects, C15:0 provides the same zombie cell-neutralizing mechanisms as metformin and rapamycin.

This means that C15:0 helps to keep our cells strong and healthy, while also helping to neutralize zombie senescent cells.

Have a wonderful week, everyone!