Spinning your cellular wheels with mTOR

May 15, 2023

Welcome to Issue 47 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

Stuck in the mud?

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

This week, let’s talk about a top troublemaker in the longevity pathway: mTOR.

This sounds familiar. What is mTOR, again?

mTOR is an enzyme that continues to spin the wheels of broken cells stuck in the mud. We’ve talked about these senescent cells over the past few weeks, and you now know that these malfunctioning cells wreak havoc on our tissues, resulting in a chronic inflammatory state. mTOR is a driver of many aging-related diseases, including:

Cancer
Neurodegenerative diseases
Type 2 diabetes

mTOR plays such a central role in causing age-related breakdown, that Papadopoli et al. describe mTOR as “a central regulator of lifespan and aging.”

Got it – mTOR speeds up aging. So, how do we block mTOR?

mTOR stands for the Mechanistic Target of Rapamycin. Yes, mTOR is called mTOR because this enzyme is effectively blocked by rapamycin, a longevity compound superstar.

In addition, Ge et al. showed that compounds that turn up AMPK (remember last week’s newsletter?) also work upstream to block mTOR. Both metformin and C15:0 are examples of compounds that turn up AMPK.

Good things happen when mTOR is blocked.

Sorrenti et al. review how compounds that block mTOR keep our malfunctioning cells from continually spinning their wheels. This results in the following beneficial activities:

Anti-cancer activities that slow or stop the proliferation of cancer cells
Anti-inflammatory activities that stem chronic inflammation of aging
Anti-senescent cell activities that allow malfunctioning cells to go to cell heaven

These mTOR-blocking benefits have been proposed by Blagosklonny et al. as approaches not only to support our overall health and longevity, but to specifically address many aging-associated conditions, including autoimmune diseases, cancer, diabetes, hypertension, osteoporosis, and neurodegenerative conditions such as Alzheimer’s and Parkinson’s diseases.

In summary, studies continue to show that getting mTOR to stop pushing bad cells to become badder can help us stay healthier, longer. Clinical trials with mTOR inhibitors, including rapamycin and metformin, are underway to help determine how long we can truly stay healthy with age and expand our longevity.

C15:0 inhibits mTOR

Important disclaimer here: This newsletter provides you with the latest peer-reviewed science on C15:0. C15:0 supplements are not intended to prevent, manage, treat or cure any disease – including cancer. With that important note, back to the science.

We covered how mTOR allows bad cells to be badder, including cancer cells. This is why blocking mTOR is not only being explored as a means to generally live healthier and longer, but to specifically stop cancer cells from proliferating.

Peer-reviewed studies have demonstrated C15:0’s anti-cancer activities, including its role as an mTOR inhibitor. Specifically, To et al. and Ediriweera et al. conducted a series of extensive, albeit early, laboratory studies demonstrating the following cell-based benefits of C15:0 (aka pentadecanoic acid):

C15:0 decreases both the growth and invasiveness of breast cancer cells. To et al. showed that C15:0 decreases the proliferation of both MCF-7 and MCF-7/SC cancer cells. MCF-7/SC cancer cells are resistant to tamoxifen, which is the most common first-line treatment for breast cancer. This is important because Ali et al. report that up to 30% of women with breast cancer have tamoxifen-resistant cancer.
C15:0 inhibits both JAK/STAT signaling and HDAC to decrease the proliferation of many cancer cell types. To et al. demonstrated that C15:0 decreased breast cancer cell growth by inhibiting JAK/STAT signaling, a targeted pathway that ramps up cancer cell proliferation and chronic inflammation. Ediriweera et al. further showed that C15:0 strongly inhibited the proliferation of multiple cancer cell types by inhibiting HDAC.
C15:0 reverses tamoxifen resistance, in part by blocking mTOR. In their latest studies, To et al. showed that C15:0 effectively reversed tamoxifen resistance in both MCF-7/SC breast cancer cells and in an in vivo model with breast cancer. C15:0 did this by directly increasing the availability of a key tamoxifen target (ER-ɑ) and inhibiting mTOR – thus allowing breast cancer cells to be readily killed.

While this is exciting news on the science front, these studies are early, and extensive clinical trials are needed to further evaluate C15:0’s potential role as an effective anticancer compound.

The ability for C15:0 to support healthy aging and longevity in many ways – including blocking mTOR – is gaining the attention of more and more scientific teams around the world. To read the latest and greatest science on C15:0, visit DiscoverC15.com.

Have a wonderful week, everyone!