C15:0 & A Younger Biological Age 

Healthy Aging

C15:0 linked to slower aging using epigenetic clocks

In this Whole Body Health Series, we are sharing the latest science on our whole body, from our cells on up.

This week, we’re covering whole-body biological aging.  Specifically, let’s talk about an exciting peer-reviewed study by Liu et al., linking C15:0 to slower biological aging.

Amazing! What is biological aging, again?

There are two ways to measure aging. The first is our chronological age, which counts how many years we have been alive. The second is our biological age, which measures how much our body has broken down over time.

As we have shared before, there’s not much we can do about controlling time. So where can we increasingly make headway? By slowing down our biological age.

I’m in. How is biological age measured?

There are a number of ways to measure our biological aging rate, including the following two:

One is declining hemoglobin over time. As we published in the Proceedings of the National Academy of Sciences, declining hemoglobin over time is a strong indicator of biological aging rates in dolphins. The same holds for people, too.

Another is the epigenetic clock. The more damage we experience throughout life, the more dust balls accumulate on our DNA (hence, the term “epigenetic”). Tests can reliably measure how many dust balls (aka methylation) we have on our DNA, which  is used to measure our biological age.

• If we have more methylated DNA than expected for our chronological age, we are aging at an accelerated rate.
• Conversely, if we have less methylated DNA than expected for our chronological age, we age at a slower rate.

Two biological aging measurements that use the epigenetic clock are called “AgeAccelPheno” and “AgeAccelGrim”. Well, someone had a grim sense of humor.

How was the Liu et al. study done?

Liu et al. determined the biological ages of 4,151 older adults using both AgeAccelPheno and AgeAccelGrim. They also measured  964 different lipid species and 267 fatty acid combinations in each person’s blood. Quick lesson: “Lipid species” are complex molecules that contain multiple fatty acids.

This study’s main question was, “Can certain lipids accelerate or slow our aging?

Got it. Where does C15:0 come in?

This study found that people with higher levels of lipids containing C15:0 had slower aging – using both AgeAccelPheno and AgeAccelGrim measurements. Specifically, people who had more of the lipid called “lysophophosphatidylethanolamide” (let’s go with “LPE”) containing C15:0 had a younger biological age compared to their chronological age. The same held for C17:0, C15:0’s odd-chain saturated fatty acid sister. That’s pretty awesome, right?

A recurring pattern with naughty even-chain saturated fats.

While people with higher odd-chain C15:0 and C17:0 were biologically younger, those with higher even-chain saturated fatty acid levels (especially C16:0 and C18:0) had accelerated aging. This science-backed pattern of “odds are good” and “evens are bad” has been found over and over again, including meta-analyses showing that people with higher C15:0 and C17:0 have better long-term metabolic and heart health, while those with higher C16:0 and C18:0 have worse long-term health.

Quick Comments from Science Says! Issue 81:

We received a helpful note about Issue 81, which focused on ferroptosis. Because conditions related to iron mishandling also include iron deficiencies, people should work closely with their doctors to guide their nutritional iron needs.