C15:0’s Multi-Tier Approach to Healthy Aging

Healthy Aging

A New Home Run Study for C15:0

Mid-last year, we published evidence of a nutritional C15:0 deficiency condition called Cellular Fragility Syndrome in the peer-reviewed journal, Metabolites. This is the first nutritional deficiency syndrome to be identified in 75 years, and may be affecting as many as 1 in 3 people globally. More importantly, we showed how C15:0 supplementation fixes this syndrome. A new extensive study from an independent team put Cellular Fragility Syndrome to the test. This week, let’s dive into what this team found (spoiler alert: C15:0 got an A+).

Amazing! What is Cellular Fragility Syndrome?

Good question. While C15:0 does a lot of good things, one of its most important jobs is to strengthen our cell membranes against age-driving lipid peroxidation.

C15:0 is a sturdy fatty acid that readily integrates into our cell membranes. Since it has no double bonds (bonds that are particularly susceptible to attack by oxygen), C15:0 helps to keep our cells protected and functioning – especially as we age.

If we don’t get enough C15:0 from our diet or supplements, our cell membranes become more fragile, resulting in:

• Increased lipid peroxidation.
• Increased fragility of red blood cells, reflected by lower hemoglobin and higher red blood cell distribution width (RDW).
• Ferroptosis, a new form of cell death caused by fragile fatty acids in cell membranes.
• Dysregulated iron metabolism & immune function throughout the body, starting with the liver.
• Accelerated age-related breakdown, including impaired liver, metabolic, heart, and cognitive function.

The good news is that our C15:0 levels are directly related to our dietary C15:0 intake. Which means that, like all nutritional deficiencies, Cellular Fragility Syndrome can be readily fixable by raising our C15:0 levels.

Got it. What was the purpose of the latest study?

Well, Aabis et al. put pure C15:0 to the test. Specifically, they used a rodent model with liver lipid peroxidation, cell death, dysregulated iron metabolism and immune function, and impaired liver function (aka induced Cellular Fragility Syndrome)… and sought what daily oral C15:0, at three different doses, could fix within 10 weeks.

And the outcomes were…

Many good benefits. Compared to the non-supplemented poorly functioning control group, the C15:0 supplemented group (especially the lower 10 mg/kg body weight dose group) demonstrated the following statistically significant benefits:

• Healthier body weight
• Lower lipid peroxidation
• Lower RDW and higher intracellular hemoglobin concentrations (markers of stabilized red blood cells)
• Improved cell survival and increased glutathione, a protector against ferroptosis
• Restored healthy iron metabolism, including stemming harmful liver iron deposition
• Lower multiple proinflammatory cytokines
• Lower AST, ALT, and GGT (aka improved liver function)

Just as we had shown in the Metabolites publication (that C15:0 supplementation reverses all components of ferroptosis and Cellular Fragility Syndrome), Aabis et al. repeated – perfectly.  Go science.