BREAKING SCIENCE NEWS: Deep Dive on Cellular Fragility Syndrome

Healthy Aging

C15:0 deficiency: What your doctor cares about

Last week, we shared our published discovery of the first nutritional deficiency syndrome found in 75 years, called Cellular Fragility Syndrome. This week, we’re diving deeper into what happens in our bodies when C15:0 levels are too low and advance to Cellular Fragility Syndrome.

It all starts with fragile cells.

When our cell membranes become fragile, we age faster. As we shared previously, the strength of our cells depends on which fatty acids are in our cell membranes.

• Fragile fatty acids (aka polyunsaturated fats) = fragile cells
• Sturdy fatty acids (aka C15:0) = sturdy cells

We now know that if our cell membranes contain less than 0.2% C15:0, our cells become fragile, including our red blood cells.

After that, fragile red blood cells are taken out by our liver.

Our liver is trained to remove fragile red blood cells. Which is great – until we have too many fragile cells. Because when our liver gathers too many fragile red blood cells, these cells leave behind iron… lots of iron.

The result? Less iron in our blood and more iron sitting in our liver.

Then, our liver becomes ground zero for ferroptosis.

So, if we have excess liver iron AND fragile cells, our liver becomes ground zero for ferroptosis – a form of cell death newly discovered by scientists at Columbia University. As we covered last week, ferroptosis causes our cells to:

• Increase bad lipid peroxidation
• Make massive amounts of damaging reactive oxygen species (ROS)
• Shut down mitochondria (aka our cells’ energy source)

Finally, ferroptosis goes systemic.

As this process advances in the liver, the following happens: lipid peroxidation, ROS, and iron spill over to negatively impact not only our liver, but our heart, pancreas, and brain health. And we age faster.

All in, this is the process of Cellular Fragility Syndrome, which is believed to affect as many as 1 in 3 of us.