Dr. Stephanie Venn-Watson

They called it fructosis.

And Dr. Jury, the best way I would explain it is, like you said, it involves this oxidation of lipids.

It's like, you know, if you have oil and it sits out in the air, it goes bad and we call it rancidity.

So it's basically our cells become, the fats in our cell membrane become susceptible to going rancid from lipid peroxidation, aka rancidity.

When that happens, it then combines with this strange iron that's showing up in the cell.

They combine together and they create all these reactive oxygen species that take out our mitochondria and kill the cell.

It's a very unique way our cells die.

The

Why we care about it is today there are over 20,000 papers, peer reviewed papers on ferroctosis showing that it creates this systemic explosion of reactive oxygen species of iron overload.

So bad iron starts seeding itself in our brain, our heart, our liver, and our lungs, our pancreas.

And while all of this has been really well described, but what nobody could understand is where did this form of cell death come from?

That's where we were finding at the same time this was happening in humans, we were seeing it happening in navy dolphins in a very clean way.

And that's where we discovered that as their C15 levels went down in their diet because of a specific type of fish that got fished out, C15 went out of their diet.

And we learned that these C15 deficiencies in their diet

cause their cells to be fragile, resulting in all these downstream proptosis, accelerated aging, fatty liver disease, all the things that come with it.

So it was a major unlock.

We're realizing we're seeing that same thing happening in people.

And in younger and younger ages, which is a big reason why since our primary source of C15 is dairy fat, we're thrilled to see the new updated guidelines with regard to getting whole fat milk back into our diet.

We need to get the C15 back in and help to stabilize our cell membranes.

That's right.