Cyclooxygenase-2

So we have these different pathways of inflammation.

Curcumin is gonna function on that NF-kappa-B or COX-2 pathway, which NSAIDs do.

But the fact that Boswellia will function on the five locks means that they're both covering that acute inflammation, that chronic inflammation in a synergistic way to support the body the best.

And so I get so excited because Ayurveda always fused everything together.

We published that And basically he points out that 600 milligrams once a day is not an anti-inflammatory dose.

If you want to use aspirin as a COX-2 inhibitor, you've got to give 600 milligrams three times a day.

And so we're always using an antiplateless dose.

Now we've just gone to the lowest level that we can.

It inhibits something called five locks.

And a lot of these act as COX-2 inhibitors and LOX inhibitors.

And they work really well when you combine them together.

And that's why we created Fortify Omega Relief Extreme because it covers all the bases.

It's called NextGen Curcumin by Fortify.

And it's a great anti-inflammatory.

It actually acts on NK, Kappa B, COX-2, LOX, cytokines.

So it lowers inflammation.

In many ways, it's the biological opposite of an NSAID.

Over-the-counter NSAIDs, they reduce pain and inflammation by inhibiting cyclooxygenase enzymes, specifically one called COX-2.

Right.

They shut down the inflammation pathway.

They do.

But here is the catch.

COX-2-derived prostaglandins are actually essential for the initial stages of muscle repair.

Oh, wait.

The deep red color comes mainly from anthocyanins, primarily cyanidin-3-glucosal rutinicide and cyanidin-3-sorbose, a class of antioxidant pigment.

What makes these particular anthocyanins interesting to researchers since the late 1990s is lab work showing they inhibit COX-1 and COX-2, the same two enzymes targeted by NSAID pain relievers like ibuprofen and naproxen.

And in some in vitro comparisons, the inhibition was in a similar range to those drugs.

That's a laboratory finding, not proof the juice works in your body the way a pill does.

Observational studies have shown that, so for the nurse's health study, for example, those who are on aspirin have lower rates of primary colon cancer and seem to have lower rates of occurrence.

So observational data has seen this a number of times, and that's through COX-2 expression or overexpression, it's thought to be the mechanism.

So people have wondered about this for a while.

There was the study by Geoffrey Mayerhart and Charles Fuchs, which is the C-LGB SWOG 80702 study that involved Celecoxib.

There was another COX-2 inhibition study as well that was negative.

And now there have been three studies randomized controlled trials of aspirin and the adjuvant use of colon cancer, all of which differ subtly but importantly.

The one many of us will know is ALESCA, which was a randomized trial of aspirin in colon and rectal cancer, colon stage 2 and 3, rectal stage 1 through 3, that had the group A and group B mutations looking at PIK3 kinase, exons 9 and 20, or group B mutations with PIK3 kinase, PIK3R1 and P10, and looked at the relevant benefit if you had those mutations that was positive, indicative.

And aspirin 200 versus placebo, the translational study was pre-planned.

The NCI, National Cancer Institute, explicitly says that researchers are continuing to investigate the mechanism.

Current research is focused heavily on COX-1 and COX-2, which we'll talk about, prostaglandins, inflammatory signaling, and potential biomarkers that might identify people who respond differently to aspirin.

There are even NCI-funded studies specifically investigating aspirin's metabolic effects in cancer prevention.

And one NIH-funded project was literally titled Aspirin, and I can't pronounce his second word, Metabolomics? Metabolomics? metabolomics there that's probably right aspirin metabolomics in colorectal cancer chemo prevention you can look that up the way that word is spelled is m-e-t-a-b-o-l-o-i-l-o-m-i-c-s it's friday i'm sorry because the researchers are trying to figure out what metabolic changes actually account for aspirin's effects So this isn't really a case of Ray Peet discovered all of this and nobody bothered researching it.