Browse evidence-based analysis of health-related claims and assertions
Even though the mice had fatty plaques and they burst, their blood fat levels didn’t change — meaning the rupture wasn’t caused by worse cholesterol, but by something else, like immune activity.
Quantitative
After the plaque burst, the number of immune cells that calm down inflammation went up — like the body’s way of trying to fix the damage after the explosion.
In the artery walls where plaques burst, the genes that make Th17 and Th1 immune cells were turned way up — showing the immune system was actively working right at the site of damage.
When scientists added IL-17 to artery muscle cells in a dish, the cells started dying off in large numbers — especially at higher doses — which could explain how plaques get weak and burst.
Mechanistic
When the plaques burst in the mice, a chemical called IL-17 showed up in high amounts in their blood and right where the plaque broke — like a warning signal at the scene of the damage.
When mice with fatty arteries were stressed, the number of a specific type of immune cell called Th17 went up dramatically — but another type, Th1, stayed the same, suggesting Th17 might be special in causing artery damage.
In mice with fatty artery buildup, a quick burst of stress (like cold, a toxin, and a blood pressure drug) caused 3 out of 4 fragile plaques to burst, but only if the plaque was already weak — strong plaques didn’t break.
Descriptive
When people ate less animal fat, their bad cholesterol went down and their belly fat became less inflamed — and heart attacks dropped fast.
Even though heart treatments didn’t get better in the early 1990s, heart disease deaths still dropped — pointing to diet as the likely reason.
When the balance of omega-3 to omega-6 fats in body fat improves, there are fewer inflammation-causing immune cells — meaning omega-3s may help calm inflammation.
Correlational
Fewer people were obese in the early 1990s in the Czech Republic, and this was linked to less body-wide inflammation and fewer heart disease deaths.
In the early 1990s, Czech doctors didn’t have access to modern heart drugs like statins or new blood pressure medications.
The drug didn’t affect blood sugar or fat levels in the blood, so its benefits aren’t due to improving how the body handles sugar or fat.
When people ate less butter and more plant oils, their overall heart disease risk score — based on good and bad cholesterol — got better.
The mice didn’t gain or lose weight or eat differently with the drug, so the benefits aren’t just because they were eating less or changing their metabolism.
After the Czech government stopped subsidizing butter and fatty meats, heart disease deaths in men dropped dramatically over the next two decades.
There was a hint that the drug might help turn some immune cells into a less inflammatory type, but the data weren’t strong enough to be sure.
More of two specific saturated fats — palmitate and palmitoleate — in fat tissue is linked to more inflammation-causing immune cells in the belly.
The drug didn’t make the fibrous cap around the plaque thicker, so its protective effect must come from other changes, like less cell death or inflammation.
Eating more omega-3 fats — like those in fish and certain oils — is linked to fewer inflammation-causing cells in belly fat.
The drug didn’t lower the mice’s overall cholesterol, so its benefits must come from something else—like reducing inflammation or cell death in plaques.
People with higher bad cholesterol tend to have more inflammation-causing immune cells in their belly fat — for every 1 mmol/L rise in cholesterol, these cells go up by about 18%.
The drug seemed to make more of the CD36 protein visible in the artery plaques, which might help the body clear dead cells better.
When people in the Czech Republic stopped eating so much butter and started using healthier oils, their bad cholesterol levels dropped by 14%.