This particular study looked at inflammation through imaging (CT scans) as part of Biograph's $17,500 program. You can get at the underlying signal fairly cheaply through a simple blood test (hs-CRP).
It's fairly well-known that inflammation is an independent risk factor for heart disease, alongside LDL cholesterol (or ApoB) and blood pressure: https://www.empirical.health/blog/inflammation-and-heart-hea...
The American College of Cardiology looked at a bunch of inflammation biomarkers and standardized on hs-CRP: https://www.jacc.org/doi/10.1016/j.jacc.2025.08.047
> Crucially, no routine blood biomarker, lipid metric, or clinical risk score could identify these individuals with inflamed coronary arteries.
I call bs on this. There are two common blood tests that are meant for it:
1) hs-CRP (High-sensitivity CRP)
2) Lp-PLA2: Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet activating factor Acetylhydrolase, is an inflammatory enzyme that circulates bound mainly to low density lipoproteins and has been found to be localized and enriched in atherosclerotic plaques. In multiple clinical trials, Lp-PLA2 activity has been shown to be an independent predictor of coronary heart disease and stroke in the general population. Measurement of Lp-PLA2 may be used along with traditional cardiovascular risk factor measures for identifying individuals at higher risk of cardiovascular disease events.
I have routinely had both of these blood tests among others, although I paid myself to get them.
As for hs-CRP, it will likely show an elevation. If you use a binary classifier with a higher threshold of what's safe, e.g. 3.0 instead of 1.0, you will miss it! I am guessing this is why they missed it.
If all the other biomarkers of inflammation "showed no correlation with the presence of coronary inflammation" as predicted by this scan, then how exactly do they assess the positive predictive value of the scan?
Before or after 2020?
I'm still surprised we don't have many physical interventions for this, knowing that it's a physical problem. I'm reminded of the older surgeon style medicine whose reputation seems to be pretty coarse now since we have so much knowledge about chemistry and non-invasive interventions.
Wonder what would happen if we pushed the envelope on physical fixes like endarterectomy like procedures and made them safer/more routine. Like getting your teeth flossed.
Recently I learned that only those with over-active immune systems survived the 14th century plagues. Therefore, inflammation is to be taken seriously, or at least understood in this historical context, depending on your ancestry.
As for the article, the findings come as no surprise given what we know about the risk factors in the post-smoking world. Nowadays nutrition, specifically saturated fats in combination with lots of sugar and salt, as found in today's artificial foods is showing up in the research (not paid for by 'big beef').
There is no need to over-think it, just stay off the corporate 'food' and cook from fresh ingredients, where you don't get 'HFSS' (UK government term for high fat/salt/sugar) held together with weird chemicals. Sure, nobody has time for that, but this is the frontier of public health, a.k.a. the 'obesity crisis', with a simple solution - actually bother to cook!
I don't see how one can spin this into a positive finding - their preprint says that the only correlate they find with their new measurement is BMI. By my reading, not even male sex is associated with more inflammation. It sounds like they've identified a fancy BMI estimator, and not a very good one.
This is in asymptomatic patients, who already have a great estimator for 10-year heart disease mortality risk in the coronary calcium score which isn't even obliquely mentioned in their abstract. Edit: the paper shows no correlation with calcium, either
https://www.medrxiv.org/content/10.64898/2026.10.19.26364786...