That isn't the a good comparison. You are describing two pathogens that can both be found to be highly correlated to risk of lung cancer in isolation. A smoker with no known asbestos exposure is still more likely to get lung cancer than a nonsmoker, and visa versa.
I don't think anyone would argue that inflammation is a cause of heart disease. Inflammation is always a body's response to some underlying condition. The cholesterol hypothesis argues that dietary cholesterol is the important factor causing heart disease.
My argument specifically is not that inflammation causes heart disease and dietary cholesterol does not. That seems to be what you were arguing against.
>The cholesterol hypothesis argues that dietary cholesterol is the important factor causing heart disease.
We know from studies that if you get your LDL low enough, such as <50 (and don't have high Lp(a)), you not only see plaque stop being deposited, you even see regression of existing soft plaque, regardless of other factors like inflammation. MR studies show people that don't produce LDL/Lp(a) in significant quantities basically just don't die of atherosclerosis related heart-disease.
We have medications that can lower systemic inflammation, but local inflammation can still allow for plaque deposition in the presence of high LDL/Lp(a) and can be caused by a wide variety of things, and then plaque deposition itself causes more local inflammation via foam cells and cytokines.
We have medications today that let us drive LDL down to extremely low levels - combo statin/pcsk9 inhibitors, statin/ezetimibe/bempedoic acid, etc. - and the current evidence points towards doing this as being extremely efficacious for prevent atherosclerosis without significant side effects. Lp(a) isn't as great of a story yet - the pcsk9 inhibitors do make a ~30% dent in it, but we have other meds in phase 3 trials right now that are more like 80-90%. We're going to be able to remove the vast majority of atherogenic particles from the bloodstream well before we have any way to prevent all of the potential ways your endothelial walls can be inflamed (if that will ever even be possible.)
What I’m arguing against is the form of the argument you’re making when you say:
> If the data here is correct and inflammation is a better indicator of heart disease than cholesterol levels, it should raise questions whether cholesterol levels are correlative rather than causal.
But, as with the asbestos and smoking example, I don’t think an argument with this structure is valid. What I’m arguing against is your claim that the existence of one exposure/outcome relationship with a stronger association entails casting doubt on other exposures’ relationship with the same outcome.
Does that make sense, and do you have a good argument as to why we should believe that it casts doubt?
I don't think anyone would argue that inflammation is a cause of heart disease. Inflammation is always a body's response to some underlying condition. The cholesterol hypothesis argues that dietary cholesterol is the important factor causing heart disease.
My argument specifically is not that inflammation causes heart disease and dietary cholesterol does not. That seems to be what you were arguing against.