For decades, LDL cholesterol has been the main target in preventive heart health.
The American College of Cardiology just started recommending that everyone measure hs-CRP, a blood test for inflammation. Why? Because inflammation now predicts cardiovascular events more accurately than cholesterol — especially in people already on statins or those without traditional risk factors.
In some ways, cholesterol has become a victim of its own success. With routine screening and statins, most heart attack patients now have artificially lowered cholesterol. That leaves the remaining risk hidden in non-traditional biomarkers — beyond the usual SMuRFs (standard modifiable risk factors).
Thanks for the summary! I haven’t read tfa yet, so my apologies if this is answered in there, but: does this mean that we’ve already reduced the contribution from cholesterol to events? Or that cholesterol was simply associated and not causative? I imagine the truth is somewhere in between, perhaps we can guess that’s it’s 70% due to one and 30% due to the other?
> The ACC is now recommending that everyone measure inflammation (specifically, hs-CRP)
Burying the lede a little, here. The ACC has decided on a standard way to measure inflammation, which decades ago was a centerpiece of some very woo-woo "following the squizledoff diet will decrease your gomperblorp"-style health 'advice'. "Systemic inflammation" was a very tricky physiological parameter to nail down.
I have genetically high cholesterol. But otherwise I exercise quite a lot and healthy. I’ve been told not to worry about cholesterol unless other indicators start to climb. So I just generally avoid high saturated fat foods (sat fat in food matters more to blood cholesterol than food cholesterol).
Anyone know how weight lifting might be related to this?
Weight lifting causes short bursts of inflammation right after training, which is part of the repair process. But in general it is considered very beneficial.
Curious about infliximab being unhelpful or even harmful for cardiovascular risk; I'm not sure if there were any confounding factors re. people on infliximab not generally being in great health to begin with. But back when I was on infliximab I had some not-awesome systemic side effects, so I wouldn't be chocked if it's just not great for your cardiovascular health in general. (And that's still probably a worthwhile tradeoff if you're the kind of person who's being prescribed infliximab.)
Before you assume that LDL isn’t a good biomarker, read the entire article. Specifically this section:
> Why? In some ways, cholesterol has become a victim of its own success. We now screen the whole population for high cholesterol, give statins to those with high LDL (or ApoB), and so then the majority of people who end up having heart attacks have lower cholesterol than they would naturally have
In other words, in the study population patients who would have had high LDL were likely to be on statins. The had a lower measured LDL value even though they might still be consuming a poor diet and living an unhealthy lifestyle, for example. Statins don't fix everything about poor diet and lifestyle, but they do help with cholesterol.
So don’t go throwing LDL out yet. It’s still the best measure we have, though you should obviously know that LDL measured while on statins is lower than it would be normally.
The headline, therefore, is somewhat clickbait from a company trying to sell these tests to you outside of your insurance. I recommend checking your insurance to see if the tests would be covered before you go the self-pay route.
Edit to add: If your doctor won't order hs-CRP for some reason, you can order it from sites like privatemdlabs.com for $50 (less if you take their 25% off coupon).
> In other words, in the study population patients who would have had high LDL were likely to be on statins. The had a lower measured LDL value even though they might still be consuming a poor diet and living an unhealthy lifestyle, for example. Statins don't fix everything about poor diet and lifestyle, but they do help with cholesterol.
The implication here is that the LDL-lowering effect of statins is greater than the CVE-reducing effect of statins. That is, if the statins lower your LDL by 30%, that doesn't bring your risk of heart disease the to the same level as someone who naturally has an identical lower LDL.
There is a theory that cholesterol elevates in response to circulating endotoxin (dead bacteria cell walls).
Lipoproteins can bind to the endotoxin, and clear it or at least stop immune cells from reacting to it.
This response increases LDL, but decreases the immune activity that would otherwise be created by letting the endotoxin circulate.
So LDL is a defense mechanism against the body's own response to circulating endotoxin as well as the endotoxin itself.
If true, that would explain the link between inflammation, LDL, and heart disease.
It would also imply that the circulating endotoxin is the thing to target.
I wonder where all the dead bacteria cell walls are coming from, probably where the dead bacteria are.
That, of course, is the gut.
I don't remember the original paper, but I found something that at least explains the theory here.
Cholesterol -> Coronary plaque -> Dormant bacteria within the plague biofilm is shielded from the immune system and antibiotics. When it ruptures, bacteria is released, sudden death.
>Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies.
Interesting that official recommendations are catching up to what some clinicians on the edge have been saying for years: inflammation may be a stronger predictor of heart disease than cholesterol. Clinician-authors like Dr. Gundry (who blame lectins/diet) have long argued inflammation is central, though their theories are more controversial and less trial-backed.
The argument, as I recall, is that the inflammation causes your body to want to treat the inflamed area and when coupled with cholesterol causes "cholesterol Band-Aids" to be plastered all over your arteries. The argument is that if you remove the inflammation, the cholesterol is not important because it's not trying to be made into a Band-Aid.
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This isn't surprising, and its refreshing to see more research that questions the cholesterol hypothesis finally gaining some traction.
You only have to read up on the history of how the cholesterol hypothesis came about to realize the science behind it was poorly defined, poorly tested, and arguably counterfeited as data was cherry picked.
I am extremely skeptical about the need for this kind of shotgun "health marker" blood panel test. Even granting the premise that whatever ML algorithm they use to interpret the results is at all accurate, the upshot is unlikely to change the general recommendations regarding heart disease anyway (control blood pressure, stop smoking, manage diabetes or pre-diabetes, maintain a healthy diet and meet the physical activity guidelines).
If I'm being extra charitable, this kind of test might show up an elevated Lp(a) level, which is a risk factor. At which point you would want to consult a qualified physician, not rely on a single blood test interpreted by an algorithm.
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[ 4.1 ms ] story [ 50.7 ms ] threadThe American College of Cardiology just started recommending that everyone measure hs-CRP, a blood test for inflammation. Why? Because inflammation now predicts cardiovascular events more accurately than cholesterol — especially in people already on statins or those without traditional risk factors.
In some ways, cholesterol has become a victim of its own success. With routine screening and statins, most heart attack patients now have artificially lowered cholesterol. That leaves the remaining risk hidden in non-traditional biomarkers — beyond the usual SMuRFs (standard modifiable risk factors).
TLDR: women who would otherwise be missed by current algorithms might be picked up by this inflammatory marker (hs-CRP)
Burying the lede a little, here. The ACC has decided on a standard way to measure inflammation, which decades ago was a centerpiece of some very woo-woo "following the squizledoff diet will decrease your gomperblorp"-style health 'advice'. "Systemic inflammation" was a very tricky physiological parameter to nail down.
https://medium.com/@petilon/cholesterol-and-statins-e7d9d8ee...
Weight lifting causes short bursts of inflammation right after training, which is part of the repair process. But in general it is considered very beneficial.
This article might be truthful, it might not. But it is absolutely trying to sell you something.
Unknown editor
No journal? Committee? Conference?
Ew.
> Why? In some ways, cholesterol has become a victim of its own success. We now screen the whole population for high cholesterol, give statins to those with high LDL (or ApoB), and so then the majority of people who end up having heart attacks have lower cholesterol than they would naturally have
In other words, in the study population patients who would have had high LDL were likely to be on statins. The had a lower measured LDL value even though they might still be consuming a poor diet and living an unhealthy lifestyle, for example. Statins don't fix everything about poor diet and lifestyle, but they do help with cholesterol.
So don’t go throwing LDL out yet. It’s still the best measure we have, though you should obviously know that LDL measured while on statins is lower than it would be normally.
The headline, therefore, is somewhat clickbait from a company trying to sell these tests to you outside of your insurance. I recommend checking your insurance to see if the tests would be covered before you go the self-pay route.
Edit to add: If your doctor won't order hs-CRP for some reason, you can order it from sites like privatemdlabs.com for $50 (less if you take their 25% off coupon).
I'm quite sure we would still see that cholesterol is useless and that inflammation drives everything.
The implication here is that the LDL-lowering effect of statins is greater than the CVE-reducing effect of statins. That is, if the statins lower your LDL by 30%, that doesn't bring your risk of heart disease the to the same level as someone who naturally has an identical lower LDL.
If true, that would explain the link between inflammation, LDL, and heart disease. It would also imply that the circulating endotoxin is the thing to target. I wonder where all the dead bacteria cell walls are coming from, probably where the dead bacteria are. That, of course, is the gut.
I don't remember the original paper, but I found something that at least explains the theory here.
https://www.sciencedirect.com/science/article/abs/pii/S01406...
Cholesterol -> Coronary plaque -> Dormant bacteria within the plague biofilm is shielded from the immune system and antibiotics. When it ruptures, bacteria is released, sudden death.
Viridans Streptococcal Biofilm Evades Immune Detection and Contributes to Inflammation and Rupture of Atherosclerotic Plaques https://www.ahajournals.org/doi/10.1161/JAHA.125.041521
>Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies.
I exercise an hour a day (resistance + cardio), eat a diet of nothing but meat + vegetables + yogurt.
Will post my lipids below. Sometimes you just get fucked by life.
https://i.imgur.com/r0nfUo3.png
For those that won't view the image:
The argument, as I recall, is that the inflammation causes your body to want to treat the inflamed area and when coupled with cholesterol causes "cholesterol Band-Aids" to be plastered all over your arteries. The argument is that if you remove the inflammation, the cholesterol is not important because it's not trying to be made into a Band-Aid.
You only have to read up on the history of how the cholesterol hypothesis came about to realize the science behind it was poorly defined, poorly tested, and arguably counterfeited as data was cherry picked.
If I'm being extra charitable, this kind of test might show up an elevated Lp(a) level, which is a risk factor. At which point you would want to consult a qualified physician, not rely on a single blood test interpreted by an algorithm.