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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).

There have always been people with high LDL who lived to a very old age and finally died of something other than a heart attack (nobody knows why). Still high LDL after controlling for everything we can think of (cholesterol is cheap to measure so we have a lot of data!) is a strong sign of a future heart attack and so anyone with high LDL should talk to their doctor: there is good reason to think statins will reduce your chance of a heart attack. Which why we measure it and control it.

If you have normal cholesterol though - we have long known that people with normal cholesterol also have heart attacks. It isn't as common as people who have high cholesterol, but it is still very common for someone normal cholesterol to have a heart attack. We don't really know what to do about this though. This article is saying we should measure inflammation and if found deal with it. Seems reasonable.

What isn't known is if we deal with inflammation will heart attacks go away or if there are more factors. If there are more factors we don't know what they are or if they are worth measuring/treating (though some researchers may have data they are trying to get out here). If dealing with inflammation is good, can we start ignoring cholesterol - another unknown (one for researchers to look into, but the rest of us should for now say no cholesterol is independently important - until data says otherwise)

(OP here) LDL is still a good biomarker, but ApoB is a better biomarker for the same undelrying risk factor -- each atherogenic particle (LDL, VLDL, IDL) has exactly one ApoB molecule.

The reason we offer the tests as cash pay is that it's the only way we can guarantee the price. In the past, when we've gone through insurance, the insurer's "negotiated rate" for the same exact panel comes out to $1,400-$1,500. If the insurer later decides to deny coverage for any of the tests, it's more expensive for the patient.

The $190 price is negotiated to be pretty low. It includes hs-CRP ($59 by itself online), but also the other major heart health biomarkers: ApoB ($69), Lp(a) ($49), A1c ($39), lipid panel ($59), eGFR ($99), other biomarkers, and a video consultation with a doctor to actually explain the results and what to do about them.

For hs-CRP in particular, it's not covered under the ACA as a preventive benefit, so you would usually need to hit your deductible before insurance kicks in at all. (That's assuming they count it as medically necessary at all -- for example, Aetna's current medical policy for hs-CRP requires 2 risk factors, LDL in a specific range, and overall cardiovascular risk to be in a certain range or the claim would simply be denied). It's possible this will change over time as the ACC/AHA recommend universal screening, and I hope it does, but it's a relatively a slow process since it depends on the US Preventive Services Task Force to issue a formal recommendation.

LDL levels is too complex to be used as the litmus test it has become.

This might dependent on how much you care about false positives and pushing wrong advice to people, but the difference in levels in non Caucasian ethnies in particular is kind of ignored in most directives.

When looking deeper into it, it's a lot more complex than a simple "higher than X is market for Y". For instance:

https://www.ahajournals.org/doi/10.1161/01.atv.19.9.2234

> In conclusion, we have found an ethnic difference in the LDL size distribution, with African Americans having the highest LDL size (“less atherogenic”) and Hispanics having the lowest LDL size; these ethnic differences in LDL size, however, appear to be primarily due to differences in triglyceride and HDL cholesterol among the ethnic groups. Similar variables (triglyceride, HDL cholesterol, insulin resistance, etc) appear to be related to LDL size in these ethnic groups. Last, ethnic differences in LDL size are not consistent with previously reported differences in their risk of CVD or atherosclerosis; in fact, the ethnic differences in LDL size may be opposite the CVD risk differences by ethnic group.

The problem I'm seeing here in Norway is that the bar to put people on statins is way too low given the severe side-effects and likely consequences of long-term statin use, even low doses.

I think LDL is a good biomarker, just not in isolation, and especially not a "one-size fits all" metric for individual humans.

> 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.

I'm not a doctor, but doesn't LDL basically just prevent the body from healing damage to the epithelium, which comes from things like high blood pressure and inflammation? Unless my understanding is wildly off base, it doesn't really make sense that a thing that merely slows down the healing process would be more predictive than the things causing the damage in the first place, given that if you aren't accumulating significant damage then your levels of cholesterol are somewhat moot.

LDL has a u shaped association with mortality , just like bmi. Statins have a lot of side effects also, lots of muscle toxicity.
> 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.

But if they have lower cholesterol and still have a heart attack, then certainly the causal link is not quite there. It seems you’re suggesting it’s a good proxy measurement if untampered by statins though
There is a detailed lipid panel (Lipofraction NMR) as along with the HDL/LDL/TriG estimates they get today. There is a lot more detail in there. Statins help reduce LDL but the detailed lipid panel may still show a very high level of LDL-P and Small LDL-P which still increase risk.

If you're going for more testing, I would definitely suggest the lipofraction.

It should be extremely easy to take this into consideration, and create cohorts of people who were not on a statin.

I'm quite sure we would still see that cholesterol is useless and that inflammation drives everything.

If you're already on statins, they may be lowering your hs-CRP. Still have that conversation with your dr.
You forgot to mention that statins are an anti-inflammatory as well. This argument itself fails on that
when a measure becomes a target etc etc
ApoB is the best measure we have.
Yes, LDL is the best we have since they won’t bother to measure oxidative stress nor inflammation in the human body.

But lowering your LDL does not prevent heart disease. There are many many people with normal LDL who have heart attacks.

In fact, it is the norm. And I can’t imagine how many people are being told. They have no heart disease risk just because their LDL is normal. It’s a crime and it needs to be stopped.

https://www.uclahealth.org/news/release/most-heart-attack-pa...

A new national study has shown that nearly 75 percent of patients hospitalized for a heart attack had cholesterol levels that would indicate they were not at high risk for a cardiovascular event, based on current national cholesterol guidelines.

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.

https://www.sciencedirect.com/science/article/abs/pii/S01406...

Why would a significant part of the population have dead bacteria circulating throughout their bloodstream? Bacteria live and die in the gut regularly, so it seems exceptional that parts of it would enter circulation and somehow avoid metabolism.

This also doesn't seem to consider how many people have altered cholesterol status due to genetics. An interesting theory, but if it were proven true, I imagine its effect on public health would be limited to a narrow subset of individuals.

Saw this the other day which may tie in with what you're saying? "Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture" : https://pubmed.ncbi.nlm.nih.gov/24917599/
I'm wary of trusting new health science from a company trying to sell me the cure to what they just discovered was the _real cause_ of my ills.

This article might be truthful, it might not. But it is absolutely trying to sell you something.

Cholesterol can hide your inflammation.

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.

Does "inflammation" refer to a general systemic thing? Or does this refer to something specific such as tendonitis or inflammation due to injury?
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).
Is this an advertisement? There's a CTA for a $190 service above the fold.
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.

This is the study that finally confirms what a lot of people in the health/bio-hacking space have suspected for years! It’s not that cholesterol is irrelevant—it's still a primary risk factor—but it's clear it's only half the story.

The headline makes sense because we've been treating the symptom (high cholesterol) so effectively with statins that for the remaining group of heart attack victims, the real driver is something else entirely: chronic inflammation.

Essentially, high LDL provides the "gunk" for the plaque, but the plaque doesn't become dangerous until inflammation sets in and makes that plaque unstable enough to burst. If your arteries are calm, that cholesterol is less likely to kill you.

The huge win here is the marker: hs-CRP (High-Sensitivity C-Reactive Protein). It's affordable, widely available, and now, officially a critical measure. If your LDL is fine but your hs-CRP is elevated, you have a massive, unaddressed "residual risk."

I hope this pushes doctors to run that test routinely. For us, the message is clear: reducing systemic inflammation through diet, sleep, and stress management is now a non-negotiable part of heart health, even if your lipid panel looks great.

So statins lower LDL; what lowers inflammation?
28 years old, had a heart attack last weekend (inferior STEMi)

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:

  LDL: 72
  HDL: 23
  Triglycerides: 49
  Apo(B): 85
No, you are all victims of a massive scheme to treat your poor habits with medications which wont create metabolic health. Stop eating all highly processed foods, like protein bars, restaurant foods cooked in seed oils and vegetables laced w pesticides. Eat pasture cattle, chicken, turkey, mozzarella, and organic fruit only. Cook in tallow or ghee only. Olive oils are fake. No more processed sugar. Learn to play pickleball, and make friends that bike, walk and are active. You will die from the normal American diet before retirement.Statins cause diabetes, GLP-1 50% reduction and Alzheimers per the CDC.
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.

is there something akin to a continuous glucose monitor but for inflammatory biomarkers? it would be so dope to be able to watch your body respond in real time to the foods you eat the way you can with a cgm
It’s important to note that hsCRP and C Reactive Protein are 2 different tests.
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.)
I am an Empirical Health customer, and the app has numerous bugs. Please, fix them before blogging! Thank you for your attention to this matter. MAKE APPS GREAT AGAIN!
> 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.

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.

It always did... even the way cholesterol recommendations have been aren't really good in and of themselves. The better marker is Triglyceride to HDL ratio, in terms of correlation to morbidity. Not total, not LDL by itself without quality tests.
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.

Very interesting recommendation - very much in line with this paper from a few weeks ago: https://pubmed.ncbi.nlm.nih.gov/40878356/

TLDR: women who would otherwise be missed by current algorithms might be picked up by this inflammatory marker (hs-CRP)

So does this mean apoB or hs-CRP is a better predictor of heart disease?
What about GLP-1 antagonists to lower inflammation / hs-CRP?
Cholesterol and statins have always been suspect science in any case:

https://medium.com/@petilon/cholesterol-and-statins-e7d9d8ee...

Single author

Unknown editor

No journal? Committee? Conference?

Ew.

How do you measure inflammation !
This is now a thing because of the covid vax no less
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).

This is clearly now a thing due to the covid "vaccine" myocarditis, pericarditis