Three main saturated fats raise your cholesterol
empirical.health
empirical.health
And it's an area where there is legitimate nuance: we only measure LDL-C partly because it's easy and available, there are other ways of looking at blood lipid particles we could be measuring that might be more effective (like ApoB), it interacts with other things like insulin, inflammation, metabolic health, blood pressure.
But all that said, the case for high LDL being bad for heart attacks and strokes is very strong.
To me the strongest short list of evidence is simply:
- People who have familial hypercholesterolemia, from different genetic causes/pathways, all have massively increased heart disease at young ages.
- People who naturally have a disabled PCSK9 gene have extremely low LDL levels, where PCSK9 is directly involved in the liver's ability to clear LDL from blood, and these people also have incredibly low incidence of heart disease.
- Modifying cholesterol levels via PCSK9 or statins both have very strong evidence that they work on people who have heart disease, we have many RCT involving people who have already had one heart attack, and they have clear dose response curves: the amount of LDL reduction is directly proportional to risk reduction. We have less clear evidence on healthy people and from diet but those people are just a lot harder to study.
It's true that not everyone with high LDL develops plaque and we don't know why, but I feel a lot of "lipid hypothesis skeptics" tend to swim around in the gray areas and just don't interact with the more smoking gun bits of evidence that have to be explained away if you are going to say that LDL has no effect.
Seeing as the threat is calcium build-up in the arteries, and because cholesterol is a vital component of health, I believe that if you are in good health, and don't have a history of heart-disease, or have diabetes or other auto-immune disease which increases risk of atherosclerosis, lowering cholesterols is an in direct measure.
It's about understanding your personal risk and making decisions based on that.
First of all, I agree with your points that you should consider the individual. My long term interest in this is also from being a very fit, low blood pressure, metabolically healthy person who always had at least somewhat elevated LDL (sometimes very elevated) that doctors would flag.
PCSK9 people are as close to a natural experiment on the effects of life time low LDL as you will get and they get near total protection, even when they have no other risk factors. People like smokers, hypertensives and diabetes have ~90% less than other high risk people, but people without any of those factors also have significantly less heart disease. People with two broken PCSK9 genes have close to zero LDL and have noticeably completely plaque free arteries as adults. I do think this does pretty fatal damage to the theory that you must have some other health issue for LDL to be bad.
It's very likely that "LDL-C" the lab measurement isn't as good as measuring ApoB, but for most people, they are concordant. And ApoB is a different way of looking at low density lipids, by particle count instead of weight. Dietary stuff like the fats in the article that lowers LDL measurements typically also lowers ApoB in most people.
So, in part, I agree that more precise biomarkers can help adjust individual risk. But most people are concordant. And the evidence that the underlying "low density lipids", no matter how you measure them, are causally part of the disease process is very strong.
i'm not sure i follow this extrapolation from low-ldl individuals to any direct statement about causes and effects at higher ldl levels.
if there was, for instance, some thought-harmless virus endemic to a large portion of the population which somehow caused plaque buildup but only at sufficiently high ldl levels, people with naturally low levels their entire lives would still have plaque free arteries and we would still, as we do, see a broader range of plaque buildup among people with high levels. how do you propose to distinguish this hypothetical (and admittedly most likely biologically incoherent) explanation from yours by only looking at people with naturally low levels?
your assertion that such individuals are an excellent approximation to an experiment on the arterial health effects of lifetime low ldl seems reasonable enough, but you then appear to draw unfounded conclusions about the nature of potential inverse effects at higher ldl levels.
You are correct that it doesn't rule out lipids + unknown additional factor(s). However: If there is a mystery factor, it must be close to universal. We know from autopsy studies of non-cardiac deaths that fatty streaks are present in virtually all children and that by 30 most people have advanced fibrous plaques (including soft plaque invisible to calcium score tests). The double variant people don't. So LDL is at minimum a necessary, limiting factor.
It also doesn't exclude that there is some more specific subset of the low density lipids that cause problems (this is what switching to ApoB testing is supposed to get at). Which is actually where we are at in the first place with LDL-C measurement being a refinement over previously looking at total cholesterol.
The challenge is that some people, like myself, have outrageously high LDL, yet no calcium build-up in arteries via calcium score testing.
This is why ApoB is the newer more common test. Molecules containing ApoB can stick to the walls of arteries, and the theory is that the more ApoB molecules in the blood, the more likelihood of a molecule sticking and then becoming calcified.
If you have an auto-immune disease or diabetes, which increases the amount of time it takes for tears in the arteries to repair, you have a longer exposure time of fats sticking to the arterial walls which increases the likleihood of calcifying.
However, that doesn't mean that everyone with high LDL and high ApoB are at higher risk.
This is why I went for the calcium score. Don't show me the things that might lead to calcium build up later, just measure my calcium levels and let's see if I am currently at risk, and we can keep monitoring this.
Doctors are still trying to push me on to statins, but without a history of heart-disease and every other biomarker being off the charts high, I am taking that risk myself, knowing that calcium score is 0, so my suspected risk is actually very low.
Long answer, but hopefully that clarifies the understanding.
I'm not a doctor, I work in neurotech so am around health and have gone through this process myself.