4 ms·

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

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)

Aurornis 1y ago
LDL is a proxy measure that's cheap and easy to measure. It's widely used for screening despite not being perfect, which confused some into thinking it's the one and only thing measure of CVD risk. It's not, though. Many of the tests we look at are proxies and markers, not actually the sole factor for a disease. More in-depth testing would check LDL-P (particle count) and ApoB along with hsCRP. Though realistically, most people could simply look at their diet and lifestyle and work on improving both before investing in any extra testing. The testing can be useful to catch cases where genetics overwhelm even healthy lifestyles, but in many cases for younger people the testing basically serves as a wake-up call to actually do something about lifestyle and diet problems. It's easier to inspire lifestyle and diet changes when you're staring at bad numbers on the test results and getting a little preview of the consequences of your decisions.
- Maxion 1y ago
  LDL is almost always talked about as a singluar thing, even in scientific studies when LDL comes in several flavors. Large bouyant LDL is not associated with CVD risk whereas small dense LDL is. You can have high HDL, high LDL and low triglycerides. This is a pretty rare pattern, but one where you do not have increase risk of CVD. In most people, having high LDL is linked to having high small dense LDL and low aounts of large boyant LDL. Hence why LDL is used as a simple risk measure - even though it's wrong. Statins in trials show benefits for secondary events, but for primary protection statins don't actually work that well.
  - KempyKolibri 1y ago
    This doesn't really seem to pan out in reality. Often people with small dense LDL have it as a result of other risk markers. There's a good discussion here - https://www.youtube.com/watch?v=kplh30RmYo8 https://www.youtube.com/watch?v=kplh30RmYo8 - the long and short of it is that when you perform mutual adjustment for number of particles, both large and small LDL particles are associated with a fairly similar risk. But if you have the same mass of cholesterol in two individuals (LDL-c) and one has SD LDL and the other has LB LDL, the latter has fewer LDL particles and therefore lower risk, so it can appear that LB LDL are less risky if you're only measuring cholesterol mass. As for statins not working well in primary prevention, I'm not sure what you mean - the JUPITER trial showed significant risk reductions for primary prevention, for example.
    - Maxion 1y ago
      The Jupiter trial clearly stated that those with low hs-crp didn’t benefit from LDL-C reduction, only those with high hs-crp had reduced CVD events due to LDL-C reduction.
      - KempyKolibri 1y ago
        The claim I was addressing was that we don’t have evidence of statin efficacy for primary prevention. My point was that JUPITER seems to be evidence this isn’t the case.
llm_nerd 1y ago
> If you have normal cholesterol though - we have long known that people with normal cholesterol also have heart attacks. Just to continue on this line, we also know that people with a genetic disposition for low cholesterol have a significantly lower risk of coronary heart disease than people with ostensibly normal cholesterol levels. It is one of the most proven, obvious correlations (more cholesterol increases the incident of CHD) in medicine. Some snake-oil merchants, usually pitching a book or supplement, have often tried to muddy the waters by pointing out that someone at death's door often has very low cholesterol (they usually aren't eating, and cancer often "eats" cholesterol and leads to low levels), trying to then extrapolate this out.
- FollowingTheDao 1y ago
  These people with genetically low cholesterol, however, have other issues. Familial hypobetalipoproteinemia (FHBL) is a disorder that impairs the body's ability to absorb and transport fats. Many individuals with FHBL develop an abnormal buildup of fats in the livercalled hepatic steatosis or fatty liver. You have to understand the point which you’re not yet able to put in your head. Yes it is true that lowering cholesterol lowers cardiovascular disease. No one here is disagreeing with that. What we are explaining is that cholesterol alone does not cause heart disease. It is cholesterol plus inflammation that causes heart disease. I don’t know why this is so hard to understand. Lowering inflammation not only would reduce cardiovascular disease, but also cancer, arthritis and a multitude of other diseases.
  - llm_nerd 1y ago
    >These people with genetically low cholesterol, however, have other issues Neat. >You have to understand the point which you’re not yet able to put in your head Nowhere did I ever dismiss other causative inputs. All I did was reply to some probably-listen-to-chiropractor people who sure are trying incredibly hard to downplay cholesterol.
    - FollowingTheDao 1y ago
      If one person with high cholesterol does not get heart disease then cholesterol is not the problem. Fact. Logic. Why don’t you stop your appeal to authority arguments and focus on the facts. It’s not that I haven’t died yet either. My calcium artery score was zero. I have no plaque in my arteries and I’ve had high cholesterol for probably 30 years of my life because of my genetics. If that is not interesting to you then you have an odd bias. I merely saying that inflammation is the risk factor that matters more than high cholesterol. You can lower cholesterol for someone who has high inflammation and reduce heart disease, but reducing inflammation is more important overall.

Aurornis 1y ago

LDL is a proxy measure that's cheap and easy to measure. It's widely used for screening despite not being perfect, which confused some into thinking it's the one and only thing measure of CVD risk. It's not, though. Many of the tests we look at are proxies and markers, not actually the sole factor for a disease. More in-depth testing would check LDL-P (particle count) and ApoB along with hsCRP. Though realistically, most people could simply look at their diet and lifestyle and work on improving both before investing in any extra testing. The testing can be useful to catch cases where genetics overwhelm even healthy lifestyles, but in many cases for younger people the testing basically serves as a wake-up call to actually do something about lifestyle and diet problems. It's easier to inspire lifestyle and diet changes when you're staring at bad numbers on the test results and getting a little preview of the consequences of your decisions.

Maxion 1y ago
LDL is almost always talked about as a singluar thing, even in scientific studies when LDL comes in several flavors. Large bouyant LDL is not associated with CVD risk whereas small dense LDL is. You can have high HDL, high LDL and low triglycerides. This is a pretty rare pattern, but one where you do not have increase risk of CVD. In most people, having high LDL is linked to having high small dense LDL and low aounts of large boyant LDL. Hence why LDL is used as a simple risk measure - even though it's wrong. Statins in trials show benefits for secondary events, but for primary protection statins don't actually work that well.
- KempyKolibri 1y ago
  This doesn't really seem to pan out in reality. Often people with small dense LDL have it as a result of other risk markers. There's a good discussion here - https://www.youtube.com/watch?v=kplh30RmYo8 https://www.youtube.com/watch?v=kplh30RmYo8 - the long and short of it is that when you perform mutual adjustment for number of particles, both large and small LDL particles are associated with a fairly similar risk. But if you have the same mass of cholesterol in two individuals (LDL-c) and one has SD LDL and the other has LB LDL, the latter has fewer LDL particles and therefore lower risk, so it can appear that LB LDL are less risky if you're only measuring cholesterol mass. As for statins not working well in primary prevention, I'm not sure what you mean - the JUPITER trial showed significant risk reductions for primary prevention, for example.
  - Maxion 1y ago
    The Jupiter trial clearly stated that those with low hs-crp didn’t benefit from LDL-C reduction, only those with high hs-crp had reduced CVD events due to LDL-C reduction.
    - KempyKolibri 1y ago
      The claim I was addressing was that we don’t have evidence of statin efficacy for primary prevention. My point was that JUPITER seems to be evidence this isn’t the case.

llm_nerd 1y ago

> If you have normal cholesterol though - we have long known that people with normal cholesterol also have heart attacks. Just to continue on this line, we also know that people with a genetic disposition for low cholesterol have a significantly lower risk of coronary heart disease than people with ostensibly normal cholesterol levels. It is one of the most proven, obvious correlations (more cholesterol increases the incident of CHD) in medicine. Some snake-oil merchants, usually pitching a book or supplement, have often tried to muddy the waters by pointing out that someone at death's door often has very low cholesterol (they usually aren't eating, and cancer often "eats" cholesterol and leads to low levels), trying to then extrapolate this out.

FollowingTheDao 1y ago
These people with genetically low cholesterol, however, have other issues. Familial hypobetalipoproteinemia (FHBL) is a disorder that impairs the body's ability to absorb and transport fats. Many individuals with FHBL develop an abnormal buildup of fats in the livercalled hepatic steatosis or fatty liver. You have to understand the point which you’re not yet able to put in your head. Yes it is true that lowering cholesterol lowers cardiovascular disease. No one here is disagreeing with that. What we are explaining is that cholesterol alone does not cause heart disease. It is cholesterol plus inflammation that causes heart disease. I don’t know why this is so hard to understand. Lowering inflammation not only would reduce cardiovascular disease, but also cancer, arthritis and a multitude of other diseases.
- llm_nerd 1y ago
  >These people with genetically low cholesterol, however, have other issues Neat. >You have to understand the point which you’re not yet able to put in your head Nowhere did I ever dismiss other causative inputs. All I did was reply to some probably-listen-to-chiropractor people who sure are trying incredibly hard to downplay cholesterol.
  - FollowingTheDao 1y ago
    If one person with high cholesterol does not get heart disease then cholesterol is not the problem. Fact. Logic. Why don’t you stop your appeal to authority arguments and focus on the facts. It’s not that I haven’t died yet either. My calcium artery score was zero. I have no plaque in my arteries and I’ve had high cholesterol for probably 30 years of my life because of my genetics. If that is not interesting to you then you have an odd bias. I merely saying that inflammation is the risk factor that matters more than high cholesterol. You can lower cholesterol for someone who has high inflammation and reduce heart disease, but reducing inflammation is more important overall.