How old are you? I'm not a doctor, but my impression is treatment for cholesterol is not considered worth it until you are "older". Depending on how high, older can range from 35 to 50. (actually a better marker is probably when did your grandparents have heart attack, start treating somewhat before then). Which is to say get regular checkups because you will likely be put on treatment in the future, but not today.
Again, I'm not a doctor. I talk to my doctor and see what others hear from their doctors and am able to make some educated guesses off of that.
The guidance has been changing significantly over the past few years. The consensus from expert organizations is now that we should be lowering it far earlier.
To the point of the original article, the consensus is probably doing people more harm than good. My mother had a heart attack at 45. My brother died of a heart attack at 48 and my other brother had a heart attack at 47. My cholesterol has been over 200 for at least 15 years and I’m in my late 50s. My calcium artery scan was zero and all heart sonograms are perfect.
I would worry more about HDL than LDL first of all, because HDL is an antioxidant. And it’s about the oxidative stress, which is only another term for inflammation, that we should be concerned about.
So why did I not get heart disease? Everyone else in my family smoked that had heart disease for a much longer period than I did. I only smoked for about five years when I was younger, but everyone else smoked for over 15.
So it wasn’t cholesterol that killed my brother. It was the smoking that caused inflammation on the body that oxidized the cholesterol that killed him.
Anecdotal data does not disprove the millions of data points from well controlled well structured RCTs that have been poured over by the brightest minds in the field.
The positive impact of lowering LDL is some of the strongest science we have on health.
The dismissal of anecdotal data is why science has been stalled and people are still sick.
The fact that you don’t care if one person who has high, LDL does not get heart disease is emblematic of the problem in healthcare. If one person who has high, LDL does not get heart disease then high LDL alone does not cause heart disease. There is amounts of evidence that LDL on its own, when it is not oxidized by inflammation, does not cause heart disease is something you’re consistently overlooking.
Again, and I don’t know why I have to repeat this, but I know that Laura LDL decreases cardiovascular disease risk, but that is only because if you have lower amounts of oxidized LDL, then you won’t get heart disease. But what do we want to lower, the LDL, which is needed by the body or the oxidative stress and inflammation which damages the LDL we need for our body?
High LDL or Lp(a) on its own causes enough localized inflammation to continue plaque deposition. We can’t drive down every cause on inflammation to 0 to the point that there is zero plaque deposition at all in the presence of high LDL, there are just too many causes. Even temporary increases in inflammation from natural processes can deposit plaque is you have high amounts of atherogenic particles. And once they deposit, they begin to cause inflammation independently. Not all inflammation can be measured by hsCRP.
Inflammation is an important causal factor for sure, and persistent high levels of inflammation will drive even more deposition of plaque.
Your body does not need serum LDL in significant quantities. I’ve commented in this post multiple times with studies that show that even driving LDL down below 20 has no impact to the systems that use LDL that people are concerned about. All of the related organs can do de novo synthesis, make use of HDL instead, etc. People that do not produce LDL at all that ends up in the bloodstream still produce all of their necessary hormones at normal rates, the brain still produces it locally de novo, etc.
No one thinks LDL and Lp(a) are the sole factors in heart disease. We know of plenty that are unrelated - blood pressure, LVH, etc. etc. etc.
But lowering LDL is one of the most powerful and broad spectrum tools we have at our disposal.
You mean the positive impact of consuming statins. Consuming statins coincides with lower LDL so I can imagine people conflating the two variables. I'm sure taking statins also has other effects on the body.
No, I mean the positive impact of lowering LDL. Statins of course show positive impact, and yes, including from also lowering inflammation. But so do other drugs that lower LDL through other mechanisms, including ezetimibe, bempedoic acid, and pcsk9 inhibitors. MR studies on genetics also show that lower LDL even without other factors that reduce inflammation significantly reduces the risk of of negative ASCVD outcomes.
Even from the inflammation standpoint, we know that lowering LDL has a causal effect on lowering inflammation in your arteries - plaque being deposited results in foam cell activation and cytokine signaling which directly increase localized inflammation which can then result in additional plaque deposition.
This is also just extremely well understood mechanistically - to have plaque deposited in your arteries, you have to have something that deposits it. This comes primarily from LDL in most individuals - though Lp(a) is a largely genetically driven carrier of atherogenic particles as well, which is why ApoB is a better measure - and with less LDL there is simply less to be deposited.
The idea that LDL is not a directly causal factor for ASCVD is one goes against mountains of evidence and the consensus of the absolutely overwhelming majority of experts in the field. That is not the same as them saying it is the only causal factor - but people trying to argue that LDL isn't causal have a huge burden of proof on them. This is some of the most studied science in health.
Heart disease progresses over decades and there's no solid evidence it can be reversed. You don't want to wait til you're 18 months out from a heart attack to do anything. I don't think this is good advice
> Heart disease progresses over decades <...> You don't want to wait til you're 18 months out from a heart attack to do anything. I don't think this is good advice
Correct. The idea is commonly referred to as "LDL-C Burden"
We do see good evidence of soft-plaque regression with very low levels of LDL-C, generally in patients undergoing high dose statin therapy or combo therapy.
Again, I'm not a doctor. I talk to my doctor and see what others hear from their doctors and am able to make some educated guesses off of that.