4 ms·

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, old

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.

deleted 1y ago
[deleted]
softwaredoug 1y ago
In my 40s
- bluGill 1y ago
  It would be worth checking to be sure your doctor is up to date. The other reply suggests younger is the latest - but I'm not a doctor.
cthalupa 1y ago
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. https://www.lipidjournal.com/article/S1933-2874%2825%2900317-4/fulltext https://www.lipidjournal.com/article/S1933-2874%2825%2900317...
- FollowingTheDao 1y ago
  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.
  - cthalupa 1y ago
    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.
    - nmsmith 1y ago
      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.
      - cthalupa 1y ago
        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.
    - FollowingTheDao 1y ago
AstroBen 1y ago
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
- cthalupa 1y ago
  > 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" https://jamanetwork.com/journals/jamacardiology/fullarticle/2784038 https://jamanetwork.com/journals/jamacardiology/fullarticle/... > no solid evidence it can be reversed 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. https://www.jacc.org/doi/10.1016/j.jacc.2021.10.035 https://www.jacc.org/doi/10.1016/j.jacc.2021.10.035 https://jamanetwork.com/journals/jama/fullarticle/2584184 https://jamanetwork.com/journals/jama/fullarticle/2584184 https://pmc.ncbi.nlm.nih.gov/articles/PMC7644491/ https://pmc.ncbi.nlm.nih.gov/articles/PMC7644491/ We don't have any real evidence of effective/widely-applicable treatments to reduce calcified plaque, though.

deleted 1y ago

[deleted]

softwaredoug 1y ago

In my 40s

bluGill 1y ago
It would be worth checking to be sure your doctor is up to date. The other reply suggests younger is the latest - but I'm not a doctor.

cthalupa 1y ago

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. https://www.lipidjournal.com/article/S1933-2874%2825%2900317-4/fulltext https://www.lipidjournal.com/article/S1933-2874%2825%2900317...

FollowingTheDao 1y ago
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.
- cthalupa 1y ago
  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.
  - nmsmith 1y ago
    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.
    - cthalupa 1y ago
      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.
  - FollowingTheDao 1y ago

AstroBen 1y ago

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

cthalupa 1y ago
> 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" https://jamanetwork.com/journals/jamacardiology/fullarticle/2784038 https://jamanetwork.com/journals/jamacardiology/fullarticle/... > no solid evidence it can be reversed 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. https://www.jacc.org/doi/10.1016/j.jacc.2021.10.035 https://www.jacc.org/doi/10.1016/j.jacc.2021.10.035 https://jamanetwork.com/journals/jama/fullarticle/2584184 https://jamanetwork.com/journals/jama/fullarticle/2584184 https://pmc.ncbi.nlm.nih.gov/articles/PMC7644491/ https://pmc.ncbi.nlm.nih.gov/articles/PMC7644491/ We don't have any real evidence of effective/widely-applicable treatments to reduce calcified plaque, though.