Is it true that below 70 LDL, cholesterol deposits recede?
October 14, 2014 8:44 AM Subscribe
A friend just had a stent put in due to 100% congestion in one blood vessel (50% congestion remains in another). He's on highest Lipitor dose (80mg), which has brought LDL down to 90. Cardiologist wants to keep him on high Lipitor plus sign him up for a trial of Alirocumab (an experimental monoclonal antibody which lowers cholesterol). The goal is an LDL of 70, because doctor says at that point the body starts a reverse process of removing cholesterol, thereby reducing the congestion. I can't find any confirmation of this anywhere. Can anyone help verify or clarify?
Best answer: I think probably something got lost in the passing along of info from doctor to friend to you, but 70 or below is indeed the current, revised in 2004, recommendation.
"The reverse process of removing cholesterol" is the function that is carried out by HDL, or "good cholesterol", which is manufactured in the liver, and which picks up LDL particles, and brings them back to the liver for reprocessing or disposal as bile salts. Details. It carries out this function regardless of the LDL level; this is not something that is somehow triggered when LDL goes below 70. But it may be that when LDL is 70 or less, HDL can do its job more effectively so that the buildup of LDL in blood vessels not only slows down or stops, but goes into reverse.
posted by beagle at 9:40 AM on October 14, 2014
"The reverse process of removing cholesterol" is the function that is carried out by HDL, or "good cholesterol", which is manufactured in the liver, and which picks up LDL particles, and brings them back to the liver for reprocessing or disposal as bile salts. Details. It carries out this function regardless of the LDL level; this is not something that is somehow triggered when LDL goes below 70. But it may be that when LDL is 70 or less, HDL can do its job more effectively so that the buildup of LDL in blood vessels not only slows down or stops, but goes into reverse.
posted by beagle at 9:40 AM on October 14, 2014
A family member of mine had hereditary hypercholesterolemia which was incredibly hard to lower despite aggressive treatment. The thing that finally worked for him was adding cholestyramine powder to his regimen. It's a bile sequestering resin that lowers cholesterol by preventing reuptake of bile from the GI tract. It's worth considering if your friend is hesitant to try a more experimental drug.
posted by quince at 11:12 AM on October 14, 2014
posted by quince at 11:12 AM on October 14, 2014
The recommendations referred to in the above comments are outdated, and the latest guidelines actually downplay absolute lipid targets. Experts do not have consensus on the subject. What you are suggesting about plaque reduction and absolute LDL levels is controversial, and mostly supported by correlated data that may lack truly causal evidence. Even in studies of treatment effects on plaque reduction and LDL level, there doesn't seem to be an absolute cutoff on beneficial effects for a given LDL. Moreover, in studies looking at plaque regression, it is actually only seen in a minority of treated patients, while the beneficial effects on clinical outcomes are more far reaching.
More importantly, there have been drugs (see ezetimibe) with presumably beneficial quantitative effects on lipid profiles that have failed to actually improve meaningful clinical outcomes like death, heart failure, heart attacks, etc. Consequently, we have no idea whether treatments like alirocumab will be helpful in humans. If we did, we wouldn't be studying it. We'd be prescribing it.
I'd be somewhat distrustful of anyone who makes strong claims that an experimental treatment is going to be helpful. Just my two cents as an academic physician who enrolls patients in clinical trials for a living.
posted by drpynchon at 11:45 AM on October 14, 2014 [6 favorites]
More importantly, there have been drugs (see ezetimibe) with presumably beneficial quantitative effects on lipid profiles that have failed to actually improve meaningful clinical outcomes like death, heart failure, heart attacks, etc. Consequently, we have no idea whether treatments like alirocumab will be helpful in humans. If we did, we wouldn't be studying it. We'd be prescribing it.
I'd be somewhat distrustful of anyone who makes strong claims that an experimental treatment is going to be helpful. Just my two cents as an academic physician who enrolls patients in clinical trials for a living.
posted by drpynchon at 11:45 AM on October 14, 2014 [6 favorites]
Response by poster: drpynchon,
I followed all but the final clause in this: "Moreover, in studies looking at plaque regression, it is actually only seen in a minority of treated patients, while the beneficial effects on clinical outcomes are more far reaching." Can you clarify?
Also, I'm not clear on the distinction you're drawing here: "I'd be somewhat distrustful of anyone who makes strong claims that an experimental treatment is going to be helpful". My friend would have no interest in joining a trial, nor would a trial have him, unless the substance being tested wasn't potentially helpful. It's obvious - and was also explicitly explained - that there are no guarantees (even insofar as whether he receives placebo, after all). My understanding (perhaps incorrect) is that LDL 70 remains the widely accepted target for high risk patients (issue of regression aside). If so, his current reading of 90 does leave him shy of ideal, ezetimibe is being tested for precisely this situation, and so his enrollment still sounds reasonable (at least to my limited understanding). Do you have serious qualms, or are you just suggesting general caution in such things?
posted by Quisp Lover at 1:55 PM on October 14, 2014
I followed all but the final clause in this: "Moreover, in studies looking at plaque regression, it is actually only seen in a minority of treated patients, while the beneficial effects on clinical outcomes are more far reaching." Can you clarify?
Also, I'm not clear on the distinction you're drawing here: "I'd be somewhat distrustful of anyone who makes strong claims that an experimental treatment is going to be helpful". My friend would have no interest in joining a trial, nor would a trial have him, unless the substance being tested wasn't potentially helpful. It's obvious - and was also explicitly explained - that there are no guarantees (even insofar as whether he receives placebo, after all). My understanding (perhaps incorrect) is that LDL 70 remains the widely accepted target for high risk patients (issue of regression aside). If so, his current reading of 90 does leave him shy of ideal, ezetimibe is being tested for precisely this situation, and so his enrollment still sounds reasonable (at least to my limited understanding). Do you have serious qualms, or are you just suggesting general caution in such things?
posted by Quisp Lover at 1:55 PM on October 14, 2014
With recent studies, the LDL situation has become a little more complicated.
Somebody on a normal or low fat diet will have hard dense LDL molecules. (Pattern B)
Somebody on a low carb style diet will have light fluffy LDL molecules. (Pattern A)
The small hard ones oxidize easily and can clog arteries. The light fluffy ones don't tend to clog the arteries.
If they are on a low carb style diet (Atkins, Paleo, Low GI, etc) the count may not lower, but the type of LDL will be different and less risky.
Wikipedia link (same article as above, direct link to section)
General pattern A and B info
The same diets increase HDL levels. HDL carries the LDL away and to the liver for processing (reuse or excretion).
I have not seen numbers/studies on it, but it seems possible that a low carb diet that helped make the pattern A LDL molecules would not deposit much/any more in the arteries. The increase in HDL from the same diet ~may~ help reduce congestion by carrying away deposits. All theoretical, but it seems possible. ALL THEORETICAL.
It might help and wouldn't hurt - but I wouldn't expect too much from it.
posted by Leenie at 2:51 PM on October 14, 2014 [1 favorite]
Somebody on a normal or low fat diet will have hard dense LDL molecules. (Pattern B)
Somebody on a low carb style diet will have light fluffy LDL molecules. (Pattern A)
The small hard ones oxidize easily and can clog arteries. The light fluffy ones don't tend to clog the arteries.
If they are on a low carb style diet (Atkins, Paleo, Low GI, etc) the count may not lower, but the type of LDL will be different and less risky.
Wikipedia link (same article as above, direct link to section)
General pattern A and B info
The same diets increase HDL levels. HDL carries the LDL away and to the liver for processing (reuse or excretion).
I have not seen numbers/studies on it, but it seems possible that a low carb diet that helped make the pattern A LDL molecules would not deposit much/any more in the arteries. The increase in HDL from the same diet ~may~ help reduce congestion by carrying away deposits. All theoretical, but it seems possible. ALL THEORETICAL.
It might help and wouldn't hurt - but I wouldn't expect too much from it.
posted by Leenie at 2:51 PM on October 14, 2014 [1 favorite]
Quisp Lover, drpynchon is making a great point about experimental drugs. If a treatment wasn't at least potentially beneficial, the study could not ethically move forward, so that's not at issue, but what he's saying is that your friend needs to recognize that there are 2 potentially sketchy things about his doctor's proposal:
1. That he must reach a level of 70 for LDL by any means necessary. The new guidelines that drpynchon refers to do not emphasize this target. Here's an article without much jargon to explain further: "Doctors have long prescribed statins based on a cholesterol number, particularly the level of “bad” LDL cholesterol.
But the guidelines advise assessing factors such as age, gender, race, whether a patient smokes, blood pressure and whether it’s being treated, whether a person has diabetes, as well as blood cholesterol levels in determining their risk. They also suggest that healthcare providers may want to consider other factors, including family history. Only after that very personalized assessment is a decision made on what treatment would work best.
“Physicians now have to shift their thinking away from only looking at cholesterol levels,” said Donald Lloyd-Jones, M.D., an American Heart Association volunteer who helped write the new guidelines. “A patient’s overall risk is really the playing field on which people need to understand whether they need statin medication.”
2. That no one should be making claims about how beneficial an experimental drug is (i.e. "this will reverse your cholesterol plaques!"), the whole point of the study is that we don't really know that it IS beneficial. Hence the need for more skepticism. Suggesting to people that an experimental drug will be helpful for them is very questionable when the fact is, it hasn't been proven that it is helpful for anyone, not to mention that specific patient and their situation.
posted by treehorn+bunny at 5:23 PM on October 14, 2014
1. That he must reach a level of 70 for LDL by any means necessary. The new guidelines that drpynchon refers to do not emphasize this target. Here's an article without much jargon to explain further: "Doctors have long prescribed statins based on a cholesterol number, particularly the level of “bad” LDL cholesterol.
But the guidelines advise assessing factors such as age, gender, race, whether a patient smokes, blood pressure and whether it’s being treated, whether a person has diabetes, as well as blood cholesterol levels in determining their risk. They also suggest that healthcare providers may want to consider other factors, including family history. Only after that very personalized assessment is a decision made on what treatment would work best.
“Physicians now have to shift their thinking away from only looking at cholesterol levels,” said Donald Lloyd-Jones, M.D., an American Heart Association volunteer who helped write the new guidelines. “A patient’s overall risk is really the playing field on which people need to understand whether they need statin medication.”
2. That no one should be making claims about how beneficial an experimental drug is (i.e. "this will reverse your cholesterol plaques!"), the whole point of the study is that we don't really know that it IS beneficial. Hence the need for more skepticism. Suggesting to people that an experimental drug will be helpful for them is very questionable when the fact is, it hasn't been proven that it is helpful for anyone, not to mention that specific patient and their situation.
posted by treehorn+bunny at 5:23 PM on October 14, 2014
Best answer: Sorry, I probably should have quoted this more to the point sentence from the article:
"For patients taking statins, the guidelines say they no longer need to get LDL cholesterol levels down to a specific target number – a significant departure from how doctors have treated cholesterol for years. While research clearly shows that lowering LDL lowers the risk for heart attack and stroke, there is no evidence to prove that one target number is best."
posted by treehorn+bunny at 5:29 PM on October 14, 2014
"For patients taking statins, the guidelines say they no longer need to get LDL cholesterol levels down to a specific target number – a significant departure from how doctors have treated cholesterol for years. While research clearly shows that lowering LDL lowers the risk for heart attack and stroke, there is no evidence to prove that one target number is best."
posted by treehorn+bunny at 5:29 PM on October 14, 2014
This thread is closed to new comments.
Here is what WebMD has to say: However, it is generally agreed that people with advanced arterial plaque or high risk of heart disease keep their LDL levels below 70. Wikipedia link.
posted by I am the Walrus at 9:40 AM on October 14, 2014