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Not from one single source but a variety of sources. I was trying to update my own understanding as to what is happening now in research. It is also observational on my part from progression of formulas used in addressing risk. It indicates the thought process of what is going on. I saw a video from a cardiologist which concluded what has been known for years and that is LDL < non-HDL < ApoB. Nothing new there but the reason for that brought up new theories in explaining why that is the case.
I make no assertions that the theories are accurate or that they will probably change in the future. I just find it interesting in what they said from a discussion point of view involving cholesterol theory.
There's no difference in clinical practice as to how to interpret the LDL, non-HDL or the ApoB levels. Those are all discussed in the various practice guidelines. What I didn't find and only assume is that ApoB levels are only done with selective patients and why that is the case brings into question my assumption. There's some disagreement with regards to the other parameters in the lipid panel and I presented those from the point of view of the newer cholesterol hypothesis.
There have been some posts on the subject in the past with debates about theories and pathophysiology, and particle studies. Some people don't want to be put on statins and they interpret the lipid panel with their spin.
Last edited by Medical Lab Guy; 10-15-2023 at 01:36 PM..
So, should I take statins or not if my #'s a slightly elevated and I have cardio risk in my family?
I'll ask for the test you menton next physical...or before.
1/2 say statins are useless (The Statin Myth book Docs), and the 1/2 say they work.
My sister in law has taken statins forever, has low hdl & ldl, & eats cleaner than anyone I know, and she just had to do angioplasty...makes me thing statins are a farce.
So, should I take statins or not if my #'s a slightly elevated and I have cardio risk in my family?
I'll ask for the test you menton next physical...or before.
1/2 say statins are useless (The Statin Myth book Docs), and the 1/2 say they work.
My sister in law has taken statins forever, has low hdl & ldl, & eats cleaner than anyone I know, and she just had to do angioplasty...makes me thing statins are a farce.
The treatment recommendations haven't changed recently. I was simply updating the cholesterol theory underlining such recommendations. One thing I did forget to mention is that one can have normal or even low LDL levels and yet have a high ApoB level which again puts a person at risk and why ApoB is better.
It's more like fine tuning rather than gross readjustments.
This is all opinion here but what happens in most cases is that people take the 5 year study for statin approval and they look at the stats and say for example 4 out 100 people come down with ASCVD. If statins are given and one sees only 2 come down with it then one sees an absolute risk reduction of 2% from 4% while one sees a relative risk reduction of 50%. That's where arguments come to play with the numbers. In reality the numbers do get better with time because it is over time that one wants to see reduction and not necessarily over just five years.
I presume she had high cholesterol which is why your SIL was put on statins. Normally one wants to address all issues pertaining to risk which includes clinical risk factors and if she had low HDL then metabolic syndrome usually causes a low HDL with a high triglycerides and so those issues should be addressed to reduce risk. If she has high blood pressure or smokes or etc then those issues should be addressed. What can't be addressed via lifestyle issues are genetic factors that cause a low HDL and coronary risk. Genetic conditions unfortunately are different. For example we have familial hyperhomocysteinemia. They have high homocysteine levels in the blood that causes risk. If one treats it with folate and B12 the homocysteine becomes normalized but the risk is still there. It is a marker and not a cause. If a person has a genetically low HDL then raising it will not ameliorate the risk because HDL is a marker and not a cause. It's not because of their low HDL that causes problems but something else that lowers HDL which also causes heart problems.
You mentioned that she has a low LDL and I presume it was based on the statins. One opinion is that blood cholesterol levels can be too low and be harmful because the body needs cholesterol. The opposing view is that each cell makes the lipids it needs on an individual level rather than being dependent on the blood lipid levels. The problem with doing LDL-C and having a low level is that it is inaccurate at assessing risk and ApoB is much more accurate in that setting. She should definitely have had an ApoB level along with an Lp(a) level done.
The other part of the argument of statins being bad and people don't trust them then there are alternatives as mentioned before by Suzy and Mike can go into that further. There is Ezetimibe (Zetia), and PCSK9 inhibitors that can lower ApoB and cardiac events have been reduced in RCT. If one has issues with muscle problems with statins then Bempedoic acid is similar to statin but affects the muscles less.
For those interested in more on the specifics of ApoB and Lp(a) with case studies then the link below is for you. They discuss the importance of ApoB and the flaws of the regular lipid panel and this Canadian researcher mentioned the 40 history of ApoB science. In his opinion, the reason why more ApoB tests are not ordered is because of perceived expense.
I have heard that insurance will not pay for ApoB. Something to verify if the expense is a hardship for you. You can order your own at various online sites also.
I have heard that insurance will not pay for ApoB. Something to verify if the expense is a hardship for you. You can order your own at various online sites also.
Thanks for that. That is probably one big determinant on why it isn't done more. I had to look it up to see exactly what the stance is and came up with this and my understanding on that.
Some important notes on government sponsored healthcare and control thereof.
Statements made with regard to the lipid panel and when it is covered by medicare.
"Note #1: There is no Medicare benefit for screening CV risk assessment testing for asymptomatic (without signs or symptoms of disease) patients. Screening asymptomatic patients for cardiovascular risk is statutorily excluded by Medicare and will not be addressed in this policy."
"NCD 190.23 covers lipid panel testing for symptomatic patients for evaluating atherosclerotic CV disease, to monitor the progress of patients on anti-lipid dietary management and pharmacologic therapy for various lipid disorders. Per NCD 190.23, “Routine screening and prophylactic testing for lipid disorders are not covered by Medicare. While lipid screening may be medically appropriate, Medicare by statue does not pay for it. Lipid testing in asymptomatic individuals is considered to be screening regardless of the presence of other risk factors such as family history, tobacco use, etc.â€
Long list of tests that are not covered at present.
"The following biomarkers, when they are included in a CV risk assessment panel, are non-covered:
Lipoprotein subclasses;
Lipoprotein(a);
Apolipoprotein B (Apo B), apo A-I and apo E;
Despite the Framingham risk-scoring tool, clinicians have sought non-traditional lipid and other biomarker measurements to predict CV events. The most promising biomarkers are the ones that closely correlate with the pathophysiological process of the disease. In general, there is evidence that some of these biomarkers may alter risk categorization (higher or lower) compared to traditional risk prediction, but it has not been established that changes in categorization provides clinically actionable information beyond that of traditional lipid measures. In addition, no study has provided high-quality evidence that measurement of non-traditional lipid and other biomarkers leads to changes in management that improve health outcomes.
To provide clinically useful knowledge, a biomarker should meet the following criteria:
Adds clinical knowledge that improves patient outcomes (criteria for Medicare “reasonable and necessaryâ€);
Provides risk information that is independent of established predictors;
Is easy to measure and interpret in the clinical setting; and
Is accurate, reproducible and standardized."
While Apo B and Apo A-I are thought to be the main structural proteins of atherogenic and anti-atherogenic lipoproteins and particles, testing for these compounds has not been validated as a tool for risk assessment. As such, the 2010 ACCF/AHA guidelines indicate that apolipoproteins testing is not recommended for CV risk assessment in asymptomatic adults. However, AACE recommends apoB testing to assess residual risk in patients for CAD (even when LDL-C levels are controlled) in patient when the triglyceride concentration is >150 mg/dL or the HDL-C concentration is Medicare expects testing to be limited to assessment of residual risk in patients with CAD with triglyceride concentrations of >150 mg/dL or HDL-C of Apo E, the major constituent of VLDL and chylomicrons, acts as the primary binding protein for LDL receptors in the liver and is thought to play a role in lipid metabolism. Although some individuals hypothesize that Apo E genotypes may be useful in the selection of drug therapy, the value of Apo E testing in the diagnosis and management of CHD is insufficient and needs further evaluation. "
My interpretation of what is being implied is that the lipid panel is cheaper and correlates with ApoB most of the time and they are saying that it doesn't impact treatment that much. That is true most of the time but not true all of the time. It also states that ApoB is not recommended for asymptomatic screening but is recommended for those with residual disease even in the presence of of LDL levels that are controlled. That implies that the standard lipid panel sucks. That is some progress from before when it wasn't approved under any circumstances.
It also explains why people are reworking the lipid panel calculated LDL formulas that are more accurate. They are not paying for ApoB.
It is confusing in one sense on when they suggest lipid panels be done. If one has symptoms of CAD then what good is the predictive value of the test if one already has succumbed to symptoms? It is appropriate only in symptomatic patients. That seems bizarre to me. The recommendations are more reactive than proactive in screening for CAD.
The Canadian guidelines state that Lp(a) be performed once in a lifetime.
Thanks for the info but lipid researchers still think of ApoB as better than the standard lipid panel. The video of one researcher is in the previous post stating that.
1/2 say statins are useless (The Statin Myth book Docs), and the 1/2 say they work.
My sister in law has taken statins forever, has low hdl & ldl, & eats cleaner than anyone I know, and she just had to do angioplasty...makes me thing statins are a farce.
The cited ref is a meta-analysis of studies following 80K+ pts. Taking statins for prmary prevention (ie- before the pt has an MI) lowerd risk by 10% RELATIVE RISK.... Because the basic risk of a pt with no risk factors is 4/1000/yr, 10% RR is only an improvement of 0.4% in ABSOLUTE RISK....That means we'd have to treat 2500 pts with statins to "save" one MI...But, the side efect risk of statins is 5-10%, meaning that for everyt 1 heart attack avoided each year, we'd make 125-250 people sick from the pills.
It's even more complicated tho, because statistics only apply to the group, NOT the individual. We know we'll save one pt and make 250 sick, but we can't predict WHO thioose will be out of the group.
Your sister's case is a good illustration of two important points-- (a) statins (or any med for any disease) don't absolutely prevent disease progression, they just improve the risk a little, and (2) it's low HDL that's the real predictor, not high LDL.....In getting back to MLG's original post, chol numbers are only useful in predictions but don't really describe the mechanism (cause) of CAD. Cf- observing cloud types can help you predict rain, but that doesn't explain why it rains or not....but then, do you really care why when chosing to take an umbrella or not?
Last edited by guidoLaMoto; 10-16-2023 at 08:46 AM..
The cited ref is a meta-analysis of studies following 80K+ pts. Taking statins for prmary prevention (ie- before the pt has an MI) lowerd risk by 10% RELATIVE RISK.... Because the basic risk of a pt with no risk factors is 4/1000/yr, 10% RR is only an improvement of 0.4% in ABSOLUTE RISK....That means we'd have to treat 2500 pts with statins to "save" one MI...But, the side efect risk of statins is 5-10%, meaning that for everyt 1 heart attack avoided each year, we'd make 125-250 people sick from the pills.
It's even more complicated tho, because statistics only apply to the group, NOT the individual. We know we'll save one pt and make 250 sick, but we can't predict WHO thioose will be out of the group.
Your sister's case is a good illustration of two important points-- (a) statins (or any med for any disease) don't absolutely prevent disease progression, they just improve the risk a little, and (2) it's low HDL that's the real predictor, not high LDL.....In getting back to MLG's original post, chol numbers are only useful in predictions but don't really describe the mechanism (cause) of CAD. Cf- observing cloud types can help you predict rain, but that doesn't explain why it rains or not....but then, do you really care why when chosing to take an umbrella or not?
"We included trials that randomly assigned participants at low cardiovascular risk to receive a statin versus a placebo or no statin. We defined low risk as an observed 10-year risk of less than 20% for cardiovascular-related death or nonfatal myocardial infarction, but we explored other definitions in sensitivity analyses."
If they studied patients at no risk at all how many would it prevent?
The other limiting factor of studies included is that they are short term studies and not over the lifetime of the person. It is compounded over time.
The SIL case illustrates the flaws in the lipid panel. Two people can have the same LDL value but have two completely different outcomes. LDL does not tell you particle number like ApoB or LDL-P does. A person with a normal LDL would have no medication or low dose in comparison to those with higher ApoB levels that would put the person on high dose statins. Right now the way it works is that they wait for the person to have a coronary event to confirm high risk.
The incidence of having a high Lp(a) is about 20% of the population at large. Statins won't work for those cases which means the person can be missed with regular lipid panels and they more than likely will be missed as having high risk. The only goal for such patients is to be have lifestyle changes and dietary changes and overall risk reduction with factors that can be changed.
The goal of testing and treating is to maximize prevention on an individual basis.
The goal of testing and treating is to maximize prevention on an individual basis.
Good post, but this sentence^^ shows the flaw in logic in the whole chol treatment paradigm. You cannot apply statistics in a meaningful way to a single individual or event....A more correct statement would be "...to maximize prevention over the group taken as a whole."
So, should I take statins or not if my #'s a slightly elevated and I have cardio risk in my family?
I'll ask for the test you menton next physical...or before.
1/2 say statins are useless (The Statin Myth book Docs), and the 1/2 say they work.
My sister in law has taken statins forever, has low hdl & ldl, & eats cleaner than anyone I know, and she just had to do angioplasty...makes me thing statins are a farce.
The small particle HDL should be high to protect against ldl, at least that's what the medical articles used to say, most people never seemed to understand that. The low HDL might have been her problem. Am I right Medical Lab Guy?
The small particle HDL should be high to protect against ldl, at least that's what the medical articles used to say, most people never seemed to understand that. The low HDL might have been her problem. Am I right Medical Lab Guy?
In the old theory it is supposedly protective of LDL effects which essentially why the ratio was developed. Back in the day the theory goes, I don't know if that part of the theory is still correct or not, that there was a competitive inhibition or effects of LCAT which is an enzyme that can bind LDL or HDL and when bound to LDL to release the payload lipids accumulate in the vessel or if it releases the HDL payload those particles are much less arthrogenic based on density.
The present theory based on clinical studies where HDL has been elevated through medication or other means has not reduced risk by itself. The researcher said you can raise it 2-3 times from its original low levels but it won't reduce risk. HDL has been reduced to marker status for other risk factors present. Those with high HDL levels due to genetic factors appear to also have genetically low risk factors for developing heart disease thus confounding. Let's not misunderstand that part. If a person has an acquired low HDL level via insulin resistance through lifestyle it is a marker for risk. If the person takes control and gets rid of that insulin resistance then the risk is reduced. It is the insulin resistance that adds risk. HDL is simply a marker. Risk reduction was not simply due to elevating HDL.
The revised theory takes that into account based on the fact that the predominant carrier lipoprotein for HDL is ApoA1 and not AopB. When one is talking about a LDL/HDL ratio one is talking about the ApoB/ApoA1 ratio. By using the ratio one implies that there is a protective effect that HDL renders. All ratios are thrown out with the new theories. It is replaced with ApoB is a causative directly correlating to heart risk. If it is high then there is risk and if it is lower then there is less risk. Even with old theories we looked at LDL goals and we looked at non-HDL cholesterol elevations as high risk. We only used the HDL levels to get at the calculated LDL and non-HDL cholesterol.
Just for example the failure of HDL raising,
"Results: A total of 3414 patients were randomly assigned to receive niacin (1718) or placebo (1696). The trial was stopped after a mean follow-up period of 3 years owing to a lack of efficacy. At 2 years, niacin therapy had significantly increased the median HDL cholesterol level from 35 mg per deciliter (0.91 mmol per liter) to 42 mg per deciliter (1.08 mmol per liter), lowered the triglyceride level from 164 mg per deciliter (1.85 mmol per liter) to 122 mg per deciliter (1.38 mmol per liter), and lowered the LDL cholesterol level from 74 mg per deciliter (1.91 mmol per liter) to 62 mg per deciliter (1.60 mmol per liter)."
ApoB correlates to particle number rather than to particular size. The reason why small particles correlate to heart disease is because most of the time one also finds particle number increased.
They base their understandings on genetic studies like those having large particle size LDL familial hypercholesterolemia and clinical interventional studies like with statins that selectively reduces large LDL particle size.
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