Please help me improve my cholesterol numbers? (pains, aches, how to)
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OK let's back up people. We need to ask what tests are done and why each test is done instead of something else. We need to define what the term independent risk factor is and how it relates to risk. Risk is defined as who will come down with coronary artery disease. One follows people for many years and then backtracks based on laboratory testing. Independent laboratory risk factors are sought to be able to predict who is coming down with CAD. They found out that total cholesterol, LDL and HDL were independent risk factors. That is each was independent between or amongst themselves. Triglycerides were not based on the large numbers but obviously small genetic clusters exist out there.
Every year new tests come out being taunted as the new better test that is able to predict. Most of these new tests are by definition new and haven't been around for years needed to catch people before they come down with CAD. It's predictive value is what we are after. One can not study people after the fact and then be able to call it predictive. There has been longitudinal studies for many decades since the 1950's going on and that's where we get predictive values.
Every so often recommendations are updated and newer tests are evaluated and the recent literature of studies are evaluated in order to see if the newer tests should be added or replace older tests. The sub particle testing has been around for a long time. There has been problems with newer technologies and tests with sub particle testing correlating with gold method ultracentrifugation. Quicker methods are shortcuts and can miss the mark as to what they are testing. The VAP panel was reporting out wrong Lp(a) levels because their method was screwed and nobody caught it. It was only when other people staritng putting up their own methods for Lp(a) were brought into the market that errors stuck out. The VAP panel the company using was taken off the market for many years until they could get their **** together.
The bottom line is that they reviewed all of the new tests and failed to see any overall beneficial value over the old tests. The newer tests are presently routinely used for detecting abnormalities in people who have already experienced a heart attack at a young age.
Keep in mind that once the cholesterol theory came about and accepted then interventions in cholesterol chemistry came about and that being statins and only statins. Statins could alter such values and outcome studies have been generated.
There is no evidence that statin drugs can alter Lp(a) levels that have been genetically predetermined. There is no evidence that anything can change or alter such levels enough clinically to make a difference.
Hyperhomocysteinemia is another similar problem where people with elevated homocysteine levels suffer events but when we lower their levels with B12 and folate to normal the risk and outcomes are the same. It does not help knowing ahead of time because we can't do anything about it. That testing is also done after the fact to determine the cause of those who have had events.
We are talking about finding predictors and being able to intervene rather than simply finding predictors and not being able to do nothing about it. People will live on egg-shells and that is not good for quality of life issues.
At present there hasn't been any change to recommendations and the basic lipid panel is still in effect unless one has had a heart attack and is using it for investigational purposes.
what about triglycides? Does that number have any value?
Even less than the predictave value of chol numbers-- and that's pretty bad. Coefficient of correlation for chol is 0.3-- not much better than flippinga coin- heads you're at risk; tails you're not.
Quote:
Originally Posted by rabbit33
The primary source of LDL and VLDL cholesterols in the body is the metabolism of saturated fat.
If you want to improve your blood fat levels, cut down on saturated fat.
Just wrong.
Chol levels are determined almost exclusively by genetics until you get down to concentration camp starvation conditions.
Even pts with Familial Hypertriglyceridemia (blood levels in the 1000s) don't have that much increased risk of MI (CAD risk is 4 per 1000 per yr in those with no risk factors and 8 per 1000 per yr in those with Familial Hypertriglyceridemia-- the same risk as chol >300mg%. https://www.ahajournals.org/doi/10.1...81777.17879.85
Last edited by guidoLaMoto; 04-19-2023 at 12:04 PM..
... They found out that total cholesterol, LDL and HDL were independent risk factors....
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Excellent post.
But we really should object to the term "risk factor" when what we really mean is factors that have a positve correlation with crtain outcomes (early CAD/MI).
As you note about homocysteine levels - treating risk factors like HTN doesn't alter CAD outcomes (it does reduce hemorrhagic stroke rates & reduce severity of CRF), and good management of BS in DM is still dissapointingly inadequate in reducing CAD...Using statins after an MI reduces the risk (a little) of a second MI, and it just happens to lower chol also-- BUT- adding niacin to reduce chol further doesn't improve the risk of that second MI at all.
More info to cogitate-- in the few "head to head" studies comparing different statins, the amount that each lowered chol did NOT correlate at all with the risk reduction....BTW- statins also have mild anticoagulant and anti-inflammatory properties.
We've been blaming the drier for all those lost socks all these years...Could it really be the washer is to blame?
But we really should object to the term "risk factor" when what we really mean is factors that have a positve correlation with crtain outcomes (early CAD/MI).
As you note about homocysteine levels - treating risk factors like HTN doesn't alter CAD outcomes (it does reduce hemorrhagic stroke rates & reduce severity of CRF), and good management of BS in DM is still dissapointingly inadequate in reducing CAD...Using statins after an MI reduces the risk (a little) of a second MI, and it just happens to lower chol also-- BUT- adding niacin to reduce chol further doesn't improve the risk of that second MI at all.
More info to cogitate-- in the few "head to head" studies comparing different statins, the amount that each lowered chol did NOT correlate at all with the risk reduction....BTW- statins also have mild anticoagulant and anti-inflammatory properties.
We've been blaming the drier for all those lost socks all these years...Could it really be the washer is to blame?
The laboratory makers were elevated rhetorically to "risk factors" to categorize them on equal footing with "clinical risk" factors like diabetes and hypertension. Indeed the formula to calculate the ten year risk assessment requires all "risk factor" data that includes laboratory markers. Some laboratory markers were eliminated in the new formula which got from negative feedback from clinicians.
The cholesterol theory is a dynamic theory because it needs to be nestled in a general theory of plaque formation and arthrogenesis. The use of statins did not prove nor disprove the cholesterol theory because of the many properties that statins contain. They may work outside of that cholesterol theory and evidence for that lies in it's anti-inflammatory properties and a lack of a linear response of statin use. Twice the dose did not elicit twice the reduction in outcome events.
I think there is a difference though in what one is trying to do and predict. The targeted research originated after WWII and the intent was to reduce the number of young adult men dying of heart attacks with the pathological findings of atherosclerosis. It sort of reminds me of Alzheimer's disease where back in the day it was called presenile dementia. Presenile to separate it from senile dementia. It was occuring in the young. Now we call somebody in their 80's as have Alzheimer's disease. There can be a problem with confounding variables if one tries to use global definitions of risk factors without taking into account age. Some people with high cholesterol do not come down with disease while others with the same levels do. There are genetic handling differences that one must take into account similar to what hibernating bears experience as they all have high cholesterol.
Laboratory markers can lose their predictive value based on age and genetics on an individual basis.
what about triglycides? Does that number have any value?
I dropped my triglycerides by 50% when I quit drinking regular soft drinks. I won't drink diet soft drinks, so no soft drinks at all for me, just water or unsweet iced tea. My doctor tells me that cutting sugars is one of the best ways to drop triglyceride levels.
Blood cholesterol is made from the saturated fat you eat, not from the cholesterol you eat. The cholesterol you eat is digested. Of course if you eat 22 eggs a day, a large amount of the cholesterol you eat won't get digested, but for normal eating habits, dietary cholesterol has little to do with blood cholesterol. It's the saturated fat that gets converted to LDL which is the dangerous stuff.
As someone pointed out above, genetics has a lot to do with your body's tendency to convert incoming fat to LDL or not. But this is really about people with genetic abnormalities that cause them to convert flippin' everything into LDL, with serious coronary artery disease and heart attacks in the 30s. For normal people, saturated fat intake will track well with LDL and VLDL levels, and LDL and VLDL levels do correlate well with the formation of plaques in arteries and subsequent heart attacks.
Cardiovascular health is a multisided affair: inflammation; blood sugar; blood fats; aerobic exercise; stress management, they all play into it. You can't just focus on one aspect and think you're all good.
The laboratory makers were elevated rhetorically to "risk factors" to categorize them on equal footing with "clinical risk" factors like diabetes and hypertension. Indeed the formula to calculate the ten year risk assessment requires all "risk factor" data that includes laboratory markers. Some laboratory markers were eliminated in the new formula which got from negative feedback from clinicians.
The cholesterol theory is a dynamic theory because it needs to be nestled in a general theory of plaque formation and arthrogenesis. The use of statins did not prove nor disprove the cholesterol theory because of the many properties that statins contain. They may work outside of that cholesterol theory and evidence for that lies in it's anti-inflammatory properties and a lack of a linear response of statin use. Twice the dose did not elicit twice the reduction in outcome events.
I think there is a difference though in what one is trying to do and predict. The targeted research originated after WWII and the intent was to reduce the number of young adult men dying of heart attacks with the pathological findings of atherosclerosis. It sort of reminds me of Alzheimer's disease where back in the day it was called presenile dementia. Presenile to separate it from senile dementia. It was occuring in the young. Now we call somebody in their 80's as have Alzheimer's disease. There can be a problem with confounding variables if one tries to use global definitions of risk factors without taking into account age. Some people with high cholesterol do not come down with disease while others with the same levels do. There are genetic handling differences that one must take into account similar to what hibernating bears experience as they all have high cholesterol.
Laboratory markers can lose their predictive value based on age and genetics on an individual basis.
interesting. Hmm.. but after a certain age, 65, 70., whatever, do the numbers even matter? If you lived that long in good health, do numbers matter?
interesting. Hmm.. but after a certain age, 65, 70., whatever, do the numbers even matter? If you lived that long in good health, do numbers matter?
I don't have a good answer for that. The original goal was to prevent deaths in young men. Since the men were young one was searching for highly arthogenic components associated with the cholesterol theory. It was correlated to LDL levels. When they looked at women they found non-HDL correlated better. There's a slight difference there. The odds of an elderly having a highly arthrogenic cholesterol is slim. A lot of that is genetically determined.
Intuitively if one dies of a heart attack at the age of 80 that it would be considered as a natural death and not a premature death. Longitudinal studies show that no all people with high cholesterol come down with CAD. Some men with normal total LDL levels can have abnormal forms of cholesterol like Lp(a) and die a premature death.
If I remember correctly the studies showing benefit to interventions with statins in the elderly are not necessarily based on cholesterol levels but more on the benefit of treatment. Those on statins had less events. Not a big difference but there was a difference. That's where anti-inflammatory effects of the drug would be beneficial regardless of cholesterol status. Once a person has a heart attack the person is put on statins and they have an immediate effect that is beneficial. Statins can lower CRP levels slightly thus reducing some inflammation as a cofactor among multiple factors.
"Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol."
So right now the numbers only matter in determining if one wants to decide to put somebody on statins. The expansion of the use of statins is based on extended properties not solely based on cholesterol lowering. Age was added to the formula and some clinicians were complaining that the drug company was trying to place everybody on statins and as one got older then just about most people would be placed on statins.
I don't have a good answer for you. There is some disagreement there among the medical community on the use of statins.
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