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  • TC/HDL ratio greater risk detector than LDL

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    Old 07-18-2003, 03:25 AM   #1
    pcovers
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    Post TC/HDL ratio greater risk detector than LDL

    This is not new info, but I haven't seen it specifically stated here for a while. So for any new folks around, you may find this interesting:

    Efficacy of cholesterol levels and ratios in predicting future coronary heart disease in a Chinese population.
    .....Our data indicate that current guidelines for lipid management may misclassify subjects with high levels of HDL and LDL cholesterol as well as those with low levels of HDL and LDL cholesterol. Using the ratio of total to HDL cholesterol as the initial screening tool can obviate this discrepancy.

    University of Pennsylvania Medical Center
    Researchers at the University of Pennsylvania Medical Center concluded that the ratio of one's total cholesterol to high-density lipoprotein (HDL) cholesterol is a superior measure of determining coronary heart disease risk. This study challenged current national guidelines that recommend physicians measure only low-density lipoprotein (LDL) levels.
    In a subsequent study, using data from a study of 3,641 men in the Lipid Research Clinics Coronary Primary Prevention Trial, the authors found that changes in the ratios, as opposed to changes in LDL levels alone, more accurately measure changes in a patient's risk of coronary heart disease. Again, the study challenges current guidelines that state physicians should use the changes in LDL levels alone as a measure of treatment success.



    There are of course other references to this position, but these two represent what they say.

    Here are how the risk factors have been classified by at least one source (where low risk is 1 and higher risk is 5):

    Risk TC/HDL
    1 <3.4
    2 3.5-4.0
    3 4.1-4.7
    4 4.8-5.5
    5 >5.5



    [This message has been edited by pcovers (edited 07-18-2003).]

     
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    Old 07-18-2003, 03:06 PM   #2
    Gooba
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    It should also be noted that the latest protocol calls for more evaluation of the actual risk factors as it pertains to history and and family history,instead of cholesterol numbers or ratios.

     
    Old 07-19-2003, 11:04 AM   #3
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    I would also go so far as to say that a person should not really utilize these ratios or cholesterol readings as an indicator for their chances of getting CAD.They need to get tested to C-RP and LP-PLA2 which has been found to be a more accurate indicator.

     
    Old 07-19-2003, 02:34 PM   #4
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    Quote:
    Originally posted by Gooba:
    It should also be noted that the latest protocol calls for more evaluation of the actual risk factors as it pertains to history and and family history,instead of cholesterol numbers or ratios.
    While I am acedotal, my personal experience does provide valid data.

    My family history:

    Paternal Grandfather - Died 65 no evidence of CAD
    Paternal Grandmother - Died 92 no evidence of CAD
    Maternal Grandfather - Died 75 no evidence of CAD
    Maternal Grandmother - Died 93 no evidence of CAD
    Father - died 47 result of a surgery - no CAD
    Mother - living 76 no known CAD
    Brothers - both living - 51 and 55 no known CAD
    Sisters - all four living - 49 to 61 known no CAD
    Seven paternal uncles and aunts - no deaths attributed to CAD

    Me - 47 - Heart Attack at 46 Ratio of 6.0

    Anecdotal for sure. Compelling nonetheless.

    Knowing and respecting my TC/HDL risk factor may just have prevented my MI. I respect your right to an opinion, but I would certainly not advise against using ratios as one tool in the process of understanding and acting on one's risk potential.


    [This message has been edited by pcovers (edited 07-19-2003).]

     
    Old 07-19-2003, 05:53 PM   #5
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    [QUOTE]Originally posted by pcovers:
    [
    Me - 47 - Heart Attack at 46 Ratio of 6.0

    Anecdotal for sure. Compelling nonetheless.

    Knowing and respecting my TC/HDL risk factor may just have prevented my MI.

    I guess I am a little confused here.You said you had a Heart attack at 46,and in the next sentence you say that the ratio prevented it.You either had a heart attack or you didn't.
    In regards to what I said.The fact of the matter is that emrging research shows that cholesterol is NOT a valid indicator of risk to the patient.As was stated here on numerous times that cholesterol readings were low but the person still had blocked arteries or suffered a heart attack.The presence of C-RP and now the presence of L-LPA2 are better indicators than cholesterol or ratios in regards to trigs and cholesterol.The latest studies in this show people who had normal or below normal cholesterol were still at a higher risk due to the presence of C-RP and L-PLA2.Both having to do with inflammation and nothing to do with cholesterol or trigs.Also,look at the research in regards to reocclusion of a stent or angio site.The emergence of the drug eluting stent has shown great strides in this area.The key to this stent is the drug that is used.It is an immuno suppressive and decreases the immune system's response to the area.The success of this proves that cholesterol or ratios are not a factor,that inflammation and the bodies response is a better indicator.As was said before also,people with low cholesterol and ideal ratios still have heart atacks.That tends to remove the importance of these ratios,and the need to spend all the time,money and energy reducing something that is not really going to help.

     
    Old 07-20-2003, 03:28 AM   #6
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    Four years ago my TC/HDL were a smidgeon under 10. I panicked and went on Lipitor, which brought the levels to a more tolerable 5 but my HDL's were still too low (though upo 20% from the statin).
    I added cod liver oil and lecithin and now enjoy TC/HDL ratios regularly around 3.0.

    I couldn't be more pleased. This kind of data may have well saved me from a death from CAD...just like my mom- too bad statins weren't available for her---best treatment she could get were NO EGGS, SKIM MILK and lots of TRANS-FAT MARGARINE..........OY!

    [This message has been edited by zip2play (edited 07-20-2003).]

     
    Old 07-20-2003, 04:34 AM   #7
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    I guess I am a little confused here. You said you had a Heart attack at 46,and in the next sentence you say that the ratio prevented it. You either had a heart attack or you didn't.

    I had a heart attack. My point was that if I had known and respected the risk factors associated with TC/HDL ratio, I might have taken action to avoid the MI.

    In regards to what I said. The fact of the matter is that emerging research shows that cholesterol is NOT a valid indicator of risk to the patient.

    There is a lot of research on a lot of things and many of them appear valid. There is current research that demonstrates that lowering cholesterol does in fact reduce risk. This is CURRENT research. However, since no one has a lock on absolute knowledge about the root cause of CAD, many researchers are still working to understand it all.

    As was stated here on numerous times that cholesterol readings were low but the person still had blocked arteries or suffered a heart attack.

    No one, not even the researchers that lean toward cholesterol as a problem source would say that cause and effect is an absolute and that if your numbers are high then you will definitely have a problem. Of course there are other factors at work in this process. The minute that they show a person with high CRP numbers and no CAD will demonstrate that inflammation is also not an absolute cause and effect.

    The presence of C-RP and now the presence of L-LPA2 are better indicators than cholesterol or ratios in regards to trigs and cholesterol. The latest studies in this show people who had normal or below normal cholesterol were still at a higher risk due to the presence of C-RP and L-PLA2.Both having to do with inflammation and nothing to do with cholesterol or trigs.

    I don't at all disagree that these might be valid and important risk factors. My problem is the absolute nature of your comments. Based on your statement, all the other scientific researchers focusing on anything other than CRP and L-PLA2 may as well pick up their toys and go home because there is no need to continue down any other road than the one you propose. You said that cholesterol is NOT a valid indicator. That is pretty definitive.

    Also, look at the research in regards to reocclusion of a stent or angio site. The emergence of the drug eluting stent has shown great strides in this area.The key to this stent is the drug that is used.It is an immuno suppressive and decreases the immune system's response to the area.The success of this proves that cholesterol or ratios are not a factor,that inflammation and the bodies response is a better indicator.

    There it is again. According to you, the "proof" is in. Everyone else with solid data can pack it up and put their efforts elsewhere.

    Specifically to your point, I don't follow your rational. The drug eluding stents work by reducing or eliminating restenosis caused by scar tissue. Stents have a 15%-25% chance of closing up after placement due specifically to the bodies attempt to "heal" itself where the stent is placed. Where restenosis occurs, it is because the body sees the stent as a foreign object and builds scar tissue inside or at the edges of the stent. This has nothing to do with your inflammation theories. It is a simple matter of the body rejecting a foreign object.

    Can you better explain how you are making a correlation between the bodies natural effort to build scar tissue around a foreign object and your position on inflammation research.

    As was said before also, people with low cholesterol and ideal ratios still have heart atacks. That tends to remove the importance of these ratios, and the need to spend all the time, money and energy reducing something that is not really going to help.

    Again, my problem with your mater of fact statements is that you present them in the manner that says all studies and research showing a link between cholesterol and heart disease is wasted. This is just too far to take the debate. The research you cite is valid, but you know as well as I that I could produce dozens of studies showing a direct and significant correlation between cholesterol and CAD. That everyone with high cholesterol does not develop CAD, or that some with low cholesterol develop CAD, does not take away from he validity demonstrated in the cholesterol research.

    I am open to many possibilities and I take supplements to try to address these various possibilities. I am open to the CRP inflammation ideas, to the Rath-Pauling ideas, to the cholesterol ideas, etc. I think it is unwise to place all one’s absolutes in any on of these theoretical baskets.

     
    Old 07-20-2003, 07:45 AM   #8
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    My statements are no more than statements by yourself and others in regards to the ratios,supplements and everything else here especially in regards to statins.I am always open to ideas and research.By your own admission there is alot of research going on in alot of areas.It tends to boil down to nobody knows anything for sure,except that we are al going to die at some point.

     
    Old 07-20-2003, 08:37 AM   #9
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    Here are some pints to consider.
    One,atherosclerosis is an inflammatory process; two, it is an inflammatory process that is mediated by the immune system; three, the immune system is tremendously redundant; so four, there will never be one cure or one answer. It will be a combination of lifestyle, medication and further understanding of this disease process.
    What we have learned over the last two decades is that inflammation is a key mechanism in atherosclerosis through all of its stages, from lesion development to plaque rupture and its clinical consequences.

    The rise in C-RP after a PCI is a valid marker for restenosis.
    As for a person who had an mI,their cholesterol levels as well as their C-RP go up because the body is trying to repair the damage.That is one of the reasons that a person who has an MI will tend to have a rise in cholesterol levels even though diet and exercise are being followed religiously.

     
    Old 07-20-2003, 09:15 AM   #10
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    Quote:
    Originally posted by Gooba:
    My statements are no more than statements by yourself and others in regards to the ratios,supplements and everything else here especially in regards to statins.I am always open to ideas and research.By your own admission there is alot of research going on in alot of areas.It tends to boil down to nobody knows anything for sure,except that we are al going to die at some point.
    You made the unqualified statement that:

    The success of this proves that cholesterol or ratios are not a factor

    I think that both inflamation and ratios are factors. I am not here to start any arguments. I am simply responding to such a matter of fact claim that proof exists that ratios are not a factor. There is tons of evidence that, at a minimum, suggests otherwise.

    I am still trying to understand your relationship between the body's propensity to scar at the location of a stent and the relationship of this phenomenon to the CRP/inflammation link to CAD.



    [This message has been edited by pcovers (edited 07-20-2003).]

     
    Old 07-20-2003, 11:00 AM   #11
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    I think that there are probably a multitude of factors involved here, and it is difficult to single out or pinpoint any one of them as being THE telling factor. The human body is a very complex mechanism, with a dizzying amount of chemical reactions occurring at all times. I do feel, however, that dietary influences are also involved, and that when the diet is adequate, and essential nutrients are readily available in sufficient quantities, then there is a greater probability of continued good health. If the diet is of poor quality, or the intake of essential nutrients is sub-optimal, then our body's natural chemistry becomes skewed, setting in motion a series of chain reactions which can manifest itself in many ways, including any number of changes pertaining to blood-lipids, etc.

    Our current epidemic of type 2 diabetes and obesity are two good examples of diet related disorders, and I believe that to a large extent, the same is probably true for atherosclerosis. Therefore, what we need to do is to determine the root cause of heart disease, and then work from there. But so far we haven't done that. We appear to be more concerned with uncovering risk factors, and developing various drugs to couteract them. This whole thing just keeps snowballing, and in essence all we are doing is treating an underlying symptom.

    So, how many risk factors are there already? Let's see now. There is total cholesterol, low HDL, high LDL, high triglycerides, homocysteine, lipoprotein(a), CRP, VLDL, high blood pressure, and now LP-PLA2. That's 10 right there. Have I missed any others? This is getting ridiculous. Every time they discover another potential risk factor, they answer the call by developing some new drug. This is enough to drive anybody crazy.


    P.S. Incidentally, I am inclined to agree that inflammation risk markers may in fact turn out to be the most valid benchmark for developing heart disease. If cholesterol alone was the culprit, then blockages would more randomly occur throughout our bodies. But it doesn't. Pauling and Rath also pointed this out, and stated that the deposition of plaque inside the artery is the body's way of repairing a crack or tear in the artery wall--sort of like the way a scab forms over an open wound.

    [This message has been edited by ARIZONA73 (edited 07-20-2003).]
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    Old 07-20-2003, 12:07 PM   #12
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    Quote:
    Originally posted by ARIZONA73:
    So, how many risk factors are there already? Let's see now. There is total cholesterol, low HDL, high LDL, high triglycerides, homocysteine, lipoprotein(a), CRP, VLDL, high blood pressure, and now LP-PLA2. That's 10 right there. Have I missed any others?
    I'll add genetics as a possible risk factor.

    All things suggest that all these are indicators. What is the root cause? Not absolutely known yet. We do know there are cultures that have extremely low incidencs of CAD. Even knowing this, there is no definitive factor identified that wraps up exactly why. For any one avenue there is proof and then there is contradiction to that proof.

    You do what you can given the information available.



    [This message has been edited by pcovers (edited 07-20-2003).]

     
    Old 07-20-2003, 10:36 PM   #13
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    Just to add to this great discussion here I will give the numbers. There is obviously more issues than cholesterol when according to recent data 75% OF ALL patients who have NORMAL cholesterol levels go on to have an event. Only time and research will tell which other factors are the next piece of this ever changing puzzle.

     
    Old 07-21-2003, 02:53 AM   #14
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    Quote:
    Originally posted by pcovers:
    I'll add genetics as a possible risk factor.
    One more big one that gets little attention but that has very strong evidence is stress. I am convinced this one gets so litte attention because it is the least factor that can easily be addressed with a pill.

    Some research on this inidicates as much as five times greater likelihood for an event for highly anxious, highly stressed people when compared to those at the other end of the stress scale.

     
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