Does anyone have experience with Welchol (colesevelam) for treating high LDL.
My doctor just prescribed it for me to treat my lipid disorder. I am now past the point of preventing CAD which 15+ years on statins did not prevent and am attempting to reduce plaque to stave off another heart attack.
Advanced lipoprotein labs reveal high LDL, high Lp(a), High LDL particle number and high VLDL size. The Welchol is an attempt to deal with the high LDL since I refuse (at this point) to go back on statins. Six MIs and two cancers convinced me of that.
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Welchol?
13 posts
• Page 1 of 1
by David Staup » Thu Aug 11, 2011 11:17 am
WMO
you need to understand that cholesterol is not the problem and that cholesterol levels between about 200 to 320 lead to longer lives see here:
http://www.spacedoc.com/cheerios_fda
if you are male 40 to 65 then LOW dose statin (5mg or less) may be helpful but not because it lowers cholesterol
in my case after 5 years on 20 mg zocor I stopped on my own and 18 months later I recovered to about 80%. 4 months after that I stupidly allowed myself to be put on welchol...5 weeks later, even though I quit the welchol, I had relapsed and in fact reached a level of adverse effects that I could not even imagine before and that had me totally disabled within 7 months. Artificially lowering cholesterol is a BAD thing.
you need to understand that cholesterol is not the problem and that cholesterol levels between about 200 to 320 lead to longer lives see here:
http://www.spacedoc.com/cheerios_fda
if you are male 40 to 65 then LOW dose statin (5mg or less) may be helpful but not because it lowers cholesterol
in my case after 5 years on 20 mg zocor I stopped on my own and 18 months later I recovered to about 80%. 4 months after that I stupidly allowed myself to be put on welchol...5 weeks later, even though I quit the welchol, I had relapsed and in fact reached a level of adverse effects that I could not even imagine before and that had me totally disabled within 7 months. Artificially lowering cholesterol is a BAD thing.
- David Staup
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- Location: granbury, texas
by lars999 » Thu Aug 11, 2011 2:44 pm
I am another that agrees totally with what David wrote "artificially lowering cholesterol is BAD". After taking Lipitor 10 mg daily for 6-7 years, I quit cold because it was steadily ruining my health, well on way to killing me. Twelve months later I am largely recovered from most of the severe adverse effects of Lipitor. Lipitor did reduce my total cholesterol from about 300 to 150 and LDL by more than 1/2 -- it must have reduced my coq10 etc. by about same amount to have caused my large number of adverse side effects, both physical and cognitive, and especially stamina.
My gross lipid profile is now more or less back to normal, which sent my then GP into highly bizzare behavior, and then into a rage when I flatly disagreed with him about the "extremely bad" picture he was presenting -- he is no longer a doctor I visit. I even wonder if he is a doctor that barely managed to get his medical license. I had done a large amount of homework about lipid profiles, going back to as many original medical journal reports, that presented full data, as I could (NO Medline abstracts!!). In point of fact, each component of my lipid profile, as well as various indicators of arterial inflammation indicated good to excellent conditions, when you disregarded the cholesterol con BS and outright lies. Arterial inflammation is the increasingly widely accepted underlying cause of plaque, NOT cholesterol, LDL, etc.
FYI, perhaps as much of 75% of heart attack victims have normal cholesteral levels.
I have one condition that you apparently do not have, that is, little or no detectable plaque in major arteries. Apparently, neither did any of my ancestors, because very few, if any, died of heart attacks, etc., going back a few hundred years. One can easily surmise that they had low levels of inflammation affecting walls of their arteries.
Strongly suggest that you read widely in articles from Dr. Graveline's Newsletters, as well as books by him and the various other MDs noted on this website -- give special attention to books by Kendrick, Ravenskov and McCully -- read them all if possible. In a few months you could become more accurately informed about CAD than your doctor, who I would label as just another of the huge population of cholesterol quacks practicing very damaging medicine.
Lars
My gross lipid profile is now more or less back to normal, which sent my then GP into highly bizzare behavior, and then into a rage when I flatly disagreed with him about the "extremely bad" picture he was presenting -- he is no longer a doctor I visit. I even wonder if he is a doctor that barely managed to get his medical license. I had done a large amount of homework about lipid profiles, going back to as many original medical journal reports, that presented full data, as I could (NO Medline abstracts!!). In point of fact, each component of my lipid profile, as well as various indicators of arterial inflammation indicated good to excellent conditions, when you disregarded the cholesterol con BS and outright lies. Arterial inflammation is the increasingly widely accepted underlying cause of plaque, NOT cholesterol, LDL, etc.
FYI, perhaps as much of 75% of heart attack victims have normal cholesteral levels.
I have one condition that you apparently do not have, that is, little or no detectable plaque in major arteries. Apparently, neither did any of my ancestors, because very few, if any, died of heart attacks, etc., going back a few hundred years. One can easily surmise that they had low levels of inflammation affecting walls of their arteries.
Strongly suggest that you read widely in articles from Dr. Graveline's Newsletters, as well as books by him and the various other MDs noted on this website -- give special attention to books by Kendrick, Ravenskov and McCully -- read them all if possible. In a few months you could become more accurately informed about CAD than your doctor, who I would label as just another of the huge population of cholesterol quacks practicing very damaging medicine.
Lars
- lars999
- Posts: 331
- Joined: Mon Sep 20, 2010 10:14 am
by lars999 » Thu Aug 11, 2011 10:30 pm
Thanks Bill for that article.
Over coming weeks I will spend some time digging into references cited. Unless I missed it in quick read through just now, there is no mention of the really dangerous type of plaque, vulnerable plaque, which can really be thought of as a plaque boil that is likely to rupture, dumping its contents into blood stream, which then triggers clotting of blood around the contents, which then often leads to blockage of smaller arteries, causing heart attacks. Most plaque is stable plaque and is of little consequence, unless it becomes really thick.
Formation of plaque is essential consequence of damage to lining or arteries, otherwise, we would develop leaky arteries -- not good. Unfortunately, plaque is really crude bandaids. Too many bandaids on bandaids, especially when plaque boils form, is bad news. Treating the real problem, chemical and physical damage to artery walls, is essential. Treating the symptoms, plaque is, as always with treating only symptoms of serious illnesses, not very effective.
One of my associates had a heart attack a few years ago. He was incredibly lucky -- he literally fell into arms of a cardiologist that was equipped to give him immediate injection of clot buster drug. He needed a stint to strengthen part of coronary artery that was damaged by blood clot. When catheter was run up from groin, attached ultrasound device found no plaque of any kind, nor did other, external, doppler ultrasound investigations. They never were able to determine location of plaque boil that ruptured. This guy met all usual criteria for a person highly unlikely to ever have a heart attack. He is now taking small amounts of aspirin to stabilize any possible additional such plaque boils.
I can say already, from just what I read quickly tonight of this article, that for many of us, high fat, protein-rich diets are not adverse, quite the contrary actually. However, I do not eat anything like the "standard american diet" of burgers and wide assortment of highly processed and junk food, replete with aggressive, oxidative chemicals. I eat pretty much what my ancestors did for 100s of years, folks that had few, in any heart attacks.
Thanks again for article with references.
Lars
Over coming weeks I will spend some time digging into references cited. Unless I missed it in quick read through just now, there is no mention of the really dangerous type of plaque, vulnerable plaque, which can really be thought of as a plaque boil that is likely to rupture, dumping its contents into blood stream, which then triggers clotting of blood around the contents, which then often leads to blockage of smaller arteries, causing heart attacks. Most plaque is stable plaque and is of little consequence, unless it becomes really thick.
Formation of plaque is essential consequence of damage to lining or arteries, otherwise, we would develop leaky arteries -- not good. Unfortunately, plaque is really crude bandaids. Too many bandaids on bandaids, especially when plaque boils form, is bad news. Treating the real problem, chemical and physical damage to artery walls, is essential. Treating the symptoms, plaque is, as always with treating only symptoms of serious illnesses, not very effective.
One of my associates had a heart attack a few years ago. He was incredibly lucky -- he literally fell into arms of a cardiologist that was equipped to give him immediate injection of clot buster drug. He needed a stint to strengthen part of coronary artery that was damaged by blood clot. When catheter was run up from groin, attached ultrasound device found no plaque of any kind, nor did other, external, doppler ultrasound investigations. They never were able to determine location of plaque boil that ruptured. This guy met all usual criteria for a person highly unlikely to ever have a heart attack. He is now taking small amounts of aspirin to stabilize any possible additional such plaque boils.
I can say already, from just what I read quickly tonight of this article, that for many of us, high fat, protein-rich diets are not adverse, quite the contrary actually. However, I do not eat anything like the "standard american diet" of burgers and wide assortment of highly processed and junk food, replete with aggressive, oxidative chemicals. I eat pretty much what my ancestors did for 100s of years, folks that had few, in any heart attacks.
Thanks again for article with references.
Lars
- lars999
- Posts: 331
- Joined: Mon Sep 20, 2010 10:14 am
by wmodavis » Thu Aug 11, 2011 11:25 pm
I'm with you on most of that Lars.
There are disadvantages to all those ways you mentioned to measure actual plaque. In short they do not do a good job of that. Using a coronary artery calcium does a much better and more accurate job of that. It is the best technology today for determining if you have plaque. It's a bit like using a stress test to determine your risk of a heart attack. It simply won't tell you that. Here is an exerpt from Dr
William Davis's book "Track Your Plaque" wherein he discusses the other ways to proportedly measure plaque.
===================================
From Chapter 4
"Other methods to detect early heart disease:
Though imaging technology is advanced rapidly, many methods are not yet ready for mainstream use. There are several alternatives, however, to coronary calcium scoring using EBT or MDCT scanners that are already available. Let’s discuss these alternatives and their strengths and weaknesses.
[b]Carotid Ultrasound [/b]
Atherosclerosis is a body-wide disease that affects all arteries of the body. That means plaque can develop simultaneously in the heart (coronary arteries), the brain (carotid arteries and cerebral circulation), the abdomen (abdominal aorta and mesenteric arteries), legs (iliac and femoral arteries), etc. Plaque develops in these parts of the body in parallel to the heart, though to varying degrees.
Most people with atherosclerotic disease tend to show evidence of disease in their heart first, i.e., they have a heart attack, or develop angina, or undergo a cardiac procedure. The other arteries of the body, though also developing plaque, tend to do so more slowly. This is partly due to the larger diameter of other arteries. Compare their relative sizes: coronary arteries generally measure 3–4 mm in diameter; carotid arteries measure 5–8 mm; femoral (thigh) arteries measure 6–9 mm, sometimes larger. Less plaque accumulation is, therefore, required in the smaller heart arteries before trouble ensues.
Nonetheless, because there is a parallel tendency for various arteries to develop plaque, some physicians have proposed that other arteries be measured in place of the heart. The imaging technique usually used is ultrasound, since it is easy, painless, and can be somewhat quantitative.
In ultrasound (like that used for intracoronary ultrasound), images are generated by a high-frequency sound-emitting crystal. The data is processed by a computer and converted into images. The best-studied technique involves ultrasound imaging of the carotid arteries, in which the device is applied gently to the neck and the carotid arteries (right and left) are examined. Using this technique, a measure called carotid intimal-medial thickness (CIMT), or the thickness of the internal lining of the arteries, is obtained. Note that CIMT is a measurement of the lining of the artery, not of carotid plaque itself. There have also been studies examining other arteries of the body (particularly the abdominal aorta, iliac, and femoral arteries), but they correlate less well to heart disease than the carotids.
Among the most experienced in this technique is Dr. Howard Hodis of the University of Southern California. His extensive experience does indeed suggest that measuring CIMT can predict heart attack risk, is correlated to a moderate degree with the extent of coronary plaque, and can be used to track the course of disease, i.e, progression or regression (Hodis HN 1996). CIMT measurement has been quite popular in research settings to examine the efficacy of various therapies.
Ultrasound is safe, since no radiation is involved. Devices capable of obtaining quality images are also very widely available. Most hospitals and even many cardiologists’ offices will have at least one if not several ultrasound units. Carotid ultrasound is already routinely performed to look for large plaques that pose risk for stroke.
So why isn’t carotid ultrasound performed more widely for identification of early heart disease?
There are several reasons. One reason is that the relationship of coronary disease to carotid IMT is not perfectly parallel. Coronary and carotid arteries respond somewhat differently to various influences and so develop plaque at different rates. Carotid IMT, for instance, is very sensitive to blood pressure effects; coronary plaque less so. The correlation of carotid IMT to coronary plaque is around 60 to 70%, meaning that a certain carotid IMT measurement will be around 60–70% accurate in predicting the extent of coronary plaque (Folsom AR 2008). It would be like buying a used car and trying to gauge the accuracy of the odometer mileage by looking at the wear on the rubber of the gas pedal—you can make relatively crude predictions, but it’s not terribly accurate.
Despite wide availability of ultrasound devices and the relative ease of obtaining this measure, the vast majority of facilities do not offer CIMT. CIMT measurement requires special software that most facilities do not have. Insurance also does not pay for CIMT. Ultrasound facilities, however, can measure carotid plaque, though in a non-quantitative way. Anyone who has undergone a conventional carotid ultrasound has likely been provided the frustratingly imprecise results, e.g., “10-49% plaque in the right internal carotid artery.â€
There are disadvantages to all those ways you mentioned to measure actual plaque. In short they do not do a good job of that. Using a coronary artery calcium does a much better and more accurate job of that. It is the best technology today for determining if you have plaque. It's a bit like using a stress test to determine your risk of a heart attack. It simply won't tell you that. Here is an exerpt from Dr
William Davis's book "Track Your Plaque" wherein he discusses the other ways to proportedly measure plaque.
===================================
From Chapter 4
"Other methods to detect early heart disease:
Though imaging technology is advanced rapidly, many methods are not yet ready for mainstream use. There are several alternatives, however, to coronary calcium scoring using EBT or MDCT scanners that are already available. Let’s discuss these alternatives and their strengths and weaknesses.
[b]Carotid Ultrasound [/b]
Atherosclerosis is a body-wide disease that affects all arteries of the body. That means plaque can develop simultaneously in the heart (coronary arteries), the brain (carotid arteries and cerebral circulation), the abdomen (abdominal aorta and mesenteric arteries), legs (iliac and femoral arteries), etc. Plaque develops in these parts of the body in parallel to the heart, though to varying degrees.
Most people with atherosclerotic disease tend to show evidence of disease in their heart first, i.e., they have a heart attack, or develop angina, or undergo a cardiac procedure. The other arteries of the body, though also developing plaque, tend to do so more slowly. This is partly due to the larger diameter of other arteries. Compare their relative sizes: coronary arteries generally measure 3–4 mm in diameter; carotid arteries measure 5–8 mm; femoral (thigh) arteries measure 6–9 mm, sometimes larger. Less plaque accumulation is, therefore, required in the smaller heart arteries before trouble ensues.
Nonetheless, because there is a parallel tendency for various arteries to develop plaque, some physicians have proposed that other arteries be measured in place of the heart. The imaging technique usually used is ultrasound, since it is easy, painless, and can be somewhat quantitative.
In ultrasound (like that used for intracoronary ultrasound), images are generated by a high-frequency sound-emitting crystal. The data is processed by a computer and converted into images. The best-studied technique involves ultrasound imaging of the carotid arteries, in which the device is applied gently to the neck and the carotid arteries (right and left) are examined. Using this technique, a measure called carotid intimal-medial thickness (CIMT), or the thickness of the internal lining of the arteries, is obtained. Note that CIMT is a measurement of the lining of the artery, not of carotid plaque itself. There have also been studies examining other arteries of the body (particularly the abdominal aorta, iliac, and femoral arteries), but they correlate less well to heart disease than the carotids.
Among the most experienced in this technique is Dr. Howard Hodis of the University of Southern California. His extensive experience does indeed suggest that measuring CIMT can predict heart attack risk, is correlated to a moderate degree with the extent of coronary plaque, and can be used to track the course of disease, i.e, progression or regression (Hodis HN 1996). CIMT measurement has been quite popular in research settings to examine the efficacy of various therapies.
Ultrasound is safe, since no radiation is involved. Devices capable of obtaining quality images are also very widely available. Most hospitals and even many cardiologists’ offices will have at least one if not several ultrasound units. Carotid ultrasound is already routinely performed to look for large plaques that pose risk for stroke.
So why isn’t carotid ultrasound performed more widely for identification of early heart disease?
There are several reasons. One reason is that the relationship of coronary disease to carotid IMT is not perfectly parallel. Coronary and carotid arteries respond somewhat differently to various influences and so develop plaque at different rates. Carotid IMT, for instance, is very sensitive to blood pressure effects; coronary plaque less so. The correlation of carotid IMT to coronary plaque is around 60 to 70%, meaning that a certain carotid IMT measurement will be around 60–70% accurate in predicting the extent of coronary plaque (Folsom AR 2008). It would be like buying a used car and trying to gauge the accuracy of the odometer mileage by looking at the wear on the rubber of the gas pedal—you can make relatively crude predictions, but it’s not terribly accurate.
Despite wide availability of ultrasound devices and the relative ease of obtaining this measure, the vast majority of facilities do not offer CIMT. CIMT measurement requires special software that most facilities do not have. Insurance also does not pay for CIMT. Ultrasound facilities, however, can measure carotid plaque, though in a non-quantitative way. Anyone who has undergone a conventional carotid ultrasound has likely been provided the frustratingly imprecise results, e.g., “10-49% plaque in the right internal carotid artery.â€
- wmodavis
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- Joined: Wed Aug 10, 2011 8:43 am
- Location: Highlands Ranch CO
by lars999 » Fri Aug 12, 2011 7:47 am
Bill,
I have not done my homework on "calcium measurement" of hearts, in part because I keep hearing low opinions of it. Perhaps the "fast scan" CAT scanners are enough better. I will take time to do some homework.
There still remains ability to distinguish between ordinary stable plaque and the dangerous vulnerable plaque boils. Last I understood, only intra arterial doppler ultrasound could do that. Can the latest, gee whiz calcium measurement CAT scanners clearly identify vulnerable plaque at all? Of course, if my friend's experience is common, calcium measurement CAT scans only on heart would miss any plaque boils elsewhere.
Detection and measurement of plaque is really monitoring symptoms, not underlying causes. By time a person has much ordinary, stable plaque, it is really quite late in game. But, that is exactly the major weakness in nearly all methods in cardiology, way too much way too late.
Lars
I have not done my homework on "calcium measurement" of hearts, in part because I keep hearing low opinions of it. Perhaps the "fast scan" CAT scanners are enough better. I will take time to do some homework.
There still remains ability to distinguish between ordinary stable plaque and the dangerous vulnerable plaque boils. Last I understood, only intra arterial doppler ultrasound could do that. Can the latest, gee whiz calcium measurement CAT scanners clearly identify vulnerable plaque at all? Of course, if my friend's experience is common, calcium measurement CAT scans only on heart would miss any plaque boils elsewhere.
Detection and measurement of plaque is really monitoring symptoms, not underlying causes. By time a person has much ordinary, stable plaque, it is really quite late in game. But, that is exactly the major weakness in nearly all methods in cardiology, way too much way too late.
Lars
- lars999
- Posts: 331
- Joined: Mon Sep 20, 2010 10:14 am
LP(a)
by BCGuy » Mon Aug 22, 2011 7:22 pm
Hello all!
It seems the excellent people here are still at their work of helping others in regards to these health issues and Statin damage.
I finally found a doctor who at least listens and is understanding about my wishes to not take Statins to lower Cholestrol.
I had several different blood tests done recently, they were C-Reactive Protein,Lp(a), Homocysteine, and Fibrinogen.
The only issues here were a very slightly increased inflamation level, but my
Lp(a) ( which I think is the small dense LP) was at 503.
My question to you good people is how does this number reflect my health? I quit smoking, don't eat sugar anymore, exercise more and take all the suggested vitamins and minerals. Could these numbers reflect something I maybe doing wrong or is it something my body creates by itself?
Does anyone have any insight or links to help me educate myself on this?
Thank you in advance
It seems the excellent people here are still at their work of helping others in regards to these health issues and Statin damage.
I finally found a doctor who at least listens and is understanding about my wishes to not take Statins to lower Cholestrol.
I had several different blood tests done recently, they were C-Reactive Protein,Lp(a), Homocysteine, and Fibrinogen.
The only issues here were a very slightly increased inflamation level, but my
Lp(a) ( which I think is the small dense LP) was at 503.
My question to you good people is how does this number reflect my health? I quit smoking, don't eat sugar anymore, exercise more and take all the suggested vitamins and minerals. Could these numbers reflect something I maybe doing wrong or is it something my body creates by itself?
Does anyone have any insight or links to help me educate myself on this?
Thank you in advance
- BCGuy
- Posts: 14
- Joined: Sat Jan 22, 2011 2:54 pm
by David Staup » Tue Aug 23, 2011 9:37 am
http://www.spacedoc.com/lipoprotein(a)_heart_disease
http://www.spacedoc.com/cardiovascular_risk_factors
http://www.spacedoc.com/stephen-sinatra-QandA-01
always search this site first!
http://www.spacedoc.com/cardiovascular_risk_factors
http://www.spacedoc.com/stephen-sinatra-QandA-01
always search this site first!
- David Staup
- Posts: 546
- Joined: Wed Nov 28, 2007 1:13 pm
- Location: granbury, texas
by lars999 » Tue Aug 23, 2011 9:44 am
BCGuy,
The Wikipedia write up on lipoprotein(a) seems like a good place to start.
*http://en.wikipedia.org/wiki/Lipoprotein(a)
Many months ago I dug as deeply into this as time permitted. Happily I was reported to have rather low Lp(a) concentration, but not the insanely low values some Cholesterol Quacks want to see. Reading as many full (NOT just abstracts!!) medical journal articles as I could find, I came away without any great conviction that my low Lp(a) concentration marked me as one of the fortunate. I did not spend any time educating myself about reliability of predictions based on high concentrations of Lp(a). However, note that Lp(a) levels are "widely" considered to be inherited. Also be aware that proponents commonly "push the limits" when touting the importance of their new "gee whiz" method, procedure, etc., while down playing utility of other methods, etc. Great chance to play "Judge and Jury" games.
I also spent a lot of time reading full articles about various analytical chemistry methods and practices used, for the more "advanced, gee whiz" tests. In a few cases this resulted in me calling the actual chemical lab that was going to do the analysis and requesting to talk to the actual chemist doing the analyses. Having been a practicing analytical chemist for a few decades, this was SOP for me, especially for methods I had never used. Results were generally good, but, I actually canceled some tests because they simply could not reliably measure what they claimed, one was even worse than that. These were all among the most expensive, least time-honored and cross-checked tests. Lp(a) measurements seemed to be OK. My contacting the chemical labs greatly enraged the "prescribing" doctor -- yea!! I did not go so far as to have any tests repeated, at least not this time. Nearly all tests I had done are well established and reliable, unless someone screws up and QC does not catch it and have analysis repeated.
Should you come to be seriously concerned, I would check into possibility of having the Lp(a) test repeated, especially if there is a second, reputedly reliable lab that does the same analysis (don't recall if there are multiple high quality labs doing this test or not).
Best wishes,
Lars
The Wikipedia write up on lipoprotein(a) seems like a good place to start.
*http://en.wikipedia.org/wiki/Lipoprotein(a)
Many months ago I dug as deeply into this as time permitted. Happily I was reported to have rather low Lp(a) concentration, but not the insanely low values some Cholesterol Quacks want to see. Reading as many full (NOT just abstracts!!) medical journal articles as I could find, I came away without any great conviction that my low Lp(a) concentration marked me as one of the fortunate. I did not spend any time educating myself about reliability of predictions based on high concentrations of Lp(a). However, note that Lp(a) levels are "widely" considered to be inherited. Also be aware that proponents commonly "push the limits" when touting the importance of their new "gee whiz" method, procedure, etc., while down playing utility of other methods, etc. Great chance to play "Judge and Jury" games.
I also spent a lot of time reading full articles about various analytical chemistry methods and practices used, for the more "advanced, gee whiz" tests. In a few cases this resulted in me calling the actual chemical lab that was going to do the analysis and requesting to talk to the actual chemist doing the analyses. Having been a practicing analytical chemist for a few decades, this was SOP for me, especially for methods I had never used. Results were generally good, but, I actually canceled some tests because they simply could not reliably measure what they claimed, one was even worse than that. These were all among the most expensive, least time-honored and cross-checked tests. Lp(a) measurements seemed to be OK. My contacting the chemical labs greatly enraged the "prescribing" doctor -- yea!! I did not go so far as to have any tests repeated, at least not this time. Nearly all tests I had done are well established and reliable, unless someone screws up and QC does not catch it and have analysis repeated.
Should you come to be seriously concerned, I would check into possibility of having the Lp(a) test repeated, especially if there is a second, reputedly reliable lab that does the same analysis (don't recall if there are multiple high quality labs doing this test or not).
Best wishes,
Lars
- lars999
- Posts: 331
- Joined: Mon Sep 20, 2010 10:14 am
by BCGuy » Tue Aug 23, 2011 10:17 am
Thanks Lars,
I did do some reading about this and found somewhat the same things.
I asked for this test not the new doctor. It seems he didn't know too much about the actual numbers and said he'd get back to me about it. Which I appreciate instead of someone who has to protect their intellectual ego and just give some kind of answer.
From what I can recall from my reading yesterday Lp(a) is similar but not the same as LDL Cholestrol, yes believed to be inherited. Lp(a) seems to be the stickiest blood component involved in plaque formation. High doses of VitaminC and Niacine seem to be the only things that might lower the amounts one might have. L-lysine ,and L-proline are other products that help to "use up" the receptors on each Lp(a) particle.
I'm not sure if low inflamation and oxidation levels makes Lp(a) more inert in a persons system. As always thanks Lars you do a great job helping others here.
BCGuy
I did do some reading about this and found somewhat the same things.
I asked for this test not the new doctor. It seems he didn't know too much about the actual numbers and said he'd get back to me about it. Which I appreciate instead of someone who has to protect their intellectual ego and just give some kind of answer.
From what I can recall from my reading yesterday Lp(a) is similar but not the same as LDL Cholestrol, yes believed to be inherited. Lp(a) seems to be the stickiest blood component involved in plaque formation. High doses of VitaminC and Niacine seem to be the only things that might lower the amounts one might have. L-lysine ,and L-proline are other products that help to "use up" the receptors on each Lp(a) particle.
I'm not sure if low inflamation and oxidation levels makes Lp(a) more inert in a persons system. As always thanks Lars you do a great job helping others here.
BCGuy
- BCGuy
- Posts: 14
- Joined: Sat Jan 22, 2011 2:54 pm
by lars999 » Tue Aug 23, 2011 1:53 pm
Thanks David for that reference to newsletter from Duane on Lp(a) -- I either missed it or maybe "old man's amnesia" is to blame.
BCGuy,
Maybe my low Lp(a) is the primary reason why my, apparently inherited, high total cholesterol is accompanied by a family history of few, if any, heart attacks. Various blood tests for arterial inflammation indicate low, but not lowest, levels of such inflammation. I like Duane's concise interpretation of role and importance of Lp(a) -- however, I could not come to such a neat interpretation after reading what, relatively few, full articles I could find on Internet. Duane surely has access to many more and better articles -- certainly, he has far better access to others in medical community than I do.
Nice to see Duane's article point out not only positive role of vitamin C but also of CoQ10, because I have been taking a few grams of vitamin C and a few 100 mg of CoQ10 (as ubiquinol) each day, since I got smart and quit Lipitor on 10 June 2010.
I have been a bit liberal with my affections for various explanations of what actually causes excessive plaque, thrombosis, etc. I grew up with Pauling and Rauth's ideas about role of vitamin C and find Kilmer McCully's writings on homocycteine quite convincing. Now it would appear that somewhere in the medical literature is similarly extensive and convincing information and interpretations of role of Lp(a). And, maybe, I can even credit Lp(a) for my blood clotting so nicely when I get cuts .......
Thank you for bringing up Lp(a) again!!
Lars
BCGuy,
Maybe my low Lp(a) is the primary reason why my, apparently inherited, high total cholesterol is accompanied by a family history of few, if any, heart attacks. Various blood tests for arterial inflammation indicate low, but not lowest, levels of such inflammation. I like Duane's concise interpretation of role and importance of Lp(a) -- however, I could not come to such a neat interpretation after reading what, relatively few, full articles I could find on Internet. Duane surely has access to many more and better articles -- certainly, he has far better access to others in medical community than I do.
Nice to see Duane's article point out not only positive role of vitamin C but also of CoQ10, because I have been taking a few grams of vitamin C and a few 100 mg of CoQ10 (as ubiquinol) each day, since I got smart and quit Lipitor on 10 June 2010.
I have been a bit liberal with my affections for various explanations of what actually causes excessive plaque, thrombosis, etc. I grew up with Pauling and Rauth's ideas about role of vitamin C and find Kilmer McCully's writings on homocycteine quite convincing. Now it would appear that somewhere in the medical literature is similarly extensive and convincing information and interpretations of role of Lp(a). And, maybe, I can even credit Lp(a) for my blood clotting so nicely when I get cuts .......
Thank you for bringing up Lp(a) again!!
Lars
- lars999
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