Nelson Vergel
Founder, ExcelMale.com
This is a very good summary table of different supplements that have been successfully studied in decreasing LDL cholesterol and triglycerides. Some also can increase HDL (good) cholesterol.
Supplements that lower LDL cholesterol and triglycerides and increase HDL.
- Thread starter Nelson Vergel
- Start date
Don Schultz
Member
Some individuals have very difficult, inherited, LDL and HCL challenge and use statins to control this. Is there any information easily available showing the results such individuals have been able to achieve using some or all of the supplements above? Actual case studies of individuals and their numbers?
Nelson Vergel
Founder, ExcelMale.com
GEORGE TOULIATOS
New Member
Phytosterols are estrogenic compounds.Supplementation that includes them among their ingredients are:
1) ''Cholesterol success plus''-TWINLAB
2) ''Lipid Stabil''-MOLECULAR NUTRITION
1) ''Cholesterol success plus''-TWINLAB
2) ''Lipid Stabil''-MOLECULAR NUTRITION
IntelligentLabs
New Member
Hen measuring LDL have any of you looked at the size of LDL particles rather than just volume?
Vince
Super Moderator
Decreases small low-density lipoprotein (small LDL) particles. Small LDL is an important yet underappreciated cause of heart disease. Niacin is the most effective agent known for correcting this abnormal pattern.
Decreases triglycerides by 30%. Niacin is especially effective when taken with fish oil (at doses of 4000 mg a day, providing 1200 mg of EPA/DHA).https://www.excelmale.com/forum/showthread.php?6159-Using-Niacin-to-Improve-Cardiovascular-Health
Although niacin is the most potent compound known as far as shifting the profile of LDL pattern, it is speculation that doing so will result in reducing the chance of a cardiovascular event. In other words, there has never been a trial designed to assess the niacin's ability to reduce CV events. In fact the trials designed to determine whether using niacin to increase HDL reduces risk has proven to be a bust. HDL looks better on paper, but it didn't reduce events. I would have to assume that the niacin used to raise HDL also shifted the LDL pattern, but yet no reduction in risk
Vince
Super Moderator
Imaging
Imaging study shows plaque regression with niacin vs placebo
October 30, 2009 Shelley Wood Oxford, UK - A new imaging study is providing a first hint at the potential for niacin to help with plaque regression when used on top of optimized statin therapy. Writing in an early online edition of the Journal of the American College of Cardiology (JACC), Dr Justin MS Lee (University of Oxford, UK) and colleagues report that 2 g of modified-release nicotinic acid (Niaspan, Abbott Laboratories) daily,on top of statin, resulted in a 1.64 mm reduction in carotid wall area on MRI, compared with placebo, in patients with vascular disease and low HDL.
The paper comes as anticipation builds for the ARBITER-HALTS6 study results. ARBITER-HALTS 6 is an imaging study comparing changes in carotid intima-media thickness in patients treated with ezetimibe (Zetia, Merck/Schering-Plough) or extended-release niacin; market analysts are already for niacin. As previously reported by heartwire, ARBITER-HALTS 6 was stopped early: full results will be presented Monday, November 16, 2009 at the American Heart Association meeting in Orlando.
In the current study, niacin-treated patients experienced increases in HDL and decreases in LDL and triglycerides, accompanied by a 1.1 mm reduction in carotid wall area over the course of the 12-month study. By contrast, HDL levels in placebo-treated patients stayed more or less static, with more modest decreases in LDL and triglycerides, while carotid wall area actually increased by 1.32 mm
"There are a number of studies before this one—HATS and ARBITER 3—that have suggested findings consistent with ours, and I think what's new and important about this study is that it is the first one to show regression in patients who were taking established best contemporary treatment," senior author on the JACC paper, Dr Robin P Choudhury (University of Oxford, UK), told heartwire. "This feeds into a bigger understanding of how this drug works, and it is very encouraging. To me, it absolutely focuses interest on those outcome studies, but we do need those studies."
Not only are large outcome trials key, but experts not involved in the study point out that an important question not answered by the imaging end points used in this study is whether nicotinic acid reduces the volume of lipid-rich core, something other MRI studies have specifically addressed. In an accompanying editorial, Dr Farouc A Jaffer (Massachusetts General Hospital, Boston) writes, "it may be important to ascertain whether [nicotinic acid] therapy reduces carotid plaque lipid-rich/necrotic cores." Likewise, Dr Roger Blumenthal (Johns Hopkins University, Baltimore, MD), commenting on the study for heartwire, said he was not so sure that a regression of 1 mm in carotid wall area is "clinically meaningful."
"Usually with MRI, you talk about volume of plaque, and they are talking about area of plaque, which is a little bit confusing. . . . It's not like 30% of the lipid-rich core has gone away—that would be meaningful. These are minute changes and, in my mind, whether those will translate into better clinical outcomes in the two ongoing niacin studies remains to be determined."
The two much-anticipated outcome studies are AIM-HIGH, due out in 2011, and HPS2-THRIVE, anticipated to wind up in 2013.
To heartwire, Choudhury agreed that the change in carotid wall area is "very modest."
"So, in terms of relieving a stenosis, for example, it is not clinically relevant. The point is the direction of change. Atherosclerosis has, for years, been considered a relentlessly progressive disease process. To bring about a demonstrable reversal, however small, in only 12 months is mechanistically significant," he said. "Furthermore, remember that the plaque is heterogeneous. We don't know what compositional changes have been induced but if, for example, the lipid component had been reduced—and there are data from other studies to suggest this happens—then even a small change in total size could be very relevant to plaque behavior."
Asked why plaque volume was not the primary end point in the study, Choudhury said that carotid wall area is "effectively the same thing" as plaque volume.
"Volume is generated in other studies by multiplying the area of the wall by the MR slice thickness," he stated.
New results
The Merck KGaA-funded study by Lee et al was investigator-initiated and randomized 71 patients with low HDL (<40 mg/dL) to 2 g daily nicotinic acid (up-titrated over the first eight weeks), or placebo, on top of statin therapy, as dosed by the treating physician. To be enrolled in the study, patients needed to have carotid atherosclerosis, peripheral arterial disease, or type 2 diabetes and coronary artery disease. MRI was performed at baseline and at six and 12 months, with blood samples taken at the time of MRI.
In addition to the primary end point of absolute change in carotid artery wall area at one year—which was statistically significant, favoring the niacin-treated patients—investigators assessed change in aortic wall area and other measures of vascular function by MRI, none of which were statistically different between the niacin and placebo groups at one year.
Known side effects of niacin—flushing, itching, and gastrointestinal upset—were common in the study, and a full 20% of patients randomized to niacin withdrew because of drug side effects or MRI claustrophobia.
As Choudhury reminded heartwire, niacin has "been around a long time," but, due largely to its side-effect profile, is now scarcely used in the UK and, to the best of his knowledge, is prescribed infrequently in the US. "It was the first drug that was demonstrated to be of benefit in secondary prevention after MI, but it fell by the wayside because the early preparations had problems with toxicity and tolerance. And in the meantime, statins came on the scene and of course were very effective in reducing mortality in a wide variety of patient groups."
Some caveats
On that background, however, Choudhury says the results of this latest study are intriguing, but with two caveats.
"One, we absolutely have to wait for the outcome studies before we make any comments on the appropriateness of niacin treatment in these patients. This is a very interesting study, but it's not definitive. Second, most patients experience some side effects with niacin, and the large majority experience some flushing. But with appropriate precautions, such as taking the drug at night, with aspirin, and perhaps having a light snack, [side effects] are manageable in most patients. So if it turns out in the outcome studies that there are, indeed, very significant benefits, then these side effects, in my view, are certainly liveable with."
Blumenthal, speaking with heartwire, was more guarded, and said he felt the discussion in Lee et al's paper "went a bit overboard [portraying] niacin as a clear winner."
"I think they were very strong in their support of niacin, based on an absolute difference of 2/100ths of a square millimetre," he noted.
My English is not good. What does Niacin "on top of statins" mean?
Does that mean niacin "tops" statin for regression?
Cardiology News & Opinion – theheart.org | Medscape
Imaging study shows plaque regression with niacin vs placebo
October 30, 2009 Shelley Wood Oxford, UK - A new imaging study is providing a first hint at the potential for niacin to help with plaque regression when used on top of optimized statin therapy. Writing in an early online edition of the Journal of the American College of Cardiology (JACC), Dr Justin MS Lee (University of Oxford, UK) and colleagues report that 2 g of modified-release nicotinic acid (Niaspan, Abbott Laboratories) daily,on top of statin, resulted in a 1.64 mm reduction in carotid wall area on MRI, compared with placebo, in patients with vascular disease and low HDL.
The paper comes as anticipation builds for the ARBITER-HALTS6 study results. ARBITER-HALTS 6 is an imaging study comparing changes in carotid intima-media thickness in patients treated with ezetimibe (Zetia, Merck/Schering-Plough) or extended-release niacin; market analysts are already for niacin. As previously reported by heartwire, ARBITER-HALTS 6 was stopped early: full results will be presented Monday, November 16, 2009 at the American Heart Association meeting in Orlando.
In the current study, niacin-treated patients experienced increases in HDL and decreases in LDL and triglycerides, accompanied by a 1.1 mm reduction in carotid wall area over the course of the 12-month study. By contrast, HDL levels in placebo-treated patients stayed more or less static, with more modest decreases in LDL and triglycerides, while carotid wall area actually increased by 1.32 mm
"There are a number of studies before this one—HATS and ARBITER 3—that have suggested findings consistent with ours, and I think what's new and important about this study is that it is the first one to show regression in patients who were taking established best contemporary treatment," senior author on the JACC paper, Dr Robin P Choudhury (University of Oxford, UK), told heartwire. "This feeds into a bigger understanding of how this drug works, and it is very encouraging. To me, it absolutely focuses interest on those outcome studies, but we do need those studies."
Not only are large outcome trials key, but experts not involved in the study point out that an important question not answered by the imaging end points used in this study is whether nicotinic acid reduces the volume of lipid-rich core, something other MRI studies have specifically addressed. In an accompanying editorial, Dr Farouc A Jaffer (Massachusetts General Hospital, Boston) writes, "it may be important to ascertain whether [nicotinic acid] therapy reduces carotid plaque lipid-rich/necrotic cores." Likewise, Dr Roger Blumenthal (Johns Hopkins University, Baltimore, MD), commenting on the study for heartwire, said he was not so sure that a regression of 1 mm in carotid wall area is "clinically meaningful."
"Usually with MRI, you talk about volume of plaque, and they are talking about area of plaque, which is a little bit confusing. . . . It's not like 30% of the lipid-rich core has gone away—that would be meaningful. These are minute changes and, in my mind, whether those will translate into better clinical outcomes in the two ongoing niacin studies remains to be determined."
The two much-anticipated outcome studies are AIM-HIGH, due out in 2011, and HPS2-THRIVE, anticipated to wind up in 2013.
To heartwire, Choudhury agreed that the change in carotid wall area is "very modest."
"So, in terms of relieving a stenosis, for example, it is not clinically relevant. The point is the direction of change. Atherosclerosis has, for years, been considered a relentlessly progressive disease process. To bring about a demonstrable reversal, however small, in only 12 months is mechanistically significant," he said. "Furthermore, remember that the plaque is heterogeneous. We don't know what compositional changes have been induced but if, for example, the lipid component had been reduced—and there are data from other studies to suggest this happens—then even a small change in total size could be very relevant to plaque behavior."
Asked why plaque volume was not the primary end point in the study, Choudhury said that carotid wall area is "effectively the same thing" as plaque volume.
"Volume is generated in other studies by multiplying the area of the wall by the MR slice thickness," he stated.
New results
The Merck KGaA-funded study by Lee et al was investigator-initiated and randomized 71 patients with low HDL (<40 mg/dL) to 2 g daily nicotinic acid (up-titrated over the first eight weeks), or placebo, on top of statin therapy, as dosed by the treating physician. To be enrolled in the study, patients needed to have carotid atherosclerosis, peripheral arterial disease, or type 2 diabetes and coronary artery disease. MRI was performed at baseline and at six and 12 months, with blood samples taken at the time of MRI.
In addition to the primary end point of absolute change in carotid artery wall area at one year—which was statistically significant, favoring the niacin-treated patients—investigators assessed change in aortic wall area and other measures of vascular function by MRI, none of which were statistically different between the niacin and placebo groups at one year.
Known side effects of niacin—flushing, itching, and gastrointestinal upset—were common in the study, and a full 20% of patients randomized to niacin withdrew because of drug side effects or MRI claustrophobia.
As Choudhury reminded heartwire, niacin has "been around a long time," but, due largely to its side-effect profile, is now scarcely used in the UK and, to the best of his knowledge, is prescribed infrequently in the US. "It was the first drug that was demonstrated to be of benefit in secondary prevention after MI, but it fell by the wayside because the early preparations had problems with toxicity and tolerance. And in the meantime, statins came on the scene and of course were very effective in reducing mortality in a wide variety of patient groups."
Some caveats
On that background, however, Choudhury says the results of this latest study are intriguing, but with two caveats.
"One, we absolutely have to wait for the outcome studies before we make any comments on the appropriateness of niacin treatment in these patients. This is a very interesting study, but it's not definitive. Second, most patients experience some side effects with niacin, and the large majority experience some flushing. But with appropriate precautions, such as taking the drug at night, with aspirin, and perhaps having a light snack, [side effects] are manageable in most patients. So if it turns out in the outcome studies that there are, indeed, very significant benefits, then these side effects, in my view, are certainly liveable with."
Blumenthal, speaking with heartwire, was more guarded, and said he felt the discussion in Lee et al's paper "went a bit overboard [portraying] niacin as a clear winner."
"I think they were very strong in their support of niacin, based on an absolute difference of 2/100ths of a square millimetre," he noted.
My English is not good. What does Niacin "on top of statins" mean?
Does that mean niacin "tops" statin for regression?
Cardiology News & Opinion – theheart.org | Medscape
THANKS VINCE
There is a lot of very interesting information there. However, whoever that person is that said that LDL below 70 is a myth and based on the fact that babies don't have plaque cannot be taken seriously. I find it astounding that someone would make such a statement. LDL below 70 is based on RCT that have shown that lowering LDL results in less events. We never had the 70 threshold of LDL before that was proven in trials. However, we have know forever that babies have low cholesterol. The JUPITER trial has even hinted that LDL as low as 50 may reverse plaque
There is a lot of very interesting information there. However, whoever that person is that said that LDL below 70 is a myth and based on the fact that babies don't have plaque cannot be taken seriously. I find it astounding that someone would make such a statement. LDL below 70 is based on RCT that have shown that lowering LDL results in less events. We never had the 70 threshold of LDL before that was proven in trials. However, we have know forever that babies have low cholesterol. The JUPITER trial has even hinted that LDL as low as 50 may reverse plaque
maxadvance
Active Member
Aren't there studies showing LDL that low can cause memory loss? At least LDL lowered by statins have shown this
Perhaps there are. Honestly, I don't know. I do know that there is an association between very low cholesterol and brain Hemorrhagic stroke. So my comment is not to say that lowering cholesterol, or LDL cholesterol for that matter, is not without side effects. Although, the aforementioned is an association, and as such does not prove causation.
However, my point is that in the post above there is a quote stating that "the myth about LDL<70 is based on the idea that babies don't have cholesterol plaques. Duh." That statement is incorrect. This is not the rationale for that threshold. And I am not commenting on whether the threshold is proper. I am just stating that the statement is so erroneous that it makes me question anything that the quoted person (john Kent or Blanchet) states.
However, my point is that in the post above there is a quote stating that "the myth about LDL<70 is based on the idea that babies don't have cholesterol plaques. Duh." That statement is incorrect. This is not the rationale for that threshold. And I am not commenting on whether the threshold is proper. I am just stating that the statement is so erroneous that it makes me question anything that the quoted person (john Kent or Blanchet) states.
Vince
Super Moderator
I read this before and thought it was interesting. http://www.examiner.com/article/hea...lesterol-of-14-due-to-a-rare-genetic-mutation
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