Have your Doctor read this before he stops your Niacin.
Dr. Dayspring on recent niacin trials link
This article no longer appears on Dr. Dayspring's site
Excerpt:
"On December 22nd a world class cardiologist, lipid thought leader, Michael Davidson, tweeted that the baseline lipids(in HPS2 THRIVE) were LDL-C = 63, TG = 120 and HDL-C 44 mg/dL with the comment “Why treat?” Bingo – whenever a trial produces a certain outcome, that outcome pertains only to patients who have the characteristics of the population that was studied. So this study shows that in patients with stable coronary artery disease who happen to have on-treatment lipids at goal, indeed exemplary values, why would anyone add any additional lipid therapy. So I could not more strongly agree with my friend and colleague’s statement!
This study almost looks like a re-run of the AIM-HIGH trial in which adding niacin to statin or statin/ezetimibe also struck out – but once again LDL-C, non-HDL-C and apoB goals had been achieved at baseline with use of high dose simvastatin or simvastatin plus ezetimibe. Of course in AIM-HIGH study the baseline HDL-C was still low and at least you can make the case that this study was well designed to show whether niacin induced-raising of HDL-C in high-risk persons with at-goal apoB (LDL-C, non-HDL-C) has any clinical benefit.
Clearly it does (did) put to bed the idea that niacin’s mechanism has anything to do with HDL-cholesterol. Niacin is primarily an apoB lowering drug.
Paradoxically niacin raises HDL-C without raising HDL-P which it would suggest niacin is simply increasing HDL size and perhaps reducing HDL-TG.
HPS2-THRIVE makes no statement about what benefit niacin/laropiprant might bring when added to on-treatment persons not at goal of therapy. It also makes no statement about what niacin monotherapy or niacin/fibrate combo therapy or niacin bile acid sequestrant therapy might do.
So all we really know right now is when treating high risk patients who are at goal additional lipid modulation with niacin is not needed.
However in my mind, I would not hesitate to add high dose niacin (cannot prescribe laropiprant in US):
1- to a statin or statin/ezetimibe regimen if the patient were not at apoB (LDL-C, non-HDL-C) goal
2- or use niacin in statin-intolerant persons."
"Further, baseline TG was 125 mg/dL and HDL-C was 44 mg/dL, so HPS2-THRIVE tested a drug in patients who, on average, had no indication to take it. "
Dr. Dayspring on recent niacin trials link
This article no longer appears on Dr. Dayspring's site
Excerpt:
"On December 22nd a world class cardiologist, lipid thought leader, Michael Davidson, tweeted that the baseline lipids(in HPS2 THRIVE) were LDL-C = 63, TG = 120 and HDL-C 44 mg/dL with the comment “Why treat?” Bingo – whenever a trial produces a certain outcome, that outcome pertains only to patients who have the characteristics of the population that was studied. So this study shows that in patients with stable coronary artery disease who happen to have on-treatment lipids at goal, indeed exemplary values, why would anyone add any additional lipid therapy. So I could not more strongly agree with my friend and colleague’s statement!
This study almost looks like a re-run of the AIM-HIGH trial in which adding niacin to statin or statin/ezetimibe also struck out – but once again LDL-C, non-HDL-C and apoB goals had been achieved at baseline with use of high dose simvastatin or simvastatin plus ezetimibe. Of course in AIM-HIGH study the baseline HDL-C was still low and at least you can make the case that this study was well designed to show whether niacin induced-raising of HDL-C in high-risk persons with at-goal apoB (LDL-C, non-HDL-C) has any clinical benefit.
Clearly it does (did) put to bed the idea that niacin’s mechanism has anything to do with HDL-cholesterol. Niacin is primarily an apoB lowering drug.
Paradoxically niacin raises HDL-C without raising HDL-P which it would suggest niacin is simply increasing HDL size and perhaps reducing HDL-TG.
HPS2-THRIVE makes no statement about what benefit niacin/laropiprant might bring when added to on-treatment persons not at goal of therapy. It also makes no statement about what niacin monotherapy or niacin/fibrate combo therapy or niacin bile acid sequestrant therapy might do.
So all we really know right now is when treating high risk patients who are at goal additional lipid modulation with niacin is not needed.
However in my mind, I would not hesitate to add high dose niacin (cannot prescribe laropiprant in US):
1- to a statin or statin/ezetimibe regimen if the patient were not at apoB (LDL-C, non-HDL-C) goal
2- or use niacin in statin-intolerant persons."
Niacin's anti-inflammatory effect
Niacin treatment in hypercholesterolemic patients with low HDL levels caused a significant decrease in their oxidative stress status. These results indicate an additional beneficial effect of niacin beyond its ability to affect the lipid profile.
Niacin treatment in hypercholesterolemic patients with low HDL levels caused a significant decrease in their oxidative stress status. These results indicate an additional beneficial effect of niacin beyond its ability to affect the lipid profile.
"Further, baseline TG was 125 mg/dL and HDL-C was 44 mg/dL, so HPS2-THRIVE tested a drug in patients who, on average, had no indication to take it. "
"Thus, ERNL has net harm in Chinese patients when added to simvastatin.
"In contrast, however, among Europeans (likely largely Caucasian) there was net MVE benefit, as well as less myopathy.
Finally, it remains possible that the use of laropiprant in the niacin arm of the study increased adverse events and/or reduced benefits."
Meanwhile, we believe that niacin
1- remains a valuable adjunct to statin treatment for LDL-C lowering,
2- a valuable statin alternative in statin intolerant patients.
3-Further, in agreement with current NCEP ATP III Guidelines, we believe that niacin should continue to be considered for use as a statin adjunct in patients with persistent low HDL-C and high TG."
"In contrast, however, among Europeans (likely largely Caucasian) there was net MVE benefit, as well as less myopathy.
Finally, it remains possible that the use of laropiprant in the niacin arm of the study increased adverse events and/or reduced benefits."
Meanwhile, we believe that niacin
1- remains a valuable adjunct to statin treatment for LDL-C lowering,
2- a valuable statin alternative in statin intolerant patients.
3-Further, in agreement with current NCEP ATP III Guidelines, we believe that niacin should continue to be considered for use as a statin adjunct in patients with persistent low HDL-C and high TG."
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