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Related: About this forumWant a way to raise HDL, in addition to exercise? Mayo Clinic says Niacin can raise HDL 30%!
http://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/in-depth/niacin/art-20046208Niacin can raise HDL cholesterol by more than 30 percent. HDL, the "good" cholesterol, picks up excess bad cholesterol in your blood and takes it back to your liver for disposal.
I don't know any substance you can take that can raise HDL like that. (Sytrinol is supposed to raise it a bit. But nothing like 30%).
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Want a way to raise HDL, in addition to exercise? Mayo Clinic says Niacin can raise HDL 30%! (Original Post)
Bill USA
Jul 2015
OP
Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct?
OKIsItJustMe
Jul 2015
#5
Shrike47
(6,913 posts)1. That's why I take it, on rec from doctor.
LiberalArkie
(15,719 posts)2. Only one type of Niacin works it is Nicotinic Acid.
TexasProgresive
(12,157 posts)3. If a man wants to experience hot flashes
that might be similar to those in menopause, take nicotine acid. I don't know if the feeling is the same but those flushes are pretty intense.
LiberalArkie
(15,719 posts)4. They only lasted about a week with me.
TexasBushwhacker
(20,196 posts)6. You have to start with a small dose
and work up. It's easiest if you can get pill form so you can split. But a heavy flush isn't fun.
womanofthehills
(8,718 posts)8. Take niacin right before you go to sleeep
I've been taking niacin for about a yr now and my HDL is up to 70
OKIsItJustMe
(19,938 posts)5. Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct?
http://www.ncbi.nlm.nih.gov/pubmed/26048725
[font face=Serif]Curr Atheroscler Rep. 2015 Aug;17(8):521. doi: 10.1007/s11883-015-0521-x.
[font size=5]Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct?[/font]
[font size=4]Abstract[/font]
[font size=3]High-density lipoprotein cholesterol (HDL-C) has been shown in epidemiologic studies to be associated with cardiovascular (CV) risk and thus significant efforts have been focused on HDL-C modulation. Multiple pharmaceutical agents have been developed with the goal of increasing HDL-C. Niacin, the most widely used medication to raise HDL-C, increases HDL-C by up to 25 % and was shown in multiple surrogate end point studies to reduce CV risk. However, two large randomized controlled trials of niacin, AIM-HIGH and HPS2-THRIVE, have shown that despite its effects on HDL-C, niacin does not decrease the incidence of CV events and may have significant adverse effects. Studies of other classes of agents such as cholesteryl ester transfer protein (CETP) inhibitors have also shown that even dramatic increases in HDL-C do not necessarily translate to reduction in clinical events. While these findings have cast doubt upon the importance of HDL-C modulation on CV risk, it is becoming increasingly clear that HDL function-related measures may be better targets for CV risk reduction. Increasing ApoA-I, the primary apolipoprotein associated with HDL, correlates with reduced risk of events, and HDL particle concentration (HDL-P) inversely associates with incident CV events adjusted for HDL-C and LDL particle measures. Cholesterol efflux, the mechanism by which macrophages in vessel walls secrete cholesterol outside cells, correlates with both surrogate end points and clinical events. The effects of niacin on these alternate measures of HDL have been conflicting. Further studies should determine if modulation of these HDL function markers translates to clinical benefits. Although the HDL cholesterol hypothesis may be defunct, the HDL function hypothesis is now poised to be rigorously tested. [/font][/font]
[font size=5]Niacin Therapy, HDL Cholesterol, and Cardiovascular Disease: Is the HDL Hypothesis Defunct?[/font]
[font size=4]Abstract[/font]
[font size=3]High-density lipoprotein cholesterol (HDL-C) has been shown in epidemiologic studies to be associated with cardiovascular (CV) risk and thus significant efforts have been focused on HDL-C modulation. Multiple pharmaceutical agents have been developed with the goal of increasing HDL-C. Niacin, the most widely used medication to raise HDL-C, increases HDL-C by up to 25 % and was shown in multiple surrogate end point studies to reduce CV risk. However, two large randomized controlled trials of niacin, AIM-HIGH and HPS2-THRIVE, have shown that despite its effects on HDL-C, niacin does not decrease the incidence of CV events and may have significant adverse effects. Studies of other classes of agents such as cholesteryl ester transfer protein (CETP) inhibitors have also shown that even dramatic increases in HDL-C do not necessarily translate to reduction in clinical events. While these findings have cast doubt upon the importance of HDL-C modulation on CV risk, it is becoming increasingly clear that HDL function-related measures may be better targets for CV risk reduction. Increasing ApoA-I, the primary apolipoprotein associated with HDL, correlates with reduced risk of events, and HDL particle concentration (HDL-P) inversely associates with incident CV events adjusted for HDL-C and LDL particle measures. Cholesterol efflux, the mechanism by which macrophages in vessel walls secrete cholesterol outside cells, correlates with both surrogate end points and clinical events. The effects of niacin on these alternate measures of HDL have been conflicting. Further studies should determine if modulation of these HDL function markers translates to clinical benefits. Although the HDL cholesterol hypothesis may be defunct, the HDL function hypothesis is now poised to be rigorously tested. [/font][/font]
Bill USA
(6,436 posts)7. very interesting. What's really interesting is this abstract is from the future (2015 Aug).!!
No, very fascinating. thanks for that informaton!