Just read this thread as I’ve been absent for a while. As someone with high lp(a) and someone who took 4g niacin / day for 30+ years it interests me greatly. Something to clarify re the effect (or lack of–) of niacin on CV mortality…
Niacin suffers from the fact that statins were on the market prior to the discovery that Niacin improves the lab values of most lipid markers (raises HDL, lowers LDL, lowers TG. The only way to ethically test Niacin’s efficacy in preventing cardiovascular events was to add Niacin to statins in patients at risk and see if their were less events. The hypothesis was that raising HDL would improve risk and reduce the number of CV events. So there were two large studies (AIM-HIGH in 2011and HPS2-THRIVE in 2014). The patients had LDL levels driven below 80 with statins and then added Niacin to the protocol and there was no significant reduction in cardiac risk and an increase in stroke risk and T2DM in a small percentage of individuals. Because Niacin is off patent (ie no financial benefit) and because it would be unethical at this point to do so (statins have been shown to lower LDL and reduce events), a study of cardiovascular risk reduction with Niacin alone to my knowledge has not been done. Most cardiologists would use Niacin to further lower LDL cholesterol in the context of patients unresponsive or intolerant to statins until pcsk9 inhibitors came out.
You can have your lp(a) gene sequenced or probably better just have your genome sequenced since you may want to go back and look for other “stuff” as new information becomes available. I’ll have to check if rs10496731 is in an exon but also possible you could just do exome sequencing.
Review the following article{link and attached is a PDF file) by the Medical Doctor who did the original trials in the US on nician for lip control. William B. Parsons, Jr., M.D., FACP.
Article
“Introduction of Niacin as the First Successful Treatment for Cholesterol Control, A Reminiscence”
The problem with niacin is that many people cannot take it in therapeutic doses.
Minimal amounts cause them to have the unpleasant “flush” effect even when taking timed-release versions, which are dangerous for other reasons.
Even so, I don’t believe niacin is a first-line treatment for high cholesterol. If you just need a modest reduction and can tolerate therapeutic levels then niacin may be okay for you.
Joseph, nothing new here. It’s well known that Niacin has a favorable affect on lipid profiles as I stated above. The study that hasn’t been done to my knowledge is a randomized controlled trial of niacin vs placebo to reduce cardiovascular events and or death.
I believe if that study were performed it would show that Niacin can effectively reduce cardiac risk but as I stated above it would be unethical to do the study at this point.
I’m considering starting Niacin again given the reports that it can lower lp(a). Having taken huge doses for years myself I know that it is a low risk proposition for me and having high lp(a) is a high risk factor for aortic valvular calcification, aortic stenosis, and CAD. My lp(a) did not reduce significantly on pcsk9 inhibitors. In addition, it will push my ApoB levels lower without me having to max out a statin, and it potentially has added longevity benefits of raising NAD+.
I get that flushing like everybody else but it reduces over time by starting with small doses and raising the amount incrementally. I got to the point where 2g would give minimal flushing (still some, but not a bother) and then I would take that dose 2x day.
Davin8r, I’ve never used or prescribed clopidogrel so I can’t say whether it would be equivalent. The studies are done with aspirin and the mechanism is ASA disrupts blood clotting by irreversibly inactivating the pathway in platelets. So unless somebody has done a side by side study and compared the efficacy to aspirin I’d be wary of just substituting it.
It might be useful to actually do some research, which is in complete opposition with a single paper, bashing niacin by Cleveland clinic. Every marker they Claim was increased inflammation in particular, is completely false. All you have to do is take Google advanced search type in niacin and VCAM.
As a matter of fact, there is a 2PY and 4PY analysis in the setting of kidney disease. It turns out neither one was estrogenic, in fact it was anti-fibrotic and anti-inflammatory.
@lsutiger On occasion I would get side effects that I attributed to Niacin but never confirmed. My WBC was consistently low and hit 2500/ul at one point and I would occasionally get gout. Both have not occurred since stopping it. WBC now in the normal range at 3900/ul. Like I stated above I think I will start back on it provided I can get my lipidologist on board. I don’t like taking meds they disagree with since I want them to take ownership of that aspect of my health. I think I will definitely try an ASO to lower my Lp(a) when they become available. Right now PCSK9i and Niacin are the best ways to lower Lp(a) outside of plasmapheresis.
Here is my update 6 weeks after taking Repatha and stopping niacin, zetia, and nexletol.
The first number after the lab item is the most recent measure pre repatha but still on niacin, nexletol, and niacin (1500 mg daily). The second number is the labs from this week–6 weeks after being on Repatha:
So it seems Dr. Tsimikas’s objective to replace three meds (Niacin, Nexletol, Zetia) with one (Repatha) seems to have worked. Thoughts? I would appreciate anyone’s input on my thinking to add Zetia back to the mix to further lower APOB and LDL? Any input on what the small LDL-P going down substantially means? I have not heard back from DR. T on the results, Just FYI. Thanks
Why stop the Nexlitol at all, would be my thought (unless insurance won’t pay for it or you’re paying out of pocket)? Risk of side effects is so small, and if you have established CAD (high calcium score and/or events), I’d advocate for the lower the LDL particle number, the better.
If cost is an issue, the at least adding back the ezetimibe seems like a no-brainer since it’s so cheap and will help to further drive down LDLp.
It’s interesting that insulin went down (generally good from longevity perspective) while A1c went down too (as sometimes the lower insulin can allow the A1c to creep up. That’s great if it sustains.
Did you have more than one pre everything measurement? Going from 130 to 52 with repatha alone seems very much above what most people experience. (And the niacin decline was very big too). Just wondering if the 130 level might have been a flukey high reading.
Agreed, that Lp(a) drop is too high for Repatha alone. How long have you been off the niacin prior to that most recent blood draw? Even though niacin half life is short, the time course for Lp(a) (and other lipids) might take a lot longer to normalize back to pre-niacin levels.
Lp(a) of 130 appeared on 2 different labs 6 months apart. I had stopped Niacin for two weeks before starting the Repatha. Did not take Niacin at any point during the past six weeks while on Repatha. Doing labs again in three months so will see what Lpa is at that time to see if it is stable at 52.