Elevated Lp(a) levels are an independent and causal risk factor for cardiovascular disease with limited treatments currently available. Oxidized Lp(a) stimulates foam cell formation, endothelial dysfunction and inflammation.
Lp(a)-enriched ApoB particles underwent time-dependent oxidation, reaching a peak oxidation value after 2 hours (27-fold, 0.45 ± 0.07 vs 12.60 ± 0.24, p <0.001) that were sustained through 4 hours. EPA significantly inhibited Lp(a) oxidation in a time-dependent manner through 3 hours. After 3 hours, EPA inhibited oxidation by 31% (8.04 ± 0.79 μM, p <0.001) while EA had no activity.
EPA inhibited oxidation of Lp(a)-enriched plasma in a time-dependent fashion consistent with a free radical scavenging mechanism. The potent antioxidant actions of EPA may contribute to reduced CV events in REDUCE-IT, including those subjects with elevated Lp(a).
I tried gemfibrozil and it did not lower my high lp(a).
Am researching the merits of the anecdotal reports of amla + lysine and Vit C + collagen reducing lp(a).
From what I understand the paper doesn’t claim Lp(a) lowering but lowering its oxidation so potentially making it less “harmful”. Could it explain the MACE reduction in REDUCE IT (pure EPA)?
Have we talked about this paper before? It’s a meta analysis of CoQ10 and Lp(a) lowering. At first, the degree of lowering seem trivial, but in the fine print:
[CoQ10 supplementation led to a]…“numerically greater reduction in plasma Lp(a) concentrations in the subset of trials with baseline Lp(a) values ≥ 30 mg/dL (WMD: -11.72 mg/dL, 95% CI: -21.01, -2.42,
p=0.013) compared with the subset with baseline values < 30 mg/dL (WMD: -3.14 mg/dL, 95% CI:
-4.92, -1.35, p=0.001”
Also: “Subgroup analysis suggested that the impact of CoQ10 on plasma Lp(a) was greater at supplemental doses < 150 mg/day (WMD: -9.24 mg/dL, 95% CI: -15.19, -3.29, p = 0.002) compared with doses ≥ 150 mg/day (WMD: -2.75 mg/dL”
So I wonder what the average reduction would be in someone using both a low dose of CoQ10 and who had a higher baseline Lp(a)?
That 11.72 reduction is significantly higher when converted to modern units (nmol/L), this is roughly 12 x 2.5 = 30 nmol/l, right? Not huge, but definitely significant.
Add a daily baby aspirin to that to knock it down a little more (along with platelet inhibition).
in the link that @adssx posted above (post 182 of this thread). I only commented because I take 200 mg and that is what I’ve found to relieve statin induced muscle soreness most effectively.
" Lilly’s drug is the only oral treatment in a field of several injectable therapies being tested to treat high Lp(a), a risk factor for heart disease that affects one in five individuals globally.
Unlike low-density lipoprotein, or LDL, the so-called bad cholesterol that can be treated with diet and statins, there are no approved treatments for Lp(a) and few individuals even know they have it."
It does seem interesting. "At week 12, the study found:
Compared to placebo, muvalaplin treatment reduced Lp(a) by up to 70% as measured by the traditional blood test […]"
That is a large reduction!
I am not sure that anyone has actually shown that reducing Lp(a) actually improves health outcomes though. I - and everyone else, I guess - suspect it does, which is the reason for the interest. Anyway, quoting a different article:
“We were encouraged by the degree of Lp(a)-lowering in these patients who are most likely to benefit from its use and by the safety and tolerability,” Nicholls said. “While muvalaplin appears to be an effective approach to lowering Lp(a) levels, we still need to study whether Lp(a) lowering will result in fewer heart attacks and strokes.”
“ The drug, muvalaplin, reduced levels of lipoprotein(a), or Lp(a), by 70% using a traditional blood test and by nearly 86% based on a more specific test developed by the company, researchers reported at the American Heart Association meeting in Chicago.”
Recent JAMA article published 18 Nov '24: Zerlasiran–A Small-Interfering RNA Targeting Lipoprotein(a). A Phase 2 Randomized Clinical Trial
Conclusion: Zerlasiran was well-tolerated and reduced time-averaged lipoprotein(a) concentration by more than 80% during 36 weeks of treatment in patients with ASCVD
Little to none adverse effects.
My question to this readership: does anyone know the average length of time from Phase 2 to being available to the public? Thanks
