Apparently no effect of high dose Rx fish oil on lowering Lp(a) itself, but seems to decrease cardiac events per the study posted previously (which is most important).
Unfortunately, high-dose fish oil also increases risk of afib, so it’s a balancing act.
I don’t want to go off-topic now, but if those are anything like nut absorption, then flax seed oil would be the healthier choice (but also eating seeds).
I appreciate that. Funnily enough I put flax seed oil on my shopping list this week! Forgot to mention I eat at least two spoons of spirulina per day too.
I wouldn’t be. The outcome data is really what matters, and that clearly demonstrates strong efficacy. I wouldn’t stop taking it because of a feared unfounded mechanism.
As far as I know in trials ezetimibe hasn’t detected decrease in cardiovascular death or all-cause mortality, which is the endpoints that measure net benefit? If ezetimibe reduces ALA absorption and if that is bad, it could reduce the benefit of ezetimibe compared to other treatments.
That was MACE or a composite of events, it doesn’t measure net benefit I think, like if the deaths are the same in both groups that could be because of low statistical power or it could be because the ezetimibe people are dying because of other reasons (like possible lower ALA absorption)?
I would rather take a low dose Praluent (PCSK9 inhibitor) than ezetimibe at this point, in addition to other treatments, but I dunno.
I have no doubts about the efficacy of Ezetimibe, in fact I have the personal test results to prove it. My concern is with the unintended potential side effects if for me it inhibits absorption of Omega 3 EFAs. I suppose all I can do is keep testing and trialling different scenarios. For the last month I have been on increased Omega 3 (4g instead of 1g) and I have stopped Ezetimibe (was 10mg). I am also titrating up to 3g of Niacin (currently stuck on 500mg though flushing is starting to improve). My Atorvastatin remains unchanged at 80mg. I am now waiting to see a cardiologist who will hopefully suggest something better like a PCSK9 inhibitor. In the meantime I shall stay on the current regime for a full three months before retesting and perhaps reintroducing Ezetimibe to see how things then change. I appreciate all the comments, viewpoints and suggestions on here though because they help me consider all the angles.
We conducted Mendelian randomization (MR) analyses using variants in several genes associated with lipid-lowering medication targets: HMGCR (statin target), PCSK9 (alirocumab target), NPC1L1 (ezetimibe target), APOB (mipomersen target), ANGPTL3 (evinacumab target), PPARA (fenofibrate target), and APOC3 (volanesorsen target), as well as LDLR and LPL. Our objective was to investigate the relationship between lipid-lowering drugs and asthma through MR. Finally, we assessed the efficacy and stability of the MR analysis using the MR Egger and inverse variance weighted (IVW) methods.
The elevated triglyceride (TG) levels associated with the APOC3, and LPL targets were found to increase asthma risk. Conversely, higher LDL-C levels driven by LDLR were found to decrease asthma risk. Additionally, LDL-C levels (driven by APOB, NPC1L1 and HMGCR targets) and TG levels (driven by the LPL target) were associated with improved lung function (FEV1/FVC). LDL-C levels driven by PCSK9 were associated with decreased lung function (FEV1/FVC).
In conclusion, our findings suggest a likely causal relationship between asthma and lipid-lowering drugs. Moreover, there is compelling evidence indicating that lipid-lowering therapies could play a crucial role in the future management of asthma.
I don’t get a lot of sunshine. Here in Hong Kong the sunlight is much harsher to the point you feel like you are frying when you are under it. I have very fair skin, burn easily and have a history of skin cancer. So, I actively avoid sunlight. Hence, I’m not too shocked by low levels of D3.
However, contrary to previous studies, we also observed that an increased LDL-C level driven by LDLR led to a decreased risk of asthma (LDLR: OR = 0.9930, 95%CI: 0.9874–0.9987).
A study might find causal relationships, but they might be so small to not matter.
You’re right, I didn’t check the HR, it’s ridiculously small and therefore clinically not relevant. Still good to know that at least these drugs are not detrimental for our lungs