I don’t think there is enough data for PCSK9i at this moment that would warrant PCSK9i in primary prevention as the first line of drug.
Finally, there is very limited evidence on any potential safety issues of both evolocumab and alirocumab. While the current evidence synthesis does not reveal any adverse signals, neither does it provide evidence against such signals. This suggests careful consideration of alternative lipid lowering treatments before prescribing PCSK9 inhibitors.
They all point to a high efficacy and safety. But they mostly look at very-high risk patients. I don’t know if we can conclude yet about statins vs PCSK9 inhibitors indeed. It would be great for Cochrane to update their review with the current evidence.
There are some signals in that direction, but think it’s again one of those where we just don’t know enough (yet).
One of the problems with the MR of PCSK9 is that we don’t know how much it matters that genetically lower PCSK9 through development and childhood AND in the brain/CNS (that are part of MR analyses) whereas the current PCSK9i antibody based drugs are probably not crossing the blood brain barrier and are not generally started until in adulthood.
For me it was enough that PCSK9i is the only Apo B lowering option that has a somewhat material Lp(a) lowering effect for it to be worth that being my base medication for now. Will keep evaluating as time goes by.
Based on that study, slight yes just because an effect was detected for PCSK9i.
If you can’t monitor desmosterol then it can be better for preventing Alzheimer’s especially if you have an apoE4 allele.
I don’t know how it would compare on vascular dementia and depression. A lipophilic statin might be good for both especially in case of genetically elevated LDL in the brain. Alzheimer’s isn’t the only dementia that exists. Desmosterol hypothesis is kind of weak anyway. Statins also have widespread use like atorvastatin and lots of data.
Several clinical studies show that adding sterols or stanols, usually incorporated in a margarine or spread, to statins results in an additional 7% to 10% reduction in LDL cholesterol. (Blair, Am J Cardiol 2000; Cabezas, J Am Diet Assoc 2006).
ConsumerLab recommends a product called CholestOff Plus
Thought this was interesting. A reminder that one answer may not fit all. Genetics can impact efficacy of cholesterol treatments
“Additionally, apoB was reduced significantly in patients with AA or GA, but not GG, with both pravastatin and policosanol (Liu et al., 2016). Policosanol is typically initiated at 5 mg/day and titrated up to 20 mg/day for hypercholesterolemia.”
I’m on my 3rd week and the most noticeable thing is my blood pressure dropped from 140/90 to 120/80. Previously my blood pressure has always been good but in the last 6 months I’m not sure why it went up. Anyway now it has normalised.
You probably aren’t crazy about Paul Mason, but in this video he shows pictures of plaque with what look like cholesterol crystals and says they are camposterol from plant oils. They lower LDL but do the same thing:
2.3% had muscle side effects compared to 1.4% for placebo.
5.3% developed diabetes compared to 4.0% for placebo.
REPRIEVE results revealed that pitavastatin, a statin medication and the heart disease prevention strategy tested in the trial, reduced major heart disease events like heart attacks and strokes in people with HIV by 35% compared to placebo. Pitavastatin also reduced major heart disease events or death from any cause by 21% compared to placebo.
Pitavastatin was effective in both men and women, and the study participants experienced very few safety events.
Adding ezetimibe improves LDL better than doubling statin dose, 2020.
Peter Attia says they think probably Pitavastatin, Rosuvastatin probably the best place to go if choosing a statin (3 months ago), but it’s all highly individualized and to try a couple if choosing a statin to the one that does the best without any collateral damage.
I might try Pitavastatin 2 mg after I run out of rosuvastatin, it seems better. He mention to start with only third generation statins, and highly potent ones.
This guy doesn’t like pitavastatin:
It’s not a very popular statin, so rosuvastatin might be better after all…
Nah. I don’t have anything against rosuvastatin, that is the one my daughter takes.
I take atorvastatin plus ezetimibe and see no reason to change based on the studies.
“According to subgroup analysis of the 11 included studies (Fig. (Fig.2),2), the combination of ezetimibe and atorvastatin (10 mg) (Sakamoto K 2017, Sakamoto K 2015, Matsue Y 2013, Okada K 2012) [MD = -16.98 mg/dL, p < 0 .0001] or simvastatin (20 mg) (Le NA 2015, Averna M 2010) [MD = -17.35 mg/dL, p < 0 .0001] also showed stronger ability of reducing LDL-C, while the combination of ezetimibe and rosuvastatin (10 mg2018,) Ran D 2017, Farnier M 2016, Saeedi R 2015) [MD = -9.29 mg/dL, p = 0.05] showed less relevant.”
I did try eating healthier as well, more Mediterranean. Surprising decrease in apoB. I did not have such good level before using 5 mg rosuvastatin. But then I was making my own capsules and grinding larger tablets and I wasn’t focusing more on healthier stuff. Liver markers improved or stayed the same.
Probably placeboooo
“You underestimate the power of faith.” - Princess Irulan
I don’t really know where to put this video. It is a talk about metabolic disorder being the root of all evil, so it covers much of what we talk about here, not just heart disease:
