Bempedoic acid is a fairly new drug and still under patent in the US (I don’t know what its status is in India, though I see lots of vendors claiming to sell it). I can imagine shady operators selling pills labeled as BEMP that are actually statins and relying on people only checking LDL-C, if that. Aside from doing repeat n-of-1 testing with known statin and putative Indian-sourced “BEMP,” does anyone have any thoughts on how one might have more confidence that one were buying real BEMP?
Isn’t desmosterol important factor in nerve myelination and responsible in regenerative processes in MS? Anyway I would not want my desmosterol levels very low in order to preserve nerve function and cognition…
Precisely. It is health optimizing for health concious people. Peter doesn’t have to take statins, he can take PCSK9 inhibitors, bempedoic acid and ezetimibe. Not everyone has the luxury to health optimize on the margin. Which optimizing for desmosterol is, because of the low expected value. Low dose statins shouldn’t decrease desmosterol by a lot. In 10 years the non-statin drugs will be cheaper and more evidence will build for or against. Until those 10 years happen I will gladly take a statin.
I don’t think that’s clear (see this and this), but even if it were, that’s exactly the kind of mechanism-based speculation that I’m tallking about. The actual outcomes data from human randomized controlled trials and prospective epidemiology find a reduction in AD risk for both kinds of statin.
Rosuvastatin has some potential advantages over atorvastatin: - Higher potency - Rosuvastatin produces greater LDL reduction milligram-for-milligram compared to atorvastatin. Lower doses of rosuvastatin can achieve lipid goals. - Higher hydrophilicity - The polar nature of rosuvastatin results in less systemic absorption and tissue penetration, potentially reducing risk of muscle toxicity. - Greater HDL increase - Meta-analyses show rosuvastatin produces slightly greater increases in HDL cholesterol compared to atorvastatin. - Improved outcomes - The JUPITER trial with rosuvastatin showed reduced cardiovascular events in a primary prevention population"
Brillo BA is made by the largest pharmaceutical company in India. It’s their Pfizer comparable. Usually the bigger the company, the better the product.
I can tell you it’s not just a statin as I am statin intolerant and I would be suffering severe muscle fatigue if it were just a statin in disguise.
Finally, if a company did repackage other drugs, that’s illegal and the government would probably notice and shut it down.
I’ll see what happens with my cholesterol the next time I measure.
LDL-cholesterol reduction is a primary goal for reducing the risk of atherosclerotic cardiovascular disease: lower is better for lifetime, earlier is better, and lowest is best.
LDL-cholesterol is a driving force for broad spectrum, progressive pathophysiology and multiple disease states adversely impacting longevity and quality of life.
Many facts suggest that a desirable, physiologic level of LDL cholesterol is far lower than previously assumed:2
Serum LDL-C in utero and in newborns averages 20–40 mg/dL (0.52–1.03 mmol/L). During gestation and after birth, humans are forming new cells at prodigious rates yet require little contribution of cholesterol from LDL.
All cells of the body make their own cholesterol (plus a small portion derived from HDL-C).
Those born with complete absence of proprotein convertase subtilisin kexin type 9 (PSCK9; loss of function mutation) suffer no ill consequences from lifelong near zero circulating LDL-C and have no atherosclerosis.
Brown and Goldstein showed that fibroblast receptors for LDL are maximized at a concentration of 25 mg/dL (0.67 mmol/L) due to feedback control. Excess cholesterol beyond that is taken up either by hepatocytes or scavenger receptors on intimal macrophages that have no feedback control and thus accumulate much larger amounts of cholesterol.
Randomized controlled trials (RCTs) and Mendelian randomization analyses demonstrate that there is log-linear relationship between atherosclerotic cardiovascular disease (ASCVD) and LDL-C at the highest levels down to near zero. The hazard ratio of 1.0 (meaning no excess risk) is achieved at an LDL-C of approximately 38 mg/dL (0.98 mmol/L).
Many RCTs show that lowering LDL-C at any stage is beneficial, but doing so as early as possible is far better.
Elevations in mid-life LDL-C also correlate with increased risk for neurologic disease, especially vascular and Alzheimer’s dementia, as well as Parkinson’s disease.
Considering this, the most desirable LDL-C appears to be that of the newborn, 20–40 mg/dL (0.52–1.03 mmol/L). Such a low level is likely not needed if LDL-C is well below 70 mg/dL (1.81 mmol/L) from birth, remains at that level through life and all other risk factors (hypertension, hyperglycaemia, obesity, inflammation, lipoprotein(a), and many others) are absent or well controlled. That is not common, but treatment can achieve it when needed.2
Unfortunately, most people are not entirely free from other risk factors.
Do the studies showing a reduction in dementia risk with statins break down between APOE4 and non-APOE4 carriers? If it had a benefit to non-carriers (75% of the population) and a negative effect on carriers, it might still have a population net benefit even if it were harming APOE4 carriers.
Update time…two months ago I went off rosuvastatin 20mg due to low desmosterol levels and started taking Praluent 150mg once every 4 weeks (as opposed to every 2 weeks, to save money). My ApoB went from 87 on rosuvastatin alone to 112 on Praluent. This test was three weeks after my last Praluent dose. I’m pretty disappointed, as I expected Praluent to perform as well or better than the statin, even at the lesser frequency.
My ApoB was 121 back when I wasn’t taking anything, so the Praluent only marginally decreased ApoB from baseline. In fairness, back when I was on nothing I ate largely a pescatarian diet and I’ve been eating a lot more meat since starting the statin and then Praluent, so possible that I’m getting a bigger decrease than the baseline would suggest. Still disappointing.
Next I’ll add my Indian bempedoic acid and zetia to the mix and see what happens. Fingers crossed.
How long ago was the 121 (and was that one single measurement or did you have multiple around that?) if we was more than a year or two (and even potentially if smaller) you are in the age range where you base line cholesterol level could start going up materially just from “aging”
I wanted to know what my apoB was in the last half of my cycle, which is why I tested at week 3. I figure that matters as much as my number one week in. Not optimal to have a high apoB for half the month, it seems to me. But yes, I’m an absorber so cautiously optimistic that zetia will make a big difference. May experiment to see if zetia/bempedoic gives me the same reduction as Praluent/zetia. The former would be a lot cheaper…
Update…added 10mg Indian zetia to my Praluent every four weeks and apoB went from 112 to 57. And this was 3.5 weeks after my last Praluent dose. That’s more like it!