Just got my blood work back after switching from EOD Atorvastatin 5 mg to daily Pitavastatin 2 mg.
ApoB 53 from 58
LDL 43 from 58
HBA1C 5.6 from 5.7
HDL 57 from 51
Overall, it’s a success. Also mild muscle soreness disappeared from my legs.
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Nice. Pita might be responsible, because at that dose the 2mg daily is more effective than 5mg ator EOD (10mg ator ~ 2mg pita; 20mg ator ~ 4mg pita), at lowering LDL/ApoB. Pita is also known to raise HDL if it’s low, and is neutral vs blood sugar levels compared to ator, so if ator raised A1c, pita allowed it to fall back down. If long term you experience no sides from pita at that dose, it looks like pita is a success for you. My only caveat would be that pita is still a statin, and sometimes in very statin intolerant people the sides don’t show up until months later, although it looks like in your case pita is fine. Congrats!
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How long ago did you switch? Did you measure apoA1 as well? I would check creatinine kinase (CK), especially if your muscles become sore again.
I switched around February, so it’s been a solid 6 months. Atorvastatin is known to cause muscle soreness for me, which is why I switched from EOD Atorvastatin to Pitavastatin.
Also my mother switched from 10 mg Atorvastatin every day to Pitavastatin 2 mg every day and muscle soreness went away for her as well. Unfortunately I don’t have new blood work for her yet to see the effects although her ApoB is 34 using Atorvastatin and Ezetemibe only. Her triglycerides are the big problem.
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Even pitavastatin turned out to be incompatible with me so I’m currently waiting for Ubeslo.
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Use RW-ApoB in the case for high trigs and/or Lp(a) for an adjusted apoB level: RW-ApoB -- Superior Metric For Lipid Related CVD Risk --- Using Lp(a), ApoB, and Triglycerides
Although I’m unsure if it’s wise to go lower than 30 mg/dl apoB so fixing the cause of the high triglycerides become more important.
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Just got labs again staying on 4mg Pitavastatin, 10mg Ezetimibe, and 2mg weekly Retatrutide. LDL further dropped from 44 to 36. HDL went from 50 to 55. Didn’t check ApoB this particular time but I would imagine it has continued to drop as well (it was 44 last time). I haven’t seen an HDL that high since pre-testosterone use. Still no muscle pains (I had some on Rosuvastatin).
Also for those worrying about A1C. Mine dropped to 5.0 (I am still on 10mg empagliflozin and 100mg Acarbose daily along with the retatrutide so no changes there).
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So we’re seeing lowered LDL and ApoB and higher HDL with lower HBA1C. That’s all excellent!
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Yes I love this particular statin. When I was only using 2mg, my LDL was 55 (same pharmacology for everything else so I know the additional drop was from a dose increase). Not to mention it showed lowered biological aging on that aging clock study Sinclair posted a few months ago that was discussed (for what that’s worth).
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https://onlinelibrary.wiley.com/doi/10.1002/jcp.27932
Interesting that CoQ10 supplementation, which appears generally to not be helpful for myalgia in most statin users, may actually be helpful in protecting the pancreas against statin toxicity.
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Discussion of mechanisms of pancreatic toxicity from statins:
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So possibly attenuate the increase risk in diabetes (what about other LLT – as genetic evidence suggest ALL LDL-c lowering drugs increase diabetes risk)?
(P.S to the readers don’t stop LLT based on this, the reward:risk is way more in favor than any risk increase from diabetes).
That would depend on the proposed mechanism. Despite the theoretical risk posed by Mendelian randomization, apparently there’s zero increased risk of diabetes in PCSK9i studies.
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Hmm, that’s right, so if there isn’t any increase in diabetes in any of the other drugs RCT’s, despite the MR data, then that means they don’t increase diabetes risk, at least relative to statins (pitavastatin also increases diabetes risk, despite any relative improvements in glucose compared to other statins).
RCT > MR, anyway.
The situation with pitavastatin and CoQ10 is more nuanced. There are some conflicting results based on either direct serum measurement or proxy effects. Here’s an example:
Comparison of effects of pitavastatin and atorvastatin on plasma coenzyme Q10 in heterozygous familial hypercholesterolemia: results from a crossover study
https://pubmed.ncbi.nlm.nih.gov/17957184/
“Under these conditions, plasma levels of CoQ10 were reduced by atorvastatin (-26.1%, P=0.0007) but not by pitavastatin (-7.7%, P=0.39), although no adverse events or abnormalities of liver and muscle enzyme were observed after either statin treatment.”
Effect of Statins (Atorvastatin, Pitavastatin, Pravastatin, Rosuvastatin and Simvastatin) and Coenzyme Q10 (CoQ10) on Adenosine Triphosphate (ATP) Levels
https://www.lipidjournal.com/article/S1933-2874(15)00112-9/fulltext
“Antimycin-A, the positive control, significantly reduced the ATP levels. The ATP levels in simvastatin and atorvastatin treated cells were not significantly different from antimycin-A. While ATP levels in rosuvastatin, pitavastatin and pravastatin (p<0.05) treated cells were significantly different from antimycin-A. Addition of CoQ10 ameliorated the negative effects of atorvastatin (p<0.001); rosuvastatin (p=0.009) and simvastatin (p=0.026) on ATP levels in the adipocytes while presence of CoQ10 in pitavastatin treated cells caused further significant reduction in ATP levels (p=0.001).”
So supplementing with CoQ10 might have some effect with simvastatin, atorvastatin and rosuvastatin, but differential effects with pitavastatin. Of course this is a cell-based mechanistic finding with antimycin-A as a readout, but interesting nonetheless. If pitavastatin does not significantly affect serum CoQ10, then it matters less for downstream effects. What we need are more rigorous long term outcome studies with CoQ10 and these statins, because the studies so far supplementing with CoQ10 in the presence of statins are not encouraging. But in general I’m not sure CoQ10 is a fruitful direction here - I don’t think it makes much if any difference. YMMV.
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The idea with CoQ10 supplementation for statin toxicity in pancreas would be purely as a mitochondrial antioxidant protecting against statin-induced oxidative damage rather than to correct a CoQ10 deficiency. One of the studies mentioned in the OpenEvidence discussion apparently showed that N-acetylcysteine also protected against the statin toxicity, so there are multiple candidates that might work including ergothioneine.
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Honestly I have a higher hope for ergothioneine than CoQ10, because in studies tracking molecules associated with good health/longevity outcomes ergo was the one that stood out. Meanwhile other than heart failure there’s not much to hang you hat on with CoQ10. Of course, either way it’s a pretty thin reed to place much weight on. I think we need better studies.
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How do you measure efficacy? IIRC it’s not possible to reverse diabetes (except its effects like elevated glucose) due to the entropic damage from exposures in e.g the pancreas.
Could you like scan the pancreas or use some biomarker (except diabetes biomarker – that’s I think a later stage finding, correct me if I’m wrong)?
Now you are moving further afield wrt, statins. Just looking at protecting pancreatic beta cells, there’s imeglimin:
Imeglimin exerts favorable effects on pancreatic β-cells by improving morphology in mitochondria and increasing the number of insulin granules
Honestly, I’m more interested in imeglimin for countering possible negative effects of rapamycin than strictly diabetic glucose control. Rapamycin might be toxic to pancreatic beta cells, which was clearly shown in mice and hinted at in human transplant patients. Big “do not want” here for me wrt. rapamycin. YMMV.
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Pancreas biopsy😂. This would be best tested first in mice/rats to demonstrate protection by a mitochondrial antioxidant from statin-induced pancreatic toxicity.
GLYNAC seems like it would have great potential here.