#678

The “any dose” of lipitor vs. placebo was pretty similar though, including muscle pain at 3.8 vs. 3.6%.

#679

+20% increase in muscle spasms in “any dose” of lipitor vs. placebo.

Again, these are averages over the cohort, per the above meta-analysis, some populations have higher rates (elderly, women, Asian and Black, obese, T2D, hypothyroidism, chronic liver, renal failure).

So for young white men without other conditions, statins probably have a safety profile better than placebo.

Conclusion: everyone is different. That’s OK: if someone is statin-intolerant, there are alternatives.

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#680

Yes, just to not confuse anyone this is relative risk, so it’s 1.2 times the regular rate of muscle spasms over the study period.

Some people’s opinion on statins make it seem like they are crack cocaine, while in reality they are quite benign medications with lots of beneficial effects for most people. I expect these people to be perfect health beings and who do not do things that are more harmful than statins.

#681

Statins reduce the amount of acetyl-CoA used to make cholesterol. Hence they increase the amount available for other purposes.

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#682

Which shouldn’t influence your decison making either way unless you have a biomarker for acetyl-CoA that can be measured and which either has mendelian randomization, clinical trial, or at least observational data showing benefits (or possibly a mice study), at least when on the other side of the scale such data exist.

#683

I have my own study of the effects of varying acetyl-CoA.

I attach the poster I have produced from this.

final poster as pdf.pdf (1.3 MB)

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#684

So your biomarker of choice is CRP? If so, both statins and bempedoic acid lowers it.

#685

CRP is only one biomarker. I am still working out how many biomarkers I consider are sufficient to get the best idea of metabolism.

In the end functional tests are key. CRP if anything (and I mean the background CRP level) indicates the burden of senescence. This is only one part and I think probably the lesser part of the aging process. More important is mitochondrial quality.

I am unaware of a simple mechanism for measuring average mitochondrial quality although average serum citrate (without supplementation) might be a good proxy for it.

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#686

CRP probably causes heart disease via IL-6 and I wonder if it also causes aging via some correlation with IL-11. Of course the increase in CRP during infection would you say is useful? And that rather, the chronic baseline CRP that is harmful that is over a certain level?

#687

I don’t know whether CRP is harmful or not. Nor do I know the knock on effects of IL-6. What (background) CRP does is indicate the presence of senescent cells. Of those IL-10 has been shown to cause further senescence.

#688

I am taking Bempedoic Acid, Ezetemibe and low dose Atorvastatin as the effects are additive. Based on my calculations, my ApoB and LDL should hit the 45-50 range which would be close to perfect for me.

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#689

Decades ago, I tried multiple statins and even tried a half a pill 3x per week and I felt awful and went off

In hindsight, if I knew then what I know now, I would have toughed it out until the advent of PCSK9, but my cardiologist said, don’t worry, you have a great diet and and a great ratio … sigh…

#690

Bempedoic Acid/Eztimibe took my ApoB from 69 to 49 in less than two months. Absolutely no side effects. Cheap as well. Well worth it.

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#691

May I ask how much it impacted your Lp(a) so far? Do you know the typical impact in others?

@Davin8r did you ever look into this?

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#692

Per this study, fenofibrate actually increases Lp(a), which probably explains why none of the lipidology experts talk about it.

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#693

I tried this to lower my Lp(a);

  • daily 400mg bezafibrate from 16 november 2023 to 16 februari 2024; Lp(a) dropped from 96 mg/dL to 54 mg/dL, so a 43% reduction.
  • daily fenofibrate nanoparticle 145mg from 17 februari to 6 june; Lp(a) dropped from 54 mg/dL to 39 mg/dL, so an additional 28% reduction

The only downside: homocysteine has increased from 8,6 to 12,2 mcmol/L, although I take a lot of supplements daily to lower it (5g creatine, 3g glycine, 0,5g TMG, methylated B vitamins).

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#694

I find it strange that there is conflicting research evidence about the effect of fenofibrate on Lp(a)…
You would almost start believing in a big pharma conspiracy :face_with_raised_eyebrow:
I found these summary paper very informing;

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#695

Seems pretty clear:

“Fibrates: Bezafibrate has been shown to reduce Lp(a) levels by approximately 13–39% [52]. A similarly modest, but not statistically significant, effect was demonstrated for gemfibrozil [53]. Thus, fibrates do not appear to influence Lp(a) concentrations significantly [54].”

Now if only I could find a source for bezafibrate. It’s unavailable in the USA or India (at least according to one vendor in India).

#696

I have added a low dose Atorvastatin to my Bempedoic Acid and Ezetemibe and my LDL and ApoB are now both 45 down from 68 and 65. HDL is 51.

My hsCRP is 1.59 though and my HBA1C is back up to 5.8 as I stopped Metformin and all supplements except Rapamycin and cholesterol meds for 2 weeks. I’ll bet they’ll be back to normal in 6 months when I check next.

I’m just ecstatic about the LDL and ApoB which are moving in lockstep.

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#697

How low should LDL go?

According to Harvard Medical, the lower the better.

“People who are at high risk for cardiovascular diseases can benefit from driving LDL levels as low as possible to help reduce their risk for heart attacks and strokes,” says cardiologist Dr. Christopher Cannon, editor in chief of the Harvard Heart Letter . “Across many large clinical trials, for LDL, the lower the better.”

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