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Statins, muscle pain experience? Mitochondrial dysfunction?

Ghoul said:
In my experience people who go down this path never escape the seductive message that high LDL is no problem so ignore it, and statins will ruin your muscles so don’t use them.

The market for telling people what they want to hear will always have charlatans willing to supply it.
Click to expand...
Well said. It's truly seductive.
 
thestruggle said:
Well said. It's truly seductive.
Click to expand...

On a practical note. Myalgia (muscle pain) can be a (reversible) side effect for a small minority of susceptible people. But this varies greatly from statin to statin. With each generation of statin this side effect has become increasingly rarer.

The TLDR is that the same pathway statins inhibit to reduce LDL production can also reduce CoQ10 production. Low CoQ10 = muscle pain and poor mitochondrial function.

It comes down to how “off target” the statin is. Does it needlessly penetrate muscle? Is it a large dose (in mg)?

If you’re nervous, take CoQ10 as an added insurance policy against the possibility. Even without CoQ10 supplementation though, the vast majority never experience muscle pain.

And the most important thing you can do is choose the correct statin:

IMG_1924.webp
 
Ghoul said:
In my experience people who go down this path never escape the seductive message that high LDL is no problem so ignore it, and statins will ruin your muscles so don’t use them.

The market for telling people what they want to hear will always have charlatans willing to supply it.
Click to expand...
I have a friend who is easily 80 pounds over weight. He also has high blood pressure. His ldl is through the roof. He won't take statins cuz bad. He wheezes when he walks and talks at the same time.
 
Reading from a wide range of sources both pro and con on an issue to try to come to an unemotional choice as to what is best for an individual seems prudent to me. When ever an individual tries to limit ones choices i tend to give less credence to their opinions. Statins have their place, especially for those that have heart issues. As a preventative they seem to be less effective at increasing life span. Seems half of all people that have heart attacks had what is considered healthy cholesterol levels last i checked. Seems there is more going on the just how much LDL-C a person has.
 
Ghoul said:
On a practical note. Myalgia (muscle pain) can be a (reversible) side effect for a small minority of susceptible people. But this varies greatly from statin to statin. With each generation of statin this side effect has become increasingly rarer.

The TLDR is that the same pathway statins inhibit to reduce LDL production can also reduce CoQ10 production. Low CoQ10 = muscle pain and poor mitochondrial function.

It comes down to how “off target” the statin is. Does it needlessly penetrate muscle? Is it a large dose (in mg)?

If you’re nervous, take CoQ10 as an added insurance policy against the possibility. Even without CoQ10 supplementation though, the vast majority never experience muscle pain.

And the most important thing you can do is choose the correct statin:

View attachment 358266
Click to expand...
Your information on statins has been a great help. Thank you.
 
buck said:
Reading from a wide range of sources both pro and con on an issue to try to come to an unemotional choice as to what is best for an individual seems prudent to me. When ever an individual tries to limit ones choices i tend to give less credence to their opinions. Statins have their place, especially for those that have heart issues. As a preventative they seem to be less effective at increasing life span. Seems half of all people that have heart attacks had what is considered healthy cholesterol levels last i checked. Seems there is more going on the just how much LDL-C a person has.
Click to expand...

With all due respect, this is not about limiting choices or silencing dissenting opinions.

One side of this issue is boring and backed by mountains of evidence, and accepted by 99.99.% of cardiologists as expressed worldwide by the organizations representing them, all sheep apparently, while dissenting from this is a guarantee of instant social media fame, cool points, and pats on the back from the people who “just knew it”.

There is no human ailment that has a higher degree of evidence between cause and effect established than LDL and cardiovascular disease. I’m not sure if that statement is strong enough so I’ll put it another way. If a handful of sensationalist outliers are enough to cast doubt in your mind that LDL is the underlying cause of cardiovascular disease because the evidence isn’t sufficient, there is no cause and effect you should believe is proven, including cigarettes to lung cancer and respiratory disease, which isn’t as strongly established as LDL and cardiovascular disease. None.

The other part that’s been definitively established is that lower LDL, achieved by any means, has a direct association with lower rates of cardiovascular disease and death.

So it’s not about shutting down another opinion, it’s about how tiresome it is arguing with people who baselessly refute the position that’s met the highest possible standards of proof, and aren’t doing any of the work to look at the evidence from “both sides”, giving each appropriate weight based on volume and strength, but taking the easy, “cooler” counter position built on sound bites and low-powered studies, that requires deliberately ignoring what amounts to incontrovertible evidence developed over 60 years, by tens of thousand of scientists (all corrupted by big pharma supposedly) following the trajectories of tens of millions of subjects, their treatments, and outcomes.

Given this is the #1 cause of death, no effort has been spared by generations of researchers, governments, and doctors to chase down every doubt and ambiguity as to what causes it and how to reduce it. This was no quick conclusion or academic theory. After jumping over every hurdle, and finally meeting the highest possible standards of proof, it’s irritating to have the occasional clown say, “Nah”, without producing 1/10000 the evidence to back their assertion, to the ready applause of an approving crowd.

I also notice the guy in this vid is very careful to pepper his statements with just enough caveats to maintain plausible deniability if someone were to follow his advice and suffer as a consequence. He’s a shrewd manipulator, I’ll give him that.
 
Last edited:
buck said:
Reading from a wide range of sources both pro and con on an issue to try to come to an unemotional choice as to what is best for an individual seems prudent to me. When ever an individual tries to limit ones choices i tend to give less credence to their opinions. Statins have their place, especially for those that have heart issues. As a preventative they seem to be less effective at increasing life span. Seems half of all people that have heart attacks had what is considered healthy cholesterol levels last i checked. Seems there is more going on the just how much LDL-C a person has.
Click to expand...

I wanted to touch on the last part of what you said, because it’s something I’ve been looking into. From what I understand, LDL can be deceptive and appear to be within an acceptable range, while an advanced cardio panel will show high LDL particles. Those small, dense particles are the most damaging.

My LDL was around 90, but when I ran an advanced cardio iq panel, my LDL particles were a mess. At the time, my ApoB was discordant with my LDL, so not helpful either. Both my HDL and trigs were very good.

As far as the ones who have heart attacks with healthy cholesterol levels, I’d theorize that group likely has dealt with other ongoing metabolic damage, or years of atherosclerosis causing inflammation. Just because they get their numbers into an acceptable range doesn’t mean they’re free from the endothelial damage that’s already been done. I would bet they have high homocysteine, hs-crp, uric acid or some combination. I don’t think there are any robust studies, but I do recall reading that lowering inflammation cut cardiovascular events independent of lowering LDL.
 
Superchicken said:
I wanted to touch on the last part of what you said, because it’s something I’ve been looking into. From what I understand, LDL can be deceptive and appear to be within an acceptable range, while an advanced cardio panel will show high LDL particles. Those small, dense particles are the most damaging.

My LDL was around 90, but when I ran an advanced cardio iq panel, my LDL particles were a mess. At the time, my ApoB was discordant with my LDL, so not helpful either. Both my HDL and trigs were very good.

As far as the ones who have heart attacks with healthy cholesterol levels, I’d theorize that group likely has dealt with other ongoing metabolic damage, or years of atherosclerosis causing inflammation. Just because they get their numbers into an acceptable range doesn’t mean they’re free from the endothelial damage that’s already been done. I would bet they have high homocysteine, hs-crp, uric acid or some combination. I don’t think there are any robust studies, but I do recall reading that lowering inflammation cut cardiovascular events independent of lowering LDL.
Click to expand...
The data points to several different things being able to cause heart disease.
So tracking any one thing is not likley to paint the whole picture. I check various things and have for decades.

All my cholesterol numbers. have been exceptionally good all my life other then HDL not being very high but with total cholesterol in the 125-140 range it is hard for me to get tit higher. Glucose , BP, inflammatory markers etc all good yet still a high CAC score. That is why i tend to say there is a lot that modern science does not yet understand.

Lipitor's own study when going from 40mg a day to 80 mg reduced cardiac events. Yet life expectancy also went down. I suggest that people look past just the number of events and also ask about longevity

Studies such as this and others show that statins can lower cholesterol levels but don't decrease small dense lipoprotein.
pubmed.ncbi.nlm.nih.gov

Statins do not decrease small, dense low-density lipoprotein - PubMed

In an observational study, we examined the effect of statins on low-density-lipoprotein (LDL) subfractions.Using density-gradient ultracentrifugation, we measured small, dense LDL density in 612 patients (mean age, 61.7 ± 12.6 yr), some with and some without coronary artery disease, who were...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
 
Ghoul said:
With all due respect, this is not about limiting choices or silencing dissenting opinions.

One side of this issue is boring and backed by mountains of evidence, and accepted by 99.99.% of cardiologists as expressed worldwide by the organizations representing them, all sheep apparently, while dissenting from this is a guarantee of instant social media fame, cool points, and pats on the back from the people who “just knew it”.

There is no human ailment that has a higher degree of evidence between cause and effect established than LDL and cardiovascular disease. I’m not sure if that statement is strong enough so I’ll put it another way. If a handful of sensationalist outliers are enough to cast doubt in your mind that LDL is the underlying cause of cardiovascular disease because the evidence isn’t sufficient, there is no cause and effect you should believe is proven, including cigarettes to lung cancer and respiratory disease, which isn’t as strongly established as LDL and cardiovascular disease. None.

The other part that’s been definitively established is that lower LDL, achieved by any means, has a direct association with lower rates of cardiovascular disease and death.

So it’s not about shutting down another opinion, it’s about how tiresome it is arguing with people who baselessly refute the position that’s met the highest possible standards of proof, and aren’t doing any of the work to look at the evidence from “both sides”, giving each appropriate weight based on volume and strength, but taking the easy, “cooler” counter position built on sound bites and low-powered studies, that requires deliberately ignoring what amounts to incontrovertible evidence developed over 60 years, by tens of thousand of scientists (all corrupted by big pharma supposedly) following the trajectories of tens of millions of subjects, their treatments, and outcomes.

Given this is the #1 cause of death, no effort has been spared by generations of researchers, governments, and doctors to chase down every doubt and ambiguity as to what causes it and how to reduce it. This was no quick conclusion or academic theory. After jumping over every hurdle, and finally meeting the highest possible standards of proof, it’s irritating to have the occasional clown say, “Nah”, without producing 1/10000 the evidence to back their assertion, to the ready applause of an approving crowd.

I also notice the guy in this vid is very careful to pepper his statements with just enough caveats to maintain plausible deniability if someone were to follow his advice and suffer as a consequence. He’s a shrewd manipulator, I’ll give him that.
Click to expand...
Thanks for your input.

Regarding this guy, he's been a controversial scientist. I see he does all sort of n=1 experiments as well, probably just to go viral. See his research:

Google Scholar

scholar.google.com scholar.google.com

The one about LMHRs phenotype:

Google Scholar

scholar.google.com scholar.google.com

—

In my personal experience leading to find about LMHRs as a potential classification of my metabolic state at the time, a lowcarb diet with not so high amount of saturated fat content (no shit load of butter on steak horror movies), but 5-6 eggs per day skyrocketed my ldl to ~400, while my TG and HDL remained in healthy.

A subsequent measurement showed low range oxidized LDL yielded, high apob as well. Running a Atherosclerosis test a few weeks later, showed no change in artery walls. But this was only a short timeperiod of exposure before I course corrected my diet.

Attaching some biomarkers for the curious.
 

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buck said:
The data points to several different things being able to cause heart disease.
So tracking any one thing is not likley to paint the whole picture. I check various things and have for decades.

All my cholesterol numbers. have been exceptionally good all my life other then HDL not being very high but with total cholesterol in the 125-140 range it is hard for me to get tit higher. Glucose , BP, inflammatory markers etc all good yet still a high CAC score. That is why i tend to say there is a lot that modern science does not yet understand.

Lipitor's own study when going from 40mg a day to 80 mg reduced cardiac events. Yet life expectancy also went down. I suggest that people look past just the number of events and also ask about longevity

Studies such as this and others show that statins can lower cholesterol levels but don't decrease small dense lipoprotein.
pubmed.ncbi.nlm.nih.gov

Statins do not decrease small, dense low-density lipoprotein - PubMed

In an observational study, we examined the effect of statins on low-density-lipoprotein (LDL) subfractions.Using density-gradient ultracentrifugation, we measured small, dense LDL density in 612 patients (mean age, 61.7 ± 12.6 yr), some with and some without coronary artery disease, who were...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
Click to expand...
The language is a bit misleading and needs nuance. Larger LDL fell more sharply in comparison to the smaller, so it made the them higher only in proportion to the original baseline, even though total was lower. That’s also an older observational study showing association, there have been newer and more robust studies done since then.

Linking in case you’re curious.

RCT showing high dose rosu reduced smaller more than low dose therapy.

pubmed.ncbi.nlm.nih.gov

High-dose statin therapy with rosuvastatin reduces small dense LDL and MDA-LDL: The Standard versus high-dose therApy with Rosuvastatin for lipiD lowering (SARD) trial - PubMed

High-dose statin therapy significantly reduced the sd-LDL and MDA-LDL components of atherosclerotic lipoproteins without adverse events in comparison with low-dose statin therapy.
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov

Study on pita showing the same thing.

www.frontiersin.org

Frontiers | Small, Dense Low-Density Lipoprotein-Cholesterol and Atherosclerosis: Relationship and Therapeutic Strategies

Abstract: Low-density lipoprotein cholesterol (LDL-C) plays an important role in the formation, incidence, and development of atherosclerosis (AS). Low-densi...
www.frontiersin.org www.frontiersin.org

I think focusing on life expectancy is too narrow a view. My fil for example is getting a stent put in next month, studies show that treatment for secondary prevention does affect life expectancy. The length of which relies on baseline health when starting. My husband otoh, is 40 and started a statin preventatively. There’s no data on that, but I am hopeful he will die with age related atherosclerosis and not early because of it. For someone like myself, the off values were hormone related and resolved without statins. I doubt my life expectancy would change significantly if I were to use statin therapy, as I don’t have the same risk factors.

Would be interested in reading the Lipitor study if you get a chance to link it.
 
BigDadd7 said:
I have a friend who is easily 80 pounds over weight. He also has high blood pressure. His ldl is through the roof. He won't take statins cuz bad. He wheezes when he walks and talks at the same time.
Click to expand...
This is like my mom who drinks like a fish, but won’t get a mammogram done because she says it causes cancer. Yk what actually does have a significant risk for preventative cancer, fucking alcohol. So she won’t get the mammogram, which means her dr won’t give her hrt. I was helping her out and sourcing for her, but nah. As soon as she has a bad health outcome, she’s going to say I did it.
 
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