I chose to leave this part out of the article but will leave this personal observation here as a conversation starter:
1) About 3% of my patients experience noticable muscle aches within days/weeks of starting statins and the feel better when statins are stopped
2) another 7% of my patients will have delayed muscle aches that takes months or even years to develop and they often miss the fact that its even related to statins. Frequently attributed to “old age”
3) A 1 month statin holiday is how I distinguish true statin myalgias. To see who improves. Today with PSCK9 inhibitors available to us. I rarely treat statin myalgias with CoQ10 anymore.
4) These days I reach for CoQ10 for the mitrochondrial function benefit (generally combined with magnesium and omega 3’s- and pomegranates to maximize urolithin a levels) to “grease the cogs of the mitrochondria” so to speak. (Assuming all general concepts of an anti inflammatory diet are already being followed). This is an emerging science we dont fully understand yet but it is fascinating.
The statin industrial complex wants everyone on statins. They made me so sick. My doctor refused to believe me. The only thing he ever said about my really high cholesterol was take statins. I exercised huge amounts, lost tons of weight and nothing brought it down. It wasn’t until I saw and endocrinologist to start hormone therapy that a doctor finally listened to me. She said, hmm I think you shouldn’t be on statins. And you might have heterozygous hipercolesterolemia. Let’s try Repatha. After 30 days, my cholesterol dropped from over 300 to below 60. I’m not saying statins are not useful, I’m saying the tidal wave of marketing has the effect that most doctors see it as the only treatment. It is not, and in my case, as well as making me sick, they would have had no effect.
Thank you for sharing your experience. I’m sorry that you felt unwell on statins and, just as importantly, that you felt your concerns were not taken seriously. Whether or not a symptom ultimately proves to be medication-related, patients deserve to be heard and to have a thoughtful discussion about options.
You are absolutely right that statins are not the only treatment for elevated LDL cholesterol. For someone with very high LDL levels—particularly an untreated LDL above 190, and certainly levels in the 300 range—clinicians should think about familial hypercholesterolemia and consider a more complete evaluation, including family history, secondary causes, lipoprotein(a), and sometimes referral to a lipid specialist. Lifestyle remains foundational for cardiovascular health, but when LDL is genetically driven, even major improvements in diet, exercise, and weight may not lower it enough on their own.[acc]
Repatha is an important option. It is a PCSK9 inhibitor, and the degree of LDL reduction you describe is consistent with the substantial reductions this class can produce, especially in people with familial hypercholesterolemia.
The one nuance I would add is that heterozygous familial hypercholesterolemia does not mean statins have no effect. Many people with FH do benefit from them, often in combination with other medications. But if a person truly cannot tolerate statins, or if statins alone do not produce enough LDL lowering, there are now several evidence-based alternatives and add-on therapies. The goal should never be to force one medication on every patient; it should be to reduce cardiovascular risk with a plan the individual can safely tolerate and sustain.
And that is why discussions about statins—and about supplements such as CoQ10—should be individualized rather than ideological.
Remember the heart is also a muscle, and also prone to the adverse effects of statin drugs. This is why statin drugs are also known for causing heart failure.
I understand why that concern can sound intuitive—skeletal muscle symptoms are a real issue for some people taking statins, and those symptoms should be taken seriously. But the conclusion that statins are known to cause heart failure is not supported by the evidence.
The heart is indeed a muscle, but it is biologically different from skeletal muscle. In large randomized trials, statins have not been shown to cause cardiomyopathy or heart failure. In fact, trials that enrolled people who already had systolic heart failure found that rosuvastatin did not worsen symptoms, increase heart-failure hospitalizations, or create a cardiac safety signal.
It is also important to distinguish two separate questions: statins are not routinely started solely to treat established heart failure, because major trials did not show that they improve survival in every patient with heart failure. That is very different from saying they cause heart failure. The available randomized-trial evidence does not support that claim.
If someone develops new shortness of breath, swelling, chest symptoms, profound fatigue, or muscle weakness after starting any medication, that deserves a clinical evaluation—not an assumption online. And for people who truly cannot tolerate a statin, there are evidence-based alternatives.
I did not say anything about established heart failure because that has nothing to do with my point.
Yes, there are different types of muscle (skeletal, cardiac, and smooth). I learned that decades ago in high school. What do muscles, especially cardiac muscle , rely heavily on? Adenosine triphosphate (ATP). What do statins reduce ATP. The reduction of ATP can lead to rhabdomyolosis. Generally, when people think of statin induced rhabdomyolosis, they think skeletal muscle. The heart is more dependent on ATP than skeletal muscle, and the heart can develop cardiac rhabdomyolosis, resulting in heart failure.
Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99.
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms
Am J Cardiovasc Drugs
. Author manuscript; available in PMC: 2010 Apr 6.
Published in final edited form as: Am J Cardiovasc Drugs. 2008;8(6):373–418
Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
Thank you for clarifying your argument and for citing the papers you are relying on. You are correct that cardiac muscle has a very high energy demand, that ATP is essential to its function, and that mitochondrial mechanisms have been proposed as one possible contributor to statin-associated muscle symptoms in susceptible individuals. Severe statin-associated skeletal-muscle injury, including rhabdomyolysis, is real—although rare—and warrants immediate evaluation, medication review, and attention to dose, drug interactions, thyroid status, kidney function, and other contributors.[pmc.ncbi.nlm.nih +1]
Where I disagree is the leap from a plausible laboratory mechanism or hypothesis to the clinical claim that statins are “known for causing heart failure.” The two articles you cite are reviews that advance a hypothesis; they are not randomized clinical-trial evidence demonstrating that statins cause cardiac rhabdomyolysis, cardiomyopathy, or heart failure in patients. The 2015 article itself describes its conclusion as a “perspective” and proposes mechanisms by which the authors believe statins may contribute to disease. It does not establish that causal relationship.[pubmed.ncbi.nlm.nih +1]
That distinction matters. In medicine, many mechanisms are biologically plausible but do not translate into a meaningful clinical outcome when tested in large, controlled trials. The broader evidence base and major safety reviews have not found statin-induced cardiomyopathy to be an established adverse effect. Serious statin muscle injury is uncommon, with the American Heart Association estimating rhabdomyolysis at less than 0.1%, and it is principally recognized as skeletal-muscle injury—not “cardiac rhabdomyolysis” as a defined, routine clinical entity.[ahajournals +1]
None of this means that every person should take a statin or that symptoms should be dismissed. It means we should take symptoms seriously, avoid absolutist claims in either direction, and tailor treatment to the person. For someone with reproducible intolerance after an appropriate evaluation and rechallenge when safe, alternatives such as ezetimibe, bempedoic acid, or PCSK9-targeting therapy may be appropriate depending on their LDL level and overall cardiovascular risk.
A major reason that rhabomyolosis is not common is because the issue of statin induced rhabdomyolosis has been known for a long time, as well as how to to reduce the risk. For this reason, many doctors recommend that patients on statin drugs take CoQ10 to increase ATP, which reduces the risk of rhabdomyolosis.
In addition, many people with heart issues also take magnesium, which is also great for heart health and blood pressure. Especially magnesium malate as both magnesium, and the malic acid increase ATP levels.
As for the studies thing, sometimes we have to look beyond the studies and apply basic common sense based on knowing how thing work in the body.
Studies are often bought and paid for. Even double blind studies can be designed or interpreted in ways to get whatever desired results that the funders wish. Happens all the time. This is why we get so many studies on the same exact thing that get totally opposite results.
As another way of looking at this, I was writing about how NSAIDs could cause heart attacks and stokes 30 years before the medical community finally admitted to this fact. How did I figure this out? Obviously not from double blind studies that had not been conducted. Instead, I applied some simple common sense based on knowing how these drugs work, and how they induce other side effects such as liver failure that killed 2 dozen people during clinical trials of ibuprofen , and kidney failure. Failure of the liver or kidneys by strong NSAIDs, such as ibuprofen are due to he vasoconstriction properties of NSAIDs, which is what prevents fluid leakage from blood vessels, thus reducing edema and pain. Same reason for some other side effects from NSAIDs, such as tinnitus and vision loss. This is all about vasoconstriction. What happens when the blood supply is cut off to organs? Failure. Why for over 30 years did the medical establishment think the heart and brain were somehow magically immune to the same vasoconstriction that can cause liver and kidney failure from these drugs? Just because there was no double blind studies to prove that the NSAIDs were causing heart attacks and strokes, that does not mean this was not happening.
Let’s get back to the statins for a minute. Are their double blind studies showing the fact that statins can raise cholesterol levels? I doubt it. Let’s again apply some common sense though. What organ regulates cholesterol levels? The liver, which produces cholesterol levels for the body when levels are low, and breaks down excess cholesterol when levels are high. A well known side effect of statin drugs is liver damage, which will prevent the liver from doing its job of breaking down excess cholesterol.
By the way, you may want to do some research in to the scandal behind the Jupiter study regarding the safety of statins. Quite interesting cover up.
In fact, much of the whole cholesterol issue is a scam. Cholesterol is essential to the body for so many reasons, and abnormally low cholesterol is detrimental to the body increasing the risk of things including dementia, and even heart attack and stroke.
Thank you so much for this info!
I chose to leave this part out of the article but will leave this personal observation here as a conversation starter:
1) About 3% of my patients experience noticable muscle aches within days/weeks of starting statins and the feel better when statins are stopped
2) another 7% of my patients will have delayed muscle aches that takes months or even years to develop and they often miss the fact that its even related to statins. Frequently attributed to “old age”
3) A 1 month statin holiday is how I distinguish true statin myalgias. To see who improves. Today with PSCK9 inhibitors available to us. I rarely treat statin myalgias with CoQ10 anymore.
4) These days I reach for CoQ10 for the mitrochondrial function benefit (generally combined with magnesium and omega 3’s- and pomegranates to maximize urolithin a levels) to “grease the cogs of the mitrochondria” so to speak. (Assuming all general concepts of an anti inflammatory diet are already being followed). This is an emerging science we dont fully understand yet but it is fascinating.
The statin industrial complex wants everyone on statins. They made me so sick. My doctor refused to believe me. The only thing he ever said about my really high cholesterol was take statins. I exercised huge amounts, lost tons of weight and nothing brought it down. It wasn’t until I saw and endocrinologist to start hormone therapy that a doctor finally listened to me. She said, hmm I think you shouldn’t be on statins. And you might have heterozygous hipercolesterolemia. Let’s try Repatha. After 30 days, my cholesterol dropped from over 300 to below 60. I’m not saying statins are not useful, I’m saying the tidal wave of marketing has the effect that most doctors see it as the only treatment. It is not, and in my case, as well as making me sick, they would have had no effect.
Thank you for sharing your experience. I’m sorry that you felt unwell on statins and, just as importantly, that you felt your concerns were not taken seriously. Whether or not a symptom ultimately proves to be medication-related, patients deserve to be heard and to have a thoughtful discussion about options.
You are absolutely right that statins are not the only treatment for elevated LDL cholesterol. For someone with very high LDL levels—particularly an untreated LDL above 190, and certainly levels in the 300 range—clinicians should think about familial hypercholesterolemia and consider a more complete evaluation, including family history, secondary causes, lipoprotein(a), and sometimes referral to a lipid specialist. Lifestyle remains foundational for cardiovascular health, but when LDL is genetically driven, even major improvements in diet, exercise, and weight may not lower it enough on their own.[acc]
Repatha is an important option. It is a PCSK9 inhibitor, and the degree of LDL reduction you describe is consistent with the substantial reductions this class can produce, especially in people with familial hypercholesterolemia.
The one nuance I would add is that heterozygous familial hypercholesterolemia does not mean statins have no effect. Many people with FH do benefit from them, often in combination with other medications. But if a person truly cannot tolerate statins, or if statins alone do not produce enough LDL lowering, there are now several evidence-based alternatives and add-on therapies. The goal should never be to force one medication on every patient; it should be to reduce cardiovascular risk with a plan the individual can safely tolerate and sustain.
And that is why discussions about statins—and about supplements such as CoQ10—should be individualized rather than ideological.
Remember the heart is also a muscle, and also prone to the adverse effects of statin drugs. This is why statin drugs are also known for causing heart failure.
I understand why that concern can sound intuitive—skeletal muscle symptoms are a real issue for some people taking statins, and those symptoms should be taken seriously. But the conclusion that statins are known to cause heart failure is not supported by the evidence.
The heart is indeed a muscle, but it is biologically different from skeletal muscle. In large randomized trials, statins have not been shown to cause cardiomyopathy or heart failure. In fact, trials that enrolled people who already had systolic heart failure found that rosuvastatin did not worsen symptoms, increase heart-failure hospitalizations, or create a cardiac safety signal.
It is also important to distinguish two separate questions: statins are not routinely started solely to treat established heart failure, because major trials did not show that they improve survival in every patient with heart failure. That is very different from saying they cause heart failure. The available randomized-trial evidence does not support that claim.
If someone develops new shortness of breath, swelling, chest symptoms, profound fatigue, or muscle weakness after starting any medication, that deserves a clinical evaluation—not an assumption online. And for people who truly cannot tolerate a statin, there are evidence-based alternatives.
I did not say anything about established heart failure because that has nothing to do with my point.
Yes, there are different types of muscle (skeletal, cardiac, and smooth). I learned that decades ago in high school. What do muscles, especially cardiac muscle , rely heavily on? Adenosine triphosphate (ATP). What do statins reduce ATP. The reduction of ATP can lead to rhabdomyolosis. Generally, when people think of statin induced rhabdomyolosis, they think skeletal muscle. The heart is more dependent on ATP than skeletal muscle, and the heart can develop cardiac rhabdomyolosis, resulting in heart failure.
Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99.
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms
Am J Cardiovasc Drugs
. Author manuscript; available in PMC: 2010 Apr 6.
Published in final edited form as: Am J Cardiovasc Drugs. 2008;8(6):373–418
Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
Thank you for clarifying your argument and for citing the papers you are relying on. You are correct that cardiac muscle has a very high energy demand, that ATP is essential to its function, and that mitochondrial mechanisms have been proposed as one possible contributor to statin-associated muscle symptoms in susceptible individuals. Severe statin-associated skeletal-muscle injury, including rhabdomyolysis, is real—although rare—and warrants immediate evaluation, medication review, and attention to dose, drug interactions, thyroid status, kidney function, and other contributors.[pmc.ncbi.nlm.nih +1]
Where I disagree is the leap from a plausible laboratory mechanism or hypothesis to the clinical claim that statins are “known for causing heart failure.” The two articles you cite are reviews that advance a hypothesis; they are not randomized clinical-trial evidence demonstrating that statins cause cardiac rhabdomyolysis, cardiomyopathy, or heart failure in patients. The 2015 article itself describes its conclusion as a “perspective” and proposes mechanisms by which the authors believe statins may contribute to disease. It does not establish that causal relationship.[pubmed.ncbi.nlm.nih +1]
That distinction matters. In medicine, many mechanisms are biologically plausible but do not translate into a meaningful clinical outcome when tested in large, controlled trials. The broader evidence base and major safety reviews have not found statin-induced cardiomyopathy to be an established adverse effect. Serious statin muscle injury is uncommon, with the American Heart Association estimating rhabdomyolysis at less than 0.1%, and it is principally recognized as skeletal-muscle injury—not “cardiac rhabdomyolysis” as a defined, routine clinical entity.[ahajournals +1]
None of this means that every person should take a statin or that symptoms should be dismissed. It means we should take symptoms seriously, avoid absolutist claims in either direction, and tailor treatment to the person. For someone with reproducible intolerance after an appropriate evaluation and rechallenge when safe, alternatives such as ezetimibe, bempedoic acid, or PCSK9-targeting therapy may be appropriate depending on their LDL level and overall cardiovascular risk.
A major reason that rhabomyolosis is not common is because the issue of statin induced rhabdomyolosis has been known for a long time, as well as how to to reduce the risk. For this reason, many doctors recommend that patients on statin drugs take CoQ10 to increase ATP, which reduces the risk of rhabdomyolosis.
In addition, many people with heart issues also take magnesium, which is also great for heart health and blood pressure. Especially magnesium malate as both magnesium, and the malic acid increase ATP levels.
As for the studies thing, sometimes we have to look beyond the studies and apply basic common sense based on knowing how thing work in the body.
Studies are often bought and paid for. Even double blind studies can be designed or interpreted in ways to get whatever desired results that the funders wish. Happens all the time. This is why we get so many studies on the same exact thing that get totally opposite results.
As another way of looking at this, I was writing about how NSAIDs could cause heart attacks and stokes 30 years before the medical community finally admitted to this fact. How did I figure this out? Obviously not from double blind studies that had not been conducted. Instead, I applied some simple common sense based on knowing how these drugs work, and how they induce other side effects such as liver failure that killed 2 dozen people during clinical trials of ibuprofen , and kidney failure. Failure of the liver or kidneys by strong NSAIDs, such as ibuprofen are due to he vasoconstriction properties of NSAIDs, which is what prevents fluid leakage from blood vessels, thus reducing edema and pain. Same reason for some other side effects from NSAIDs, such as tinnitus and vision loss. This is all about vasoconstriction. What happens when the blood supply is cut off to organs? Failure. Why for over 30 years did the medical establishment think the heart and brain were somehow magically immune to the same vasoconstriction that can cause liver and kidney failure from these drugs? Just because there was no double blind studies to prove that the NSAIDs were causing heart attacks and strokes, that does not mean this was not happening.
Let’s get back to the statins for a minute. Are their double blind studies showing the fact that statins can raise cholesterol levels? I doubt it. Let’s again apply some common sense though. What organ regulates cholesterol levels? The liver, which produces cholesterol levels for the body when levels are low, and breaks down excess cholesterol when levels are high. A well known side effect of statin drugs is liver damage, which will prevent the liver from doing its job of breaking down excess cholesterol.
By the way, you may want to do some research in to the scandal behind the Jupiter study regarding the safety of statins. Quite interesting cover up.
In fact, much of the whole cholesterol issue is a scam. Cholesterol is essential to the body for so many reasons, and abnormally low cholesterol is detrimental to the body increasing the risk of things including dementia, and even heart attack and stroke.