I started taking statins (rosuvastatin 40 and ezetimibe 10) about a decade ago. I should have started sooner, but I was too healthy to be prescribed statins according to the UK's NHS "matrix". I had high cholesterol, but low BMI, low BP, was fit, ate well, not pre-diabetic... so it was left to a "foreign" cardiologist to identify my Familial Hypercholesterolemia. Thankfully. My Apo-B was so high his first question was "How are you still here?"
I did have leg cramps when I started taking Rosuvastatin. I don't think this was coincidental - I am talking wake-you-up with a steel-rod-in-your-leg cramp - something I'd not experienced previously. However, I found that adequate daily exercise alleviated the incidence and that the cramps were IMO preferable to further artery clogging. And eventually, the cramps went away completely. And I can say that I really cannot identify any unwelcome effects of my statin use. My cholesterol level is now low-normal and my other metrics remain good. I have also modified my diet to reduce carb intake (not to a keto level, but minimal starches and sugars)
I would like to challenge the thought that because someone reads of an adverse event means that they can and will manifest it. And, secondly, when their doctor "encourages" them to stay on the drug, the adverse events
Picked up my first prescription and the pharmacist made a point of warning me that it could cause soreness, specifically in the shoulders but it would pass in a week or so. I wonder how many people wind up with shoulder pain because they were told this? I'm waiting to start until after I finish some big running events so that if I do feel sore muscles it's clear why.
I think more importantly the risk of diabetes needs to be cautioned. Two people I know blame their diabetes on statin use. I think some people take the statin to mean they can just eat whatever and that still isn't really the case but could be related to the higher rate of diabetes in statin users.
Such important information. I gave up on statins for primary prevention due to perceived muscle pains, and when my risk profile increased with age and I tried them again years later, I had no problems. Nocebo plus concurrent soreness likely due to competitive sports fooled me despite years of teaching others about the impact of cognitive bias in medicine!
Well written and well reasoned. Also your replies to comments are very insightful. Probably the most difficult arena to discuss with patients when I was in practice. The most difficult patients were those with symptoms from statins and unable to afford or unwilling to take the PCSK9 inhibitors.
Not sure why a statin crossing the blood brain barrier is much of a concern, as LDL also crosses, and brain cells can up-regulate the IDL/LDL receptor to maintain intracellular cholesterol levels, just as occurs in the liver. Hence no effect on brain function.
Statin effect on Lp(a) levels varies from individual to individual. Some studies show an increase, some a decrease. A large recent meta-analysis suggested no significant change.
Kahn exhibits the #1 red flag of quackery: promoting and selling tons of useless supplements. At the shop on his website you can buy unproven supplements in 20 different categories. He has been added to the list of candidates for America's greatest purveyors of humbuggery
I have long joked with all my doctors over the years that I get side effects from every medication up to and including baby aspirin. If a medication has side effects. I typically get them. Prior to becoming a patient of Doctor P, my PCP at the time prescribed me atorvastatin for high cholesterol. I had ZERO prior knowledge about the drug or its possible side effects. Almost immediately after starting the drug , the only way I can describe it is my entire body “locked up “. Walking even a few feet felt like torture. I contacted my pharmacist immediately who advised to stop taking it, contact my prescribing doctor, and informed me I was in the 5 percent of people with severe reactions to it. Subsequent bloodwork indicated my muscle enzymes were more than triple above the normal range. It took over a year for it to return to normal and pain to dissipate. They even did a muscle biopsy of my right thigh to ensure I didn’t have a muscular disease of some kind. I wish it was different but I for one will NEVER take a statin for ANY reason! I’ve since been on both Praulent and Repatha (at different times) which control my cholesterol with no noticeable problems.
Hmmmm... I wouldn't call Malcolm Kendrick someone with little or no scientific expertise and he's not selling anything... And recently won a court case against a newspaper libelling him as responsible for the deaths of zillions because he contested the utility of statins... using the truth defence. Are you sure you have no association with the pharmaceutical companies that deal in statins? I'm not casting aspersions, I genuinely don't know your personal affiliation, but would suggest statin proponents are typically just as monetarily invested in their products as the 'deniers', at least if Kendrick is anything to go by
Since I began writing the skeptical cardiologist blog in 2013 I have had no association of any kind with pharmaceutical companies. My sole aim in writing (as in my medical practice) is to disseminate information that helps save lives, reduce disability, and increase happiness.
Almost all the statin prescriptions I write are for generics which cost for most around 5$ per month and don't make big Pharma any money.
I have spent thousands of hours researching and writing on the optimal approach to reducing atherosclerotic cardiovascular and haven't taken a penny from Pharma, Big AG, supplement selling, product placement or anyone for that work.
I have read much of what Kendrick has written. He is a PCP in the UK, an independent thinker and a good writer. But what a judge decides in a libel suit should not determine whether his opinions on statins is correct or incorrect.
The couple of articles I've read have been appreciated. Doctors don't typically have time to have these indepth discussions this is an efficient way to educate many more than just the patient sitting in your office.
Fourteen years ago I spent the better part of four months being ill. It was a generalized feeling of ill health with very low energy and the moderate aches and pains associated with a low grade fever. I became concerned that this seemed to be a self perpetuating situation and I started to think seriously about what was going on. I reviewed all supplements and medications I was taking and came across the atorvastatin I had started not long before the malaise. I had been a profoundly statin naive and trusting patient with no fore knowledge of positive or negative side effects beyond cholesterol lowering. I stopped the statin. It took about ten days for me to feel well again. I was reluctant, but I knew that re-challenging myself would be wise. It took a few days, but that illness returned. I deny that nocebo could possibly be the initial cause of my statin illness. I grant you that placebo and nocebo might have been working during the initial quitting and re-challenging. That said, I contend that there is no way of proving anything concerning an individual's response to drugs. Double blind randomized controlled trials with many subjects is not an approach open to a single individual. On the subject of pro- and nocebo, I would ask you if you yourself take a statin and if you think you are immune to these effects – as the individual that you are.
I have suffered months of diarrhea associated with lymphocytic colitis several times in my career. NSAIDS including aspirin, omeprazole, and rosuvastatin have been my triggers.
I send you this comment not as a challenge, but as one man's experience, in hopes of improving everyone's knowledge base.
As a psychologist, I know that both placebo and nocebo effects are real. With muscle soreness, one can test creatinine kinase levels to make sure the patient doesn't suffer from rhabdomyolysis. For cognition, it is more subjective (unless one does a full cognitive battery pre and post statins, which nobody does). While population-level observational studies indicate statins do not negatively impact cognition ON AVERAGE, they might not tell the whole story about INDIVIDUAL differences. (I can't wait for precision medicine). I finally decided to take a statin after getting a CAC score AND listening to lipidologist Thomas Dayspring on Peter Attia's podcast. When my doctor upped my dose, I really noticed an increase in memory issues, and wondered if it was just a nocebo effect, but I knew what to do because of Dayspring. Research has shown that low desmosterol is associated with dementia, and Dayspring thinks it's plausible that low desmosterol might negatively impact cognitive functioning. (It's unlikely anybody will fund an RCT to demonstrate causality with certainty). Dayspring recommends stopping or reducing the dose of your statin if your desmosterol is below the 20th percentile and going on a different cholesterol lowering medication (statins are the only cholesterol lowering drug that affect desmosterol). So I had my desmosterol tested, and it was below the 20th PR; it turns out I'm a cholesterol hyper-absorber. So I reduced my statin dose and started Zettia and will adjust as needed after further testing. Since my mother had dementia, I will not take chances with low desmosterol, since there are other drugs I can take to bring my LDL-C into a healthy range. If interested, I recommend Googling "Thomas Dayspring desmosterol cognition." He's the true expert on lipids and has posted a lot on Twitter and LinkedIn, but Peter Attia has written the best article for laymen in the link below.
I have great respect for Dr. Dayspring but he is an outlier in the world of lipidologists, most of whom do not measure desmosterol routinely.
Likewise, as I've written in the past, I have great respect for Peter Attia but he definitely has a tendency to go overboard in many areas and get ahead of the science.
A careful read on his 2021 article (which is a good one) notes that he says
One of the most common causes of reduced desmosterol is statin therapy. Statins can cross the BBB — and while the data is conflicting — a recent study confirmed the hypothesis that lipophilic versions including simvastatin (Zocor) and atorvastatin (Lipitor) may more easily cross the BBB than hydrophilic ones including rosuvastatin (Crestor) and pravastatin (Pravachol), and therefore may inhibit cholesterol synthesis in the brain. Is low desmosterol a cause of cognitive impairment and dementia or the result of it? The short answer is we don’t know. What we do know is that cholesterol is critical to brain function and there are observational studies like the ones above (and more recent ones) suggesting low plasma desmosterol is a biomarker for MCI and AD. Unfortunately, the 2012 and 2015 papers discussed above don’t include patients on statins, which would be helpful for us to elucidate any links between statin use, desmosterol levels, and cognitive decline. It may sound cliché to hear this, but more, and better, research is needed to understand whether statins have an effect on cognition or neurological disorders like AD, in at least a subset of users. "
Yes, we don't know whether low desmosterol contributes to cognitive impairment or dementia.
But we do know that markedly lowered desmosterol which happens with statins is not associated with MCI or AD.
So, routinely measuring desmosterol and stopping statin at an arbitrarily determined cut point is not warranted in asymptomatic individuals.
If a patient is experiencing a sense of brain fog or cognitive impairment in clinical practice we would end up in the same place as you have ended up but without measuring desmosterol-if patient felt better on lower dosage we would add ezetimibe to get to goal without side effects.
As an orthopedic sports medicine specialist (a surgeon by training), I frequently see patients who develop tendinopathy and who happen to have been on statins for several years, usually at low doses. Tendinopathy is always very slow to improve (i.e., 6-9 months) and quite difficult to treat. It significantly reduces the quality of life during this time, and often prevents patients from exercising as their cardiologist has recommended. There are many studies tying statins to tendon changes, but the relationship does not appear to be as well accepted as for fluoroquinolones.
My questions:
Based on your reading of the literature, do you believe that tendinopathy is a side effect of statins?
If a patient informed you that their orthopedist wanted them to be off their statin for 3-6 months, to see if they can recover from their tendinopathy, what would you advise? If you agreed for a respite, would you prescribe a substitute temporarily?
I'm particular sensitive to this topic as my dad developed tendinopathy and rupture on a fluoroquinolone.
As I indicated in the post I am always open to stopping statins for perceived side effects. Depending on the patient's cardiac risk I would offer a substitute if off for 3-6 months.
In cases where side effects are real, I would compare the side effect to the consequence of not taking statins. Muscle soreness compared to a heart attack is insignificant. However, I recognize that comparing an issue I have now to a possible issue in the future is difficult. We like to solve the problem in front of us, not the possible problem down the road.
I respect your opinion but I also respectfully disagree with your premise. My “muscle soreness “ from taking the statin went completely beyond that. It was debilitating. My personal choice would be to take my chances on a heart attack rather than continue living like I was. Fortunately, Doctor P became my cardiologist and got me started on Praulent which was life changing and possibly life saving.
I understand your perspective. You compared the pain (debilitating) vs heart attack and made a decision that fit your needs. Reviewing my comment, I realized I was only considering those that want a pain-free life no matter how minor the pain may be. I should have added to my second sentence “unless the pain becomes so debilitating that it impacts quality of life.” Thank you and the family doc for helping me see a broader perspective.
I have had a number of patients who note that muscle aches are worse at higher intensity statins but when we halve or quarter the dosage they have a minimal ache that they find tolerable because they understand the benefits in reducing their lifelong risk of atherosclerotic complications
Family doc here — while it may be true we tend to try to solve immediate problems over future ones, I have a handful of patients (including myself) where aching precludes exercise…and I definitely want people to exercise! Had I not experienced the pain myself I’d be more in the “compare the consequences” camp, but it was real and it was debilitating. For myself I took a year to work up to 5 mg rosuvastatin (ldl 2.02) but couldn’t tolerate higher, so I added ezetimibe. For patients I take the same approach: start low, go slow, don’t be afraid of adding a different agent.
Clear Outcomes has added advantage of specifically enrolling those who were “statin intolerant”. Sadly, not yet available in Canada.
I have had less luck with drug on/off trials. As with many aspects of “misinformation “, it’s tough slogging pushing back against the Internet.
Also great point that, regardless of trial data, there will be some individuals who truly have some (at times idiosyncratic) adverse response to a drug that will never be borne out by “data” but is nonetheless very real.
Clear Outcomes being the RCT that established bempedoic acid as improving MACE outcomes in diabetics(Over a median of 3·4 years follow up, patients with diabetes had significant relative and absolute cardiovascular risk reductions in MACE-4 endpoints with bempedoic acid (HR 0·83; 95% CI 0·72–0·95; absolute risk reduction of 2·4%) compared to placebo, with no statistical evidence of effect modification across glycaemic strata (interaction p=0·42) )without increasing risk of DM.
It takes a lot of time and effort to convince some patients to rechallenge with statin and some have pretty much decided before they enter the exam room that they aren't going to either take them or tolerate them. I've learned to recognize this latter group and move quickly to the good alternatives we have.
I started taking statins (rosuvastatin 40 and ezetimibe 10) about a decade ago. I should have started sooner, but I was too healthy to be prescribed statins according to the UK's NHS "matrix". I had high cholesterol, but low BMI, low BP, was fit, ate well, not pre-diabetic... so it was left to a "foreign" cardiologist to identify my Familial Hypercholesterolemia. Thankfully. My Apo-B was so high his first question was "How are you still here?"
I did have leg cramps when I started taking Rosuvastatin. I don't think this was coincidental - I am talking wake-you-up with a steel-rod-in-your-leg cramp - something I'd not experienced previously. However, I found that adequate daily exercise alleviated the incidence and that the cramps were IMO preferable to further artery clogging. And eventually, the cramps went away completely. And I can say that I really cannot identify any unwelcome effects of my statin use. My cholesterol level is now low-normal and my other metrics remain good. I have also modified my diet to reduce carb intake (not to a keto level, but minimal starches and sugars)
Can you provide citations that demonstrate or have investigated the stabilization of CAC scores after starting statins? Thanks.
Sorry, comment continued:
.... the adverse event stops. I can say from experience that a patient gets tired of "trying to convince" their doctor that their symptoms are real.
I would like to challenge the thought that because someone reads of an adverse event means that they can and will manifest it. And, secondly, when their doctor "encourages" them to stay on the drug, the adverse events
Picked up my first prescription and the pharmacist made a point of warning me that it could cause soreness, specifically in the shoulders but it would pass in a week or so. I wonder how many people wind up with shoulder pain because they were told this? I'm waiting to start until after I finish some big running events so that if I do feel sore muscles it's clear why.
I think more importantly the risk of diabetes needs to be cautioned. Two people I know blame their diabetes on statin use. I think some people take the statin to mean they can just eat whatever and that still isn't really the case but could be related to the higher rate of diabetes in statin users.
Such important information. I gave up on statins for primary prevention due to perceived muscle pains, and when my risk profile increased with age and I tried them again years later, I had no problems. Nocebo plus concurrent soreness likely due to competitive sports fooled me despite years of teaching others about the impact of cognitive bias in medicine!
Well written and well reasoned. Also your replies to comments are very insightful. Probably the most difficult arena to discuss with patients when I was in practice. The most difficult patients were those with symptoms from statins and unable to afford or unwilling to take the PCSK9 inhibitors.
Not sure why a statin crossing the blood brain barrier is much of a concern, as LDL also crosses, and brain cells can up-regulate the IDL/LDL receptor to maintain intracellular cholesterol levels, just as occurs in the liver. Hence no effect on brain function.
Hello Dr. P! Dr. Kahn writes that statins often raise Lp(a) levels. Is this true and are there any statin types that do not do this?
Statin effect on Lp(a) levels varies from individual to individual. Some studies show an increase, some a decrease. A large recent meta-analysis suggested no significant change.
We need more data on optimal treatment of patients with high Lp(a) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098730/
I wouldn't take any advice from joel kahn. He's a vegan wacko.
Kahn exhibits the #1 red flag of quackery: promoting and selling tons of useless supplements. At the shop on his website you can buy unproven supplements in 20 different categories. He has been added to the list of candidates for America's greatest purveyors of humbuggery
In regards to him , I will agree with you 100 percent. I was hoping you weren't going to defend him.
I have long joked with all my doctors over the years that I get side effects from every medication up to and including baby aspirin. If a medication has side effects. I typically get them. Prior to becoming a patient of Doctor P, my PCP at the time prescribed me atorvastatin for high cholesterol. I had ZERO prior knowledge about the drug or its possible side effects. Almost immediately after starting the drug , the only way I can describe it is my entire body “locked up “. Walking even a few feet felt like torture. I contacted my pharmacist immediately who advised to stop taking it, contact my prescribing doctor, and informed me I was in the 5 percent of people with severe reactions to it. Subsequent bloodwork indicated my muscle enzymes were more than triple above the normal range. It took over a year for it to return to normal and pain to dissipate. They even did a muscle biopsy of my right thigh to ensure I didn’t have a muscular disease of some kind. I wish it was different but I for one will NEVER take a statin for ANY reason! I’ve since been on both Praulent and Repatha (at different times) which control my cholesterol with no noticeable problems.
What makes you certain Repatha and Praluent are safe? I know personally they are effective but what are their long-term side effects???
Hmmmm... I wouldn't call Malcolm Kendrick someone with little or no scientific expertise and he's not selling anything... And recently won a court case against a newspaper libelling him as responsible for the deaths of zillions because he contested the utility of statins... using the truth defence. Are you sure you have no association with the pharmaceutical companies that deal in statins? I'm not casting aspersions, I genuinely don't know your personal affiliation, but would suggest statin proponents are typically just as monetarily invested in their products as the 'deniers', at least if Kendrick is anything to go by
Heather,
Since I began writing the skeptical cardiologist blog in 2013 I have had no association of any kind with pharmaceutical companies. My sole aim in writing (as in my medical practice) is to disseminate information that helps save lives, reduce disability, and increase happiness.
Almost all the statin prescriptions I write are for generics which cost for most around 5$ per month and don't make big Pharma any money.
I have spent thousands of hours researching and writing on the optimal approach to reducing atherosclerotic cardiovascular and haven't taken a penny from Pharma, Big AG, supplement selling, product placement or anyone for that work.
I have read much of what Kendrick has written. He is a PCP in the UK, an independent thinker and a good writer. But what a judge decides in a libel suit should not determine whether his opinions on statins is correct or incorrect.
The couple of articles I've read have been appreciated. Doctors don't typically have time to have these indepth discussions this is an efficient way to educate many more than just the patient sitting in your office.
That's a fair question and a good point.
See above.
I find the question insulting and the point without merit.
Dr. P
Don't know why you would be insulted.It was still respectful and fair question in my opinion
And I respect your honest answer
Dear Dr. Skep,
Fourteen years ago I spent the better part of four months being ill. It was a generalized feeling of ill health with very low energy and the moderate aches and pains associated with a low grade fever. I became concerned that this seemed to be a self perpetuating situation and I started to think seriously about what was going on. I reviewed all supplements and medications I was taking and came across the atorvastatin I had started not long before the malaise. I had been a profoundly statin naive and trusting patient with no fore knowledge of positive or negative side effects beyond cholesterol lowering. I stopped the statin. It took about ten days for me to feel well again. I was reluctant, but I knew that re-challenging myself would be wise. It took a few days, but that illness returned. I deny that nocebo could possibly be the initial cause of my statin illness. I grant you that placebo and nocebo might have been working during the initial quitting and re-challenging. That said, I contend that there is no way of proving anything concerning an individual's response to drugs. Double blind randomized controlled trials with many subjects is not an approach open to a single individual. On the subject of pro- and nocebo, I would ask you if you yourself take a statin and if you think you are immune to these effects – as the individual that you are.
With respect to statins and diarrhea, I refer you to this search: https://pubmed.ncbi.nlm.nih.gov/?term=%28%28statin%5BTitle%2FAbstract%5D%29+AND+%28colitis%5BTitle%2FAbstract%5D%29%29+AND+%28microscopic%5BTitle%2FAbstract%5D%29&sort=
I have suffered months of diarrhea associated with lymphocytic colitis several times in my career. NSAIDS including aspirin, omeprazole, and rosuvastatin have been my triggers.
I send you this comment not as a challenge, but as one man's experience, in hopes of improving everyone's knowledge base.
As a psychologist, I know that both placebo and nocebo effects are real. With muscle soreness, one can test creatinine kinase levels to make sure the patient doesn't suffer from rhabdomyolysis. For cognition, it is more subjective (unless one does a full cognitive battery pre and post statins, which nobody does). While population-level observational studies indicate statins do not negatively impact cognition ON AVERAGE, they might not tell the whole story about INDIVIDUAL differences. (I can't wait for precision medicine). I finally decided to take a statin after getting a CAC score AND listening to lipidologist Thomas Dayspring on Peter Attia's podcast. When my doctor upped my dose, I really noticed an increase in memory issues, and wondered if it was just a nocebo effect, but I knew what to do because of Dayspring. Research has shown that low desmosterol is associated with dementia, and Dayspring thinks it's plausible that low desmosterol might negatively impact cognitive functioning. (It's unlikely anybody will fund an RCT to demonstrate causality with certainty). Dayspring recommends stopping or reducing the dose of your statin if your desmosterol is below the 20th percentile and going on a different cholesterol lowering medication (statins are the only cholesterol lowering drug that affect desmosterol). So I had my desmosterol tested, and it was below the 20th PR; it turns out I'm a cholesterol hyper-absorber. So I reduced my statin dose and started Zettia and will adjust as needed after further testing. Since my mother had dementia, I will not take chances with low desmosterol, since there are other drugs I can take to bring my LDL-C into a healthy range. If interested, I recommend Googling "Thomas Dayspring desmosterol cognition." He's the true expert on lipids and has posted a lot on Twitter and LinkedIn, but Peter Attia has written the best article for laymen in the link below.
https://peterattiamd.com/does-low-cholesterol-cause-cognitive-impairment-part-ii/
I have great respect for Dr. Dayspring but he is an outlier in the world of lipidologists, most of whom do not measure desmosterol routinely.
Likewise, as I've written in the past, I have great respect for Peter Attia but he definitely has a tendency to go overboard in many areas and get ahead of the science.
A careful read on his 2021 article (which is a good one) notes that he says
One of the most common causes of reduced desmosterol is statin therapy. Statins can cross the BBB — and while the data is conflicting — a recent study confirmed the hypothesis that lipophilic versions including simvastatin (Zocor) and atorvastatin (Lipitor) may more easily cross the BBB than hydrophilic ones including rosuvastatin (Crestor) and pravastatin (Pravachol), and therefore may inhibit cholesterol synthesis in the brain. Is low desmosterol a cause of cognitive impairment and dementia or the result of it? The short answer is we don’t know. What we do know is that cholesterol is critical to brain function and there are observational studies like the ones above (and more recent ones) suggesting low plasma desmosterol is a biomarker for MCI and AD. Unfortunately, the 2012 and 2015 papers discussed above don’t include patients on statins, which would be helpful for us to elucidate any links between statin use, desmosterol levels, and cognitive decline. It may sound cliché to hear this, but more, and better, research is needed to understand whether statins have an effect on cognition or neurological disorders like AD, in at least a subset of users. "
Yes, we don't know whether low desmosterol contributes to cognitive impairment or dementia.
But we do know that markedly lowered desmosterol which happens with statins is not associated with MCI or AD.
So, routinely measuring desmosterol and stopping statin at an arbitrarily determined cut point is not warranted in asymptomatic individuals.
If a patient is experiencing a sense of brain fog or cognitive impairment in clinical practice we would end up in the same place as you have ended up but without measuring desmosterol-if patient felt better on lower dosage we would add ezetimibe to get to goal without side effects.
As an orthopedic sports medicine specialist (a surgeon by training), I frequently see patients who develop tendinopathy and who happen to have been on statins for several years, usually at low doses. Tendinopathy is always very slow to improve (i.e., 6-9 months) and quite difficult to treat. It significantly reduces the quality of life during this time, and often prevents patients from exercising as their cardiologist has recommended. There are many studies tying statins to tendon changes, but the relationship does not appear to be as well accepted as for fluoroquinolones.
My questions:
Based on your reading of the literature, do you believe that tendinopathy is a side effect of statins?
If a patient informed you that their orthopedist wanted them to be off their statin for 3-6 months, to see if they can recover from their tendinopathy, what would you advise? If you agreed for a respite, would you prescribe a substitute temporarily?
I would very much appreciate your input.
David
thanks for your comments/questions
Clinically, I have not seen tendinopathy in my statin patients. This analysis ()https://www.mja.com.au/journal/2016/204/3/statins-and-tendinopathy-systematic-review#:~:text=Tendon%20rupture%20was%20the%20primary,reduces%20the%20risk%20of%20tendinopathy.)suggests no increased frequency of tendon rupture with statins over placebo. Also, that simvastatin may reduce tendinopathy prevalence.
I'm particular sensitive to this topic as my dad developed tendinopathy and rupture on a fluoroquinolone.
As I indicated in the post I am always open to stopping statins for perceived side effects. Depending on the patient's cardiac risk I would offer a substitute if off for 3-6 months.
Dr. P
In cases where side effects are real, I would compare the side effect to the consequence of not taking statins. Muscle soreness compared to a heart attack is insignificant. However, I recognize that comparing an issue I have now to a possible issue in the future is difficult. We like to solve the problem in front of us, not the possible problem down the road.
I respect your opinion but I also respectfully disagree with your premise. My “muscle soreness “ from taking the statin went completely beyond that. It was debilitating. My personal choice would be to take my chances on a heart attack rather than continue living like I was. Fortunately, Doctor P became my cardiologist and got me started on Praulent which was life changing and possibly life saving.
I understand your perspective. You compared the pain (debilitating) vs heart attack and made a decision that fit your needs. Reviewing my comment, I realized I was only considering those that want a pain-free life no matter how minor the pain may be. I should have added to my second sentence “unless the pain becomes so debilitating that it impacts quality of life.” Thank you and the family doc for helping me see a broader perspective.
True.
I have had a number of patients who note that muscle aches are worse at higher intensity statins but when we halve or quarter the dosage they have a minimal ache that they find tolerable because they understand the benefits in reducing their lifelong risk of atherosclerotic complications
I would never take a high dose stat for any reason. I take 5 mg. Crestor every other day for the anti-inflammatory benefits not ldl.
Family doc here — while it may be true we tend to try to solve immediate problems over future ones, I have a handful of patients (including myself) where aching precludes exercise…and I definitely want people to exercise! Had I not experienced the pain myself I’d be more in the “compare the consequences” camp, but it was real and it was debilitating. For myself I took a year to work up to 5 mg rosuvastatin (ldl 2.02) but couldn’t tolerate higher, so I added ezetimibe. For patients I take the same approach: start low, go slow, don’t be afraid of adding a different agent.
Clear Outcomes has added advantage of specifically enrolling those who were “statin intolerant”. Sadly, not yet available in Canada.
I have had less luck with drug on/off trials. As with many aspects of “misinformation “, it’s tough slogging pushing back against the Internet.
Also great point that, regardless of trial data, there will be some individuals who truly have some (at times idiosyncratic) adverse response to a drug that will never be borne out by “data” but is nonetheless very real.
Clear Outcomes being the RCT that established bempedoic acid as improving MACE outcomes in diabetics(Over a median of 3·4 years follow up, patients with diabetes had significant relative and absolute cardiovascular risk reductions in MACE-4 endpoints with bempedoic acid (HR 0·83; 95% CI 0·72–0·95; absolute risk reduction of 2·4%) compared to placebo, with no statistical evidence of effect modification across glycaemic strata (interaction p=0·42) )without increasing risk of DM.
It takes a lot of time and effort to convince some patients to rechallenge with statin and some have pretty much decided before they enter the exam room that they aren't going to either take them or tolerate them. I've learned to recognize this latter group and move quickly to the good alternatives we have.