Statins: experience training and racing on them

My advice would be to try not to focus too much on the side effetcs of your statin medication. Sure, statins can cause the side effects you Mentorin nur there is extensive research indicating a big nocebo component to them. Maybe your shoulder is sore from the Swimming Break you probably had with your extensive leg injury. The more you focus on the side effects by doing research etc the more the nocebo components plays a role. And as you dont have many alternatives in keeping your cholesterol in check, there is no positive uphand from finding out statins are not for you.

In other words, I would worry much more about the condition requiring you to take the statins and not about Potential side effects from them. My Impression is you got it the other way around.

Thanks for the feedback…I am well familiar with nocebo effects especially in my area of work.
It is not as you state unfortunately…the condition requiring the statins is relatively minor and not something that would bother me for about 15 years if I did not treat it. There are some unique side effects to statins and dosing etc is important.

Amnesia,

There is much good info on this thread but I will add my own experience as that seems to be what you asked for.

FWIW, I have been on various brands /doses of statins for almost ten years now. At the same time I have been taking a low dose aspirin daily as well. I tend to have both cramping and muscle pain since I started taking statins.

My experience is that my body does not react to all statins/doses in the same way. One year I ran a spring marathon. After I experienced muscle soreness. In the past, after running a marathon, the muscle soreness would last 2 to 3 days. After this race the muscle soreness did not go away for over two weeks. After consulting with my Doc we decided to stop the statins. Immediately the muscle soreness went away.

I have also experienced severe hamstring cramps since being on statins. This can happen both while running, the middle of the night while sleeping and occasionally in the pool while swimming.

Since then we have experimented with different brands and different doses and found what seems to work for me.

Good luck

Steve

A few years ago, I was put on Atorvastatin (don’t remember the dosage), and after a few weeks I started experiencing temporary extreme weakness and burning in my legs. This would come typically after driving, I would get out of my car, walk a few dozen yards, and then it would hit. I would have to stand still and wait for about a minute to recover, and then I was fine. I told my cardiologist, and he immediately took me off it, and the problem disappeared right away. Last year I was put back on a lower dose (10mg), and have not noticed anything unusual…

Last year I started on Atorvastatin 10mg and ended up with near constant pain in my glutes and calves. Switched to Lovastatin 10mg. Glute pain went away quick but calf pain lasted a few months.

I am on Crestor 20mg no issues at all but a doctor in the med tent at Ironman world championship told me to stop taking it 3 days before before the race can lead to cramps
.

What a terrific response by dtoce.

Amnesia,
I am also a cardiologist, and have developed a number of cholesterol medications in my career—including having designed and run a statin intolerance study.
I agree very much with what dtoce said, and also happy to provide a few tips that you might consider also—please make sure to partner with your physician(s), since you should smartly question anything provided on a public we forum.

  1. Partner with your doc, as you are. You can also see a cardiologist who specializes in “statin intolerance”—these do exist! Given triathlon is important for your quality of life, taking this extra measure is a reasonable choice.
  2. It appears unclear whether you are having statin myalgia (only symptoms) or statin myopathy (with or without injury measured by significant increased in muscle enzymes (ie, CK)). The latter means taking some more deliberate steps. Measuring CK is not considered routine management of statin associated muscle symptoms unless severe, as you know, but I think you can make the argument this is a special case in extremely impactful activities for your quality of life. An empathic doctor should work with you on this.
  3. There are some medical conditions that may predispose to statin myalgia/myopathy, which might be subclinical. For example, hypothyroidism and Vitamin D deficiency—these are very easy to check and low hanging fruit to address.
  4. There are very effective ways of managing statin choice and administration schedule to improve your symptoms. For example, change to daily fluvastatin or pravasatin, which are associated with lower muscle symptoms. I have personally found switching to weekly (or 2-3 times weekly depending upon LDL-C goals) rosuvastatin works quite well, and can resolve symptoms in the majority of patients.

Good luck!

Edit.
Realizing how patronizing it might sound advising another doctor to “partner with your doc”—I didn’t mean for it to come across that way. As physicians we tend to be tempted self-diagnose and self-treat-I know I have been guilty of it!

4x heart bypass . Bata blocker, ace inhibitor, statin. I am 1.5 years out . I have been racing (cycling) I have beaten people who beat me before surgery. I do have to warm up really REALLY good before a race. Raced 5 months after surgery and have never stopped. I am 65.
I posted this before and some jerk accused me of not eating correctly before the heart attack. I do not ever post now. I decided to respond this one time to try to help.

What a terrific response by dtoce.

Amnesia,
I am also a cardiologist, and have developed a number of cholesterol medications in my career—including having designed and run a statin intolerance study.
I agree very much with what dtoce said, and also happy to provide a few tips that you might consider also—please make sure to partner with your physician(s), since you should smartly question anything provided on a public we forum.

  1. Partner with your doc, as you are. You can also see a cardiologist who specializes in “statin intolerance”—these do exist! Given triathlon is important for your quality of life, taking this extra measure is a reasonable choice.
  2. It appears unclear whether you are having statin myalgia (only symptoms) or statin myopathy (with or without injury measured by significant increased in muscle enzymes (ie, CK)). The latter means taking some more deliberate steps. Measuring CK is not considered routine management of statin associated muscle symptoms unless severe, as you know, but I think you can make the argument this is a special case in extremely impactful activities for your quality of life. An empathic doctor should work with you on this.
  3. There are some medical conditions that may predispose to statin myalgia/myopathy, which might be subclinical. For example, hypothyroidism and Vitamin D deficiency—these are very easy to check and low hanging fruit to address.
  4. There are very effective ways of managing statin choice and administration schedule to improve your symptoms. For example, change to daily fluvastatin or pravasatin, which are associated with lower muscle symptoms. I have personally found switching to weekly (or 2-3 times weekly depending upon LDL-C goals) rosuvastatin works quite well, and can resolve symptoms in the majority of patients.

Good luck!

Edit.
Realizing how patronizing it might sound advising another doctor to “partner with your doc”—I didn’t mean for it to come across that way. As physicians we tend to be tempted self-diagnose and self-treat-I know I have been guilty of it!

All amazing advice thanks.
For the moment, just FYI-I have halved my atorvastatin dose over the weekend and see how it feels with swimming this week. (FYI thyroid and Vit D are all good).
Question-if switching to weekly or 2-3 times weekly rosuvastatin, what dose would you normally recommend and is there any advice around dosing and exercise? I have not looked at the various half lives etc, but was just wondering if there was recommendations around when to dose and exercise.
Thanks for this.

4x heart bypass . Bata blocker, ace inhibitor, statin. I am 1.5 years out . I have been racing (cycling) I have beaten people who beat me before surgery. I do have to warm up really REALLY good before a race. Raced 5 months after surgery and have never stopped. I am 65.
I posted this before and some jerk accused me of not eating correctly before the heart attack. I do not ever post now. I decided to respond this one time to try to help.

Yep. That feedback is really uncalled for and unwelcome.
The plant based zealots can go a bit overboard at times.

I’m not an MD.

Did you have a coronary calcium scan? Personally, I would not go on a statin without seeing the results of one first.

Hi Amnesia,
This is where we move away from evidence-base medicine. As you are aware, the CV outcomes trials for statins were evaluated with on-label regimens, which were daily administration. However, the totality of evidence strongly supports the LDL hypothesis, and intermittent regimens, so long as LDL is efficaciously reduced, should translate into reduced CV events.

There are so many permutations of intermittent statin regimens, and are in balance with what you can tolerate versus your LDL-C goals. This is why partnering with an experienced lipidologist who specializes in statin intolerance can help. Your case is even more special because your regimen needs to fit an endurance athlete’s lifestyle (I refuse to believe your tibia fracture can permanently set you back! We will cheer you from the sidelines to start running again once recovered!!!). Again, with the usual caveats to take anything a stranger online will say with a grain of salt and to partner with your doc:

  1. Since your presentation is primary prevention and not secondary prevention due to ACS, it means you can probably afford to go “low and slow”.
  2. Depending upon your level of intolerance: if very intolerant, might start with 2.5 mg or 5 mg rosuvastatin once weekly. If you can tolerate, can start or titrate to twice weekly (eg. Mon/Thurs) or 3 times weekly (eg. Mon/Wed/Fri) 2.5 to 5 mg rosuvastatin. Switching to fluvastatin or pravastain is also on the table if the above does not work. Also, you can further titrate rosuvastatin dose to achieve your goals or add ezetimibe help achieve LDL-C goals if needed. PCSK9 inhibitors are also available, but is much more expensive and not sure if it is cost-effective for you.
  3. The elimination half-life of rosuvastatin is ~19 hours. It will take about 3-5 doses on whichever regimen to achieve “steady-state”, to see where you land before making further changes or titrations. Suffice to say, intermittent regimens will result in higher “peak trough fluctuations” in plasma concentration. You can leverage this peak trough fluctuation to your benefit in terms of timing your exercise sessions!
  4. I would take the statin at night (ie, before bedtime). While long duration statins like rosuvastatin tend to allow time of administration at any time of day, you are trying to get the most “bang for your buck”—most cholesterol synthesis occurs at night, which means at least on those days you take the statin, the highest concentrations of the nightly-administered statin occurs at the time when it is most needed. Taking the statin at night also gives you a practical way to manage exercise… next bullet
  5. Taking the statin at night on an intermittent regimen means the daytimes on the days you take the statin are “trough” or nadir levels of statin in your body and may be the ideal days for your higher intensity exercise sessions. For example, if you are due to take your statin Monday night, Monday morning could be you higher intensity or longer training session day.
  6. Preface—this is REALLY anecdotal and NOT evidence-based: but for really big exercise days, eg a triathlon race, you might consider pausing your statin for 3 or more days before (which is >3 elimination half-lives). Big races result in CK releases (or muscle injury pattern) in even healthy people without medical conditions, and people on statins are shown to have even higher CK releases. SInce you are in the primary prevention category, you might consider this since races are few and far in between and should not unduly affect your overall “time under the curve” on LDL-C reduction.

Take care and good luck!

you guys are terrific. i have added this to our HOT FORUM TOPICS. if you don’t know about this, hunt for it, it’s on this page a couple of times, turn down the arrow, you’ll see a bunch of cool navigational helps, including on the medical end of things.

I’m not an MD.

Did you have a coronary calcium scan? Personally, I would not go on a statin without seeing the results of one first.
See above…calcium score of 2 so low risk, but you don’t see the soft plaques on a calcium score, which is why if you can you need to get a CT coronary angiogram, and that is what showed the soft plaques and hence the reason for the statin.

Hi Amnesia,
This is where we move away from evidence-base medicine. As you are aware, the CV outcomes trials for statins were evaluated with on-label regimens, which were daily administration. However, the totality of evidence strongly supports the LDL hypothesis, and intermittent regimens, so long as LDL is efficaciously reduced, should translate into reduced CV events.

There are so many permutations of intermittent statin regimens, and are in balance with what you can tolerate versus your LDL-C goals. This is why partnering with an experienced lipidologist who specializes in statin intolerance can help. Your case is even more special because your regimen needs to fit an endurance athlete’s lifestyle (I refuse to believe your tibia fracture can permanently set you back! We will cheer you from the sidelines to start running again once recovered!!!). Again, with the usual caveats to take anything a stranger online will say with a grain of salt and to partner with your doc:

  1. Since your presentation is primary prevention and not secondary prevention due to ACS, it means you can probably afford to go “low and slow”.
  2. Depending upon your level of intolerance: if very intolerant, might start with 2.5 mg or 5 mg rosuvastatin once weekly. If you can tolerate, can start or titrate to twice weekly (eg. Mon/Thurs) or 3 times weekly (eg. Mon/Wed/Fri) 2.5 to 5 mg rosuvastatin. Switching to fluvastatin or pravastain is also on the table if the above does not work. Also, you can further titrate rosuvastatin dose to achieve your goals or add ezetimibe help achieve LDL-C goals if needed. PCSK9 inhibitors are also available, but is much more expensive and not sure if it is cost-effective for you.
  3. The elimination half-life of rosuvastatin is ~19 hours. It will take about 3-5 doses on whichever regimen to achieve “steady-state”, to see where you land before making further changes or titrations. Suffice to say, intermittent regimens will result in higher “peak trough fluctuations” in plasma concentration. You can leverage this peak trough fluctuation to your benefit in terms of timing your exercise sessions!
  4. I would take the statin at night (ie, before bedtime). While long duration statins like rosuvastatin tend to allow time of administration at any time of day, you are trying to get the most “bang for your buck”—most cholesterol synthesis occurs at night, which means at least on those days you take the statin, the highest concentrations of the nightly-administered statin occurs at the time when it is most needed. Taking the statin at night also gives you a practical way to manage exercise… next bullet
  5. Taking the statin at night on an intermittent regimen means the daytimes on the days you take the statin are “trough” or nadir levels of statin in your body and may be the ideal days for your higher intensity exercise sessions. For example, if you are due to take your statin Monday night, Monday morning could be you higher intensity or longer training session day.
  6. Preface—this is REALLY anecdotal and NOT evidence-based: but for really big exercise days, eg a triathlon race, you might consider pausing your statin for 3 or more days before (which is >3 elimination half-lives). Big races result in CK releases (or muscle injury pattern) in even healthy people without medical conditions, and people on statins are shown to have even higher CK releases. SInce you are in the primary prevention category, you might consider this since races are few and far in between and should not unduly affect your overall “time under the curve” on LDL-C reduction.

Take care and good luck!

Thanks Jae K, this is fantastic advice.
FYI-15 year specialist anaesthetist here (using our down under vernacular here rather than the USA system of Anesthesiologist!). Mainly clinical and part academic with a clinical professorship, so understand the PK aspects of what you are talking about re dosing and half lives etc.
I really appreciate your advice. I am not sure if there is a cardiologist in my area that has a special interest in statin intolerance but I will make some enquiries. So far, with a dose reduction by 50%, I have to say I am feeling less general muscle aching, but I will know more by the end of the week once we reach a new steady state and have some more swimming under my belt.

you guys are terrific. i have added this to our HOT FORUM TOPICS. if you don’t know about this, hunt for it, it’s on this page a couple of times, turn down the arrow, you’ll see a bunch of cool navigational helps, including on the medical end of things.

Thanks Dan,
This is very valuable medical information that you will absolutely struggle to find easily elsewhere (all the little pointers about how to manage the dosing and how to manage them around racing etc).

Amnesia

“4) There are very effective ways of managing statin choice and administration schedule to improve your symptoms. For example, change to daily fluvastatin or pravasatin, which are associated with lower muscle symptoms. I have personally found switching to weekly (or 2-3 times weekly depending upon LDL-C goals) rosuvastatin works quite well, and can resolve symptoms in the majority of patients.”

Having tried several, I can second this choice. Rosuvastatin has worked well with me.

I would add that this can be a difficult choice to think about. On the one hand, most physicians believe in the beneficial effects of statins although the evidence that they prevent events is seemingly unclear.

And on the other hands, for some of us faced with that choice there is a quality of life question that enters the equation.

My compromise has been a low enough dose, three times a week, so that I can remain physically active.

Good luck and best wishes in your search.

Steve

Not an MD, but my question is, why do you think a statin will help you reduce your risk for CVD? I’d suggest you apply critical thinking to this problem, which I have found, is often lacking within the medical profession. Critical thinking has 3 components: 1. Challenge Assumptions, 2. Reason through Logic. 3. Get diversified opinions.

I would challenge the “Lipid Hypothesis”, that elevated cholesterol causes heart disease. In fact, from what I have read, this hypothesis has been proven false. The correlation between elevated LDL and total cholesterol and heart disease is not convincing. For those that are metabolically healthy, a triglyceride to HDL ratio of close to 1:1, and normal fasting blood glucose, and other factors, there is even lower correlation. In a recent discussion between Dr. Peter Attia and Dr. Thomas Dayspring they discussed that heart disease is, “multi complex, multi factor.” It’s not just cholesterol. As the physicist Richard Feynman would say, if your prediction does not match your experiment, your hypothesis is false. It’s just that simple. In fact, lowering LDL can have many negative health side effects.

The hypothesis that I have found to be most supported by data is that insulin resistance is a driver of heart disease, not elevated cholesterol. Interesting that Type 2 diabetics are 60% more likely to develop heart disease.

I would suggest you listen to a recent podcast discussion with the Cardiologist Dr. Nadir Ali, on the “Fat Emperor Podcast”, Episode 60 (march 16, 2020). He does a far better discussion of this than I can.

Why do I care about this. In my late 30’s and early 40’s, I was doing 15 to 20 hours of endurance exercise, and eating a high carb, low fat diet, because the “experts” said you need carbs and you shouldn’t eat animal meats and fat. I had a physical. BP 140 over 90. Triglycerides over 150, HDL below 40, and fasting glucose above 100. MY PCP wasn’t that worried, because “you exercise and eat healthy”. However, I ended up seeing a cardiologist, and I had something thickening of my septum, and as a result, I was put on BP medication and he said, “I might want to put you on a statin”. I never went on a statin.

At that time, a friend sent me an essay on “Evolutionary Fitness” by Art De Vany. This started me down the path of a paleo diet. I also did less endurance training and more weight training and high intensity training (i.e. sprinting). About two years ago, after a soft tissue injury, I met a guy who went on the “carnivore diet” after rotator cuff surgery.

Cut to the chase. My hypothesis is that the epidemic of chronic disease, heart disease, obesity, Type 2 diabetes is being driven by processed food. Grains, sugar, and processed vegetable/seed oils (canola, vegetable, etc…) are the primary culprits. If you want to be healthy, those should be eliminated. If man made, don’t eat it.

My N=1 results. 18 months ago I went on a 90% carnivore diet, primarily, red meat (lots of it), organ meats, fish, some chicken, eggs, a little dairy, lots of bone broth. The other 10% is the occasional vegetable, fruit or treats (ice cream, cake, pizza once a month). This is also a low carb diet, so I am now “fat adapted.”

My wife and kids thought I was crazy. They said wait until your next physical or colonoscopy. Here are the results: BP went from 130’s over high 80’s to no higher than 120 over 80. HDL from 45 to 56 (good). Triglycerides from 129 to 76 (good). TRI/HDL ratio from 2.86 to 1.35 (good). Fasting glucose from 101 to 92. LDL from 118 to 148 (I don’t see this as bad). As for the colonoscopy, I’m in my 50’s and have one every 5 years because of family history. My doctor said, “looks great, even better than last time”. So much for needing fiber (that hypothesis is just wrong). The thickening in my septum has resolved. I am on NO meds.

Other benefits, I’m stronger than I’ve ever been, stubborn belly fat has melted away, and at my last eye appointment, my eyesite had actually improved. Since I’m fat adapted, I don’t need food to have energy and can easily go all day without eating. Lastly, the “morning wood” is more common than it used to be.

I’m not telling you to NOT take a statin. I don’t know your details. But I do know this. I was told from a very good cardiologist at one of the best hospitals in the country that I would be on BP medication for the rest of my life, and that my septum would likely never normalize. WRONG. 4 primary care physicians and 3 cardiologists only offered me medications, none told me how to actually determine the root cause and cure the problem.

I used critical thinking. I tend to be skeptical. I do my own research. When I have an acute injury, I have confidence in my doctors ability to fix it. But when it comes to “chronic” health conditions, the medical industrial complex is failing us. As Chris Rock would say, “they don’t cure shit. They get you on the comeback.” Follow the money.

I suspect I will get a bunch of doctors accusing me of spreading disinformation. They’ll point to this study, or that study. But I know how that game works. Everything I’ve said here is what I’ve learned from doctors, who are actually using critical thinking. At the end of the day, all I know is this, I’m healthier in my mid 50’s than I’ve ever been, and compared to most 20 year olds, and getting better everyday. I strongly urge you to investigate alternatives. I doubt you will regret it.

I will say it again. No grains, no sugar, no vegetable/seed oils.

Good luck. I hope you find a good solution that works for you, and keeps you healthy.

I am an MD and a board certified cardiologist with over 25 years of experience taking care of thousands of patients.

Your assessment of ‘critical thinking’ is somewhat flawed, IMO. And I am saddened to see you have gotten rather poor medical advice and needed to seek out alternate treatment that you believe is superior. One should always 'challenge assumptions and ‘reason through logic’ to appropriate conclusions. The problem is with #3…diversified opinions. That is not evidence based and is totally unsupported. Opinion is simply that-opinion.

The literature is quite clear and I’m not going to recite it for you. I’m disappointed that I must come back to this thread to again dispel misinformation perpetuated by one with no real evidence. You even said your N=1. That is a unique observation, not a study. You can eat whatever you want and be happy with that behavior. Your numbers are part of your risk profile. Good luck with that.

One does not ‘challenge the lipid hypothesis’ because you don’t believe it. You do it by conducting studies to prove alternate theories. You should discuss your concerns with your doctors and really should refrain from giving advice you are not trained to give. Septal thickening has nothing to do with CAD, BTW…apples and oranges…not the same type of problem. Resolution of one problem does not mitigate risk elsewhere…

I have had so many patients who have no other reason for their CAD and want an explanation for why they developed ischemic heart disease and often an elevated LDL is the only explanation. Sometimes it is one of the major contributors. We treat the best we can based on the evidence we have and that does evolve and change with time.

You did say a few thing correctly. Diabetes is a driver for risk of CAD. In fact, it is considered a ‘risk equivalent’ for ischemic heart disease or CAD. We treat it very similarly. Also, CAD is truly multifactorial-smoking/sedentary lifestyle/diet/family history/DM/age etc all can play a role. And an appropriate diet is truly very important.

One other thing we know a great deal about and that is how heart attacks happen. That is from atherosclerotic plaque rupture. If you don’t have plaque, you are at very low risk for CAD events-ie myocardial infarct (MI) and sudden cardiac death (SCD).

The treatment for known CAD/plaque/ischemic CAD is statin and aspirin in 2021. Secondary statin therapy is simply not in doubt.

I will not comment on other md opinions. You can decide for yourself, but please, please don’t give medical advice.

Reader’s Digest version

Not an MD … the medical profession is stupid. Critical thinking has 3 components: 1. Google, 2. Challenge actual science and medicine, 3. Believe everyone in the camp I’ve chosen, 3. Get diversified opinions only within my camp.

The hypothesis that I have found to be most supported by my gurus is that insulin resistance is a driver of heart disease, not elevated cholesterol.

I would suggest you listen to a recent podcast discussion with the Cardiologist Dr. Nadir Ali, on the “Unhinged angry conspiracy theorist Podcast”,

I met a guy who went on the “carnivore diet”

(standard HFLC talking points ad infinitum)

N=1

I’m a zealot.

All science and medicine is part of a giant nefarious conspiracy.

ntsa.jpg

I know there are those that are really hot on a totally plant based diet. I don’t really know to much about that. I do know that a Mediterranean diet has a more powerful effect in terms of reducing overall mortality than a statin in both primary and secondary prevention. In well conducted studies published in major journals.

Not surprising not much effort expended on recommending to pts given very little money to be made doing this and it is a lot more time consuming to prescribe a specific diet vs the 30sec or less to prescribe a statin. The effect of a statin in primary prevention is not particularly strong. You have to treat a lot of people to prevent at death. More than prescribing an anti hypertensive for example. I have prescribed truckloads of statins.