Unsure About Taking A Statin For High Cholesterol? Consider A Compromise Approach

In an earlier post the skeptical cardiologist introduced Geo, a 61 year old male with no risk factors for heart attack or stroke other than a high cholesterol. His total cholesterol was 249, LDL (bad) 154, HDL (good) 72 and triglycerides 116.
His doctor had recommended that he take a statin drug but Geo balked at taking one due to concerns about side effects and requested my input. My first steps were to gather more information.
-I calculated his 10 year risk of stroke or heart attack at 8.4% (treatment with statin typically felt to benefit individuals with 10 year risk >7.5%) and as I have previously noted, this is not unusual for a man over age 60.
-I assessed him for any hidden  or subclinical atherosclerosis and found

The vascular ultrasound showed below normal carotid thickness and no plaque and his coronary calcium score was 18,  putting him at the 63rd  percentile. This is slightly higher than average white men his age.

So Geo definitely has atherosclerotic plaque in his coronary arteries. This puts him at risk for heart attack and stroke but not a lot higher risk than most men his age.
Strictly speaking, since he hasn’t already had a heart attack or stroke, treating him with a statin is a form of primary prevention. However, we know that atherosclerotic plaque has already developed in his arteries and at some point, perhaps years from now it will have consequences.

What is the best approach to reduce Geo’s risk?

It’s essential  to look closely at lifestyle changes in everyone to reduce cardiac risk.
The lifestyle components that influence risk are

  1. Cigarette Smoking (by far the strongest)
  2. Diet
  3. Exercise
  4. Obesity (Obviously related to #1 and #2)
  5. Stress
  6. Sleep

Patients who try to change to what they perceive as a heart healthy diet by switching to non-fat dairy and eliminating all red meat will not substantially lower risk (see here.) Even if you are possess the rock-hard discipline to stay on a radically low fat diet like the Esselstyn diet or the Pritikin diet there are no good data supporting their  efficacy in preventing cardiac disease.
Geo was not far from theMediterranean diet I recommend but would probably benefit from increased veggie and nut consumption. He was not overweight and he doesn’t smoke. I encouraged him to engage in 150 minutes of moderate exercise weekly.

Low Dose, Intermittent Rosuvastatin

I engaged in shared decision-making with Geo.  Informing him, as best I could, of the potential side effects and benefits of statin therapy.

After a long discussion we decided to try a compromise between no therapy and the guideline recommended moderate intensive dose statin therapy.

This approach utilizes a low dose of rosuvastatin taken intermittently with the goal of minimizing any statin side effect but obtaining some of the benefits of statin drugs on  cardiovascular risk reduction.

I have many patients who have been unable to tolerate other statin drugs in any dosage due to statin related muscle aches but who tolerate this particular  treatment and I  see substantial reductions in the LDL (bad) cholesterol with this approach.
Studies have shown that rosuvastatin 5–10 mg or atorvastatin 10–20 mg given every other day produce LDL-C reduction of 20–40 %
Studies have also shown that In patients with previous statin intolerance, rosuvastatin administered once or twice weekly (at a mean dose of 10 mg per week) achieved an LDL-C reduction of 23–29% and was well tolerated by 74–80 % of patients.
In a recent report from a specialized lipid clinic, 90 % of patients referred for intolerance to multiple statins were actually able to tolerate statin therapy, although the majority was at a reduced dose and less-than-daily dosing.

Results in Geo

After several months of taking 5 mg rosuvastatin twice weekly Geo felt fine with no discernible side effects. He obtained repeat cholesterol  levels:

His LDL had dropped 52% from 140 to 92.
Hopefully, this LDL reduction plus the non-cholesterol lowering beneficial properties of statins (see here) will substantially lower Geo’s risk of heart attack and stroke.
We need randomized studies testing long-term outcomes using this approach to make it evidence-based. But in medicine we frequently don’t have studies that apply to  specific patient situations. In these cases shared decision-making in order to find solutions that fit the individual patient’s concerns and experience becomes paramount.
Faithfully Yours,


8 thoughts on “Unsure About Taking A Statin For High Cholesterol? Consider A Compromise Approach”

  1. Hello,
    Read your blog eagerly. Thank you for your thoughtful, reasoned postings. I’m a 52yo well controlled diabetic male (A1C 5.7) on a mediterranean diet, eating plenty of walnuts/hazelnuts/almonds (your post reinforced that!), on a healthy low carb diet for years now. I exercise regularly >150 mins/week. I also have stage 3 kidney dz. My Dr would like me to start a statin. My statin side effect concerns are rhabdomyolisis leading to kidney failure and worsening diabetes. Are my fears overblown?
    Also, playing with the ACC/AHA calculator, I noticed that diabetes is a yes/no question, with no accounting for well-controlled or not. It’s hard to believe that an out of control diabetic with an A1c of 12 would not have a higher risk.
    Appreciate your thoughts!

  2. What are your thoughts about this test
    SLCO1B1 Genotype Predicts Ability to Metabolize Statins
    Three SLCO1B1 genotypes have been identified and classified in terms of their effect on statin metabolism in the liver—normal (T/T), decreased (T/C), and markedly decreased (C/C):
    The T/T genotype (valine/valine) is classified as normal statin metabolizers. These patients have a normal ability to metabolize statins (about 75% of the population). Standard doses of statins, if indicated, are recommended for LDL-C lowering.
    The T/C genotype (valine/alanine) is classified as a decreased statin metabolizer. These patients have a decreased ability to metabolize statins (about 23% of the population). They have up to a 4.5-fold increased risk for developing statin induced myopathy.
    The C/C genotype (alanine/alanine) is classified as a markedly decreased statin metabolizer. These patients have a significantly decreased ability to metabolize statins (about 2% of the population). They have up to a 17-fold increased risk of developing myopathy on statin therapy.
    Additionally, individuals carrying the T/C or C/C genotype are less responsive to statins for LDL-C lowering than those carrying the T/T genotype.

    • I’ve been using the Boston Heart panel in select patients for the last year. I hope to put a post together on it soon.
      The ability to identify patients with potential higher risk of myopathy on statin therapy is intriguing but more work needs to be done before we know what to do with the information. In particular, I would not deny a patient statin therapy due to a high risk genotype.

  3. I am a 50 year old man with a calcium score of 240 in the last 10 months I lost over 60 lbs got my ldl down to 68 my triglycerides under 100 and total cholesterol under 150 I exercise at least 4 days a week doing cardio and weight training I eat a very low fat low carb diet and drink nothing but water except for a decaf coffee couple days a week I eat alot of vegetables and fruits oatmeal and plenty of chicken whole grain brown rice black beans. Also is there anyway to lower your calcium score

    • Well – Dr William (Wheat Belly) Davis published this in 2009
      Effect of a Combined Therapeutic Approach of Intensive Lipid Management, Omega-3 Fatty Acid Supplementation, and Increased Serum 25 (OH) Vitamin D on Coronary Calcium Scores in Asymptomatic Adults
      The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS).
      Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of ≥ 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides ≤60 mg/dL; high-density lipoprotein ≥60 mg/dL; and vitamin D3 supplementation to achieve serum levels of ≥50 ng/mL 25(OH) vitamin D, in addition to diet advice.
      Lipid profiles of subjects were significantly changed as follows: total cholesterol −24%, low-density lipoprotein −41%; triglycerides −42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%.
      After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of −14.5% (range 0% to −64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

      • The study by Dr. Wheat Belly is of poor quality in a low quality journal. There are way too many factors and there is no suitable control group. I would consider it hypothesis-generating only. I would not base my treatment on this kind of study. Neither Vitamin D or fish oil seems to be panning out as useful in the prevention of atherosclerosis.

    • It’s natural if you have been identified as having a higher than normal calcium score (and recognize that this is associated with more than typical for age/gender build up of atherosclerotic plaque in the coronary arteries and a higher risk of heart attack) to seek ways to lower that score.
      However, we haven’t clearly established that lowering the calcium score improves outcomes in any way.
      And treatment that clearly lowers risk (statin therapy) appears in some studies to accelerate deposition of calcium into plaque.
      A calcified plaque may be a healed plaque, less likely to rupture and cause sudden heart attack.


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