CoQ10 Stops Statin Damage, Helps Reclaim Heart Health
CoQ10 is found naturally in the body everywhere, making it ubiquitous. In fact, that’s why the names for the two types of CoQ10 are called ubiquinone and ubiquinol. The first is a stable supplemental form that has been in use for some time. The second is an active form that, while more expensive, seems to have wide approval.
Ultimately, after ubiquinone is ingested, it becomes ubiquinol in the body. And this nutrient helps power the body at a microscopic level. Since the heart is a muscle that always needs to keep moving, CoQ10 is essential for it to remain healthy.
But statin drugs, under the guise of being heart health, actually decrease our natural levels of CoQ10. This can lead to the heart muscles becoming weaker and less able to pump blood throughout the body, a condition known as statin cardiomyopathy. Fortunately, clinical studies have found that supplemental CoQ10 can restore heart health, especially when this supplementation is accompanied by discontinuing statin drugs.
In one clinical study, after stopping statins and supplementing with CoQ10, patients noticed a reduction in fatigue from 84 percent to 16 percent, muscle pain from 64 percent to 6 percent, peripheral neuropathy from 10 percent to 2 percent, and shortness of breath from 58 percent to 12 percent.
In another study, patients who would have been classified as heart healthy, with no physical limitations like fatigue or shortness of breath, increased from 8 percent to 79 percent. The benefits of stopping statins and supplementing with CoQ10 also included normalization or improvement of diastolic blood pressure numbers, reduced memory loss, and less muscle pain.
Abstracts:
Langsjoen PH, Langsjoen JO, Langsjoen AM, Lucas LA. Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation. Biofactors. 2005;25(1-4):147-52.
Fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ(10) at an average of 240 mg/day upon initial visit. Patients have been followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients. We conclude that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ(10). We saw no adverse consequences from statin discontinuation.
Langsjoen PH, Langsjoen JO, Langsjoen AM, Rosenfeldt F. Statin-associated cardiomyopathy responds to statin withdrawal and administration of coenzyme q10. Perm J. 2019;23:18.257.
Context: Heart failure (HF) is rapidly increasing in incidence and is often present in patients receiving long-term statin therapy.
Objective: To test whether or not patients with HF on long-term statin therapy respond to discontinuation of statin therapy and initiation of coenzyme Q10 (CoQ10) supplementation.
Design: We prospectively identified patients receiving long-term statin therapy in whom HF developed in the absence of any identifiable cause. Treatment consisted of simultaneous statin therapy discontinuation and CoQ10 supplementation (average dosage = 300 mg/d).
Main Outcome Measures: Baseline and follow-up physical examination findings, symptom scores, echocardiograms, and plasma CoQ10 and cholesterol levels.
Results: Of 142 identified patients with HF, 94% presented with preserved ejection fraction (EF) and 6% presented with reduced EF (< 50%). After a mean follow-up of 2.8 years, New York Heart Association class 1 increased from 8% to 79% (p < 0.0001). In patients with preserved EF, 34% had normalization of diastolic function and 25% showed improvement (p < 0.0001). In patients with reduced EF at baseline, the EF improved from a mean of 35% to 47% (p = 0.02). Statin-attributable symptoms including fatigue, muscle weakness, myalgias, memory loss, and peripheral neuropathy improved (p < 0.01). The 1-year mortality was 0%, and the 3-year mortality was 3%.
Conclusion: In patients receiving long-term statin therapy, statin-associated cardiomyopathy may develop that responds safely to statin treatment discontinuation and CoQ10 supplementation. Statin-associated cardiomyopathy may be a contributing factor to the current increasing prevalence of HF with preserved EF.
