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Owen Linder, MD, FACP

Internal Medicine

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May 2025

This introduces a compilation of de-identified patient information from which I have correlated the effects of treatment of hyperlipidemia with statin drugs, coenzyme Q ten and a genome CYP450 2D6.

My interest began  in 2009. At that time I cared for a hyperlipidemic patient who developed rhabdomyolysis. This is the most severe of adverse effects of statin drugs

The illness began after prescribing a statin drug for her hyperlipidemia. I observed her muscle fasciculations and elevated CPK  after that  prescription. The treatment was given per textbook. It was oral coenzyme Q ten, as well as cessation of the statin drug. See citationxx

In treating hundreds of patients with statins, patterns of adverse effects came to my attention. I began making assays of the coenzyme Q ten blood levels to correlate with the adverse effects and to alleviate the adverse effects in the individual patients. The first compilation was titled Cramps in Seniors, written in 2011(*1).

In 2023 I became aware that other professionals had been correlating statin adverse effects to certain genomes.  After looking at those findings involving genomes, which were unavailable to Labcorp patients in 2024-2025, I found the genomes which were readily available to patients in their health maintenance organization’s laboratory contractual services. The commercially available genomes are CYP450 2D6, CYP450 2C9 and CYP450 2C19.

Other  writers have published compilations of other genomes, those genomes available in research settings, SLCO1B1, ABCG2, and CYP 450 2C9. ( *2) No one has made public a longitudinal compilation of the coenzyme Q ten blood assays correlated with any group of genomes. Nor also adding in adverse effects of statins. In the spread sheet available upon request one can see  the lower; and the later (highest) Coenzyme Q ten assays. of each patient. Lower assays found before prescribing Coenzyme Q ten are generally indigenous levels. In general prescribed doses of Coenzyme Q ten result in higher assays . The spread sheet shows the change in Coenzyme Q ten assay levels.

 I term this replenishment. This is based on the sustained increase in blood assay level while the person is under statin influences and Coenzyme Q ten prescription. Of course genomes are set at the inception of  life. In this compilation the genomes of greatest correlation to coenzyme Q ten replenishment: is the genome among the three genomes available under the Labcorp contract This is  to say the difference between earliest and later, the highest coenzyme Q ten assays.  The genome appears to be CYP 450 2D6; not CYP4502C9 nor CYP450 2C19.

In one column I have calculated the difference between earliest (lowest) and highest Coenzyme Q ten assays. In the 41 patients for whom I have two or more assays the average increase is three fold (x2.8). This three fold increase was also found in the prior series of 44 patients in 2011(*1).

The genomes affect the processing of a statin in the hepatic enzyme systems. Many medicines are processed in the hepatic enzymes' systems. {*3}

 Some genomes of some persons have variant alleles. The variant alleles of interest have either slow or no processing capacity for statin drugs.{*3). One may observe in the column of genomes a predominance of variant alleles of genome CYP450 2D6. 

The reasoning for displaying rosuvastatin doses in a separate column is because only this statin is among the statins in use in this practice not processed in hepatic enzyme systems. Citation ?

Rosuvastatin works in the liver without going through a  hepatic transformation. So I have followed the implication of variant alleles in CYP450 2D6. The variant alleles may not affect the effect of rosuvastatin perhaps relatively or perhaps absolutely. Nor, I infer, as greatly  affect the onset of depletion of Coenzyme Q ten. Thus there is less need for Coenzyme Q ten supplementation. This is a hypothesis. 

For illustration in the spread sheet of clinical findings available on request line 49 is for person “SM”. She had post exertional leg cramps as a child. She had been on simvastatin 20 mg many years as an adult before her entry to this practice in 2017. Her cramps upon exertion were worse with simvastatin. She experienced progressively less frequent and less intense leg cramps as her dose of coenzyme Q ten was increased up to 800 mg a day by 2023.

Her genomic analysis of CYP450 2D6 revealed alleles *1  and *4. *1 has normal processing of medications. *4 allele function is characterized by slow processing  of medications in the liver. (*3) This includes statin drugs. The statin mechanism of action  is inhibition of hepatic hydroxymethylglutaryl Coenzyme A  (HMG CoA reductase.) This inhibition diminishes production of cholesterol. Most statins are metabolized in the liver  into a follow on biochemical form of the statin before inhibiting HMGCo A reductase. Cite? .

Coenzyme Q ten is synthesized in the same biochemical pathway as cholesterol in the liver.

Despite patient “SM” having a very useful replenishment dose of coenzyme Q ten, 800mg, reflected by a high assay of serum Coenzyme Q ten :3.4 she still had some exertional and post exertional cramps in her calves.

The inferred diagnosis was a relative deficiency in coenzyme Q ten due to the potency of simvastatin 20mg  three nights a week. Evidence of this potency lie in the complete remission of cramps when  simvastatin was replaced with rosuvastatin 5mg nightly. Her LDL remained the same. On simvastatin 20 mg 3 evenings a week in 2024 LDL was 85; on rosuvastatin 5mg nightly  in 2025 LDL was 81.

 The percentage of persons in the cohort collected in my practice with slow processing alleles of genome CYP2D6 is 80%.  I will statistically correlate the persons with alleles of

subnormal processing with the group of the largest rise in the blood level of coenzyme Q ten after supplementation.   Owen Linder, MD, FACP

1.      Cramps in Seniors, Pinellas County Medical Journal 2011

2.The Clinical Pharmacogenetics Implementation Consortium Guideline for SLCO1B1, ABCG2, and CYP2C9 genotypes and Statin -Associated Musculoskeletal Symptoms in Clin Pharmacol Ther, 2022 May , 111(5): 1007-1021 doi; 10.1002/cpt.2557 Epub2022 Mar 11 by Rhonda M. Cooper-DeHoff and twenty other coauthors PMID 35152405

3, “ Cytochrome P 450 2D6 is a drug metabolizing enzyme involved in the metabolism of more than 65 clinically important drugs including some….”  Laboratory Corporation of America Holdings, Weidong Huang, MD PhD Director Monogram Biosciences

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