Owen Linder, MD, FACP

Internal Medicine

960 Main St # 1, Safety Harbor, FL 34695 (map)

(727) 726-4721

(727) 797-6316 FAX

Owen Linder, MD FACP
September 2024

This introduces a compilation of patient information.

The information is not identified by name.

My interest began  in 2009. I came to treat a person with rhabdomyolysis. This is the most severe manifestation of adverse effects of statin drugs

The treatment had been a statin drug for hyperlipidemia. I observed the connection  at that time. The treatment was given per textbook. The treatment was oral coenzyme Q ten, as well as cessation of the statin drug.

In treating hundreds of patients with statins, patterns of ill effects were observed. I began making assays of the coenzyme Q ten blood levels to correlate with the adverse effects and alleviation of the adverse effects in the individual patients.

In 2023 I became aware that other medical persons had been correlating statin side effects to certain genomes. 1. After looking at this finding I was informed of the genomes commercially available to patients in a health maintenance organization contracted with Labcorp. The commercially available genomes are CYP450 2D6, CYP450 2C9 and CYP 2C19.

The academic researchers had the option of taking assays of other genomes.  Their inferences have been published. They have not published a longitudinal compilation of the coenzyme Q ten blood assays. In the spread sheet below one can look at the early and most recent Coenzyme Q ten assays. In this compilation you can see the genomes of greatest connection to the difference in earliest and most recent coenzyme Q ten assays. It appears to be CYP2D6.

In one column I have calculated the difference in earliest and last Coenzyme Qten assays. In the 35 patients for whom I have two assays the average increase is three fold.

The genomes affect the processing of statin in the hepatic enzyme systems. Many medicines are processed in the hepatic enzymes' systems.

Some genomes of some persons have variant alleles. The variant alleles of interest have either slow or no processing capacity for statin drugs.

One may observe in the column of genomes a predominance of variant alleles of genome CYP2D6. 

As part of the consideration of adverse effects of statins there is a list of the statin(s) used for patients in this practice.

The reasoning for displaying rosuvastatin doses separately is because only this statin is one among the statins in use in this practice which are not processed in hepatic enzyme systems. Rosuvastatin works in the liver without going through a  hepatic transformation. So variant alleles in CYP450 2D6 may not affect the effect of rosuvastatin. Nor, I infer, as greatly  affect the onset of depletion of Coenzyme Q ten and the need for Coenzyme Q ten supplementation. This is a hypothesis worth testing.

In the future I should calculate the percentage of persons in the cohort collected in my practice with slow processing alleles of genome CYP2D6. Then I should get a statistician’s guidance on  the correlation of persons with subnormal processing with the group of the largest rise in the blood level of coenzyme Q ten after supplementation.  

Owen Linder MD FACP

1.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

Linder, Owen M.D. FACP (2024). The Importance Of Coenzyme Q Ten In Adverse Effects Of Statin Drugs. Unpublished manuscript.

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