Coenzyme Q10

Abnormally high levels of coenzyme Q10 are only practically possible through the use of supplements. It is unclear whether moderately excessive amounts of coenzyme Q10 are harmful to humans. While it is fat soluble, CoQ10 does not accumulate after supplementation has stopped.

Coenzyme Q 10 deficiency may occur in three ways: primary coenzyme Q10 deficiency, secondary coenzyme Q10 deficiency, or related to another drug or disease. Primary coenzyme Q10 deficiency is rare and caused by genetic disorder that affects the CoQ10 molecule. Secondary coenzyme Q 10 deficiency, on the other hand, is caused by a problem in the mitochondria. Mitochondrial diseases cause a variety of symptoms but most are related to muscle weakness and neurological symptoms. This can lead to breathing problems, heart muscle problems, seizures, and cognitive problems.

Some specific causes of low coenzyme Q10 levels are:

- Mitochondrial diseases

- Primary CoQ10 deficiency (rare)

- Secondary CoQ10 deficiency

- Cerebellar ataxia

- Severe infantile multisystem disease

- Nephropathy

- Isolated myopathy

- Encephalomyopathy

- Statin use

Treatment considerations:

These treatment considerations are for educational purposes only. Specific treatment plans should be provided and reviewed by the treating practitioner.

→ Assess dietary intake of CoQ10. Dietary sources of CoQ10 include animal products such as beef, pork or chicken, and vegetables such as spinach, cauliflower and broccoli.

→ Consider CoQ10 supplementation. If currently taking, consider adjusting dosage and retest in 1-2 months.

→ Assess ApoA1 and/or HDL levels. If low, consider treatment with niacin or fenofibrate therapy.

CoQ10 is a fat-soluble, vitamin-like substance present in most cells, primarily in the mitochondria. CoQ10 plays an integral role in the generation of cellular energy through aerobic cellular respiration. In addition, CoQ10 is a powerful antioxidant at physiologic concentrations.