How Genetics Can Affect the Body's Use of CoenzymeQ10 and Ubiquinol sponsored by Kaneka

By Risa Schulman, PhD

November 18, 2019

A holistic read of an individual’s health provides us with the clues needed to tailor treatment recommendations. But one of the less accessible parts of the total picture is the role of genetics. We know that SNPs (single nucleotide polymorphisms) can affect an individual’s ability to utilize dietary supplements. Could this factor be at work when taking coenzyme Q10?

It turns out the answer is yes. There is a SNP called NQ01 that affects the body’s ability to convert coenzyme Q10 to Ubiquinol. Let's take a closer look at what happens there.

If you saw our last post “Ubiquinol and Bioavailability: A 70% Better Solution,” we noted that Ubiquinol is the preferred form of coenzyme Q10 in the blood, and the form in which it is best transported to the cell, where it plays out its crucial role in the generation of energy from food. When coenzyme Q10 is ingested, the body quickly transforms it into Ubiquinol.1

Coenzyme Q10 becomes Ubiquinol by the addition of two electrons and two hydrogens. This transformation cannot happen without the help of a specific enzyme called coenzyme Q10 reductase, which facilitates the two-electron reduction (both for coenzyme Q10 and other substrates). About 95% of the coenzyme Q10 in circulation exists in its reduced form (Ubiquinol) in young, healthy indiviuals.2,3 If coenzyme Q10 reductase is manufactured incorrectly, it can cause that transformation to occur less efficiently. Not surprisingly, people with the NQO1 SNP are more susceptible to oxidative stress as a result of the decreased antioxidant activity and have increased predisposition to disease.

With the advent of the sequenced human genome, we can now examine the blueprints for many genes. We can see the different, normal variations between people in given genes. There can be SNPs in genes that code for enzymes as well, such as our enzyme of interest, coenzyme Q10 reductase. These SNPs can make small, or sometimes not so small, changes in the function of the enzyme. The gene that codes for coenzyme Q10 reductase is called NQ01. There is a SNP for the NQ01 gene that makes a version of coenzyme Q10 reductase that is less efficient than other versions, because the SNP causes this version to be broken down in the body much faster than usual.4

People who have this SNP therefore have less coenzyme Q10 reductase around, and as a result, the conversion of coenzyme Q10 to Ubiquinol is greatly compromised. Therefore, these people's bodies will have a hard time transporting the coenzyme Q10 to the cells that need it and will get little benefit from taking coenzyme Q10 as a supplement.

The frequency of the NQ01 polymorphism in the population varies with ethnicity: it is found in the homozygous state (both the genes) at a frequency of 4% in Caucasians, 5% in African–Americans, 16% in Mexican Hispanics, and 22% in Chinese populations.5

Taking Ubiquinol gives the body the preferred and active form from the get-go, circumventing the whole SNP problem by bypassing the need for the coenzyme Q10 reductase enzyme altogether. This allows not only for improved efficacy in the mitochondria, but increases oxidative potential, since Ubiquinol is an important lipid-soluble antioxidant.

Testing for a SNP in the NQ01 gene is not yet routine, but hopefully will be in the future. A prudent course of action is to prescribe Ubiquinol from the start, particularly if coenzyme Q10 has been ineffective in the past.

About the Author

Risa Schulman, PhD, is founder and president of Tap~Root (Tap-Root.biz), a functional food and dietary supplement expert, professional speaker and writer, and an industry leader with over 20 years of experience. Her particular expertise is in straddling the science-regulatory-marketing axis and bridging these areas for successful product development and launch. Schulman also serves as an advisor to investment bankers and sits on science advisory boards. She holds a PhD in Plant Biology from Rutgers University, an MES in Environmental Science from Yale University, and a BS in Biology and Environmental Science from Tufts University. Schulman serves as a scientific consultant for Kanika UbiquinolTM.

References

  1. Mohr D, Bowry VW, Stocker R. Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. Biochim Biophys Acta. 1992 Jun 26;1126(3):247-54.
  2. Yamashita S, Yamamoto Y. Simultaneous detection of ubiquinol and ubiquinone in human plasma as a marker of oxidative stress. Anal Biochem. 1997 Jul 15;250(1):66-73.
  3. Tang PH, Miles MV, DeGrauw A, Hershey A, Pesce A. HPLC analysis of reduced and oxidized coenzyme Q(10) in human plasma. Clin Chem. 2001 Feb;47(2):256-65.
  4. Ross D, Kepa JK, Winski SL, Beall HD, Anwar A, Siegel D. NAD(P)H:quinone oxidoreductase 1 (NQO1): chemoprotection, bioactivation, gene regulation and genetic polymorphisms. Chem Biol Interact. 2000 Dec 1;129(1-2):77-97.
  5. Kelsey KT, Ross D, Traver RD et al. Ethnic variation in the prevalence of a common NAD(P)H:quinone oxidoreductase polymorphism and its implications for anticancer chemotherapy. Br J Cancer 1997;76:852–854.