NQO1: why CoQ10 does very little for 9% of people

• GeneNQO1, NAD(P)H quinone oxidoreductase 1
• Variant testedrs1800566 (Pro187Ser)
• What it controlsReducing ubiquinone to ubiquinol, the usable form of CoQ10
• If reducedHomozygotes have close to no functional enzyme, about 9% of people
• What changesCoQ10 deprioritised, antioxidants routed around it

What the gene does

NQO1 catalyses a two-electron reduction that turns ubiquinone into ubiquinol. That's the step that makes CoQ10 an antioxidant rather than an inert molecule. The enzyme also recycles other antioxidants, so it sits at a junction rather than serving one pathway.

What the variant changes

Pro187Ser doesn't stop the enzyme being made. It makes the protein unstable, so the cell degrades it rapidly and very little functional enzyme accumulates. People carrying two copies have close to none.

In a study of 54 healthy men given ubiquinol at 150 mg a day for two weeks, genotype shaped the response. The variant has also been examined in larger case-control work on gastrointestinal cancer and in studies of skin ageing.

What it means for you

CoQ10 is one of the more expensive things in a supplement stack, and it's widely recommended from about age 40 onward as natural production declines. Output peaks around 23 and drops by roughly half by 80.

If you carry the reduced-function variant, standard ubiquinone CoQ10 is poor value, because the conversion step it depends on barely runs. The useful response is to work around it with antioxidants that don't need NQO1: vitamins C and E, selenium, and alpha-lipoic acid, which regenerates others in the chain.

What your formula does

Where the reduced-function genotype shows up, your formula deprioritises CoQ10 and raises the independent antioxidants instead. Where NQO1 is intact, CoQ10 earns its place, particularly from your forties on.

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