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Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes

J M Hodgson, G F Watts, D A Playford, V Burke, K D Croft
European Journal of Clinical Nutrition 2002 56(11):1137-1142

Bibliography

PubMed
PMID 12428181
DOI
10.1038/sj.ejcn.1601464
Funding
Supported by a grant from the National Health and Medical Research Council (NH&MRC), Australia.
Competing interests
A specific author conflict-of-interest statement was not identified in the accessible publication record checked during this audit.

Study snapshot

DesignRandomized, double-blind, placebo-controlled 2x2 factorial trial
ModelRandomized, double-blind, placebo-controlled 2×2 factorial trial in 74 adults with uncomplicated type 2 diabetes and dyslipidaemia at Royal Perth Hospital/University of Western Australia.
Sample74 randomized participants. The CoQ10 factor compared participants assigned to CoQ10 with those assigned to no CoQ10 within a 2×2 factorial design that also independently tested fenofibrate.
InterventionCoQ10 100 mg twice daily (200 mg/day) versus matching placebo/no CoQ10 factor for 12 weeks; the factorial trial simultaneously randomized fenofibrate 200 mg each morning versus its control.
Duration12 weeks
EndpointsSystolic blood pressure; Diastolic blood pressure; HbA1c; Plasma CoQ10 concentration; Plasma F2-isoprostanes; Factorial interaction with fenofibrate

What the study showed, in plain terms

This randomized double-blind 2×2 factorial trial enrolled 74 adults with type 2 diabetes and dyslipidaemia. The CoQ10 comparison tested 100 mg twice daily (200 mg/day) for 12 weeks while a separate factorial assignment tested fenofibrate.

CoQ10 increased plasma CoQ10 about threefold and produced modest but statistically significant reductions in systolic blood pressure, diastolic blood pressure and HbA1c. The reported CoQ10 main effects were -6.1 ± 2.6 mmHg for systolic BP (p=0.021), -2.9 ± 1.4 mmHg for diastolic BP (p=0.048), and -0.37 ± 0.17 percentage points for HbA1c (p=0.032).

Plasma F2-isoprostanes did not significantly change, so the observed blood-pressure and glycemic signals were not accompanied by improvement in this measured oxidative-stress marker. The study is best interpreted as a small, short-duration metabolic RCT rather than evidence for long-term diabetes or cardiovascular outcomes.

Key findings

Plasma CoQ10: approximately threefold increase to 3.4 ± 0.3 µmol/L with supplementation (p<0.001).

Systolic BP: CoQ10 main effect -6.1 ± 2.6 mmHg (p=0.021).

Diastolic BP: CoQ10 main effect -2.9 ± 1.4 mmHg (p=0.048).

HbA1c: CoQ10 main effect -0.37 ± 0.17 percentage points (p=0.032).

Oxidative stress: plasma F2-isoprostanes changed by 0.14 ± 0.15 nmol/L (p=0.345), not statistically significant.

Fenofibrate did not significantly alter BP, HbA1c or F2-isoprostanes in the reported factorial analysis.

What this study can and cannot tell us

Only 74 participants and 12 weeks of treatment, limiting statistical power and preventing assessment of durable clinical outcomes.

Participants had uncomplicated type 2 diabetes plus dyslipidaemia, so generalizability to other diabetes populations is uncertain.

The study used a 2×2 factorial design with concomitant fenofibrate randomization. Although factorial designs efficiently estimate main effects, interpretation requires attention to the second intervention and any interactions.

Outcomes were intermediate risk factors and biomarkers rather than microvascular events, cardiovascular events, hospitalization or mortality.

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