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Effects of Coenzyme Q10 Supplementation on Biomarkers of Oxidative Stress in Adults: A GRADE-Assessed Systematic Review and Updated Meta-Analysis of Randomized Controlled Trials

Suming Dai, Zezhong Tian, Dan Zhao, Ying Liang, Meitong Liu, Zhihao Liu, Shanshan Hou, Yan Yang
Antioxidants (Basel) 2022 11(7):1360

Bibliography

PubMed
PMID 35883851
PubMed Central
PMC9311997
DOI
10.3390/antiox11071360
Funding
Key Program of the National Natural Science Foundation of China (82030098); National Natural Science Foundation of China (81872617); Shenzhen Science, Technology and Innovation Commission (JCYJ20180307153228190); Chinese Nutrition Society Research Fund for Dietary Reference Intakes.
Competing interests
The authors declared no conflict of interest.

Study snapshot

DesignSystematic review and updated meta-analysis of randomized controlled trials
ModelGRADE-assessed systematic review and updated meta-analysis of randomized controlled trials evaluating CoQ10 supplementation and circulating oxidative-stress biomarkers in adults.
Sample34 randomized controlled trial comparisons; 2,012 participants.
InterventionCoQ10 supplementation versus placebo/control across adult randomized trials; dose, formulation, population and treatment duration varied. Prespecified subgroup analyses explored dose and disease status.
Duration
EndpointsTotal antioxidant capacity (TAC); Malondialdehyde (MDA); Superoxide dismutase (SOD); GRADE certainty; Dose subgroup; Disease subgroup; Risk of bias; Sensitivity/publication-bias analyses

What the study showed, in plain terms

This 2022 GRADE-assessed meta-analysis pooled 34 randomized trials involving 2,012 adults to evaluate whether CoQ10 alters commonly used blood markers of oxidative stress.

CoQ10 significantly increased total antioxidant capacity (SMD 1.83, 95% CI 1.07–2.59; p<0.001) and reduced malondialdehyde, a lipid-peroxidation marker (SMD -0.77, 95% CI -1.06 to -0.47; p<0.001). Superoxide dismutase showed only borderline statistical significance (SMD 0.47, 95% CI 0.00–0.94; p=0.05).

Subgroup analyses suggested larger antioxidant-marker changes in coronary artery disease or type 2 diabetes and around 100–150 mg/day. Those subgroup findings are useful for hypothesis generation but should not be treated as proof of an optimal dose, because they compare different trials and populations rather than randomized doses head-to-head.

Key findings

Total antioxidant capacity (TAC): SMD +1.83, 95% CI 1.07–2.59, p<0.001.

Malondialdehyde (MDA): SMD -0.77, 95% CI -1.06 to -0.47, p<0.001.

Superoxide dismutase (SOD): SMD +0.47, 95% CI 0.00–0.94, p=0.05; the authors considered this borderline rather than secure evidence of increase.

Disease subgroups: signals appeared stronger in participants with coronary artery disease or type 2 diabetes than in some other populations.

Dose subgroup: 100–150 mg/day showed favorable subgroup effects for TAC, MDA and SOD (all subgroup p<0.01), but this is between-trial evidence and not definitive randomized dose optimization.

Search date: PubMed, Embase and Cochrane Library through 30 March 2022. Certainty was formally assessed using GRADE.

What this study can and cannot tell us

The pooled trials varied widely in disease state, age, dose, formulation, duration and baseline oxidative stress, limiting the interpretation of a single average effect.

TAC, MDA and SOD are biochemical surrogate markers. Changes do not automatically demonstrate improved symptoms, organ function or reduced clinical events.

The apparent 100–150 mg/day ‘optimal’ subgroup is not a direct randomized comparison of doses and can be confounded by trial characteristics.

SOD reached only the conventional p=0.05 threshold with a confidence interval touching the null, so that endpoint is substantially less secure than the TAC and MDA results.

The authors called for larger studies, broader elderly populations and longer supplementation periods to clarify dose and clinical relevance.

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology