Tier 3 — preclinical

Selenium and coenzyme Q10 improve the systemic redox status while reducing cardiovascular mortality in elderly population-based individuals

Belinda J Dunning, Arno R Bourgonje, Marian L C Bulthuis, Jan Alexander, Jan O Aaseth, Anders Larsson, Harry van Goor, Urban Alehagen
Free Radical Biology and Medicine 2023 204:207-214

Bibliography

PubMed
PMID 37179031
DOI
10.1016/j.freeradbiomed.2023.04.024
Trial registry
View on ClinicalTrials.gov Registered trial — results not yet published in a peer-reviewed journal.
Funding
Part of the analysis costs was supported by grants from Pharma Nord A/S, the County Council of Östergötland and Linköping University. The funding organizations were reported to have no role in study management, analysis, interpretation or manuscript preparation.
Competing interests
No author conflict statement indicating a personal financial conflict was identified in the accessible publication record used for this audit; Pharma Nord's support of the KiSel-10 program and supply of intervention products remains relevant context.

Study snapshot

DesignSecondary redox-biomarker analysis of the randomized double-blind placebo-controlled KiSel-10 combination trial, plus prospective association of free-thiol status with cardiovascular mortality.
ModelOlder community-dwelling Swedish adults from KiSel-10, characterized by low selenium status.
Sample434 participants with serum free-thiol measurements at baseline and after 48 months.
InterventionSelenoPrecise selenium yeast 200 µg/day + Bio-Quinon CoQ10 200 mg/day versus placebo for 48 months.
Duration48-month intervention; cardiovascular mortality association evaluated over median 10 years (IQR 6.8–10.5).
EndpointsAlbumin-adjusted serum free thiols (R-SH); Change in systemic redox status at 48 months; Cardiovascular mortality by baseline R-SH quartile; Adjusted mortality association

What the study showed, in plain terms

This 2023 analysis asked whether the KiSel-10 selenium+CoQ10 combination changed serum free thiols (R-SH), a marker of systemic redox status, and whether thiol status predicted later cardiovascular mortality.

Among 434 participants with measurements, albumin-adjusted serum free thiols increased after 48 months with the active combination versus placebo (p=0.002), consistent with a shift toward a less oxidized systemic redox state.

Lower baseline free-thiol status was associated with higher cardiovascular mortality during a median 10-year follow-up. The paper reports an adjusted HR of 1.98 per SD (95% CI 1.34–2.91; p<0.001) for the modeled baseline free-thiol/mortality relationship and the highest mortality in the lowest R-SH quartile.

This supports a plausible redox pathway for the selenium+CoQ10 combination, but it is not proof that CoQ10 alone improves redox status or that changing this biomarker causes the mortality difference.

Key findings

  • Serum free thiols increased with selenium+CoQ10 compared with placebo after 48 months; p=0.002.
  • The highest cardiovascular mortality rate occurred in the lowest baseline free-thiol quartile.
  • The adjusted baseline R-SH/mortality model reported HR 1.98 per SD (95% CI 1.34–2.91; p<0.001), consistent with materially higher risk at poorer redox status.
  • The intervention result is randomized for the combined treatment, while the relationship between biomarker level and mortality is a prospective association and should not be interpreted as proof of mediation.

What this study can and cannot tell us

  • Secondary analysis of the same KiSel-10 cohort rather than an independent trial.
  • Selenium and CoQ10 were co-administered; the redox effect cannot be assigned to CoQ10 alone.
  • Free thiols are a biomarker, not a direct clinical endpoint.
  • The prospective association between baseline R-SH and mortality can be confounded and does not prove that R-SH mediates treatment benefit.
  • Older low-selenium Swedish population limits generalizability.

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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