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Effects of CoQ10 Supplementation on Lipid Profiles and Glycemic Control in Patients with Type 2 Diabetes: a randomized, double blind, placebo-controlled trial

Hoda Zahedi, Shahryar Eghtesadi, Soroush Seifirad, Neshat Rezaee, Farzad Shidfar, Iraj Heydari, Banafsheh Golestan, Shima Jazayeri
Journal of Diabetes & Metabolic Disorders 2014 13:81

Bibliography

PubMed
PMID 26413493
PubMed Central
PMC4583053
Funding
Supported by the Vice-Chancellor for Research, Iran University of Medical Sciences, Tehran, Iran.
Competing interests
The authors declared no conflict of interests.

Study snapshot

DesignRandomized, double-blind, placebo-controlled trial
ModelRandomized, double-blind, placebo-controlled parallel trial in adults with type 2 diabetes.
Sample50 randomized; 40 completed the 12-week protocol (20 CoQ10, 20 placebo). Ten were excluded: four lost to follow-up and six consumed less than 70% of assigned supplements.
InterventionCoQ10 150 mg/day versus placebo for 12 weeks.
Duration12 weeks
EndpointsSerum CoQ10; Fasting plasma glucose; Insulin; HOMA-IR; HbA1c; Triglycerides; Total cholesterol; LDL-C; HDL-C; Adherence/attrition

What the study showed, in plain terms

This randomized double-blind trial assigned 50 adults with type 2 diabetes to CoQ10 150 mg/day or placebo for 12 weeks; 40 participants completed the protocol. Serum CoQ10 rose significantly in the active group, confirming biological exposure.

At 12 weeks, fasting plasma glucose and HbA1c were lower in the CoQ10 group than placebo after baseline adjustment (FPG p=0.02; HbA1c p=0.01). Insulin and HOMA-IR did not differ significantly between groups.

The lipid results were not favorable overall. LDL-C rose from 74.55 ± 15.3 to 90.65 ± 18.7 mg/dL in the CoQ10 group (within-group p=0.001) and was higher than placebo at follow-up (p<0.001). HDL-C also fell within the CoQ10 group. The authors therefore concluded that glycemic control may improve, but the lipid profile did not.

Key findings

Attrition/adherence: 10/50 randomized participants did not complete—4 lost to follow-up and 6 with <70% supplement consumption—leaving 20 per arm.

FPG: CoQ10 131.45 ± 36.3 to 115.95 ± 20.7 mg/dL; placebo 132.75 ± 38.2 to 152.55 ± 65.2; adjusted between-group p=0.02 at follow-up. The within-CoQ10 change was not significant.

HbA1c: CoQ10 6.83 ± 0.8% to 6.44 ± 0.9%; placebo 6.95 ± 1.1% to 7.18 ± 1.1%; between-group p=0.01 at follow-up, while within-group changes were not significant.

Insulin and HOMA-IR: no significant between-group differences.

LDL-C: CoQ10 74.55 ± 15.3 to 90.65 ± 18.7 mg/dL (p=0.001 within group); placebo 76.40 ± 21.6 to 71.15 ± 20.3; between-group p<0.001 at follow-up.

HDL-C: CoQ10 42.40 ± 8.7 to 37.15 ± 10.7 mg/dL (p=0.002 within group); no significant between-group difference at follow-up. Triglycerides fell within CoQ10 (136.90 ± 53.1 to 113.10 ± 50.3; p=0.004) but not significantly versus placebo. Total cholesterol was higher than placebo at follow-up (p=0.02).

Trial registration: IRCT138806102394N1.

What this study can and cannot tell us

Only 40/50 randomized participants completed the study; excluding low-adherence participants and losses rather than relying solely on a modern intention-to-treat analysis can introduce attrition bias.

Wide inclusion criteria were identified by the authors as a major limitation.

Diet was assessed using a one-day 24-hour recall; the authors noted that a three-day recall would have been preferable.

C-peptide and proinsulin—potentially more informative measures of beta-cell function—were not measured.

The unfavorable LDL-C/HDL-C pattern and small sample mean the study should not be represented simply as a positive diabetes trial.

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