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Coenzyme Q10 for heart failure.
Al Saadi, T, Assaf, Y, Farwati, M, Turkmani, K, Al-Mouakeh, A, Shebli, B, Khoja, M, Essali, A, Madmani, ME
The Cochrane database of systematic reviews. 2021;(2):CD008684
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As per the definition given by the NHS, heart failure happens when the heart fails to pump blood around the body due to stiffness or weakness of the heart muscle. Coenzyme Q10 reduces oxidative stress and toxic effects in the body by acting as a fat-soluble antioxidant nutrient. Due to these beneficial effects, CoQ10 may effectively reduce damage to cardiac cells and disruption to cellular signalling. CoQ10 is also a cell membrane stabiliser, and previous studies have shown a correlation between the severity of heart failure and CoQ10 deficiency. In addition, dietary absorption of CoQ10 is relatively slow and ineffective; therefore, supplementation is effective and safe with no side effects. This review included eleven randomised controlled studies to compare the beneficial effects of Coenzyme Q10 for the treatment of people with heart disease. This review showed that Coenzyme Q10 might reduce all-cause mortality and hospitalisation due to heart failure. In addition, CoQ10 may stabilise myocardial calcium‐dependent ion channels and encourage adenosine‐5'‐triphosphate (ATP) synthesis. However, the effectiveness of CoQ10 in lowering the risk of myocardial infarction or stroke, left ventricular ejection fraction and exercise capacity is inconclusive. Healthcare professionals can use this study's results to understand the potential beneficial effects of CoQ10 supplementation on maintaining heart health. However, due to the high heterogeneity in the current research, further robust long-term studies are required to evaluate the therapeutic value of Coenzyme Q10 in managing heart disease.
Abstract
BACKGROUND Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria, and as a coenzyme for mitochondrial enzymes. Coenzyme Q10 deficiency may be associated with a multitude of diseases, including heart failure. The severity of heart failure correlates with the severity of coenzyme Q10 deficiency. Emerging data suggest that the harmful effects of reactive oxygen species are increased in people with heart failure, and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity. Coenzyme Q10 may also have a role in stabilising myocardial calcium-dependent ion channels, and in preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. Coenzyme Q10, although not a primary recommended treatment, could be beneficial to people with heart failure. Several randomised controlled trials have compared coenzyme Q10 to other therapeutic modalities, but no systematic review of existing randomised trials was conducted prior to the original version of this Cochrane Review, in 2014. OBJECTIVES To review the safety and efficacy of coenzyme Q10 in heart failure. SEARCH METHODS We searched CENTRAL, MEDLINE, Embase, Web of Science, CINAHL Plus, and AMED on 16 October 2020; ClinicalTrials.gov on 16 July 2020, and the ISRCTN Registry on 11 November 2019. We applied no language restrictions. SELECTION CRITERIA We included randomised controlled trials of either parallel or cross-over design that assessed the beneficial and harmful effects of coenzyme Q10 in people with heart failure. When we identified cross-over studies, we considered data only from the first phase. DATA COLLECTION AND ANALYSIS We used standard Cochrane methods, assessed study risk of bias using the Cochrane 'Risk of bias' tool, and GRADE methods to assess the quality of the evidence. For dichotomous data, we calculated the risk ratio (RR); for continuous data, the mean difference (MD), both with 95% confidence intervals (CI). Where appropriate data were available, we conducted meta-analysis. When meta-analysis was not possible, we wrote a narrative synthesis. We provided a PRISMA flow chart to show the flow of study selection. MAIN RESULTS We included eleven studies, with 1573 participants, comparing coenzyme Q10 to placebo or conventional therapy (control). In the majority of the studies, sample size was relatively small. There were important differences among studies in daily coenzyme Q10 dose, follow-up period, and the measures of treatment effect. All studies had unclear, or high risk of bias, or both, in one or more bias domains. We were only able to conduct meta-analysis for some of the outcomes. None of the included trials considered quality of life, measured on a validated scale, exercise variables (exercise haemodynamics), or cost-effectiveness. Coenzyme Q10 probably reduces the risk of all-cause mortality more than control (RR 0.58, 95% CI 0.35 to 0.95; 1 study, 420 participants; number needed to treat for an additional beneficial outcome (NNTB) 13.3; moderate-quality evidence). There was low-quality evidence of inconclusive results between the coenzyme Q10 and control groups for the risk of myocardial infarction (RR 1.62, 95% CI 0.27 to 9.59; 1 study, 420 participants), and stroke (RR 0.18, 95% CI 0.02 to 1.48; 1 study, 420 participants). Coenzyme Q10 probably reduces hospitalisation related to heart failure (RR 0.62, 95% CI 0.49 to 0.78; 2 studies, 1061 participants; NNTB 9.7; moderate-quality evidence). Very low-quality evidence suggests that coenzyme Q10 may improve the left ventricular ejection fraction (MD 1.77, 95% CI 0.09 to 3.44; 7 studies, 650 participants), but the results are inconclusive for exercise capacity (MD 48.23, 95% CI -24.75 to 121.20; 3 studies, 91 participants); and the risk of developing adverse events (RR 0.70, 95% CI 0.45 to 1.10; 2 studies, 568 participants). We downgraded the quality of the evidence mainly due to high risk of bias and imprecision. AUTHORS' CONCLUSIONS The included studies provide moderate-quality evidence that coenzyme Q10 probably reduces all-cause mortality and hospitalisation for heart failure. There is low-quality evidence of inconclusive results as to whether coenzyme Q10 has an effect on the risk of myocardial infarction, or stroke. Because of very low-quality evidence, it is very uncertain whether coenzyme Q10 has an effect on either left ventricular ejection fraction or exercise capacity. There is low-quality evidence that coenzyme Q10 may increase the risk of adverse effects, or have little to no difference. There is currently no convincing evidence to support or refute the use of coenzyme Q10 for heart failure. Future trials are needed to confirm our findings.
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Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes.
Orlando, P, Silvestri, S, Galeazzi, R, Antonicelli, R, Marcheggiani, F, Cirilli, I, Bacchetti, T, Tiano, L
Redox report : communications in free radical research. 2018;23(1):136-145
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Strenuous exercise or overtraining increases the production of reactive oxygen species (ROS), especially in mitochondria. ROS production in excess leads to oxidative stress, cellular dysfunction, and oxidation of molecules such as DNA, polyunsaturated fatty acids, amino acids, and proteins. Previous research has shown that antioxidant supplementation might lead to the downregulation of ROS production. Coenzyme Q10 is an antioxidant believed to be effective in downregulating the effects of oxidative stress and preventing cellular damage. However, most previous studies have used ubiquinone, an oxidised form of Coenzyme Q10. Ubiquinol, a reduced form of Coenzyme Q10, is highly bioavailable, stable and in a form that the body can readily use. This randomised, double-blinded, crossover-controlled trial investigated ubiquinol's antioxidant and anti-inflammatory effects on biochemical and oxidative stress indexes after an intense bout of exercise in trained athletes. Twenty-one male athletes in constant training were randomly taking 200 mg/day of ubiquinol for a month. After a single bout of intense aerobic and endurance exercise, the participants showed a rapid and significant reduction in ubiquinol levels, especially lipoprotein CoQ10 and increased muscle damage markers such as Creatine kinase (CK) and Myoglobin (Mb). Ubiquinol supplementation prevented exercise-induced CoQ10 scarcity and reduced the activity of paraoxonase, an anti-inflammatory and antioxidant enzyme protective against oxidative stress in lipoprotein and circulating cells. Ubiquinol supplementation was associated with a significant decrease in cytosolic ROS in peripheral blood mononuclear cells. Ubiquinol supplementation enhanced plasma and cellular antioxidant levels. Healthcare professionals can use the results of this study to understand the antioxidant effects of ubiquinol supplementation and its buffering effect on plasma CoQ10 balances and exercise-induced CoQ10 depletion. However, further robust studies are required to evaluate the therapeutic potential of ubiquinol supplementation in sports nutrition.
Abstract
OBJECTIVES Physical exercise significantly impacts the biochemistry of the organism. Ubiquinone is a key component of the mitochondrial respiratory chain and ubiquinol, its reduced and active form, is an emerging molecule in sport nutrition. The aim of this study was to evaluate the effect of ubiquinol supplementation on biochemical and oxidative stress indexes after an intense bout of exercise. METHODS 21 male young athletes (26 + 5 years of age) were randomized in two groups according to a double blind cross-over study, either supplemented with ubiquinol (200 mg/day) or placebo for 1 month. Blood was withdrawn before and after a single bout of intense exercise (40 min run at 85% maxHR). Physical performance, hematochemical parameters, ubiquinone/ubiquinol plasma content, intracellular reactive oxygen species (ROS) level, mitochondrial membrane depolarization, paraoxonase activity and oxidative DNA damage were analyzed. RESULTS A single bout of intense exercise produced a significant increase in most hematochemical indexes, in particular CK and Mb while, on the contrary, normalized coenzyme Q10 plasma content decreased significantly in all subjects. Ubiquinol supplementation prevented exercise-induced CoQ deprivation and decrease in paraoxonase activity. Moreover at a cellular level, in peripheral blood mononuclear cells, ubiquinol supplementation was associated with a significant decrease in cytosolic ROS while mitochondrial membrane potential and oxidative DNA damage remained unchanged. DISCUSSION Data highlights a very rapid dynamic of CoQ depletion following intense exercise underlying an increased demand by the organism. Ubiquinol supplementation minimized exercise-induced depletion and enhanced plasma and cellular antioxidant levels but it was not able to improve physical performance indexes or markers of muscular damage.