ID 1911 -
Koenzym Q10
PL: Koenzym Q10
EN: Co-Enzyme Q 10
Pdf: coenzyme Q10
Oświadczenie (2)
- utrzymaniu i promocji zdrowia serca
- zdrowie serca
- ciśnienie krwi
1. Charakterystyka żywności / składnika
The food constituent that is the subject of the health claim is coenzyme Q10 (ubiquinone).
Coenzyme Q10 (CoQ10) is part of the ubiquinone family of compounds, all containing 1,4 benzoquinone as the functional group with a side chain of isoprenyl units, which is 10 units in the case of coenzyme Q10. Coenzyme Q10 can exist in three oxidation states: the fully reduced ubiquinol form (CoQ10H2), the radical semiquinone intermediate (CoQ10H) and the fully oxidised ubiquinone form (CoQ10). Coenzyme Q10 can be synthesised in most human tissues and occurs widely in nature, including foods, mainly in meat, poultry and fish. Coenzyme Q10 is measurable in foods by established methods.
The Panel considers that the food constituent, coenzyme Q10 (ubiquinone), which is the subject of the health claims, is sufficiently characterised.
2.2. Utrzymanie prawidłowego ciśnienia tętniczego (ID 1509, 1721, 1911)
The claimed effects are “blood pressure”, “heart health” and “maintenance and promotion of heart health”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel notes that the claimed effect relates to the maintenance of normal blood pressure.
Blood pressure is the pressure (force per unit area) exerted by circulating blood on the walls of blood
vessels. Elevated blood pressure, by convention 140 mmHg (systolic) and/or 90 mmHg (diastolic), may compromise the normal function of the arteries.
The Panel considers that maintenance of normal blood pressure is a beneficial physiological effect.
3. Naukowe uzasadnienia wpływu na zdrowie człowieka
Coenzyme Q10 (ubiquinone) is found in high concentrations in the mitochondria, it is involved in the mitochondrial electron transport chain as an electron acceptor/donor, and is known to play a role in oxidative mitochondrial phosphorylation (ATP production). Coenzyme Q10 can be synthesised by the body and there is no need for coenzyme Q10 in human diets (SCF, 1993).
3.2. Utrzymanie prawidłowego ciśnienia tętniczego (ID 1509, 1721, 1911)
A total of 54 references were presented in the consolidated list in relation to this claim. One meta- analysis focused on coenzyme Q10 supplementation as a therapy in patients with heart failure. In three non-controlled intervention studies and seven randomised controlled trials in humans, oral coenzyme Q10 intake was studied in patients with clinical heart disease, mainly heart failure. Subjects in these studies cannot be considered representative of the general population in relation to the claimed effect. There were 21 review papers and eight textbook chapters that discussed the role of coenzyme Q10 in heart disease, coenzyme Q10 status in relation to statin treatment, and/or the role of coenzyme Q10 in human health from a mechanistic or physiological viewpoint. These papers and textbook chapters did not contain original data on the health effects of oral coenzyme Q10 intake in non-clinical populations. Furthermore, there was one conference abstract on the effect of coenzyme Q10 in heart failure patients, one animal study (in mice) on the relation between age and mitochondrial coenzyme Q10 concentrations and one biopsy study assessing coenzyme Q10 concentrations in the heart tissue of patients with cardiomyopathy. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
The US Institute of Medicine (IoM, 2005) report on dietary reference intakes for vitamins and minerals was cited in the consolidated list, but no information on coenzyme Q10 in relation to blood pressure could be retrieved.
Two systematic reviews and one meta-analysis on the health effects of coenzyme Q10, including blood pressure, were presented. Tran et al. (2001) performed a systematic review on the safety and efficacy of oral coenzyme Q10 as co-adjuvant in the pharmacological treatment of different clinical conditions, including hypertension. The Panel considers that no scientific conclusions can be drawn from this systematic review for the scientific substantiation of the claim. A systematic review (Rosenfeldt et al., 2003) on the effects of coenzyme Q10 in the treatment of hypertension and a meta-analysis (Rosenfeldt, 2007) of clinical trials on coenzyme Q10 consumption in the treatment of hypertension were provided. The meta-analysis included a number of human intervention studies on the effects of coenzyme Q10 on blood pressure, of which four had a randomised controlled design (Yamamagi et al., 1986; Burke et al., 2001; Digiesi et al., 1990; Singh et al., 1999) and are described below. Three of these have also been cited individually in the consolidated list (Yamamagi et al., 1986; Burke et al., 2001; Digiesi et al., 1990).
Six intervention studies in humans were provided on the effects of coenzyme Q10 intake on blood pressure. One was a one arm, uncontrolled human study on the effects of coenzyme Q10 supplementation (100 mg/day) for 10 weeks on blood pressure in 26 subjects with essential hypertension (Diegisi et al., 1994), from which no conclusions could be drawn for the scientific substantiation of the claimed effect owing to the uncontrolled nature of the study.
Two randomised controlled trials (Singh et al., 1999; Yamagami et al., 1986) on the effect of coenzyme Q10 consumption on blood pressure included subjects who were on conventional (pharmacological) antihypertensive treatment before and during the studies. The Panel considers that no conclusions can be drawn from these studies for the substantiation of the claim as the evidence provided does not establish that interactions between coenzyme Q10 and antihypertensive treatment can be excluded.
A placebo-controlled cross-over study was conducted by Digiesi et al. (1990) including 18 Italian patients (four women, mean age 56 years) with baseline blood pressure of 167/103 mmHg on antihypertensive pharmacological treatment, which was suspended two weeks prior to enrolment. Patients were not selected for low coenzyme Q10 status. Coenzyme Q10 (100 mg/day) and placebo were administered for 10 weeks with a 2-week washout period in between. Blood pressure values were recorded weekly. The Panel notes the small size of the study, that differences in blood pressure changes between interventions were not reported, that intermediate blood pressure measurements were not reported nor considered in the statistical analysis, and that carry-over effects were not assessed. The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claimed effect.
In a placebo-controlled, parallel intervention, 76 older patients (35 women, mean age 68 years) with isolated systolic hypertension (ISH), who were asked to discontinue antihypertensive medications 10 days before enrolment, were randomised to consume 120 mg/day coenzyme Q10 or placebo for 12 weeks (Burke, 2001). Nine normotensive subjects were also recruited and all received coenzyme Q10 (120 mg/day) for 12 weeks. The Panel notes that differences in blood pressure changes between treatment and placebo ISH groups were not reported. The Panel considers that no conclusions can be drawn from this study for the scientific substantiation of the claim.
In a 12-week placebo-controlled intervention, 80 subjects (mean age 53 years) with type 2 diabetes, dyslipidaemia and blood pressure <160/90 mmHg who were not on antihypertensive medication were randomised to consume coenzyme Q10 (200 mg/day) and fenofibrate (200 mg/day), coenzyme Q10 and fenofibrate placebo, coenzyme Q10 placebo and fenofibrate, or double placebo (Hodgson et al., 2002). The primary outcome of the study was endothelial dysfunction. Secondary outcomes were blood lipids, blood pressure, glycaemic control and markers of oxidative stress. A total of 74 subjects completed the study and entered data analysis. A significant reduction in systolic (-6.1±2.6 mmHg, p=0.021) and diastolic (-2.9±1.4 mmHg, p=0.048) blood pressure was observed in subjects consuming 200 mg/day coenzyme Q10 with or without fenofibrate (n = 36) compared to subjects not consuming coenzyme Q10 (n = 38). No interaction between coenzyme Q10 and fenofibrate was observed for any of the variables studied. The Panel notes that change in blood pressure was not the primary outcome of the study, that no statistical adjustment for multiple outcomes was considered, that data analysis was only provided for completers, that a direct comparison between the double placebo group and the CoQ10 and fenofibrate placebo groups was not reported, and that in a more recent publication the same research group found an interaction between CoQ10 and fenofibrate for blood pressure (Chew et al., 2008). The Panel considers that these weaknesses greatly limit the conclusions that can be drawn from this study with respect to an independent effect of CoQ10 on blood pressure.
No evidence for a mechanism by which CoQ10 could exert the claimed effect has been provided.
In weighing the evidence, the Panel took into account that most of the studies presented have been conducted in hypertensive patients on pharmacological treatment for hypertension, that the evidence provided does not establish that interactions between coenzyme Q10 and antihypertensive treatment can be excluded, and that only one intervention study with considerable weaknesses reported a significant effect of coenzyme Q10 supplementation on blood pressure.
The Panel concludes that a cause and effect relationship has not been established between the consumption of coenzyme Q10 (ubiquinone) and the maintenance of normal blood pressure.
Warunki i możliwe ograniczenia stosowania oświadczenia
15 mg/day;(15% of the lower therapeutic dose 100 mg)