Scientific Documents

Lycopene-whey complex (bioavailable lycopene) and risk of atherosclerotic plaques Scientific substantiation of a health claim related to Lycopene-whey complex (bioavailable lycopene) and reduction of the risk of atherosclerotic plaques pursuant to Article 14 of Regulation (EC) No 1924/2006 [1]

Summary (152 KB)

Opinion (96 KB)

Summary

Following an application from Cambridge Theranostics Ltd. submitted pursuant to Article 14, of Regulation (EC) No 1924/2006 via the Competent Authority of United Kingdom, the Panel on Dietetic Products, Nutrition and Allergies was asked to deliver an opinion on the scientific substantiation of a health claim related to lycopene-whey complex (bioavailable lycopene) and reduction of the risk of atherosclerotic plaques.

The scope of the application was proposed to fall under a health claim referring to disease risk reduction.

The food constituent that is the subject of the health claim is a lycopene-whey complex (bioavailable lycopene). Lycopene-whey complex is prepared using a patented process by mixing tomato extract containing 10% lycopene with whey protein to form a granulated product. The amount of the active constituent, lycopene, is 2% in the final product. The lycopene-whey complex has been shown to have bioavailability similar to tomato paste in human subjects.

The Panel considers that this substantiation applies to all lycopene sources of similar bioavailability. The Panel considers that the food constituent “lycopene” which is the subject of the health claim is sufficiently characterized.

The claimed effect is “prevents oxidative damage of plasma lipoproteins, which reduces the build up of arterial plaques and reduces the risk of heart disease, stroke and other clinical complications of atherosclerosis”. The target population is adults.

The Panel considers that the evidence provided does not establish that the claimed effect, the prevention of oxidation of plasma lipoproteins, is beneficial to human health by reducing the risk of atherosclerotic diseases.

The applicant identified 80 publications as pertinent to the relationship between the consumption of the food/constituent and the claimed effect. Six of the studies were experimental intervention studies, 22 were observational studies, 44 were other human studies, and there were eight reviews.

In four of the six human intervention studies, ex vivo lipoprotein oxidisability or oxidised serum LDL were measured as the primary outcomes, endpoints which have not been established to be independent predictors of risk of atherosclerotic diseases. In addition the Panel notes various other limitations of the four studies. The Panel considers that the other two human intervention studies did not measure specific markers of oxidative damage of plasma lipoproteins and do not provide evidence for the claimed effect.

The 22 observational studies presented address the association between either dietary intake of tomato/lycopene or serum concentrations of lycopene and incident myocardial infarction, stroke or arterial plaque development assessed as intima-media thickness, incident new plaque or aortic sclerosis. The Panel considers that these studies do not establish a relationship between the intake of lycopene and the oxidation of plasma lipoproteins, or between the oxidation of plasma lipoproteins and the incidence/progression of atherosclerosis.

The 44 other human studies describe mechanistic effects of lycopene, tomato products, carotenoids, antioxidants in general, or bioavailability of lycopene. The Panel considers that the evidence provided does not establish that lycopene can reduce oxidative damage of plasma lipoproteins in vivo.

In weighing the evidence the Panel took into account the limitations of the intervention studies, i.e. the primary endpoints measured have not been established to be independent predictors of risk of atherosclerotic diseases, the higher doses used in some studies compared to those in the conditions of use proposed by the applicant, the small number of subjects, the short duration of studies and/or lack of controls in the study design, and the performance of some studies in patients for whom it was not established that the results can be extrapolated to the general population, as well as the limited evidence from observational and other human studies.

On the basis of the data presented, the Panel concludes that a cause and effect relationship has not been established between the consumption of lycopene and the claimed effect.