Lycopene Embedded into Cocoa Butter Micelles of Dark Chocolate Causes Dose-dependent Decrease in Serum Lipids of Hypercholesterolemic Volunteers
Ivan M. Petyaev, Pavel Y. Dovgalevsky, Natalia E. Chalyk, Victor A . Klochkov, Nigel H. Kyle
Journal of Advances in Medicine and Medical Research · pp. 1–11 · Published 22 Feb 2016
10.9734/BJMMR/2016/23623Abstract
Aim: To investigate if different amounts of lycopene embedded into cocoa butter micelles of dark chocolate affect serum lipid profile of hypercholesterolemia patients. Study Design: 32 clinically healthy volunteers with borderline hyperlipidemia were enrolled in a 4 week dietary trial. The study participants ingested daily one 10 g bar of L-tug dark chocolate (DC) which contained 0, 2, 3.5 or 7 mg of lycopene with no other restrictions/modifications to their habitual diet. Serum specimens were collected at the outset and after the second and fourth weeks of the trial. The study was conducted at the Saratov’s Institute of Cardiology (Russian Federation) using dark chocolate specimens provided by Lycotec Ltd (Cambridge, UK) during January-March 2013 under approved and registered protocol. Results: It was found that even the lowest concentration of lycopene tested (2 mg) caused a statistically significant (p<0.05) decline in the total cholesterol value at the end of the trial [from a median of 230.5 mg/dl (95% CI: 243.6, 204.8) to 210.5 mg/dl (95%CI: 221.7, 200.1)]. Consumption of higher amounts of lycopene embedded into L-tug DC caused an even more significant step-wise decline in total cholesterol values which were observable from the second week of the trial. There was a corresponding decline in LDL-cholesterol and triglyceride values. Consumption of L-tug DC with the highest amount of lycopene (7 mg) caused a small but statistically significant (P<0.05) increase in HDL values at the end of the interventional period [from a median of 40 mg/dl (95% CI: 43.65, 39) to 42 (95%CI: 43.65, 40.35)]. Conclusion: Lycopene-containing L-tug DC can be used for dietary management of abnormalities of lipid homeostasis in mild hyperlipidemia.
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