Lycopene reduces inflammation and improves HDL functionality in overweight individuals

Type Article

Journal Article

Authors

J. McEneny; L. Wade; A. McGinty; I. Young; F. Thies

Year of publication

2011

Publication/Journal

Atherosclerosis supplements

Volume

12

Issue

1

Pages

44

Abstract

Background: Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the developed world, and its incidence increases with increasing BMI. Dietary factors, such as increased lycopene intake, may lower CVD risk. Objectives: To assess if increasing lycopene intake reduces the inflammatory marker serum amyloid‐A (SAA) and its incorporation into high density lipoprotein (HDL), helping to restore HDL's anti‐atherogenic functionality. Design: Following a 4‐week washout, serum was collected before and after an 8‐week intervention from 54‐overweight (25.6+0.47Kgm2) middleaged (50.4+1.0years) individuals. Subjects were randomised to one of three groups, Group‐1) lycopene‐rich diet (equivalent to 70 mg/week); Group‐2) lycopene supplement (10 mg/day); Group‐3) lycopene‐deplete diet (18 per group). HDL was subfractionated into HDL2&3 by rapid ultracentrifugation. Serum and HDL2&3 were assessed for lycopene incorporation (HPLC) and SAA levels (ELISA). The arylesterase activity of HDL2&3 (PON‐1) was assessed spectrophotometrically. Results: Within group analyses found that lycopene was significantly increased in serum and HDL2&3 in both treatment groups, but was unaltered in the control group. Furthermore, SAA decreased in HDL3 in the diet group (p = 0.026) and in serum and HDL2&3 in the supplement group (all p < 0.05). Additionally, PON‐1 activity increased in HDL2&3 in both treatment groups (Group‐1, p = 0.000 & 0.035: Group‐2, p = 0.018 & 0.000, respectively). Between group analyses found that, compared to the control group, SAA was lower in HDL3 (p < 0.05), while PON‐1 activity was higher in HDL2 (p < 0.006) in both treatment groups. Discussion: These results demonstrate that increasing lycopene intake produced beneficial changes within HDL which helped restore its antiatherogenic functionality.