BackgroundThe consumption of lycopene-rich foods may lower cardiovascular disease (CVD) risk. Lycopene circulates in the blood bound to lipoproteins, including high-density lipoproteins (HDLs). Preliminary data from our group showed that increased consumption of tomato-based food or lycopene supplement in middle-aged subjects led to functional changes to HDL's sub-fractions, HDL2 and HDL3. These changes were also associated with a decrease in serum amyloid A (SAA), potentially enhancing their anti-atherogenic properties.ObjectiveWe carried out a comprehensive randomized controlled intervention trial with healthy middle-aged volunteers to assess whether the consumption of tomato-based foods or lycopene supplements affects HDL functionality and associated inflammatory markers, and lipoprotein subfractions size and distribution.DesignVolunteers (225, aged 40–65 years) were randomly assigned to one of three dietary intervention groups and asked to consume a control diet (low in tomato-based foods, <10 mg lycopene/week), a lycopene-rich diet (224–350 mg lycopene/week), or the control diet with a lycopene supplement (70 mg lycopene/week). HDL2 and HDL3 were isolated by ultracentrifugation. Compliance was monitored by assessing lycopene concentration in serum. Systemic and HDL-associated inflammation was assessed by measuring SAA concentrations. HDL functionality was determined by monitoring paraoxonase-1 (PON-1), cholesteryl ester transfer protein (CETP), and lecithin cholesterol acyltransferase (LCAT) activities. The lipoprotein subfractions profile was assessed by NMR.ResultsLycopene in serum and HDL significantly increased following consumption of both the high tomato diet and lycopene supplement (p ≤ 0.001 for both). Lycopene, either as a tomato-rich food or a supplement, enhanced both serum- and HDL3-PON-1 activities (p ≤ 0.001 and p = 0.036, respectively), while significantly reducing HDL3-SAA-related inflammation (p = 0.001). Lycopene supplement also significantly increased HDL3-LCAT activity (p = 0.05), and reduced the activity of both HDL2- and HDL3-CETP (p = 0.005 and p = 0.002, respectively). These changes were not associated with changes in the subclasses distribution for all lipoprotein fractions or the size of lipoprotein subclasses.ConclusionOur results showed that dietary lycopene can significantly enhance HDL functionality, without associated changes in particle size and distribution, by modulating the activity of HDL-associated enzymes. Concomitantly, dietary lycopene significantly decreased serum- and HDL3-associated SAA, confirming that SAA may represent a sensitive inflammatory biomarker to dietary change.Clinical Trial Register(https://www.isrctn.com), ISRCTN34203810.
An increased intake of fruit and vegetables has been associated with decreased risk of cardiovascular disease (CVD). However, it is currently unclear as to whether particular fruits and vegetables convey more benefit than others, and if the form in which a particular fruit or vegetable is delivered, for example, depending on polyphenol content or the degree of processing, affects potential health benefits. The aim of this study was to conduct a pilot randomised placebo-controlled trial (RCT) with the ultimate aim of assessing if different apple products differentially affect CVD risk factors. The RCT was conducted in those at elevated risk of CVD. Participants were randomised to receive high polyphenol apples, low polyphenol apples, capsules containing apple extract, dried apple pieces or placebo capsules to take for four weeks. A range of risk factors and biomarkers associated with CVD were measured before and after the intervention period. A total of 55 participants were randomised and completed the study. Change in hip circumference was significantly different across the groups after 4 weeks (P=0.02) Change in fibre intake was also statistically significant between groups, with those consuming high polyphenol apples having a higher intake than those on the apple extract (P=0.01). There was a significant within-group change in fasting oxidised LDL in the apple extract group (P=0.008). A significant difference in change in volume-corrected epicatechin was observed (P=0.03), with those on apple extract having higher levels than those on placebo capsule (P=0.002) or low polyphenol apples (P=0.01) Overall, interventions were generally acceptable to participants. Apple products appeared to have a positive effect on some risk factors for CVD in this pilot study, which indicated a definitive RCT is feasible. Further adequately powered studies need to be conducted to definitively test these findings.
Chronic heart failure (CHF) is a global term for the physiological state in which cardiac output is insufficient to meet the needs of the body and lungs. While oxidative stress, defined as an excess production of reactive oxygen species relative to antioxidant defence, has been shown to play an important role in the pathophysiology of CHF. However, although high density lipoproteins (HDL) have important cardioprotective properties, inflammation and oxidative stress can induce dramatic changes, which negate their antiatherogenic properties. Thus, such impairment to HDL may provide an important link between inflammation and oxidative stress in the pathogenesis of CHF. This pilot study investigated the antiatherogenic properties of HDL in CHF. Ten control subjects (BNP<100 nM) were matched for age and gender with 22 CHF subjects (BNP>100 nM). HDL 2 and HDL 3 were isolated from serum by rapid ultracentrifugation. SAA was measured by an ELISA procedure, paraoxonase-1 (PON-1) activity, hydroperoxide (HPO) and conjugated diene (CD) concentration were measured by spectrophotometric assays. Results: Compared to the control subjects, BNP was higher in the CHF subjects [50 (11) vs. 2439 (900) nM; p=0.015] and in HDL 2 and HDL 3 , SAA-related inflammation was increased, while the activity of the antioxidant enzyme PON-1 was decreased and CDs, one of the markers of lipid peroxidation, were increased (see table). Conclusion: This pilot study has shown that HDL displayed a proatherogenic phenotype in CHF subjects, which we suggest may be biologically relevant in the pathophysiology of CHF.
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