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Diet, kiwifruit and genotypes : their influence on lipid profiles and CVD-related metabolic markers in hypercholesterolaemic men : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Nutritional Science at Massey University, Albany, New Zealand
In New Zealand, cardiovascular disease (CVD) is a major public health concern
and a leading cause of death. Lifestyle modification, including dietary change, is
a crucial element in the prevention of CVD, with fruit and vegetables key
elements of a cardioprotective diet. Kiwifruit is a commonly-consumed, nutrientdense
fruit that contains many components individually shown to have positive
effects on CVD risk factors. This study investigated the effects on plasma lipid
profiles and other CVD-related metabolic markers of consuming kiwifruit daily in
conjunction with a healthy diet. Further, plasma lipid responses were examined
according to inflammatory status, APOE genotype, and additional high-density
lipoprotein cholesterol (HDL-C)-related gene polymorphisms.
Eighty-five hypercholesterolaemic men (low-density cholesterol (LDL-C) >3.0
mmol/L and triglycerides (TG) <3 mmol/L) completed a 4-week healthy diet runin
before randomisation to a controlled cross-over study of two 4-week
interventions of two green kiwifruit/day plus healthy diet (intervention), or
healthy diet alone (control). Anthropometric measures, blood pressure (BP),
heart rate (HR), stroke volume (SV), cardiac output (CO), total peripheral
resistance (TPR) and fasting blood samples (lipid profile, insulin, glucose, highsensitivity
C-reactive protein (hs-CRP), interleukin (IL)-6, tumour necrosis factor
alpha (TNF-α) and IL-10) were taken at baseline, 4 and 8 weeks. An additional
blood sample was taken for genetic testing: APOE, CETP Taq1B; APOA1
-75G/A; LIPC-514C→T; LIPG I24582. Subjects were divided into low and
medium inflammatory groups, using pre-intervention hs-CRP concentrations
(hs-CRP <1 and 1-3 mg/L, respectively). Repeated measures ANOVA was
used to examine genotype/inflammatory status x treatment interactions.
After the kiwifruit intervention, plasma HDL-C concentrations were significantly
higher (mean difference 0.04 [95% CI: 0.01, 0.07] mmol/L [P=0.004]) and the
total cholesterol (TC)/HDL-C ratio was significantly lower (-0.15 [-0.24, -0.05]
mmol/L [P=0.002]), compared to control. For the total group, there were no
significant differences between the interventions for TC, LDL-C, insulin,
glucose, hs-CRP, BP, HR, SV, CO and TPR. Lipid responses were modulated
according to inflammatory status and APOE and CETP Taq1B genotypes. The
medium inflammatory group had a significant improvement in CRP with kiwifruit
compared to control. Significant inflammatory group x intervention interactions
were seen for TC/HDL-C (P=0.02), TG/HDL-C (P=0.05), and plasma IL-6
(P=0.04). Examined by genotype, APOE4 carriers had significantly decreased
TG (-0.18 [-0.34, -0.02] mmol/L [P=0.03]) with kiwifruit compared to control. A
significant CETP Taq1B genotype x intervention interaction was seen for the
TG/HDL-C ratio (P=0.03), and B1/B1 homozygotes had a significantly lower
TG/HDL-C (-0.23±0.58 mmol/L, P=0.03) ratio after the kiwifruit intervention,
compared to control. Lipid response was not affected by other polymorphisms.
In conclusion, kiwifruit independently of a healthy diet containing fruit improved
dyslipidaemic profiles, significantly improving mean HDL-C concentration and
TC/HDL-C ratio compared with the control intervention. Effects were even more
pronounced in men with phenotypes and genotypes which placed them at
higher risk of CVD, with more sizeable improvements in HDL-C and TC/HDL-C
ratio, and significant decreases in TG concentrations and TG/HDL-C ratio.
Although modest, the improvements suggest that regular inclusion of green
kiwifruit as part of a healthy diet could translate into a significant reduction of
CVD risk in men with high cholesterol concentrations.