Role of human nutrition in the pathophysiology of cardiovascular disease; effects of diet on blood lipids and lipoprotein metabolism; genetic and environmental determinants of coronary atherosclerosis.
Research Studies 1996-2009
1996: Can the metabolic effects of dietary N-3 PUFA be explained by changes in the expression of lipase genes in adipose tissue?
1997: The influence of dietary N-3 PUFA on the structure, function and metabolism of TAG-rich lipoproteins in healthy individuals.
1998: Importance of alpha-linolenic acid as a source of long chain N-3 PUFA and its influence on risk factors of cardiovascular disease.
2000: Vitamin E biokinetics and metabolism in dyslipidaemia.
2000: Quantification of the optimal N-6 / N-3 ratio in the UK diet. The OPTILIP study
2003: Effect of low glycaemic index foods on blood lipids in type 2 diabetes
Impact of the amount and composition of dietary fat and carbohydrate on metabolic syndrome and CVD risk; The ‘RISCK’ Study.
2005: Effects of increased egg consumption on a weight-reducing diet on blood cholesterol & related biomarkers of CHD risk
2008: Dietary intervention study to determine the effects of prawns on serum cholesterol and related biomarkers of CHD risk
2009: How does dietary carbohydrate influence the formation of an atherogenic lipoprotein phenotype?
I teach and examine on five undergraduate modules associated with BSc Degree programmes in Nutrition, Nutrition & Dietetics, Nutrition & Food Science and Biochemistry, and three MSc programmes.
Admissions Tutor for MSc in Clinical biochemistry
Supervise MSc and PhD research programmes
Chairman for the Exam Board in Nutritional Medicine 2006 to date
Degree programme review panel member for BSc Undergraduate Framework for Lifelong Learning in Health and Social Care Practice, EIHMS, University of Surrey (2007)
Member of the Faculty’s Research Advisory Board, FHMS, University of Surrey
Editorial board membership:
Find me on campus Room: 32 PG 00
Objective SNPs identified from genome-wide association studies associate with lipid risk markers of cardiovascular disease. This study investigated whether these SNPs altered the plasma lipid response to diet in the ‘RISCK’ study cohort. Methods Participants (n = 490) from a dietary intervention to lower saturated fat by replacement with carbohydrate or monounsaturated fat, were genotyped for 39 lipid-associated SNPs. The association of each individual SNP, and of the SNPs combined (using genetic predisposition scores), with plasma lipid concentrations was assessed at baseline, and on change in response to 24 weeks on diets. Results The associations between SNPs and lipid concentrations were directionally consistent with previous findings. The genetic predisposition scores were associated with higher baseline concentrations of plasma total (P = 0.02) and LDL (P = 0.002) cholesterol, triglycerides (P = 0.001) and apolipoprotein B (P = 0.004), and with lower baseline concentrations of HDL cholesterol (P < 0.001) and apolipoprotein A-I (P < 0.001). None of the SNPs showed significant association with the reduction of plasma lipids in response to the dietary interventions and there was no evidence of diet-gene interactions. Conclusion Results from this exploratory study have shown that increased genetic predisposition was associated with an unfavourable plasma lipid profile at baseline, but did not influence the improvement in lipid profiles by the low-saturated-fat diets.
Objective: The PPARG SNP rs1801282 (Pro12Ala C>G) has shown variable association with metabolic syndrome traits in healthy subjects. We investigated genotype association with plasma lipids and the influence of dietary polyunsaturated:saturated fat ratio (P:S) in subjects at increased cardiometabolic risk. Methods: Habitual dietary intake was recorded at recruitment to the RISCK Study. PPARG rs1801282 was genotyped in 466 subjects aged 30-70 y. Genotype associations with plasma lipids were assessed at recruitment, after a 4-wk high-SFA (HS) diet and a 24-wk intervention with reference (HS), high-MUFA (HM) and low-fat (LF) diets. The interaction of habitual P:S intake x genotype on plasma lipid concentrations was investigated. Results: PPARG rs1801282 G-allele frequency was 0.09. At recruitment, G-allele carriers had higher plasma total cholesterol concentration (n=415; P=0.05) after adjustment for BMI, gender, age and ethnicity. Dietary P:S ratio x genotype interaction influenced plasma LDLcholesterol (P=0.02) and triglyceride (P=0.03) concentrations. At P:S ratio 0.33, mean LDLcholesterol concentration in G-allele carriers was higher than in non-carriers, but fell between 0.34-0.65. Triglyceride concentration followed a similar pattern. After the 4-wk HS diet, Gallele carriers had higher concentrations of total cholesterol (P=0.03), LDL-cholesterol (P=0.04) and apo B (P=0.04) than non-carriers, after adjustments. After the 24-wk interventions, diet x genotype interaction did not significantly influence either LDLcholesterol (P=0.58) or triglyceride (P=0.57) concentrations. Conclusion: A high dietary P:S ratio would help to reduce plasma LDL-cholesterol and triglyceride concentrations in PPARG rs1801282 G-allele carriers at increased cardiometabolic risk.
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