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Articles by N. J Wareham
Total Records ( 6 ) for N. J Wareham
  H Ward , P. N Mitrou , R Bowman , R Luben , N. J Wareham , K. T Khaw and S. Bingham

Background  The risk of coronary heart disease (CHD) may be related to genetic mutations in the production of apolipoprotein E via alterations to the metabolism of CHD-related blood lipids such as low-density lipoprotein cholesterol and triglycerides.

Methods  The relationship between APOE genotype (*E3/*E3, *E3/*E4, *E2/*E3, *E4/*E4, *E2/*E4, and *E2/*E2) and fatal and nonfatal CHD was examined among 10 035 men and 12 134 women, aged 440 to 79 years, from the Norfolk, England, arm of the European Prospective Into Nutrition and Cancer Study (1993-2007). During an average of 11 years of follow-up, 2712 CHD events were documented.

Results  The hazard ratio for CHD was 0.88 (95% confidence interval, 0.77-0.99) for *E2 carriers (*E2/*E2 and *E2/*E3) and 1.09 (1.00-1.19) for *E4 carriers (*E3/*E4 and *E4/*E4) compared with homozygous *E3/*E3 individuals after age and sex adjustment. Similar values were obtained when systolic blood pressure, body mass index, diabetes mellitus, alcohol intake, physical activity, and smoking were added to the model. After additional adjustment for baseline levels of the ratio of low- to high-density lipoprotein cholesterol, the hazard ratios (and 95% confidence intervals) for *E2 and *E4 carriers were 0.97 (0.85-1.10) and 1.06 (0.97-1.15), respectively, when compared with *E3 homozygotes. No interactions by sex, smoking status, or age groups were observed.

Conclusion  In the largest prospective cohort study to date, CHD risk was not associated with APOE genotype after controlling for a variety of cardiovascular risk factors, particularly the ratio of low- to high-density lipoprotein cholesterol.

  A. G Semb , T Ueland , P Aukrust , N. J Wareham , R Luben , L Gullestad , J. J.P Kastelein , K. T Khaw and S. M. Boekholdt

Objective— The purpose of this study was to examine the association between serum levels of osteoprotegerin (OPG) and receptor activator of nuclear factor-B ligand (RANKL) and future coronary artery disease (CAD) in apparently healthy individuals. The identification of OPG as a novel cardiovascular risk marker suggests an association between mediators of bone homeostasis and cardiovascular disease.

Methods and Results— Serum levels of OPG and RANKL were analyzed in a prospective case–control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC-Norfolk) study, a cohort study of 25 663 men and women, where 951 apparently healthy individuals who developed a coronary event during 6 years’ follow-up were matched by sex and age with 1705 healthy controls. Baseline OPG, but not RANKL, was higher in cases than in controls, and OPG was higher in women than in men. Both men and women in the highest OPG quartile had a higher risk for future CAD. These associations were independent of established cardiovascular risk factors, and when using OPG as a continuous variable, also after adjustment for CRP. In contrast, RANKL showed no association with coronary events.

Conclusion— OPG is associated with the risk of future CAD in apparently healthy men and women, independent of established cardiovascular risk factors.

  A. Q Reuwer , M. T Twickler , B. A Hutten , F. W Molema , N. J Wareham , G. M Dallinga Thie , R. L Bogorad , V Goffin , M Smink Bol , J. J.P Kastelein , S. M Boekholdt and K. T. Khaw

Background— Prolactin is increasingly recognized to play a stimulatory role in the inflammatory response. Because inflammation is considered of crucial importance in the development of atherosclerosis, we aimed to evaluate whether prolactin levels are associated with the occurrence of coronary artery disease (CAD).

Methods and Results— We performed a nested case-control study in the prospective EPIC-Norfolk cohort. Cases were apparently healthy men and women, aged 45 to 79 years, who developed fatal or nonfatal CAD (n=882). Controls remained free of CAD (n=1490). Overall, systemic prolactin levels did not differ between cases and controls, and people in the highest prolactin tertile did not have a significantly increased risk of developing future CAD (in men, odds ratio, 1.21; 95% CI, 0.92 to 1.61; in women, odds ratio, 1.12; 95% CI, 0.76 to 1.64). However, in a separate immunohistochemical study, the presence of prolactin receptors could be demonstrated in postmortem human coronary artery plaques (preliminary data).

Conclusions— Elevated systemic prolactin levels do not predict CAD in the general population. However, prolactin receptors were found in human coronary artery plaques. This observation may indicate a role of prolactin within atherosclerotic plaques. More studies are needed to define the possible role of prolactin in atherosclerotic plaque development.

  B. J Arsenault , I Lemieux , J. P Despres , N. J Wareham , E. S. G Stroes , J. J. P Kastelein , K. T Khaw and S. M. Boekholdt

Background: Gradient gel electrophoresis (GGE) and nuclear magnetic resonance (NMR) spectroscopy are both widely accepted methods for measuring LDL and HDL particle size. However, whether or not GGE- or NMR-measured LDL or HDL particle size predicts coronary heart disease (CHD) risk to a similar extent is currently unknown.

Methods: We used GGE and NMR to measure LDL and HDL particle size in a nested case-control study of 1025 incident cases of CHD and 1915 controls from the EPIC (European Prospective Investigation into Cancer and Nutrition)-Norfolk study. The study sample included apparently healthy men and women age 45–79 years followed for an average of 6 years.

Results: Pearson correlation coefficients showed that the overall agreement between NMR and GGE was better for the measurement of HDL size (r = 0.78) than for LDL size (r = 0.47). The odds ratio for future CHD among participants in the bottom tertile of LDL size (smallest LDL particles) was 1.35 (95% CI, 1.12–1.63) for GGE and 1.74 (1.41–2.15) for NMR. For HDL size, these respective odds ratios were 1.41 (1.16–1.72) and 1.85 (1.47–2.32). After adjustment for potential confounders, the relationship between small LDL or HDL particles and CHD was no longer significant, irrespective of the method.

Conclusions: In this prospective population study, we found that the relationships between NMR-measured LDL and HDL sizes and CHD risk were slightly higher than those obtained with GGE.

  U Ekelund , S Brage , S. J Griffin , N. J Wareham and the ProActive UK Research Group

Low levels of physical activity appear to be associated with insulin resistance. However, the detailed associations of these complex relationships remain elusive. We examined the prospective associations between self-reported TV viewing time, objectively measured time spent sedentary, at light-intensity activity, and at moderate- and vigorous-intensity physical activity (MVPA) with insulin resistance.


In 192 individuals (81 men and 111 women) with a family history of type 2 diabetes, we measured physical activity and anthropometric and metabolic variables at baseline and after 1 year of follow-up in the ProActive UK trial. Physical activity was measured objectively by accelerometry. Insulin resistance was expressed as fasting insulin and the homeostasis model assessment score (HOMA-IR).


Baseline MVPA was a significant predictor of fasting insulin at follow-up (β = –0.004 [95% CI –0.007 to –0.0001], P = 0.022), and the association approached significance for HOMA-IR (β = –0.003 [–0.007 to 0.000002], P = 0.052), independent of time spent sedentary, at light-intensity activity, sex, age, smoking status, waist circumference, and self-reported TV viewing. Time spent sedentary and at light-intensity activity were not significantly associated with insulin resistance. The change in MVPA between baseline and follow-up was inversely related to fasting insulin (β = –0.003 [–0.007 to –0.0003], P = 0.032) and the HOMA-IR score (β = –0.004 [–0.008 to –0.001], P = 0.015) at follow-up, after adjustment for baseline phenotype in addition to the same confounders as above.


These results highlight the importance of promoting moderate-intensity activity such as brisk walking for improving insulin sensitivity and possibly other metabolic risk factors to prevent type 2 diabetes.

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