Elizabeth A Spencer

University of Oxford, Oxford, England, United Kingdom

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Publications (55)357.93 Total impact

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    ABSTRACT: To assess the diagnostic accuracy of three personal breathalyser devices available for sale to the public marketed to test safety to drive after drinking alcohol. Prospective comparative diagnostic accuracy study comparing two single-use breathalysers and one digital multiuse breathalyser (index tests) to a police breathalyser (reference test). Establishments licensed to serve alcohol in a UK city. Of 222 participants recruited, 208 were included in the main analysis. Participants were eligible if they were 18 years old or over, had consumed alcohol and were not intending to drive within the following 6 h. Sensitivity and specificity of the breathalysers for the detection of being at or over the UK legal driving limit (35 µg/100 mL breath alcohol concentration). 18% of participants (38/208) were at or over the UK driving limit according to the police breathalyser. The digital multiuse breathalyser had a sensitivity of 89.5% (95% CI 75.9% to 95.8%) and a specificity of 64.1% (95% CI 56.6% to 71.0%). The single-use breathalysers had a sensitivity of 94.7% (95% CI 75.4% to 99.1%) and 26.3% (95% CI 11.8% to 48.8%), and a specificity of 50.6% (95% CI 40.4% to 60.7%) and 97.5% (95% CI 91.4% to 99.3%), respectively. Self-reported alcohol consumption threshold of 5 UK units or fewer had a higher sensitivity than all personal breathalysers. One alcohol breathalyser had sensitivity of 26%, corresponding to false reassurance for approximately one person in four who is over the limit by the reference standard, at least on the evening of drinking alcohol. The other devices tested had 90% sensitivity or higher. All estimates were subject to uncertainty. There is no clearly defined minimum sensitivity for this safety-critical application. We conclude that current regulatory frameworks do not ensure high sensitivity for these devices marketed to consumers for a decision with potentially catastrophic consequences. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    BMJ Open 12/2014; 4(12):e005811. DOI:10.1136/bmjopen-2014-005811 · 2.06 Impact Factor
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    Cancer Causes and Control 09/2011; 22(9):1351. DOI:10.1007/s10552-011-9815-7 · 2.96 Impact Factor
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    ABSTRACT: To describe the development of the Oxford WebQ, a web-based 24 h dietary assessment tool developed for repeated administration in large prospective studies; and to report the preliminary assessment of its performance for estimating nutrient intakes. We developed the Oxford WebQ by repeated testing until it was sufficiently comprehensive and easy to use. For the latest version, we compared nutrient intakes from volunteers who completed both the Oxford WebQ and an interviewer-administered 24 h dietary recall on the same day. Oxford, UK. A total of 116 men and women. The WebQ took a median of 12·5 (interquartile range: 10·8-16·3) min to self-complete and nutrient intakes were estimated automatically. By contrast, the interviewer-administered 24 h dietary recall took 30 min to complete and 30 min to code. Compared with the 24 h dietary recall, the mean Spearman's correlation for the 21 nutrients obtained from the WebQ was 0·6, with the majority between 0·5 and 0·9. The mean differences in intake were less than ±10 % for all nutrients except for carotene and vitamins B12 and D. On rare occasions a food item was reported in only one assessment method, but this was not more frequent or systematically different between the methods. Compared with an interviewer-based 24 h dietary recall, the WebQ captures similar food items and estimates similar nutrient intakes for a single day's dietary intake. The WebQ is self-administered and nutrients are estimated automatically, providing a low-cost method for measuring dietary intake in large-scale studies.
    Public Health Nutrition 06/2011; 14(11):1998-2005. DOI:10.1017/S1368980011000942 · 2.48 Impact Factor
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    ABSTRACT: Hip fracture risk is known to increase with physical inactivity and decrease with obesity, but there is little information on their combined effects. We report on the separate and combined effects of body mass index (BMI) and physical activity on hospital admissions for hip fracture among postmenopausal women in a large prospective UK study. Baseline information on body size, physical activity, and other relevant factors was collected in 1996-2001, and participants were followed for incident hip fractures by record linkage to National Health Service (NHS) hospital admission data. Cox regression was used to calculate adjusted relative risks of hip fracture. Among 925,345 postmenopausal women followed for an average of 6.2 years, 2582 were admitted to hospital with an incident hip fracture. Hip fracture risk increased with decreasing BMI: Compared with obese women (BMI of 30+ kg/m(2) ), relative risks were 1.71 [95% confidence interval (CI) 1.47-1.97)] for BMI of 25.0 to 29.9 kg/m(2) and 2.55 (95% CI 2.22-2.94) for BMI of 20.0 to 24.9 kg/m(2). The increase in fracture risk per unit decrease in BMI was significantly greater among lean women than among overweight women (p < .001). For women in every category of BMI, physical inactivity was associated with an increased risk of hip fracture. There was no significant interaction between the relative effects of BMI and physical activity. For women who reported that they took any exercise versus no exercise, the adjusted relative risk of hip fracture was 0.68 (95% CI 0.62-0.75), with similar results for strenuous exercise. In this large cohort of postmenopausal women, BMI and physical activity had independent effects on hip fracture risk.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 06/2011; 26(6):1330-8. DOI:10.1002/jbmr.315 · 6.59 Impact Factor
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    ABSTRACT: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive. To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (RII), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region. Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to level of education was small and not statistically significant (RII=1.14, 95% CI 0.80-1.62). Adjustment for known risk factors reduced the inequality estimates to only a small extent. In addition, no statistically significant associations were observed for age groups (adjusted RII(≤ 60 years)=0.85, 95% CI 0.44-1.64, adjusted RII(>60 years)=1.18, 95% CI 0.73-1.90), gender (adjusted RII(male)=1.20, 95% CI 0.68-2.10, adjusted RII(female)=0.96, 95% CI 0.56-1.62) or geographical region (adjusted RII(Northern Europe)=1.14, 95% CI 0.81-1.61, adjusted RII(Middle Europe)=1.72, 95% CI 0.93-3.19, adjusted RII(Southern Europe)=0.75, 95% CI 0.32-1.80). Despite large educational inequalities in many risk factors within the EPIC study, we found no evidence for an association between educational level and the risk of developing pancreatic cancer in this European cohort.
    12/2010; 34(6):696-701. DOI:10.1016/j.canep.2010.08.004
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    ABSTRACT: Epidemiologic evidence for an association between colorectal cancer (CRC) risk and total dietary fat, saturated fat (SF), monounsaturated fat (MUFA) and polyunsaturated fat (PUFA) is inconsistent. Previous studies have used food frequency questionnaires (FFQ) to assess diet, but data from food diaries may be less prone to severe measurement error than data from FFQ. We conducted a case-control study nested within seven prospective UK cohort studies, comprising 579 cases of incident CRC and 1996 matched controls. Standardized dietary data from 4- to 7-day food diaries and from FFQ were used to estimate odds ratios for CRC risk associated with intake of fat and subtypes of fat using conditional logistic regression. We also calculated multivariate measurement error corrected odds ratios for CRC using repeated food diary measurements. We observed no associations between intakes of total dietary fat or types of fat and CRC risk, irrespective of whether dietary data were obtained using food diaries or FFQ. Our results do not support the hypothesis that intakes of total dietary fat, SF, MUFA or PUFA are linked to risk of CRC.
    10/2010; 34(5):562-7. DOI:10.1016/j.canep.2010.07.008
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    ABSTRACT: The authors investigated associations between serum C-reactive protein (CRP) concentrations and colon and rectal cancer risk in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (1992-2003) among 1,096 incident cases and 1,096 controls selected using risk-set sampling and matched on study center, age, sex, time of blood collection, fasting status, menopausal status, menstrual cycle phase, and hormone replacement therapy. In conditional logistic regression with adjustment for education, smoking, nutritional factors, body mass index, and waist circumference, CRP showed a significant nonlinear association with colon cancer risk but not rectal cancer risk. Multivariable-adjusted relative risks for CRP concentrations of > or = 3.0 mg/L versus <1.0 mg/L were 1.36 (95% confidence interval (CI): 1.00, 1.85; P-trend = 0.01) for colon cancer and 1.02 (95% CI: 0.67, 1.57; P-trend = 0.65) for rectal cancer. Colon cancer risk was significantly increased in men (relative risk = 1.74, 95% CI: 1.11, 2.73; P-trend = 0.01) but not in women (relative risk = 1.06, 95% CI: 0.67, 1.68; P-trend = 0.13). Additional adjustment for C-peptide, glycated hemoglobin, and high density lipoprotein cholesterol did not attenuate these results. These data provide evidence that elevated CRP concentrations are related to a higher risk of colon cancer but not rectal cancer, predominantly among men and independently of obesity, insulin resistance, and dyslipidemia.
    American journal of epidemiology 08/2010; 172(4):407-18. DOI:10.1093/aje/kwq135 · 4.98 Impact Factor
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    ABSTRACT: Results of epidemiological studies of dietary fiber and colorectal cancer risk have not been consistent, possibly because of attenuation of associations due to measurement error in dietary exposure ascertainment. To examine the association between dietary fiber intake and colorectal cancer risk, we conducted a prospective case-control study nested within seven UK cohort studies, which included 579 case patients who developed incident colorectal cancer and 1996 matched control subjects. We used standardized dietary data obtained from 4- to 7-day food diaries that were completed by all participants to calculate the odds ratios for colorectal, colon, and rectal cancers with the use of conditional logistic regression models that adjusted for relevant covariates. We also calculated odds ratios for colorectal cancer by using dietary data obtained from food-frequency questionnaires that were completed by most participants. All statistical tests were two-sided. Intakes of absolute fiber and of fiber intake density, ascertained by food diaries, were statistically significantly inversely associated with the risks of colorectal and colon cancers in both age-adjusted models and multivariable models that adjusted for age; anthropomorphic and socioeconomic factors; and dietary intakes of folate, alcohol, and energy. For example, the multivariable-adjusted odds ratio of colorectal cancer for highest vs the lowest quintile of fiber intake density was 0.66 (95% confidence interval = 0.45 to 0.96). However, no statistically significant association was observed when the same analysis was conducted using dietary data obtained by food-frequency questionnaire (multivariable odds ratio = 0.88, 95% confidence interval = 0.57 to 1.36). Intake of dietary fiber is inversely associated with colorectal cancer risk. Methodological differences (ie, study design, dietary assessment instruments, definition of fiber) may account for the lack of convincing evidence for the inverse association between fiber intake and colorectal cancer risk in some previous studies.
    CancerSpectrum Knowledge Environment 05/2010; 102(9):614-26. DOI:10.1093/jnci/djq092 · 15.16 Impact Factor
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    ABSTRACT: Some but not all epidemiological studies have reported that high intakes of red and processed meat are associated with an increased risk of colorectal cancer. In the UK Dietary Cohort Consortium, we examined associations of meat, poultry and fish intakes with colorectal cancer risk using standardised individual dietary data pooled from seven UK prospective studies. Four- to seven-day food diaries were analysed, disaggregating the weights of meat, poultry and fish from composite foods to investigate dose-response relationships. We identified 579 cases of colorectal cancer and matched with 1,996 controls on age, sex and recruitment date. Conditional logistic regression models were used to estimate odds ratios for colorectal cancer associated with meat, poultry and fish intakes, adjusting for relevant covariables. Disaggregated intakes were moderately low, e.g. mean red meat intakes were 38.2 g/day among male and 28.7 g/day among female controls. There was little evidence of association between the food groups examined and risk for colorectal cancer: Odds ratios (95% confidence intervals) for a 50 g/day increase were 1.01 (0.84-1.22) for red meat, 0.88 (0.68-1.15) for processed meat, 0.97 (0.84-1.12) for red and processed meat combined, 0.80 (0.65-1.00) for poultry, 0.92 (0.70-1.21) for white fish and 0.89 (0.70-1.13) for fatty fish. This study using pooled data from prospective food diaries, among cohorts with low to moderate meat intakes, shows little evidence of association between consumption of red and processed meat and colorectal cancer risk.
    Cancer Causes and Control 05/2010; 21(9):1417-25. DOI:10.1007/s10552-010-9569-7 · 2.96 Impact Factor
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    ABSTRACT: Colorectal cancer (CRC) is the third most common malignant tumor and the fourth leading cause of cancer death worldwide. The crucial role of fatty acids for a number of important biological processes suggests a more in-depth analysis of inter-individual differences in fatty acid metabolizing genes as contributing factor to colon carcinogenesis. We examined the association between genetic variability in 43 fatty acid metabolism-related genes and colorectal risk in 1225 CRC cases and 2032 controls participating in the European Prospective Investigation into Cancer and Nutrition study. Three hundred and ninety two single-nucleotide polymorphisms were selected using pairwise tagging with an r(2) cutoff of 0.8 and a minor allele frequency of >5%. Conditional logistic regression models were used to estimate odds ratios and corresponding 95% confidence intervals. Haplotype analysis was performed using a generalized linear model framework. On the genotype level, hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD), phospholipase A2 group VI (PLA2G6) and transient receptor potential vanilloid 3 were associated with higher risk for CRC, whereas prostaglandin E receptor 2 (PTGER2) was associated with lower CRC risk. A significant inverse association (P < 0.006) was found for PTGER2 GGG haplotype, whereas HPGD AGGAG and PLA2G3 CT haplotypes were significantly (P < 0.001 and P = 0.003, respectively) associated with higher risk of CRC. Based on these data, we present for the first time the association of HPGD variants with CRC risk. Our results support the key role of prostanoid signaling in colon carcinogenesis and suggest a relevance of genetic variation in fatty acid metabolism-related genes and CRC risk.
    Carcinogenesis 03/2010; 31(3):466-72. DOI:10.1093/carcin/bgp325 · 5.27 Impact Factor
  • Miranda E. Armstrong, Elizabeth A. Spencer, Valerie Beral
    Medicine &amp Science in Sports &amp Exercise 01/2010; 42. DOI:10.1249/01.MSS.0000385561.58902.ad · 4.46 Impact Factor
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    Timothy J Key, Elizabeth A Spencer, Gillian K Reeves
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    ABSTRACT: Epidemiological studies have provided convincing evidence that obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colon, pancreas, breast (post-menopausal), endometrium and kidney. The magnitude of the increase in risk varies between cancer sites. For an increase in BMI of 10 kg/m2 relative risks are approximately 2.3 for adenocarcinoma of the oesophagus, 1.5 for colon cancer in men, 1.2 for colon cancer in women, 1.4 for post-menopausal breast cancer, 2.9 for endometrial cancer and >1.5 for kidney cancer, while the size of the effect on cancer of the pancreas is uncertain. There is also evidence that obesity increases the risks for cancers of the gallbladder, malignant melanoma, ovary, thyroid, non-Hodgkin lymphoma, multiple myeloma and leukaemia. Estimates of the percentage of cancers that can be attributed to excess body weight suggest that in the UK and similar countries approximately 5% of all cancers are attributable to overweight and obesity.
    Proceedings of The Nutrition Society 12/2009; 69(1):86-90. DOI:10.1017/S0029665109991698 · 4.94 Impact Factor
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    ABSTRACT: We examined the associations of measured anthropometric factors, including general and central adiposity and height, with ovarian cancer risk. We also investigated these associations by menopausal status and for specific histological subtypes. Among 226,798 women in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, there were 611 incident cases of primary, malignant, epithelial ovarian cancer diagnosed during a mean 8.9 years of follow-up. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for potential confounders. Compared to women with body mass index (BMI) < 25 kg/m2, obesity (BMI > or = 30 kg/m2) was associated with excess ovarian cancer risk for all women combined (HR = 1.33, 95% CI = 1.05-1.68; p(trend) = 0.02) and postmenopausal women (HR = 1.59, 95% CI = 1.20-2.10; p(trend) = 0.001), but the association was weaker for premenopausal women (HR = 1.16, 95% CI = 0.65-2.06; p(trend) = 0.65). Neither height or weight gain, nor BMI-adjusted measures of fat distribution assessed by waist circumference, waist-hip ratio (WHR) or hip circumference were associated with overall risk. WHR was related to increased risk of mucinous tumors (BMI-adjusted HR per 0.05 unit increment = 1.17, 95% CI = 1.00-1.38). For all women combined, no other significant associations with risk were observed for specific histological subtypes. This large, prospective study provides evidence that obesity is an important modifiable risk factor for epithelial ovarian cancer, particularly among postmenopausal women.
    International Journal of Cancer 10/2009; 126(10):2404-15. DOI:10.1002/ijc.24952 · 5.01 Impact Factor
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    ABSTRACT: The present study investigates the cross-sectional relationship between tobacco smoking and body fatness. This cross-sectional study consisted of 469,543 men and women who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) study between 1992 and 2000 providing anthropometric measurements and information on smoking. Adjusted multilevel mixed-effects linear regression models were used to assess the association between smoking and body fat mass. The analyses showed that BMI and WC were positively associated with smoking intensity in current smokers but negatively associated with time since quitting in former smokers. When compared to never smokers, average current smokers (17 and 13 cig/day for men and women, respectively) showed a lower BMI. When average former smokers (men and women who had stopped smoking for 16 and 15 years, respectively) were compared to never smokers, higher BMI and WC were observed in men, whereas no significant associations were observed in women. This cross-sectional study suggests that smoking may be associated with body fatness and fat distribution. Although our findings cannot establish cause and effect, they suggest that providing information and support to those who want to stop may help in preventing weight gain and therefore weaken a barrier against stopping smoking.
    Preventive Medicine 09/2009; 49(5):365-73. DOI:10.1016/j.ypmed.2009.08.009 · 2.93 Impact Factor
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    ABSTRACT: Increasing evidence suggests that general obesity [measured by body mass index (BMI)] is positively associated with risk of esophageal adenocarcinoma (EAC). In contrast, previous studies have shown inverse relations with esophageal squamous cell carcinoma (ESCC). However, it is still unclear whether body fat distribution, particularly abdominal obesity, is associated with each type of esophageal cancer. We applied multivariable adjusted Cox proportional hazards regression to investigate the association between anthropometric measures and risk of EAC and ESCC among 346,554 men and women participating in the European Prospective Investigation into Cancer and Nutrition. All statistical tests were two sided. During 8.9 years of follow-up, we documented 88 incident cases of EAC and 110 cases of ESCC. BMI, waist circumference, and waist-to-hip ratio (WHR) were positively associated with EAC risk [highest versus lowest quintile; relative risk (RR), 2.60; 95% confidence interval (95% CI), 1.23-5.51; P(trend) < 0.01; RR, 3.07; 95% CI, 1.35-6.98; P(trend) < 0.003; and RR, 2.12; 95% CI, 0.98-4.57; P(trend) < 0.004]. In contrast, BMI and waist circumference were inversely related to ESCC risk, whereas WHR showed no association with ESCC. In stratified analyses, BMI and waist circumference were significantly inversely related to ESCC only among smokers but not among nonsmokers. However, when controlled for BMI, we found positive associations for waist circumference and WHR with ESCC, and these associations were observed among smokers and nonsmokers. General and abdominal obesity were associated with higher EAC risk. Further, our study suggests that particularly an abdominal body fat distribution might also be a risk factor for ESCC.
    Cancer Epidemiology Biomarkers & Prevention 07/2009; 18(7):2079-89. DOI:10.1158/1055-9965.EPI-09-0265 · 4.32 Impact Factor
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    ABSTRACT: A Western diet is associated with breast cancer risk. We investigated the relation of meat, egg, and dairy product consumption with breast cancer risk by using data from the European Prospective Investigation into Cancer and Nutrition (EPIC). Between 1992 and 2003, information on diet was collected from 319,826 women. Disease hazard ratios were estimated with multivariate Cox proportional hazard models. Breast cancer cases (n = 7119) were observed during 8.8 y (median) of follow-up. No consistent association was found between breast cancer risk and the consumption of any of the food groups under study, when analyzed by both categorical and continuous exposure variable models. High processed meat consumption was associated with a modest increase in breast cancer risk in the categorical model (hazard ratio: 1.10; 95% CI: 1.00, 1.20; highest compared with lowest quintile: P for trend = 0.07). Subgroup analyses suggested an association with butter consumption, limited to premenopausal women (hazard ratio: 1.28; 95% CI: 1.06, 1.53; highest compared with lowest quintile: P for trend = 0.21). Between-country heterogeneity was found for red meat (Q statistic = 18.03; P = 0.05) and was significantly explained (P = 0.023) by the proportion of meat cooked at high temperature. We have not consistently identified intakes of meat, eggs, or dairy products as risk factors for breast cancer. Future studies should investigate the possible role of high-temperature cooking in the relation of red meat intake with breast cancer risk.
    American Journal of Clinical Nutrition 07/2009; 90(3):602-12. DOI:10.3945/ajcn.2008.27173 · 6.92 Impact Factor
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    ABSTRACT: Risk factors for pancreatic cancer, other than smoking and diabetes, are not well-established, especially for women. In a cohort of 1.3 million middle-aged women, followed for 9.2 million person-years for cancer incidence and 11.5 million person-years for mortality, there were 1,338 incident pancreatic cancer cases and 1,710 deaths from the disease. Using proportional hazards models, we calculated adjusted relative risks (RRs) and 95% confidence intervals (CIs) by smoking, height, body mass index (BMI), alcohol consumption, physical activity and history of diabetes. Pancreatic cancer incidence was greater in current than never smokers (RR 2.39, CI 2.10–2.73), the risk increasing with the number of cigarettes smoked. The incidence of pancreatic cancer also increased with increasing BMI (RR 1.34, CI 1.13–1.57 for BMI ≥ 30 vs. 22.5–25 kg/m2), and with a history of diabetes (RR 1.58, CI 1.22–2.03, with vs. without such a history). These factors were also associated with increased mortality from pancreatic cancer. Height, alcohol consumption and physical activity showed little or no association with pancreatic cancer risk. © 2008 Wiley-Liss, Inc.
    International Journal of Cancer 05/2009; 124(10):2400 - 2405. DOI:10.1002/ijc.24196 · 5.01 Impact Factor
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    ABSTRACT: Few prospective studies have examined the mortality of vegetarians. We present results on mortality among vegetarians and nonvegetarians in the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford). We used a prospective study of men and women recruited throughout the United Kingdom in the 1990s. Among 64,234 participants aged 20-89 y for whom diet group was known, 2965 had died before age 90 by 30 June 2007. The death rates of participants are much lower than average for the United Kingdom. The standardized mortality ratio for all causes of death was 52% (95% CI: 50%, 54%) and was identical in vegetarians and in nonvegetarians. Comparing vegetarians with meat eaters among the 47,254 participants who had no prevalent cardiovascular disease or malignant cancer at recruitment, the death rate ratios adjusted for age, sex, smoking, and alcohol consumption were 0.81 (95% CI: 0.57, 1.16) for ischemic heart disease and 1.03 (95% CI: 0.90, 1.16) for all causes of death. The mortality of both the vegetarians and the nonvegetarians in this study is low compared with national rates. Within the study, mortality from circulatory diseases and all causes is not significantly different between vegetarians and meat eaters, but the study is not large enough to exclude small or moderate differences for specific causes of death, and more research on this topic is required.
    American Journal of Clinical Nutrition 04/2009; 89(5):1613S-1619S. DOI:10.3945/ajcn.2009.26736L · 6.92 Impact Factor
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    ABSTRACT: Few prospective studies have examined cancer incidence among vegetarians. We report cancer incidence among vegetarians and nonvegetarians in the European Prospective Investigation into Cancer and Nutrition-Oxford (EPIC-Oxford) study. This was a prospective study of 63,550 men and women recruited throughout the United Kingdom in the 1990s. Cancer incidence was followed through nationwide cancer registries. The standardized incidence ratio for all malignant neoplasms for all participants was 72% (95% CI: 69%, 75%). The standardized incidence ratios for colorectal cancer were 84% (95% CI: 73%, 95%) among nonvegetarians and 102% (95% CI: 80%, 129%) among vegetarians. In a comparison of vegetarians with meat eaters and after adjustment for age, sex, and smoking, the incidence rate ratio for all malignant neoplasms was 0.89 (95% CI: 0.80, 1.00). The incidence rate ratio for colorectal cancer in vegetarians compared with meat eaters was 1.39 (95% CI: 1.01, 1.91). The overall cancer incidence rates of both the vegetarians and the nonvegetarians in this study are low compared with national rates. Within the study, the incidence of all cancers combined was lower among vegetarians than among meat eaters, but the incidence of colorectal cancer was higher in vegetarians than in meat eaters.
    American Journal of Clinical Nutrition 04/2009; 89(5):1620S-1626S. DOI:10.3945/ajcn.2009.26736M · 6.92 Impact Factor

Publication Stats

4k Citations
357.93 Total Impact Points

Institutions

  • 2005–2014
    • University of Oxford
      • Cancer Epidemiology Unit
      Oxford, England, United Kingdom
  • 2008–2010
    • German Institute of Human Nutrition
      • Department of Epidemiology
      Potsdam, Brandenburg, Germany
  • 2009
    • Fondazione IRCCS Istituto Nazionale dei Tumori di Milano
      Milano, Lombardy, Italy
  • 2002
    • Catalan Institute of Oncology
      • Cancer Epidemiology Research Programme (PREC)
      Badalona, Catalonia, Spain