| 1. |
- Bao, Ying, et al.
(författare)
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Folate Intake and Risk of Pancreatic Cancer : Pooled Analysis of Prospective Cohort Studies
- 2011
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Ingår i: Journal of the National Cancer Institute. - : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 103:24, s. 1840-1850
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Forskningsöversikt (refereegranskat)abstract
- Background Epidemiological studies evaluating the association between folate intake and risk of pancreatic cancer have produced inconsistent results. The statistical power to examine this association has been limited in previous studies partly because of small sample size and limited range of folate intake in some studies. Methods We analyzed primary data from 14 prospective cohort studies that included 319 716 men and 542 948 women to assess the association between folate intake and risk of pancreatic cancer. Folate intake was assessed through a validated food-frequency questionnaire at baseline in each study. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models and then pooled using a random effects model. All statistical tests were two-sided. Results During 7-20 years of follow-up across studies, 2195 pancreatic cancers were identified. No association was observed between folate intake and risk of pancreatic cancer in men and women (highest vs lowest quintile: dietary folate intake, pooled multivariable RR = 1.06, 95% CI = 0.90 to 1.25, P-trend = .47; total folate intake [dietary folate and supplemental folic acid], pooled multivariable RR = 0.96, 95% CI = 0.80 to 1.16, P-trend = .90). No between-study heterogeneity was observed (for dietary folate, P-heterogeneity = .15; for total folate, P-heterogeneity = .22). Conclusion Folate intake was not associated with overall risk of pancreatic cancer in this large pooled analysis.
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| 2. |
- de Gonzalez, Amy Berrington, et al.
(författare)
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Body-Mass Index and Mortality among 1.46 Million White Adults.
- 2010
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Ingår i: New England Journal of Medicine. - : MASSACHUSETTS MEDICAL SOC. - 0028-4793 .- 1533-4406. ; 363:23, s. 2211-2219
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Tidskriftsartikel (refereegranskat)abstract
- Background: A high body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) is associated with increased mortality from cardiovascular disease and certain cancers, but the precise relationship between BMI and all-cause mortality remains uncertain. Methods: We used Cox regression to estimate hazard ratios and 95% confidence intervals for an association between BMI and all-cause mortality, adjusting for age, study, physical activity, alcohol consumption, education, and marital status in pooled data from 19 prospective studies encompassing 1.46 million white adults, 19 to 84 years of age (median, 58). Results: The median baseline BMI was 26.2. During a median follow-up period of 10 years (range, 5 to 28), 160,087 deaths were identified. Among healthy participants who never smoked, there was a J-shaped relationship between BMI and all-cause mortality. With a BMI of 22.5 to 24.9 as the reference category, hazard ratios among women were 1.47 (95 percent confidence interval [CI], 1.33 to 1.62) for a BMI of 15.0 to 18.4; 1.14 (95% CI, 1.07 to 1.22) for a BMI of 18.5 to 19.9; 1.00 (95% CI, 0.96 to 1.04) for a BMI of 20.0 to 22.4; 1.13 (95% CI, 1.09 to 1.17) for a BMI of 25.0 to 29.9; 1.44 (95% CI, 1.38 to 1.50) for a BMI of 30.0 to 34.9; 1.88 (95% CI, 1.77 to 2.00) for a BMI of 35.0 to 39.9; and 2.51 (95% CI, 2.30 to 2.73) for a BMI of 40.0 to 49.9. In general, the hazard ratios for the men were similar. Hazard ratios for a BMI below 20.0 were attenuated with longer-term follow-up. Conclusions: In white adults, overweight and obesity (and possibly underweight) are associated with increased all-cause mortality. All-cause mortality is generally lowest with a BMI of 20.0 to 24.9. N Engl J Med 2010;363:2211-9.
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| 3. |
- Hjern, Fredrik, et al.
(författare)
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Obesity, Physical Inactivity, and Colonic Diverticular Disease Requiring Hospitalization in Women : A Prospective Cohort Study
- 2012
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Ingår i: American Journal of Gastroenterology. - : NATURE PUBLISHING GROUP. - 0002-9270 .- 1572-0241. ; 107:2, s. 296-302
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Lifestyle factors other than dietary fiber intake and risk for colonic diverticular disease have only been examined in few studies. The objective of this study was to investigate the association between obesity and physical inactivity and diverticular disease in a population-based cohort of women. METHODS: This was a prospective population-based cohort study. In all, 36,592 women, born 1914-1948, in the Swedish Mammography Cohort were followed 1997-2009. Body mass index (BMI; kg/m(2)), physical activity, diet, smoking, and other lifestyle factors were collected at baseline through questionnaires. Cases of diverticular disease were identified from the Swedish Patient and Death Registers. Relative risks (RRs) of diverticular disease requiring hospitalization (or being the cause of death) according to BMI and physical activity were estimated using Cox proportional hazards models. The multivariable models were adjusted for age; intake of dietary fiber; diabetes; hypertension; use of acetylsalicylate acid, non-steroid anti-inflammatory drug, or steroid medication; alcohol consumption; smoking; and educational level. RESULTS: During 12 years, 626 cases of incident diverticular disease requiring hospitalization were found. Two women were registered in the National Death Register only. In multivariable analysis, women with BMI 25-29.99 had 29% increased risk (RR=1.29; 95% confidence interval (CI): 1.08, 1.54) and obese women (BMI >= 30) had 33% (1.33; 95% CI: 1.03-1.72) increased risk of diverticular disease compared to women with BMI 20-24.99. Exercise <= 30 min/day increased the risk for disease with 42% (1.42; 95% CI: 1.18-1.69) compared with exercise >30 min/day in multivariable analysis. Ninety-eight subjects were hospitalized due to complications; perforation or abscess. Women with BMI >= 30 had a twofold (RR=2.00; 95% CI: 1.08-3.73; P=0.028) increased risk for complicated disease. CONCLUSIONS: Overweight, obesity, and physical inactivity among women increase diverticular disease requiring hospitalization.
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| 4. |
- Jung, Seungyoun, et al.
(författare)
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Fruit and Vegetable Intake and Risk of Breast Cancer by Hormone Receptor Status
- 2013
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP): Policy B1. - 0027-8874 .- 1460-2105. ; 105:3, s. 219-236
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Tidskriftsartikel (refereegranskat)abstract
- Estrogen receptornegative (ER) breast cancer has few known or modifiable risk factors. Because ER tumors account for only 15% to 20% of breast cancers, large pooled analyses are necessary to evaluate precisely the suspected inverse association between fruit and vegetable intake and risk of ER breast cancer. less thanbrgreater than less thanbrgreater thanAmong 993 466 women followed for 11 to 20 years in 20 cohort studies, we documented 19 869 estrogen receptor positive (ER) and 4821 ER breast cancers. We calculated study-specific multivariable relative risks (RRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression analyses and then combined them using a random-effects model. All statistical tests were two-sided. less thanbrgreater than less thanbrgreater thanTotal fruit and vegetable intake was statistically significantly inversely associated with risk of ER breast cancer but not with risk of breast cancer overall or of ER tumors. The inverse association for ER tumors was observed primarily for vegetable consumption. The pooled relative risks comparing the highest vs lowest quintile of total vegetable consumption were 0.82 (95% CI 0.74 to 0.90) for ER breast cancer and 1.04 (95% CI 0.97 to 1.11) for ER breast cancer (Pcommon-effects by ER status andlt; .001). Total fruit consumption was non-statistically significantly associated with risk of ER breast cancer (pooled multivariable RR comparing the highest vs lowest quintile 0.94, 95% CI 0.85 to 1.04). less thanbrgreater than less thanbrgreater thanWe observed no association between total fruit and vegetable intake and risk of overall breast cancer. However, vegetable consumption was inversely associated with risk of ER breast cancer in our large pooled analyses.
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| 5. |
- Kaluza, Joanna, et al.
(författare)
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Heme iron intake and acute myocardial infarction : A prospective study of men
- 2014
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Ingår i: International Journal of Cardiology. - : ELSEVIER IRELAND LTD. - 0167-5273 .- 1874-1754. ; 172:1, s. 155-160
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Tidskriftsartikel (refereegranskat)abstract
- Background: Epidemiologic studies of heme iron and non-heme iron intake in relation to risk of acute myocardial infarction (AMI) are lacking. Therefore, we examine the associations between heme iron and non-heme iron intake and fatal and nonfatal AMI in men. Moreover, we investigated whether the associations were modified by intake of minerals (calcium, magnesium, and zinc) that decreases iron absorption. Methods: The population-based prospective cohort of Swedish Men (COSM) included 36 882 men, aged 45-79 years, who completed a self-administered questionnaire on diet and had no history of coronary heart disease, stroke, diabetes, or cancer at baseline. Results: During an 11.7 year follow-up, 678 fatal and 2593 nonfatal AMI events were registered. The hazard ratio (HR) of fatal AMI among men in the highest compared with the lowest quintile of heme iron intake was 1.51 (95% CI: 1.07-2.13, P-trend = 0.02). The association was confined to men with a low intake of minerals that can decrease iron absorption. Among men with combined intakes of calcium, magnesium, and zinc below the medians, the HR of fatal AMI was 2.89 (95% CI: 1.43-5.82) for the highest vs. the lowest quintile of heme iron intake. There was no association between heme iron intake and nonfatal AMI, or between non-heme iron intake and fatal or nonfatal AMI. Conclusions: Findings from this prospective study indicate that a high heme iron intake, particularly with simultaneous low intake of minerals that can decrease iron absorption, may increase the risk of fatal AMI. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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| 6. |
- Kitahara, Cari M., et al.
(författare)
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Association between Class III Obesity (BMI of 40-59 kg/m(2)) and Mortality : A Pooled Analysis of 20 Prospective Studies
- 2014
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Ingår i: PLoS Medicine. - : PUBLIC LIBRARY SCIENCE. - 1549-1277 .- 1549-1676. ; 11:7
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Tidskriftsartikel (refereegranskat)abstract
- Background: The prevalence of class III obesity (body mass index [BMI]>= 40 kg/m(2)) has increased dramatically in several countries and currently affects 6% of adults in the US, with uncertain impact on the risks of illness and death. Using data from a large pooled study, we evaluated the risk of death, overall and due to a wide range of causes, and years of life expectancy lost associated with class III obesity. Methods and Findings: In a pooled analysis of 20 prospective studies from the United States, Sweden, and Australia, we estimated sex-and age-adjusted total and cause-specific mortality rates (deaths per 100,000 persons per year) and multivariable-adjusted hazard ratios for adults, aged 19-83 y at baseline, classified as obese class III (BMI 40.0-59.9 kg/m(2)) compared with those classified as normal weight (BMI 18.5-24.9 kg/m(2)). Participants reporting ever smoking cigarettes or a history of chronic disease (heart disease, cancer, stroke, or emphysema) on baseline questionnaires were excluded. Among 9,564 class III obesity participants, mortality rates were 856.0 in men and 663.0 in women during the study period (19762009). Among 304,011 normal-weight participants, rates were 346.7 and 280.5 in men and women, respectively. Deaths from heart disease contributed largely to the excess rates in the class III obesity group (rate differences = 238.9 and 132.8 in men and women, respectively), followed by deaths from cancer (rate differences = 36.7 and 62.3 in men and women, respectively) and diabetes (rate differences = 51.2 and 29.2 in men and women, respectively). Within the class III obesity range, multivariable-adjusted hazard ratios for total deaths and deaths due to heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory disease, and influenza/pneumonia increased with increasing BMI. Compared with normal-weight BMI, a BMI of 40-44.9, 45-49.9, 50-54.9, and 55-59.9 kg/m(2) was associated with an estimated 6.5 (95% CI: 5.7-7.3), 8.9 (95% CI: 7.4-10.4), 9.8 (95% CI: 7.4-12.2), and 13.7 (95% CI: 10.5-16.9) y of life lost. A limitation was that BMI was mainly ascertained by self-report. Conclusions: Class III obesity is associated with substantially elevated rates of total mortality, with most of the excess deaths due to heart disease, cancer, and diabetes, and major reductions in life expectancy compared with normal weight.
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| 7. |
- Levitan, Emily B., et al.
(författare)
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alpha-Linolenic acid, linoleic acid and heart failure in women
- 2012
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Ingår i: British Journal of Nutrition. - : CAMBRIDGE UNIV PRESS. - 0007-1145 .- 1475-2662. ; 108:7, s. 1300-1306
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Tidskriftsartikel (refereegranskat)abstract
- alpha-Linolenic acid (18: 3n-3) intake and linoleic acid (18: 2n-6) intake have been associated with lower rates of CHD, though results have not been consistent. The relationship of these fatty acids with incident heart failure (HF) is not well established. We examined the hypothesis that women with higher intakes of 18: 3n-3 and 18: 2n-6 would have lower rates of HF hospitalisation and mortality. We measured 18 : 3n-3 and 18: 2n-6 intake in 36 234 Swedish Mammography Cohort participants aged 48-83 years using FFQ and followed participants through Swedish inpatient and cause-of-death registers from 1 January 1998 until 31 December 2006. Cox models were used to calculate incidence rate ratios (RR) and 95% CI. Because of multicollinearity, 18: 3n-3 and 18: 2n-6 were examined separately. Over 9 years, 596 women were hospitalised and fifty-five died due to HF. In models accounting for age and other covariates, the RR for HF comparing the top quintile of 18 : 3n-3 (median 1.50 g/d) with the bottom quintile (median 0.88 g/d) was 0.91 (95% CI 0.71, 1.17, P-trend = 0.41). The RR comparing the top quintile of 18: 2n-6 (median 7.8 g/d) with the bottom quintile (median 4.6 g/d) was 1.14 (95% CI 0.88, 1.46, P-trend = 0.36). We did not find evidence for the interaction of 18: 3n-3 and 18: 2n-6 with each other or with long-chain n-3 fatty acids. In conclusion, these data do not support our hypothesis that 18: 3n-3 and 18: 2n-6 are associated with HF. However, these results may not be generalisable to populations with higher intakes of 18: 3n-3.
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| 8. |
- Lin, Yulan, et al.
(författare)
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Dietary Intake of Lignans and Risk of Esophageal and Gastric Adenocarcinoma : A Cohort Study in Sweden
- 2013
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 22:2, s. 308-312
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Tidskriftsartikel (refereegranskat)abstract
- High intake of phytoestrogen lignans has been found to be associated with decreased risk of esophageal adenocarcinoma in our previous population-based case-control study in Sweden. To further evaluate this possible association, we tested the hypothesis of an inverse association between dietary lignan intake and risk of esophageal and gastric adenocarcinoma using a prospective design. In a population-based cohort study in Sweden, 81,670 participants who were cancer-free at baseline were followed up during 1998 to 2009. All participants completed a 96-item food frequency questionnaire (FFQ), which was used to assess dietary exposure to lignans (secoisolariciresinol, matairesinol, lariciresinol, pinoresinol, medioresinol, and syringaresinol). All cases of esophageal, gastroesophageal junctional, and gastric adenocarcinoma were identified through linkage to the Swedish Cancer Register. Cox proportional hazard models were used to estimate HRs and 95% confidence intervals (CI), with adjustment for potential confounding factors. During an average follow-up of 9.9 years, a total of 211 cases were identified, including 83 cases of esophageal or junctional adenocarcinoma, and 128 cases of gastric adenocarcinoma. There was no statistically significant association between dietary intake of lignans and any of the studied adenocarcinomas. Compared with participants in the lowest quartile of lignan intake, the adjusted HR of the highest quartile was 0.96 (95% CI, 0.46-2.00; P-trend = 0.70) for adenocarcinoma of the esophagus or gastroesophageal junction, and 0.89 (95% CI, 0.52-1.55: P-trend = 0.78) for gastric adenocarcinoma. No clear support for a protective role of dietary intake of lignans in the development of esophageal or gastric adenocarcinoma was found. Cancer Epidemiol Biomarkers Prev; 22(2); 308-12. (c) 2012 AACR.
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| 9. |
- Lin, Yulan, et al.
(författare)
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Validation of FFQ-based assessment of dietary lignans compared with serum enterolactone in Swedish women
- 2013
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Ingår i: British Journal of Nutrition. - : CAMBRIDGE UNIV PRESS. - 0007-1145 .- 1475-2662. ; 109:10, s. 1873-1880
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Tidskriftsartikel (refereegranskat)abstract
- The validity of using FFQ to assess dietary lignans is uncertain. We aimed to validate the use of FFQ for the assessment of dietary intake of lignans compared to the serum biomarker enterolactone, the main product of dietary lignans' metabolism in human subjects. A random sample of women, aged 55-75 years, from the Swedish Mammography Cohort was selected. Information from two FFQ, the FFQ-87 (sixty-seven food items) and the FFQ-97 (ninety-three food items), and blood samples were collected. Dietary intake of lignans (secoisolariciresinol, matairesinol, lariciresinol, pinoresinol, medioresinol and syringaresinol) was assessed by the FFQ. Serum concentrations of enterolactone were analysed by time-resolved fluoroimmunoassay. The correlation coefficient between energy-adjusted lignan intake and serum enterolactone was estimated in crude and multivariable-adjusted models, taking into account the factors potentially influencing the serum enterolactone. Among the 135 participants aged 55-75 years, with a mean BMI of 26.7 kg/m(2), the average energy-adjusted intake of total lignans was 1616 (SD 424) and 1516 (SD 409) mu g/d according to the FFQ-87 (forty-five food items containing lignans) and the FFQ-97 (sixty-five food items containing lignans), respectively. The mean concentration of serum enterolactone was 23.2 (SD 15.4) nmol/l. The adjusted Pearson's correlation between dietary intake of lignans assessed by the FFQ-97 and serum enterolactone was statistically significant (r 0.22, P=0.01). No significant correlation was observed for the FFQ-87 (r 0.09, P=0.30). The present study indicates that the FFQ-97 might be better than the FFQ-87 for assessing dietary intake of lignans, although the correlation was low.
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| 10. |
- Tetens, Inge, et al.
(författare)
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Dietary intake and main sources of plant lignans in five European countries
- 2013
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Ingår i: Food & Nutrition Research. - : TAYLOR & FRANCIS LTD. - 1654-6628 .- 1654-661X. ; 57
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Tidskriftsartikel (refereegranskat)abstract
- Background: Dietary intakes of plant lignans have been hypothesized to be inversely associated with the risk of developing cardiovascular disease and cancer. Earlier studies were based on a Finnish lignan database (Fineli (R)) with two lignan precursors, secoisolariciresinol (SECO) and matairesinol (MAT). More recently, a Dutch database, including SECO and MAT and the newly recognized lignan precursors lariciresinol (LARI) and pinoresinol (PINO), was compiled. The objective was to re-estimate and re-evaluate plant lignan intakes and to identify the main sources of plant lignans in five European countries using the Finnish and Dutch lignan databases, respectively. Methods: Forty-two food groups known to contribute to the total lignan intake were selected and attributed a value for SECO and MAT from the Finnish lignan database (Fineli (R)) or for SECO, MAT, LARI, and PINO from the Dutch database. Total intake of lignans was estimated from food consumption data for adult men and women (19-79 years) from Denmark, Finland, Italy, Sweden, United Kingdom, and the contribution of aggregated food groups calculated using the Dutch lignin database. Results: Mean dietary lignan intakes estimated using the Dutch database ranged from 1 to 2 mg/day, which was approximately four-fold higher than the intakes estimated from the Fineli (R) database. When LARI and PINO were included in the estimation of the total lignan intakes, cereals, grain products, vegetables, fruit and berries were the most important dietary sources of lignans. Conclusion: Total lignin intake was approximately four-fold higher in the Dutch lignin database, which includes the lignin precursors LARI and PINO, compared to estimates based on the Finnish database based only on SECO and MAT. The main sources of lignans according to the Dutch database in the five countries studied were cereals and grain products, vegetables, fruit, berries, and beverages.
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