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| 2. |
- Lindblad, Birgitta Ejdervik, 1955-, et al.
(författare)
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Alcohol consumption and risk of cataract extraction : a prospective cohort study of women
- 2007
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Ingår i: Ophthalmology. - Sundsvall Hosp, Dept Ophthalmol, SE-85186 Sundsvall, Sweden. Karolinska Inst, Inst Environm Med, Stockholm, Sweden. HM Queen Sophia Hosp, Stockholm Eye Clin, Stockholm, Sweden. : Elsevier. - 0161-6420 .- 1549-4713. ; 114:4, s. 680-685
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: To investigate the association between alcohol consumption and the risk of cataract extraction.DESIGN: Population-based prospective cohort study.PARTICIPANTS: A total of 34,713 women participating in the Swedish Mammography Cohort, age 49 to 83 years, completed in 1997 a self-administered questionnaire about alcohol, smoking, and other lifestyle factors.METHODS: The women were followed from September 1997 through September 2004. The cohort was matched with registers of cataract extraction from the study area.MAIN OUTCOME MEASURES: Incident surgical extraction of age-related cataract.RESULTS: During 84 months of follow-up, we found 3587 incident cases of age-related cataract extraction. Compared with never drinkers, the relative risk of cataract extraction among current drinkers was 1.11 (95% confidence interval [CI] 1.02-1.21) after adjustment for age and other potential risk factors. In multivariate analysis, an increment of 13 g alcohol intake per day (corresponding to 1 drink = 330 ml of beer, 150 ml of wine, or 45 ml of liquor) was associated with a 7% increased risk of cataract extraction (relative risk, 1.07; 95% CI 1.02-1.12). Mean age at cataract extraction among nonsmoking women who used alcohol was 75 years, compared with 77.6 years among never drinkers.CONCLUSIONS: These prospective data suggest that daily use of >/=1 alcoholic drinks was associated with a modest increase of risk for cataract extraction. The risk increased with increasing alcohol consumption.
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| 3. |
- Akesson, Agneta, et al.
(författare)
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Combined effect of low-risk dietary and lifestyle behaviors in primary prevention of myocardial infarction in women
- 2007
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Ingår i: Archives of Internal Medicine. - Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, S-17177 Stockholm, Sweden. Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA. : AMER MEDICAL ASSOC. - 0003-9926 .- 1538-3679. ; 167:19, s. 2122-2127
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Tidskriftsartikel (refereegranskat)abstract
- Background: Limited data are available on the benefit of combining healthy dietary and lifestyle behaviors in the prevention of myocardial infarction (MI) in women. Methods: We used factor analysis to identify a lowrisk behavior - based dietary pattern in 24 444 postmenopausal women from the population- based prospective Swedish Mammography Cohort who were free of diagnosed cancer, cardiovascular disease, and diabetes mellitus at baseline (September 15, 1997). We also defined 3 low- risk lifestyle factors: nonsmoking, waist- hip ratio less than the 75th percentile (< 0.85), and being physically active (at least 40 minutes of daily walking or bicycling and 1 hour of weekly exercise). Results: During 6.2 years (151 434 person- years) of followup, we ascertained 308 cases of primary MI. Two major identified dietary patterns, "healthy" and "alcohol," were significantly associated with decreased risk of MI. The low- risk diet (high scores for the healthy dietary pattern) characterized by a high intake of vegetables, fruit, whole grains, fish, and legumes, in combination with moderate alcohol consumption (>= 5 g of alcohol per day), along with the 3 low-risk lifestyle behaviors, was associated with 92% decreased risk (95% confidence interval, 72%- 98%) compared with findings in women without any low-risk diet and lifestyle factors. This combination of healthy behaviors, present in 5%, may prevent 77% of MIs in the study population. Conclusion: Most MIs in women may be preventable by consuming a healthy diet and moderate amounts of alcohol, being physically active, not smoking, and maintaining a healthy weight.
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| 4. |
- Burgaz, Ann, et al.
(författare)
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Associations of diet, supplement use, and ultraviolet B radiation exposure with vitamin D status in Swedish women during winter
- 2007
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 86:5, s. 1399-1404
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Vitamin D is produced endogenously after sun exposure but can also be obtained from natural food sources, food fortification, and dietary supplements. OBJECTIVE: We aimed to determine the vitamin D status of women (61-86 y old) living in central Sweden (latitude 60 degrees ) during winter and its relation with vitamin D intake and exposure to ultraviolet B radiation. DESIGN: In a cross-sectional study, we assessed the vitamin D status (serum 25-hydroxyvitamin D [25(OH)D]) of 116 women by using an enzyme immunoassay. The women completed questionnaires covering food habits, use of dietary supplements, and sun-related behavior. RESULTS: In a multiple linear regression model, the main determinants of serum 25(OH)D concentrations (x +/- SD: 69 +/- 23 mmol/L) were dietary vitamin D (6.0 +/- 1.8 mug/d), travel to a sunny location during winter within the previous 6 mo (26%), and the use of dietary supplements (16%). There was no association between serum 25(OH)D status during the winter and age, time spent outdoors, the use of sunscreen, or skin type. Serum 25(OH)D concentrations increased by 25.5 nmol/L with 2-3 servings (130 g/wk) fatty fish/wk, by 6.2 nmol/L with the daily intake of 300 g vitamin D-fortified reduced-fat dairy products, by 11.0 nmol/L with regular use of vitamin D supplements, and by 14.5 nmol/L with a sun vacation during winter. Among nonsupplement users without a wintertime sun vacation, 2-3 servings fatty fish/wk increased serum vitamin D concentrations by 45%. CONCLUSION: Fatty fish, vitamin D-fortified reduced-fat dairy products, regular supplement use, and taking a sun vacation are important predictors for serum concentrations of 25(OH)D during winter at a latitude of 60 degrees .
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| 5. |
- Friberg, Emilie, et al.
(författare)
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Diabetes and risk of endometrial cancer : A population-based prospective cohort study
- 2007
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, SE-17177 Stockholm, Sweden. Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Endocrinol Diabet & Metab,Dept Med, Boston, MA 02215 USA. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 16:2, s. 276-280
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Tidskriftsartikel (refereegranskat)abstract
- Although there is accumulating evidence that hyperinsulinemia in the context of insulin resistance is associated with carcinogenesis, only one prospective study of endometrial cancer incidence, in relation to diabetes, addressed this issue and showed no significant positive association. No previous study has investigated whether physical activity can modify the association between diabetes and endometrial cancer. We examined the association between diabetes and incidence of endometrial cancer and the potential effect modification by obesity and physical activity in the Swedish Mammography Cohort, a prospective cohort of 36,773 women, including 225 incident endometrial adenocarcinoma cases. After adjustments, the relative risk (RR) for endometrial cancer among women with diabetes comparing with nondiabetic women was 1.94 [95% confidence interval (95% CI), 1.23-3.08]. Among obese diabetics, the RR was 6.39 (95% CI, 3.28-12.06) compared with nonobese nondiabetic women. Among diabetics with low physical activity, the RR for endometrial cancer was 2.80 (95% CI, 1.62-4.85) compared with physically active nondiabetic women. Obese diabetics with low physical activity had a RR of 9.61 (95% CI, 4.66-19.83) compared with normal weight nondiabetic women with high physical activity. Diabetes was associated with a 2-fold increased risk, and combination of diabetes with obesity and low physical activity was associated with a further increased risk for endometrial cancer. Interventions to reduce body weight and increase physical activity may have important implications in terms of prevention of endometrial cancer and future management of diabetic subjects.
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| 6. |
- Koushik, Anita, et al.
(författare)
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Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies
- 2007
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Ingår i: Journal of the National Cancer Institute. - Univ Montreal, CHUM, Ctr Rech, Dept Social & Prevent Med, Montreal, PQ H2W 1V1, Canada. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Loma Linda Univ, Ctr Hlth Res, Loma Linda, CA 92350 USA. Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands. Amer Canc Soc, Atlanta, GA 30329 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Univ Buffalo State Univ New York, Dept Social & Prevent Med, Buffalo, NY 14222 USA. Roswell Pk Canc Inst, Dept Canc Prevent & Populat Sci, Buffalo, NY 14263 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA USA. TNO, Dept Food & Chem Risk Anal, Zeist, Netherlands. Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA. Wayne State Univ, Sch Med, Dept Pathol, Karmanos Canc Inst, Detroit, MI 48201 USA. Natl Canc Inst, Nutr Epidemiol Unit, I-20133 Milan, Italy. Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. AZJ, Div Epidemiol, Dept Environm Med, New York, NY USA. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 99:19, s. 1471-1483
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Tidskriftsartikel (refereegranskat)abstract
- Background Fruit and vegetable intakes have been associated with a reduced risk of colon cancer; however, in more recent studies associations have been less consistent. Statistical power to examine associations by colon site has been limited in previous studies. Methods Fruit and vegetable intakes in relation to colon cancer risk were examined in the Pooling Project of Prospective Studies of Diet and Cancer. Relative risks (RRs) and 95% confidence intervals (Cis) were estimated separately in 14 studies using Cox proportional hazards model and then pooled using a randomeffects model. Intakes of total fruits and vegetables, total fruits, and total vegetables were categorized according to quintiles and absolute cutpoints. Analyses were conducted for colon cancer overall and for proximal and distal colon cancer separately. All statistical tests were two-sided. Results Among 756217 men and women followed for up to 6 to 20 years, depending on the study, 5838 were diagnosed with colon cancer. The pooled multivariable RRs (95% Cis) of colon cancer for the highest versus lowest quintiles of intake were 0.91 (0.82 to 1-01 1 P-trend =.19) for total fruits and vegetables, 0.93 (0.85 to 1.02, P-trend =.28) for total fruits, and 0.94 (0.86 to 1.02, P-trend =.17) for total vegetables. Similar results were observed when intakes were categorized by identical absolute cut points across studies (pooled multivariable FIR = 0.90, 95% CI = 0.77 to 1.05 for 800 or more versus <200 g/day of total fruits and vegetables, P-trend =.06). The age-standardized incidence rates of colon cancer for these two intake categories were 54 and 61 per 100000 person-years, respectively. When analyzed by colon site, the pooled multivariable RRs (95% Cis) comparing total fruit and vegetable intakes of 800 or more versus less than 200 g/day were 0.74 (0.57 to 0.95, P-trend =.02) for distal colon cancers and 1.02 (0.82 to 1.27, P-trend =.57) for proximal colon cancers. Similar site-specific associations were observed for total fruits and total vegetables. Conclusion Fruit and vegetable intakes were not strongly associated with colon cancer risk overall but may be associated with a lower risk of distal colon cancer.
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| 7. |
- Larsson, Susanna C., et al.
(författare)
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Alcoholic beverage consumption and gastric cancer risk : A prospective population-based study in women
- 2007
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Ingår i: International Journal of Cancer. - Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. : WILEY. - 0020-7136 .- 1097-0215. ; 120:2, s. 373-377
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Tidskriftsartikel (refereegranskat)abstract
- The association between alcohol consumption and risk of gastric cancer remains controversial. Moreover, prospective data on the role of alcoholic beverage type are sparse. We prospectively investigated the association between total alcohol (ethanol) intake as well as specific alcoholic beverages and risk of gastric cancer in the Swedish Mammography Cohort, a population-based cohort of 61,433 women. Alcohol intake and other dietary exposures were assessed at baseline (1987-1990) and again in 1997 using a food-frequency questionnaire. Incident gastric cancer cases were ascertained through the Swedish Cancer Register. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During 966,807 person-years of follow-up, through June 2005, 160 incident cases of gastric cancer occurred. Total alcohol intake was not significantly associated with risk of gastric cancer. Compared with nondrinkers, the multivariate HR of gastric cancer for women with an alcohol intake of 40 g or more per week was 1.33 (95% CI, 0.79-2.25). Consumption of medium-strong/strong beer was associated with a statistically significant increased risk of gastric cancer; the multivariate HR for women who consumed more than one serving of medium-strong/strong beer per week (median, 2.5 drinks/week) was 2.09 (95% CI, 1.11-3.93; p-trend = 0.02) compared with no consumption. Consumption of light beer, wine, and hard liquor was not significantly associated with gastric cancer risk. Our findings suggest that constituents of beer other than alcohol may be associated with an increased risk of gastric cancer. (c) 2006 Wiley-Liss, Inc.
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| 8. |
- Larsson, Susanna C., et al.
(författare)
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Body mass index and pancreatic cancer risk : A meta-analysis of prospective studies
- 2007
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Ingår i: International Journal of Cancer. - Karolinska Inst, Natl Inst Environm Med, Div Nutrit Epidemiol, S-17177 Stockholm, Sweden. : WILEY. - 0020-7136 .- 1097-0215. ; 120:9, s. 1993-1998
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Tidskriftsartikel (refereegranskat)abstract
- A number of studies have examined the association between body mass index (BMI) and risk of pancreatic cancer, but uncertainty about the relationship remains. We performed a meta-analysis to summarize the evidence from prospective studies investigating this association. We searched MEDLINE for studies published in any language from 1966 to November 2006. Prospective studies were included if they reported relative risks (RRs) with 95% confidence intervals (CIs) for the association between BMI and pancreatic cancer incidence or mortality. Study-specific RR estimates were combined by use of a random-effects model. A total of 21 independent prospective studies, involving 3,495,981 individuals and 8,062 pancreatic cancer cases, met the inclusion criteria. The estimated summary RR of pancreatic cancer per 5 kg/m(2) increase in BMT was 1.12 (95% CI, 1.06-1.17; p-heterogeneity = 0.13) in men and women combined, 1.16 (95% CI, 1.05-1.28; p-heterogeneity = 0.001) in men, and 1.10 (95% CI, 1.02-1.19; p-heterogeneity = 0.12) in women. There was no evidence of publication bias (p = 0.58). Findings from this meta-analysis of prospective studies support a positive association between BMI and risk of pancreatic cancer in men and women. (c) 2007 Wilely-Liss, Inc.
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| 9. |
- Larsson, Susanna C., et al.
(författare)
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Carbohydrate intake, glycemic index and glycemic load in relation to risk of endometrial cancer : A prospective study of Swedish women
- 2007
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Ingår i: International Journal of Cancer. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. : WILEY. - 0020-7136 .- 1097-0215. ; 120:5, s. 1103-1107
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Tidskriftsartikel (refereegranskat)abstract
- The associations of carbohydrate intake, glycemic index and glycemic load with endometrial cancer risk were examined among 61,226 participants of the Swedish Mammography Cohort who were cancer-free at enrollment between 1987 and 1990 and completed a food frequency questionnaire. During a mean follow-up of 15.6 years, through June 2005, 608 incident cases of endometrial adenocarcinoma were diagnosed. We observed no overall association between carbohydrate intake, glycemic index or glycemic load and incidence of endometrial cancer; the rate ratios (RRs) for the highest versus the lowest quintile were 1.12 (95% CI, 0.85-1.47) for carbohydrate intake, 1.00 (95% CI, 0.77-1.30) for glycemic index and 1.15 (95% CI, 0.88-1.51) for glycemic load. However, among obese women (body mass index, BMI >= 30 kg/m(2)), endometrial cancer incidence was nonsignificantly elevated in the top versus bottom quintiles of carbohydrate intake (RR, 1.68; 95% CI, 0.86-3.29) and glycemic load (RR, 1.57; 95% CI, 0.82-2.99). In a subanalysis of women who completed a follow-up questionnaire in 1997, which collected information on physical activity, carbohydrate intake and glycemic load were positively related to endometrial cancer risk among overweight women (BMI >= 25 kg/m(2)) with low physical activity. In this subgroup, the multivariate RRs comparing extreme quartiles were 1.90 (95% CI, 0.84-4.31) for carbohydrate intake and 2.99 (95% CI, 1.17-7.67) for glycemic load. Results from this cohort study suggest that a high carbohydrate intake and a high glycemic load may increase the risk of endometrial cancer among overweight women with low physical activity. (c) 2006 Wiley-Liss, Inc.
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| 10. |
- Larsson, Susanna C., et al.
(författare)
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Dietary carbohydrate, glycemic index, and glycemic load in relation to risk of colorectal cancer in women
- 2007
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Ingår i: American Journal of Epidemiology. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. : OXFORD UNIV PRESS INC. - 0002-9262 .- 1476-6256. ; 165:3, s. 256-261
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Tidskriftsartikel (refereegranskat)abstract
- Diets with a high glycemic index and glycemic load have been hypothesized to be implicated in the etiology of colorectal cancer owing to their potential to increase postprandial glucose and insulin levels. Prospective data on glycemic index and glycemic load in relation to colorectal cancer risk are limited and inconsistent. Therefore, the authors prospectively investigated the associations of dietary carbohydrate, glycemic index, and glycemic load with the incidence of colorectal cancer among 61,433 Swedish women who were free of cancer in 1987-1990 and completed a 67-item food frequency questionnaire. During follow-up through June 2005, 870 incident cases of colorectal adenocarcinoma were diagnosed. Carbohydrate intake, glycemic index, and glycemic load were not associated with risk of colorectal cancer, colon cancer, or rectal cancer. The multivariate hazard ratios for colorectal cancer comparing the highest with the lowest quintile were 1.10 (95% confidence interval: 0.85, 1.44) for carbohydrate intake, 1.00 ( 95% confidence interval: 0.75, 1.33) for glycemic index, and 1.06 ( 95% confidence interval: 0.81, 1.39) for glycemic load. Results did not vary by body mass index. The findings from this prospective study do not support the hypothesis that a high carbohydrate intake, a high glycemic index, and a high glycemic load increase the risk of colorectal cancer.
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