| 1. |
- Gaudet, Mia M., et al.
(författare)
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Anthropometry and head and neck cancer : a pooled analysis of cohort data
- 2015
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Ingår i: International Journal of Epidemiology. - : OXFORD UNIV PRESS. - 0300-5771 .- 1464-3685. ; 44:2, s. 673-681
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Tidskriftsartikel (refereegranskat)abstract
- Background: Associations between anthropometry and head and neck cancer (HNC) risk are inconsistent. We aimed to evaluate these associations while minimizing biases found in previous studies. Methods: We pooled data from 1 941 300 participants, including 3760 cases, in 20 cohort studies and used multivariable-adjusted Cox proportional hazard regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association of anthropometric measures with HNC risk overall and stratified by smoking status. Results: Greater waist circumference (per 5cm: HR = 1.04, 95% CI 1.03-1.05, P-value for trend = <0.0001) and waist-to-hip ratio (per 0.1 unit: HR = 1.07, 95% CI 1.05-1.09, P-value for trend = <0.0001), adjusted for body mass index (BMI), were associated with higher risk and did not vary by smoking status (P-value for heterogeneity = 0.85 and 0.44, respectively). Associations with BMI (P-value for interaction = <0.0001) varied by smoking status. Larger BMI was associated with higher HNC risk in never smokers (per 5 kg/m(2): HR = 1.15, 95% CI 1.06-1.24, P-value for trend = 0.0006), but not in former smokers (per 5 kg/m(2): HR = 0.99, 95% CI 0.93-1.06, P-value for trend = 0.79) or current smokers (per 5 kg/m(2): HR = 0.76, 95% CI 0.71-0.82, P-value for trend = <0.0001). Larger hip circumference was not associated with a higher HNC risk. Greater height (per 5cm) was associated with higher risk of HNC in never and former smokers, but not in current smokers. Conclusions: Waist circumference and waist-to-hip ratio were associated positively with HNC risk regardless of smoking status, whereas a positive association with BMI was only found in never smokers.
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| 2. |
- Gaudet, Mia M, et al.
(författare)
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Pooled analysis of active cigarette smoking and invasive breast cancer risk in 14 cohort studies.
- 2017
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 46:3, s. 881-893
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Tidskriftsartikel (refereegranskat)abstract
- Background: The 2014 US Surgeon General's report noted research gaps necessary to determine a causal relationship between active cigarette smoking and invasive breast cancer risk, including the role of alcohol consumption, timing of exposure, modification by menopausal status and heterogeneity by oestrogen receptor (ER) status.Methods: To address these issues, we pooled data from 14 cohort studies contributing 934 681 participants (36 060 invasive breast cancer cases). Cox proportional hazard regression models were used to calculate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).Results: Smoking duration before first birth was positively associated with risk ( P -value for trend = 2 × 10 -7 ) with the highest HR for initiation >10 years before first birth (HR = 1.18, CI 1.12-1.24). Effect modification by current alcohol consumption was evident for the association with smoking duration before first birth ( P -value=2×10 -4 ); compared with never-smoking non-drinkers, initiation >10 years before first birth was associated with risk in every category of alcohol intake, including non-drinkers (HR = 1.15, CI 1.04-1.28) and those who consumed at least three drinks per day (1.85, 1.55-2.21). Associations with smoking before first birth were limited to risk of ER+ breast cancer ( P -value for homogeneity=3×10 -3 ). Other smoking timing and duration characteristics were associated with risk even after controlling for alcohol, but were not associated with risk in non-drinkers. Effect modification by menopause was not evident.Conclusions: Smoking, particularly if initiated before first birth, was modestly associated with ER+ breast cancer risk that was not confounded by amount of adult alcohol intake. Possible links with breast cancer provide additional motivation for young women to not initiate smoking.
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| 3. |
- Holmberg, Lars, et al.
(författare)
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A search for recall bias in a case-control study of diet and breast cancer
- 1996
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Ingår i: International Journal of Epidemiology. - 0300-5771 .- 1464-3685. ; 25:2, s. 235-244
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND. In retrospective studies of dietary habits and breast cancer risk, recall bias is a concern since diet has been publicized as a cause of breast cancer. METHODS. In a case-control study of diet and breast cancer risk nested within a cohort of women screened with mammography, we contrasted answers to a retrospective dietary interview with answers to a dietary questionnaire which was filled out before any diagnostic procedures for breast cancer were undertaken. The source population was all women aged 40-74 in two counties in Sweden invited to mammographic screening and asked to fill out a questionnaire before the screening. Cases and controls were subsequently defined -- matched on age, county of residence, and time of mammography -- and approached for an interview. RESULTS. In all, 265 cases and 431 controls participated in the study. Means of frequencies differed between the agreement in the questionnaire's and the interview's classifications of study subjects into quartiles of monthly intake varied between 31 percent and 57 percent. Kappa statistics in all food groups were below 0.41. In a regression analysis, case subjects with low responses on the questionnaire about intake of meat, snacks, and coffee and tea gave higher responses on interview than did controls who had low questionnaire responses for these food groups. The reverse was also true: cases' responses that were high on the questionnaire were lower on interview for these food groups than were controls' responses. CONCLUSIONS. We found few signs of recall bias, and the few indications of a differential misclassification that we found were not in food groups that have been publicly discussed as causes of breast cancer.
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| 4. |
- Jung, Seungyoun, et al.
(författare)
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Alcohol consumption and breast cancer risk by estrogen receptor status : in a pooled analysis of 20 studies.
- 2016
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 45:3, s. 916-928
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Breast cancer aetiology may differ by estrogen receptor (ER) status. Associations of alcohol and folate intakes with risk of breast cancer defined by ER status were examined in pooled analyses of the primary data from 20 cohorts.METHODS: During a maximum of 6-18 years of follow-up of 1 089 273 women, 21 624 ER+ and 5113 ER- breast cancers were identified. Study-specific multivariable relative risks (RRs) were calculated using Cox proportional hazards regression models and then combined using a random-effects model.RESULTS: Alcohol consumption was positively associated with risk of ER+ and ER- breast cancer. The pooled multivariable RRs (95% confidence intervals) comparing ≥ 30 g/d with 0 g/day of alcohol consumption were 1.35 (1.23-1.48) for ER+ and 1.28 (1.10-1.49) for ER- breast cancer (Ptrend ≤ 0.001; Pcommon-effects by ER status: 0.57). Associations were similar for alcohol intake from beer, wine and liquor. The associations with alcohol intake did not vary significantly by total (from foods and supplements) folate intake (Pinteraction ≥ 0.26). Dietary (from foods only) and total folate intakes were not associated with risk of overall, ER+ and ER- breast cancer; pooled multivariable RRs ranged from 0.98 to 1.02 comparing extreme quintiles. Following-up US studies through only the period before mandatory folic acid fortification did not change the results. The alcohol and folate associations did not vary by tumour subtypes defined by progesterone receptor status.CONCLUSIONS: Alcohol consumption was positively associated with risk of both ER+ and ER- breast cancer, even among women with high folate intake. Folate intake was not associated with breast cancer risk.
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| 5. |
- Kaluza, Joanna, et al.
(författare)
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Long-term consumption of fruits and vegetables and risk of chronic obstructive pulmonary disease : a prospective cohort study of women
- 2018
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 47:6, s. 1897-1909
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Tidskriftsartikel (refereegranskat)abstract
- Background: Fruits and vegetables, due to high antioxidant capacity, may protect the lung from oxidative damage caused by tobacco smoke and potentially prevent chronic obstructive pulmonary disease (COPD). Only one study based on baseline diet has examined fruit and vegetable consumption in relation to risk of COPD, and no previous studies have examined long-term diet.Methods: We investigated whether long-term fruit and vegetable consumption was associated with COPD incidence among 34 739 women (age 48-83 years) in the population-based prospective Swedish Mammography Cohort. Fruit and vegetable consumption was assessed twice (1987, 1997) with a self-administered questionnaire. Cases of COPD were identified by linkage to the Swedish health register. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs).Results: During follow-up from 2002 to 2014, 1512 women were diagnosed with COPD. Long-term fruit was associated with lower risk of COPD; women in the highest vs lowest quintile of consumption (≥2.5 vs <0.8 servings/day) had a 37% lower risk of COPD (95% CI: 25-48%; P-trend < 0.0001). No association was observed with long-term vegetable intake. Current and ex-smokers with low long-term consumption of fruits (<1 serving/day) in comparison to never smokers with high consumption (≥3 servings/day) had a 38-fold (HR: 38.1; 95% CI: 20.2-71.7) and 13-fold (HR: 12.5, 95% CI: 6.5-24.1) higher risk of COPD, respectively. However, no significant interaction between smoking status and fruit intake in relation to COPD incidence was observed (P-interaction = 0.95).Conclusions: In this prospective cohort of middle-age and older women, long-term consumption of fruits but not vegetables was inversely associated with COPD incidence.
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| 6. |
- Kitahara, Cari M., et al.
(författare)
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Association between adult height, genetic susceptibility and risk of glioma
- 2012
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Ingår i: International Journal of Epidemiology. - : OXFORD UNIV PRESS. - 0300-5771 .- 1464-3685. ; 41:4, s. 1075-1085
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Tidskriftsartikel (refereegranskat)abstract
- Background Some, but not all, observational studies have suggested that taller stature is associated with a significant increased risk of glioma. In a pooled analysis of observational studies, we investigated the strength and consistency of this association, overall and for major sub- types, and investigated effect modification by genetic susceptibility to the disease. Methods We standardized and combined individual-level data on 1354 cases and 4734 control subjects from 13 prospective and 2 case-control studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for glioma and glioma sub-types were estimated using logistic regression models stratified by sex and adjusted for birth cohort and study. Pooled ORs were additionally estimated after stratifying the models according to seven recently identified glioma-related genetic variants. Results Among men, we found a positive association between height and glioma risk (epsilon 190 vs 170-174 cm, pooled OR = 1.70, 95% CI: 1.11-2.61; P-trend = 0.01), which was slightly stronger after restricting to cases with glioblastoma (pooled OR = 1.99, 95% CI: 1.17-3.38; P-trend = 0.02). Among women, these associations were less clear (epsilon 175 vs 160-164 cm, pooled OR for glioma = 1.06, 95% CI: 0.70-1.62; P-trend = 0.22; pooled OR for glioblastoma = 1.36, 95% CI: 0.77-2.39; P-trend = 0.04). In general, we did not observe evidence of effect modification by glioma-related genotypes on the association between height and glioma risk. Conclusion An association of taller adult stature with glioma, particularly for men and stronger for glioblastoma, should be investigated further to clarify the role of environmental and genetic determinants of height in the etiology of this disease.
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| 7. |
- Larsson, Susanna C., et al.
(författare)
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Urinary cadmium and mortality from all causes, cancer and cardiovascular disease in the general population : systematic review and meta-analysis of cohort studies
- 2016
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 45:3, s. 782-791
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Cadmium is a toxic heavy metal distributed in the environment. We conducted a systematic review and meta-analysis to examine the association between urinary cadmium concentration and mortality from all causes, cancer and cardiovascular disease (CVD) in the general population.METHODS: Studies were identified by searching PubMed and Embase (to 30 March 2015) and the reference lists of retrieved articles. We included prospective studies that reported hazard ratios (HR) with 95% confidence intervals (CI) for the association between urinary cadmium concentration and all-cause, cancer or CVD mortality. A random-effects model was used to combine study-specific results.RESULTS: Nine cohort studies, including 5600 deaths from all causes, 1332 deaths from cancer and 1715 deaths from CVD, were eligible for inclusion in the meta-analysis. The overall HRs for the highest vs lowest category of urinary cadmium were1.44 (95% CI, 1.25-1.64; I(2 )= 40.5%) for all-cause mortality (six studies), 1.39 (95% CI, 0.96-1.99; I(2 )= 75.9%) for cancer mortality (four studies) and 1.57 (95% CI, 1.27-1.95; I(2 )= 34.0%) for CVD mortality (five studies). In an analysis restricted to six cohort studies conducted in populations with a mean urinary cadmium concentration of ≤1 µg/g creatinine, the HRs were 1.38 (95% CI, 1.17-1.63; I(2 )= 48.3%) for all-cause mortality, 1.56 (95% CI, 0.98-2.47; I(2 )= 81.0%) for cancer mortality and 1.50 (95% CI, 1.18-1.91; I(2 )= 38.2%) for CVD mortality.CONCLUSIONS: Even at low-level exposure, cadmium appears to be associated with increased mortality. Further large prospective studies of cadmium exposure and mortality are warranted.
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| 8. |
- Michaëlsson, Karl, et al.
(författare)
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Diet and Hip Fracture Risk - A Case-control Study : Study Group of the Multiple Risk Survey on Swedish Women for Eating Assessment
- 1995
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Ingår i: International Journal of Epidemiology. - 0300-5771 .- 1464-3685. ; 24:4, s. 771-782
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- BACKGROUND. The role of diet as a risk factor for osteoporotic fractures is unclear. Earlier studies have yielded conflicting results. METHODS. In two counties in central Sweden we investigated the association between dietary intake and the risk of proximal femoral fractures in a case-control study nested in a cohort. Women born in 1914-1948 were asked to fill out a food frequency questionnaire when invited to attend for mammographic screening between the years 1987 and 1990. More than 65,000 women completed the questionnaire. Those who had participated in the enquiry and subsequently sustained a first hip fracture were defined as cases. For every case, four individually matched controls, by age and county of residence, were selected from the cohort. A second questionnaire concerning confounding factors was mailed to controls and cases. In all, 247 cases and 893 controls could finally be included. Monthly intake of foods and daily intake of nutrients were calculated. RESULTS. When highest quartile of intake was compared to lowest, intakes of iron (adjusted odds ratio [OR] of 3.3, 95% confidence interval [CI]: 1.6-6.9), magnesium (adjusted OR = 2.7, 95% CI: 1.3-6.0) and vitamin C (adjusted OR = 1.9, 95% CI: 1.2-3.1) were found to be independent risk factors for hip fracture. High calcium intake did not protect against hip fracture. Smoking, low physical activity in leisure time, low body mass index, earlier fracture of the distal forearm and diabetes were all risk factors while postmenopausal hormone replacement therapy protected against hip fracture. DISCUSSION. This large study indicates new dietary risk factors for hip fracture. The association between high dietary intake of iron, magnesium and vitamin C and risk of hip fracture has not been reported previously. Further clinical and experimental studies are needed to confirm these findings and to investigate their mechanism of action.
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| 9. |
- Michaëlsson, Karl, 1959-, et al.
(författare)
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Effect of prefracture versus postfracture dietary assessment on hip fracture risk estimates
- 1996
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 25:2, s. 403-10
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND. Dietary factors are presumed to have influence on bone mass and hence fracture susceptibility. Most information in this respect is based on retrospective assessment of previous dietary habits. In a population-based case-control study nested within a cohort, we collected dietary information both before and after a first hip fracture. Thus it was possible to study reported changes in dietary habits, intentional as well as unintentional, among hip fracture patients after a first hip fracture and to compare postfracture with prefracture dietary information. METHODS. More than 65 000 women born 1914-1948 in two counties in central Sweden completed a food frequency questionnaire regarding their usual current dietary habits, before attending a mammographic screening between the years 1987 and 1990. Subsequently 123 of them sustained a first hip fracture and were defined as cases in the present study. For every case, one control, individually matched by age and county of residence, was selected from the cohort. A second identical food frequency questionnaire was mailed to both cases and controls on average 2 years after the hip fracture event. In total 98 case/control pairs could be included in the analysis. The association between diet and hip fracture was evaluated and the results from the two dietary assessments were contrasted. Women who themselves claimed that they had not changed their diet in recent years were analysed separately. RESULTS. The hip fracture cases, compared with the controls, had reduced their reported dietary intake of dairy products after the fracture. Apparently this was not intentional since this effect was more pronounced among those cases who claimed that their diet was unchanged. The changes were most apparent among the younger cases with a more recent hip fracture and with a body mass index above the median. Half of the cases, more than twice the frequency in controls, who were initially classified as having high intake of dairy products were classified as having low intake (<800 mg calcium/day) after the hip fracture. This also lowered, in fact reversed, the relative risk estimates of hip fracture both for intake of dairy products and calcium. Crude odds ratios of highest quartile of intake versus lowest, changed from 3.0 to 0.6 for dairy products and from 2.6 to 0.9 for calcium. No other foods or nutrients displayed such notable differences between the two surveys. CONCLUSION. We conclude that the use of current and retrospective dietary information after a hip fracture can lead to a differential misclassification in dietary studies and to biased estimates of hip fracture risk as compared with prospectively collected dietary information.
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| 10. |
- Mitchell, Adam, 1991-, et al.
(författare)
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Is the Effect of Mediterranean Diet on Hip Fracture Mediated Through Type 2 Diabetes and Body Mass Index?
- 2021
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Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 50:1, s. 234-244
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Tidskriftsartikel (refereegranskat)abstract
- Background: We examined whether the inverse association between adherence to a Mediterranean diet and hip fracture risk is mediated by incident type 2 diabetes mellitus (T2DM) and body mass index (BMI).Methods: We included 50,755 men and women from the Cohort of Swedish Men and Swedish Mammography Cohort who answered lifestyle and medical questionnaires in 1997 and 2008 (used for calculation of the Mediterranean diet score [mMED; low, medium, high] and BMI in 1997, and incident T2DM in 1997-2008). The cumulative incidence of hip fracture from the National Patient Register (2009-2014) was considered as outcome.Results: We present conditional odds ratios (OR) [95% confidence interval, CI] of hip fracture for medium and high adherence to mMED, compared to low adherence. The total effect ORs were 0.82 [0.71, 0.95] and 0.75 [0.62, 0.91], respectively. The controlled direct effect of mMED on hip fracture (not mediated by T2DM, considering BMI as an exposure-induced confounder), calculated using inverse-probability weighting of marginal structural models, rendered ORs of 0.82 [0.72, 0.95] and 0.73 [0.60, 0.88], respectively. The natural direct effect ORs (not mediated by BMI or T2DM, calculated using flexible mediation analysis) were 0.82 [0.71, 0.95] and 0.74 [0.61, 0.89], respectively. The path-specific indirect and partial indirect natural effects ORs (through BMI or T2DM) were close to 1.Conclusions: Mediterranean diet has a direct effect on hip fracture risk via pathways other than through T2DM and BMI. We cannot exclude mediating effects of T2DM or BMI, or that their effects cancel each other out.
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