A healthy Nordic dietary pattern has shown beneficial effects in relation to several chronic diseases. However, no study has evaluated the association between a healthy Nordic food index (HNFI) and risk of breast cancer.
We conducted a prospective cohort study including 44,296 women, aged 29-49 at baseline in 1991-1992, who completed a food frequency questionnaire at baseline, and have been followed up ever since, through the Swedish Cancer Registry and Cause of Death Registry. Each woman was assigned a HNFI score ranging from 0 to 6. We calculated multivariable relative risks (RRs) and 95% confidence intervals (CIs) using Poisson regression models with attained age as the underlying timescale. The association between the HNFI and risk of breast cancer was assessed both overall, by menopausal status and by hormone receptor status.
A total of 1,464 breast cancer cases were diagnosed during a median follow-up time of 20 years. A higher adherence to the HNFI was not associated with a lower risk of breast cancer overall, nor of varied hormone receptor status, or when we examining premenopausal and postmenopausal women separately. The multivariable RRs (95% CI) for breast cancer per 1-point increment in the HNFI were 1.02 (95% CI 0.98-1.06) for all women, 1.01 (95% CI 0.95-1.08) for premenopausal women, and 1.02 (95% CI 0.97-1.07) for postmenopausal women.
Adherence to a HNFI was not associated with breast cancer incidence in this cohort of relatively young women, regardless of menopausal status or hormone receptor status.
Several healthy dietary patterns have been linked to longevity. Recently, a Nordic dietary pattern was associated with a lower overall mortality. No study has, however, investigated this dietary pattern in relation to cause-specific mortality. The aim of the present study was to examine the association between adherence to a healthy Nordic food index (consisting of wholegrain bread, oatmeal, apples/pears, root vegetables, cabbages and fish/shellfish) and overall mortality, and death by cardiovascular disease, cancer, injuries/suicide and other causes. We conducted a prospective analysis in the Swedish Women's Lifestyle and Health cohort, including 44,961 women, aged 29-49 years, who completed a food frequency questionnaire between 1991-1992, and have been followed up for mortality ever since, through Swedish registries. The median follow-up time is 21.3 years, and mortality rate ratios (MRR) were calculated using Cox Proportional Hazards Models. Compared to women with the lowest index score (0-1 points), those with the highest score (4-6 points) had an 18% lower overall mortality (MRR 0.82; 0.71-0.93, p
We aimed to estimate the effect of alcohol consumption on breast cancer risk and to test whether overweight and obesity modifies this association.
We included in the analysis 45,233 women enrolled in the Swedish Women's Lifestyle and Health study between 1991 and 1992. Participants were followed for occurrence of breast cancer and death until December 2009. Poisson regression models were used, and analyses were done for overall breast cancer and for estrogen receptor positive or negative (ER+, ER-) and progesterone receptor positive and negative (PR+, PR-) tumors separately.
A total of 1,385 breast cancer cases were ascertained during the follow-up period. Overall, we found no statistically significant association between alcohol intake and breast cancer risk after adjustment for confounding, with an estimated relative risk (RR) of 1.01 (95 % CI: 0.98-1.04) for an increment in alcohol consumption of 5 g/day. A statistically significant elevated breast cancer risk associated with higher alcohol consumption was found only among women with BMI =25 (RR 1.03, 95 % CI 1.0-1.05 per 5 g/day increase).
An increase in breast cancer risk with higher alcohol consumption was found for breast cancers in women with a BMI =25 kg/m(2).
Cites: Cancer Epidemiol Biomarkers Prev. 2012 Jul;21(7):1203-1222564867
Alcohol consumption is steadily increasing in high-income countries but the harm and possible net benefits of light-to-moderate drinking remain controversial. We prospectively investigated the association between time-varying alcohol consumption and overall and cause-specific mortality among middle-aged women.
Among 48 249 women at baseline (33 404 at follow-up) in the prospective Swedish Women's Lifestyle and Health cohort, age 30-49 years at baseline, we used repeated information on alcohol consumption and combined this method with multiple imputation in order to maximise the number of participants and deaths included in the analyses. Multivariable Cox regression models were used to calculate HRs for overall and cause-specific mortality.
During >900 000 person/years, a total of 2100 deaths were recorded through Swedish registries. The median alcohol consumption increased from 2.3 g/day in 1991/1992 (baseline) to 4.7 g/day in 2004 (follow-up). Compared with light drinkers (0.1-1.5 g/day), a null association was observed for all categories of alcohol consumption with the exception of never drinkers. The HR comparing never with light drinkers was 1.46 (95% CI 1.22 to 1.74). There was a statistically significant negative trend between increasing alcohol consumption and cardiovascular and ischaemic heart diseases mortality. The results were similar when women with prevalent conditions were excluded.
In conclusion, in a cohort of young women, light alcohol consumption was protective for cardiovascular and ischaemic heart disease mortality but not for cancer and overall mortality.
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BACKGROUND: It is unknown whether the association of alcohol consumption with prostate cancer risk varies between localized and advanced cases, or between sporadic and familial cases.METHODS: We assessed recent alcohol drinking in a population-based case--control study of Swedish men, including 1499 cases and 1130 controls. Drinking status and average volume, frequency, and type of alcohol consumed were evaluated. Unconditional logistic regression was performed to estimate the odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for associations between alcohol consumption and prostate cancer risk.RESULTS: Prostate cancer cases were more likely than controls to be current or former, rather than never, drinkers. However, there was no association between recent total alcohol, beer, wine, and liquor consumption and risk of overall prostate cancer, nor advanced, sporadic, or familial prostate cancer. The OR for risk of overall disease among men who drank more than 135 g of total alcohol per week versus non-drinkers was 1.2 (95% CI: 0.9, 1.5), p(trend)=0.12. There was a marginal positive association between alcohol intake and risk of localized disease.CONCLUSIONS: We detected no association between recent alcohol consumption and risk of advanced, sporadic, or familial prostate cancer, and a borderline positive association with localized disease.
Our purpose was to investigate whether alcohol (ethanol) consumption could have an influence on the metabolism of acrylamide to glycidamide in humans exposed to acrylamide through food. We studied a subsample from a population-based case-control study of prostate cancer in Sweden (CAPS). Questionnaire data for alcohol intake estimates was compared to the ratio of hemoglobin-adduct levels for acrylamide and glycidamide, used as a measure of individual differences in metabolism. Data from 161 non-smoking men were processed with regard to the influence of alcohol on the metabolism of acrylamide to glycidamide. A negative, linear trend of glycidamide-adduct to acrylamide-adduct-level ratios with increasing alcohol intake was observed and the strongest association (p-value for trend=0.02) was obtained in the group of men with the lowest adduct levels (47 pmol/g globin) when alcohol intake was stratified by acrylamide-adduct levels. The observed trend is likely due to a competitive effect between ethanol and acrylamide as both are substrates for cytochrome P450 2E1. Our results, strongly indicating that ethanol influence metabolism of acrylamide to glycidamide, partly explain earlier observations of only low to moderate associations between questionnaire data on dietary acrylamide intake and hemoglobin-adduct levels.
OBJECTIVE: The effect of alcohol intake on risk of NHL is unclear. We therefore conducted a population-based case-control study to examine the association between alcohol and NHL risk. METHODS: 613 NHL cases and 480 population controls in Sweden reported their average consumption of beer, wine, and liquor 2 years before the study. Unconditional logistic regression was used to estimate the odds ratios (OR) and corresponding 95% confidence intervals (CI) for associations between alcohol intake and NHL risk. RESULTS: Intake of total alcohol, beer, wine, or liquor was not associated with risk of overall NHL. There was no difference in risk of NHL among those who habitually consumed above 19.1 g of ethanol per day, compared to those who consumed on average 0-2.2 g of ethanol per day (OR = 1.2 (95% CI: 0.8, 1.7); Ptrend = 0.29). However, the association was significantly positive among males (OR = 1.8 (95% CI: 1.1, 2.9); Ptrend = 0.06). Total alcohol, beer, wine, or liquor intake was not associated with any major histopathologic subtype of NHL examined, apart from an association between high wine consumption and increased risk of chronic lymphocytic leukemia. CONCLUSIONS: Alcohol does not appear to be a major etiologic factor for overall NHL, nor its common subtypes.
Aspirin (ASA) use has been associated with improved breast cancer survival in several prospective studies.
We conducted a nested case-control study of ASA use after a breast cancer diagnosis among women using Swedish National Registries. We assessed prospectively recorded ASA exposure during several different time windows following cancer diagnosis using conditional logistic regression with breast cancer death as the main outcome. Within each six-month period of follow-up, we categorized dispensed ASA doses into three groups: 0, less than 1, and 1 or more daily doses.
We included 27,426 women diagnosed with breast cancer between 2005 and 2009; 1,661 died of breast cancer when followed until Dec 31, 2010. There was no association between ASA use and breast cancer death when exposure was assessed either shortly after diagnosis, or 3-12 months before the end of follow-up. Only during the period 0-6 months before the end of follow-up was ASA use at least daily compared with non-use associated with a decreased risk of breast cancer death: HR (95% CI)?=0.69 (0.56-0.86). However, in the same time-frame, those using ASA less than daily had an increased risk of breast cancer death: HR (95% CI)?=1.43 (1.09-1.87).
Contrary to other studies, we did not find that ASA use was associated with a lower risk of death from breast cancer, except when assessed short term with no delay to death/end of follow-up, which may reflect discontinuation of ASA during terminal illness.
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Although light to moderate alcohol intake may reduce cardiovascular disease (CVD) mortality, the effect on total mortality requires further study, particularly among young and middle-aged women. We studied the association between alcohol consumption and mortality from all causes, from cancer, and from CVD in the Swedish Women's Lifestyle and Health Study, a cohort of 47,921 female residents of Sweden aged 30-49 years at baseline in 1991/1992 and followed up to 2006. We estimated the relative risk (RR) of mortality associated with alcohol intake using Cox regression adjusted for age, smoking, BMI, saturated fat intake, physical activity, and education. During 713,295 person-years of follow-up, 1,119 deaths occurred, including 158 deaths from CVD, 673 deaths from cancer, and 288 deaths from other causes. Compared with non-drinking, light to moderate drinking (0.1-19.9 g of alcohol per day) showed a statistically significant inverse association with total mortality (RR = 0.83, 95% CI = 0.71-0.98). Analyses of cause-specific mortality revealed an RR for CVD mortality of 0.69 (95% CI = 0.46-1.01) and an RR for cancer mortality of 0.92 (95% CI = 0.75-1.15). These results suggest that in younger women, a possibly beneficial effect of light to moderate drinking on future risk of mortality is limited to a prevention of CVD mortality but not cancer mortality.