During half of the year, cutaneous synthesis of 25-hydroxyvitamin D (25(OH)D) is not detectable at northern latitudes, leaving the population dependent on other sources for optimal vitamin D status. During April to September, 25(OH)D status may be improved by solar exposure. In this study, we measured seasonal differences in serum 25(OH)D concentrations and identified the major predictors of summer 25(OH)D concentrations.
We assessed serum 25(OH)D concentrations during both winter and summer amongst 100 women, aged 61-83 years, randomly sampled from the Swedish Mammography Cohort. Participants completed two detailed questionnaires covering diet, use of dietary supplements and sun-related behaviour, the first in January through March and a second time in August through September.
The mean seasonal increase in serum 25(OH)D concentrations was 38% from mean 72 +/- 23 nmol L(-1) during winter to 99 +/- 29 nmol L(-1) in summer. High summer 25(OH)D concentrations were associated with higher winter concentrations, preference of staying in sun instead of shade, having a nonsensitive skin type and normal body mass index. Based on multiple linear regression modelling, preferring sun, having nonsensitive skin type and normal weight as compared with preferring shade, having sensitive skin type and being obese, was associated with a 64 nmol L(-1) higher 25(OH)D concentrations during summer.
Women with high winter 25(OH)D serum concentrations, with preference of staying in the sun instead of shade during summer, a skin type allowing for longer sun exposure and a normal weight had the highest summer 25(OH)D concentrations.
OBJECTIVE: To assess the risk of invasive breast cancer associated with total and beverage-specific alcohol consumption and to evaluate whether dietary and nondietary factors modify the association. DATA SOURCES: We included in these analyses 6 prospective studies that had at least 200 incident breast cancer cases, assessed long-term intake of food and nutrients, and used a validated diet assessment instrument. The studies were conducted in Canada, the Netherlands, Sweden, and the United States. Alcohol intake was estimated by food frequency questionnaires in each study. The studies included a total of 322647 women evaluated for up to 11 years, including 4335 participants with a diagnosis of incident invasive breast cancer. DATA EXTRACTION: Pooled analysis of primary data using analyses consistent with each study's original design and the random-effects model for the overall pooled analyses. DATA SYNTHESIS: For alcohol intakes less than 60 g/d (reported by >99% of participants), risk increased linearly with increasing intake; the pooled multivariate relative risk for an increment of 10 g/d of alcohol (about 0.75-1 drink) was 1.09 (95% confidence interval [CI], 1.04-1.13; P for heterogeneity among studies, .71). The multivariate-adjusted relative risk for total alcohol intakes of 30 to less than 60 g/d (about 2-5 drinks) vs nondrinkers was 1.41 (95% CI, 1.18-1.69). Limited data suggested that alcohol intakes of at least 60 g/d were not associated with further increased risk. The specific type of alcoholic beverage did not strongly influence risk estimates. The association between alcohol intake and breast cancer was not modified by other factors. CONCLUSIONS: Alcohol consumption is associated with a linear increase in breast cancer incidence in women over the range of consumption reported by most women. Among women who consume alcohol regularly, reducing alcohol consumption is a potential means to reduce breast cancer risk.
Comment In: JAMA. 1998 Oct 7;280(13):1138-99777807
Alcohol consumption and cigarette smoking are modifiable lifestyle factors with important impact on public health. It is unclear whether these factors influence the risk of aortic valve stenosis (AVS).
To investigate the associations of alcohol consumption and smoking, including smoking intensity and time since cessation, with AVS incidence in two prospective cohorts.
This analysis was based on data from the Swedish Mammography Cohort and the Cohort of Swedish Men, comprising 69 365 adults without cardiovascular disease at baseline. Participants were followed for AVS incidence and death by linkage to the Swedish National Patient and Causes of Death Registers. Hazard ratios (HR) with 95% confidence intervals (CI) were estimated by Cox proportional hazards regression.
Over a mean follow-up of 15.3 years, 1249 cases of AVS (494 in women and 755 in men) were recorded. Compared with never drinkers of alcohol (lifelong abstainers), the risk of AVS was significantly lower in current light drinkers (1-6 drinks per week [1 drink = 12 g alcohol]; multivariable HR 0.82; 95% CI: 0.68-0.99). The risk of AVS increased with increasing smoking intensity. Compared with never smokers, the HR was 1.46 (95% CI: 1.16-1.85) in current smokers of =30 pack-years. Former smokers who had quit smoking 10 or more years previously had similar risk for AVS as never smokers.
This study suggests that current light alcohol consumption is associated with a lower risk of AVS, and indicates that the association between smoking and AVS risk is reversible.
Using a mailed questionnaire, we investigated the risk of renal cell cancer in relation to different types of alcoholic beverages, and to total ethanol in a large population-based case-control study among Swedish adults, including 855 cases and 1204 controls. Compared to non-drinkers, a total ethanol intake of >620 g month(-1) was significantly related to a decreased risk of renal cell cancer (odds ratio (OR) 0.6, 95% confidence interval (CI) 0.4-0.9; P-value for trend=0.03). The risk decreased 30-40% with drinking more than two glasses per week of red wine (OR 0.6, 95% CI 0.4-0.9), white wine (OR 0.7, 95% CI 0.4-1.0), or strong beer (OR 0.6, 95% CI 0.4-1.0); there was a clear linear trend of decreasing risk with increasing consumption of these beverages (P-values for trends
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Research regarding the relationship between alcohol intake and breast cancer risk has suggested an association between the two, although the data are inconsistent regarding dose effects and susceptible populations. To clarify these issues, we investigated the association of breast cancer risk with alcohol intake at various ages in a population-based case-control study nested within a screening cohort in Sweden. Subjects were women 40-75 years old who participated in a screening program in central Sweden. Information about personal characteristics, diet, and alcohol intake was obtained by a questionnaire sent out at the invitation to the screening interview and at a supplementary interview conducted among a sample of women who did and did not develop breast cancer. Alcohol intake did not affect breast cancer risk among women under 50 years old. However, among those over 50 years of age, ever-drinking conferred a relative risk of 1.8 (95% confidence interval = 1.2-2.6). Current and former drinkers had similar increases in risk. No particular latent period of alcohol effect was identified, but drinking later in life to have a bigger effect than did drinking earlier in life.
Alcohol intake has consistently been associated with increased breast cancer incidence in epidemiological studies. However, the relation between alcohol and survival after breast cancer diagnosis is less clear.
We investigated whether alcohol intake was associated with survival among 3146 women diagnosed with invasive breast cancer in the Swedish Mammography Cohort. Alcohol consumption was estimated using a food frequency questionnaire. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs).
From 1987 to 2008 there were 385 breast cancer-specific deaths and 860 total deaths. No significant association was observed between alcohol intake and breast cancer-specific survival. Women who consumed 10 g per day (corresponding to approximately 0.75 to 1 drinks) or more of alcohol had an adjusted HR (95% CI) of breast cancer-specific death of 1.36 (0.82-2.26;p(trend)=0.47) compared with non-drinkers. A significant inverse association was observed between alcohol and non-breast cancer deaths. Those who consumed 3.4-9.9 g per day of alcohol had a 33% lower risk of death compared with non-drinkers (95% CI 0.50-0.90;p(trend)=0.04).
Our findings suggest that alcohol intake up to approximately one small drink per day does not negatively impact breast cancer-specific survival and a half drink per day is associated with a decreased risk of mortality from other causes.
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The incidence of cancer was studied in a population-based cohort of 9,353 individuals (8,340 men and 1,013 women) with a discharge diagnosis of alcoholism in 1965-83, followed up for 19 years (mean 7.7). After exclusion of cancers in the first year of follow-up, 491 cancers were observed cf 343.2 expected through 1984 (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.3-1.6). A similar excess risk of cancer was seen among men (SIR = 1.4, CI = 1.3-1.6) and among women (SIR = 1.5, CI = 1.1-2.0). We observed the established associations with cancers of the oral cavity and pharynx (SIR = 4.1, CI = 2.9-5.7), esophagus (SIR = 6.8, CI = 4.5-9.9), larynx (SIR = 3.3, CI = 1.7-6.0), and lung (SIR = 2.1, CI = 1.7-2.6), although confounding by smoking likely increased these risk estimates. While there was evidence of increased risk for pancreatic cancer (SIR = 1.5, CI = 0.9-2.3), alcoholism did not elevate the incidence of cancer of the stomach (SIR = 0.9, CI = 6-1.4), large bowel (SIR = 1.1, CI = 0.8-1.5), prostate (SIR = 1.0, CI = 0.8-1.3), urinary bladder (SIR = 1.0, CI = 0.6-1.5), or of malignant melanoma (SIR = 0.9, CI = 0.3-1.9). Among women, the number of breast cancers observed was close to expected (SIR = 1.2, CI = 0.6-2.2), although a significant excess number of cervical cancers occurred (SIR = 4.2, CI = 1.5-9.1).(ABSTRACT TRUNCATED AT 250 WORDS)
Antioxidant intake may reduce the risk of allergic disease by protecting against oxidative tissue damage. Major sources of antioxidants in the Western world are fruits, vegetables (vitamin C, ß-carotene, a-tocopherol), meat and milk (selenium, magnesium, zinc). Children may exclude or eat less of some fruits and vegetables due to cross-reactivity between pollen and these foods, complicating assessment of causal relationships.
To investigate the association between dietary antioxidant intake and allergic disease, taking potential reverse causation into account.
Data on 2442 8-year-old children from the Swedish birth cohort study BAMSE were analysed. Children with completed parental questionnaires on exposures and health, including a food-frequency questionnaire and who provided a blood sample were included. Associations between antioxidant intake during the past year and current allergic disease were analysed using logistic regression.
An inverse association was observed between intake of ß-carotene and rhinitis (OR(adj), highest vs. lowest quartile, 0.67, 95% CI 0.49-0.93). Magnesium intake was inversely related to asthma (OR(adj), 0.65, 95% CI 0.42-1.00) and atopic sensitisation (OR(adj), 0.78, 95% CI 0.61-1.00). Following exclusion of children who avoided certain fruits, vegetables or milk due to allergic symptoms (n = 285), the inverse association remained between magnesium intake and asthma (OR(adj), 0.58, 95% CI 0.35-0.98), whereas all other associations became non-significant.
Diet modifications due to allergy may affect the antioxidant intake and needs to be considered when investigating the relationship between diet and allergic disease. Magnesium intake seems to have a protective effect on childhood asthma.
Antioxidant vitamins have attracted considerable attention in previous studies of esophageal squamous-cell carcinoma, but dietary studies of adenocarcinoma of the esophagus and gastric cardia remain sparse. Treating these tumors as distinct diseases, we studied intakes of vitamin C, beta-carotene and alpha-tocopherol in a nationwide population-based case-control study in Sweden, with 185, 165, and 258 cases of esophageal adenocarcinoma, esophageal squamous-cell carcinoma, and gastric cardia adenocarcinoma, respectively, and 815 controls. Subjects with a high parallel intake of vitamin C, beta-carotene, and alpha-tocopherol showed a 40-50% decreased risk of both histological types of esophageal cancer compared with subjects with a low parallel intake. Antioxidant intake was not associated with the risk of gastric cardia adenocarcinoma. Separately, vitamin C and beta-carotene reduced the risk of esophageal cancers more than alpha-tocopherol. We found that antioxidant intake is associated with similar risk reductions for both main histological types of esophageal cancer. Our findings indicate that antioxidants do not explain the diverging incidence rates of the 2 histological types of esophageal cancer. Moreover, our data suggest that inverse associations with esophageal squamous-cell carcinoma and adenocarcinoma may be stronger among subjects under presumed higher oxidative stress due to smoking or gastroesophageal reflux, respectively. Our results may be relevant for the implementation of focused, cost-effective preventive measures.
We assessed the relation between beta-carotene consumption at various times in life and breast cancer risk by conducting a case-control study nested within a population-based cohort of women screened for breast cancer in Sweden. We conducted a telephone interview with 273 incident breast cancer cases and 371 controls about their diet at various ages throughout their lifetime. Controls were frequency matched to cases on age, month and year of mammography, and county of residence. We used unconditional logistic regression to measure the association between beta-carotene intake and breast cancer risk while adjusting for total energy intake, recency of intake, and the matching variables. Women were at lower risk with increasing levels of reported intake of beta-carotene. This pattern of association between breast cancer and beta-carotene intake was similar at various times before screening. These findings indicate that although diets high in beta-carotene may be associated with lower breast cancer risk, there does not seem to be evidence of a critical time period during which such diets are more relevant.