Circulating zearalenone and its metabolites differ in women due to body mass index and food intake.

The environmental estrogen, zearalenone (ZEA), is found in the food supply from Fusarium fungal contamination in grains and sometimes used as a growth promoter for beef cattle. Long-term exposure to ZEA and its metabolites may present health risk due to higher estrogenic activity. Serum ZEA metabolites were measured to determine the exposure and the association with food intake in 48 overweight/obese women (52 ±â€¯9 years). The free and conjugated ZEA indicated the highest detection rate of all the metabolites. Conjugated ZEA and total ZEA metabolites were lower (p = 0.02) in overweight/obese than normal weight women, and free metabolites were either the same or showed a trend to be higher. In addition, those with highest (280-480 g/d) compared those with lowest (<115 g/d) meat consumption had higher conjugated serum ZEA metabolite concentrations (p < 0.05). Intakes of other food groups (i.e., dairy, cereal, etc.) were not associated with ZEA metabolites. These findings indicate that ZEA and its metabolites are detectable in nearly all women and concentrations are associated with greater meat intake, and influenced by body mass index. Determining how the food supply influences human concentrations of ZEA metabolites is warranted, as well as determining vulnerable populations.

Obesity and survival among women with ovarian cancer: results from the Ovarian Cancer Association Consortium.

BACKGROUND: Observational studies have reported a modest association between obesity and risk of ovarian cancer; however, whether it is also associated with survival and whether this association varies for the different histologic subtypes are not clear. We undertook an international collaborative analysis to assess the association between body mass index (BMI), assessed shortly before diagnosis, progression-free survival (PFS), ovarian cancer-specific survival and overall survival (OS) among women with invasive ovarian cancer. METHODS: We used original data from 21 studies, which included 12 390 women with ovarian carcinoma. We combined study-specific adjusted hazard ratios (HRs) using random-effects models to estimate pooled HRs (pHR). We further explored associations by histologic subtype. RESULTS: Overall, 6715 (54%) deaths occurred during follow-up. A significant OS disadvantage was observed for women who were obese (BMI: 30-34.9, pHR: 1.10 (95% confidence intervals (CIs): 0.99-1.23); BMI: ⩾35, pHR: 1.12 (95% CI: 1.01-1.25)). Results were similar for PFS and ovarian cancer-specific survival. In analyses stratified by histologic subtype, associations were strongest for women with low-grade serous (pHR: 1.12 per 5 kg m(-2)) and endometrioid subtypes (pHR: 1.08 per 5 kg m(-2)), and more modest for the high-grade serous (pHR: 1.04 per 5 kg m(-2)) subtype, but only the association with high-grade serous cancers was significant. CONCLUSIONS: Higher BMI is associated with adverse survival among the majority of women with ovarian cancer.

Anthropometric factors and endometrial cancer risk: a systematic review and dose-response meta-analysis of prospective studies.

BACKGROUND: Greater body mass index (BMI) has been convincingly related to increased endometrial cancer risk, however, whether adiposity earlier in life or abdominal fatness is an independent risk factor and whether weight gain or greater height increases the risk is not clear. METHODS: As part of the Continuous Update Project of the World Cancer Research Fund International, we conducted a systematic review and meta-analysis of prospective studies of the association between anthropometric measures and endometrial cancer risk and searched PubMed and several other databases up to February 2015. Summary relative risks (RRs) were calculated using a random-effects model. RESULTS: Thirty prospective studies of BMI and endometrial cancer risk with 22 320 cases among 6 445 402 participants were included. The summary RR for a 5-unit increment was 1.54 [95% confidence interval (CI) 1.47-1.61, I(2) = 81%]. Although the test for non-linearity was significant, Pnon-linearity < 0.0001, and the curve was steeper within the overweight and obese BMI ranges, there was evidence of increased risk even within the high normal BMI range. The summary RR was 1.45 (95% CI 1.28-1.64, I(2) = 76%) per 5 BMI units for BMI in young adulthood, 1.18 (95% CI 1.14-1.23, I(2) = 67%) per 5 kg increase of weight, and 1.16 (95% CI 1.12-1.20, I(2) = 51%) per 5 kg of weight gained between young adulthood and study baseline, 1.27 (95% CI 1.17-1.39, I(2) = 71%) per 10 cm increase in waist circumference, 1.21 (95% CI 1.13-1.29, I(2) = 0%) per 0.1-unit increment in waist-to-hip ratio and 1.30 (95% CI 1.19-1.41, I(2) = 0%) per 10-cm increase in hips circumference. The summary RR was 1.15 (95% CI 1.09-1.22, I(2) = 61%) for a 10-cm increase in height. CONCLUSIONS: All measures of adiposity were associated with increased risk of endometrial cancer, and in addition increasing height was associated with increased risk.

Body mass index and survival in women with breast cancer-systematic literature review and meta-analysis of 82 follow-up studies.

BACKGROUND: Positive association between obesity and survival after breast cancer was demonstrated in previous meta-analyses of published data, but only the results for the comparison of obese versus non-obese was summarised. METHODS: We systematically searched in MEDLINE and EMBASE for follow-up studies of breast cancer survivors with body mass index (BMI) before and after diagnosis, and total and cause-specific mortality until June 2013, as part of the World Cancer Research Fund Continuous Update Project. Random-effects meta-analyses were conducted to explore the magnitude and the shape of the associations. RESULTS: Eighty-two studies, including 213 075 breast cancer survivors with 41 477 deaths (23 182 from breast cancer) were identified. For BMI before diagnosis, compared with normal weight women, the summary relative risks (RRs) of total mortality were 1.41 [95% confidence interval (CI) 1.29-1.53] for obese (BMI >30.0), 1.07 (95 CI 1.02-1.12) for overweight (BMI 25.0-<30.0) and 1.10 (95% CI 0.92-1.31) for underweight (BMI <18.5) women. For obese women, the summary RRs were 1.75 (95% CI 1.26-2.41) for pre-menopausal and 1.34 (95% CI 1.18-1.53) for post-menopausal breast cancer. For each 5 kg/m(2) increment of BMI before, <12 months after, and ≥12 months after diagnosis, increased risks of 17%, 11%, and 8% for total mortality, and 18%, 14%, and 29% for breast cancer mortality were observed, respectively. CONCLUSIONS: Obesity is associated with poorer overall and breast cancer survival in pre- and post-menopausal breast cancer, regardless of when BMI is ascertained. Being overweight is also related to a higher risk of mortality. Randomised clinical trials are needed to test interventions for weight loss and maintenance on survival in women with breast cancer.

Does alcohol increase breast cancer risk in African-American women? Findings from a case-control study.

BACKGROUND: Alcohol is an important risk factor for breast cancer in Caucasian women, but the evidence in African-American (AA) women is limited and results are inconclusive. METHODS: Associations between recent and lifetime drinking and breast cancer risk were evaluated in a large sample of AA women from a case-control study in New York and New Jersey. Multivariable logistic regression models provided odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: There was no association between recent drinking and breast cancer risk, even when stratified by menopausal status or by hormone receptor status. A borderline decreased risk with increased lifetime consumption was found (OR=0.77; 95% CI: 0.58-1.03), which was stronger among women who drank when under 20 years of age (OR=0.65; 95% CI: 0.47-0.89), regardless of menopausal or hormone receptor status. CONCLUSION: Breast cancer risk associated with recent alcohol consumption was not apparent in AA women, while early age drinking seemed to decrease risk. This is the first investigation on recent and lifetime drinking in subgroups and drinking during different age periods in AA women. If findings are replicated, racial differences in biological pathways involving alcohol and its metabolites should be explored.

Genome-wide meta-analyses of smoking behaviors in African Americans.

The identification and exploration of genetic loci that influence smoking behaviors have been conducted primarily in populations of the European ancestry. Here we report results of the first genome-wide association study meta-analysis of smoking behavior in African Americans in the Study of Tobacco in Minority Populations Genetics Consortium (n = 32,389). We identified one non-coding single-nucleotide polymorphism (SNP; rs2036527[A]) on chromosome 15q25.1 associated with smoking quantity (cigarettes per day), which exceeded genome-wide significance (ß = 0.040, s.e. = 0.007, P = 1.84 × 10(-8)). This variant is present in the 5'-distal enhancer region of the CHRNA5 gene and defines the primary index signal reported in studies of the European ancestry. No other SNP reached genome-wide significance for smoking initiation (SI, ever vs never smoking), age of SI, or smoking cessation (SC, former vs current smoking). Informative associations that approached genome-wide significance included three modestly correlated variants, at 15q25.1 within PSMA4, CHRNA5 and CHRNA3 for smoking quantity, which are associated with a second signal previously reported in studies in European ancestry populations, and a signal represented by three SNPs in the SPOCK2 gene on chr10q22.1. The association at 15q25.1 confirms this region as an important susceptibility locus for smoking quantity in men and women of African ancestry. Larger studies will be needed to validate the suggestive loci that did not reach genome-wide significance and further elucidate the contribution of genetic variation to disparities in cigarette consumption, SC and smoking-attributable disease between African Americans and European Americans.

The macrobiotic diet in cancer.

Macrobiotics is one of the most popular alternative or complementary comprehensive lifestyle approaches to cancer. The centerpiece of macrobiotics is a predominantly vegetarian, whole-foods diet that has gained popularity because of remarkable case reports of individuals who attributed recoveries from cancers with poor prognoses to macrobiotics and the substantial evidence that the many dietary factors recommended by macrobiotics are associated with decreased cancer risk. Women consuming macrobiotic diets have modestly lower circulating estrogen levels, suggesting a lower risk of breast cancer. This may be due in part to the high phytoestrogen content of the macrobiotic diet. As with most aspects of diet in cancer therapy, there has been limited research evaluating the effectiveness of the macrobiotic diet in alleviating suffering or prolonging survival of cancer patients. The few studies have compared the experience of cancer patients who tried macrobiotics with expected survival rates or assembled series of cases that may justify more rigorous research. On the basis of available evidence and its similarity to dietary recommendations for chronic disease prevention, the macrobiotic diet probably carries a reduced cancer risk. However, at present, the empirical scientific basis for or against recommendations for use of macrobiotics for cancer therapy is limited. Any such recommendations are likely to reflect biases of the recommender. Because of its popularity and the compelling evidence that dietary factors are important in cancer etiology and survival, further research to clarify whether the macrobiotic diet or similar dietary patterns are effective in cancer prevention and treatment is warranted.

Alcohol consumption and lung cancer: a review of the epidemiologic evidence.

A role for alcohol consumption in lung cancer etiology has been suggested in some studies, but this possible relationship has been often regarded with skepticism, with any indication of an association being attributed to confounding by cigarette smoking. The purpose of this work was to review the epidemiological evidence for an association of alcohol and lung cancer and to identify gaps in that research. The studies reviewed here provide some indication that alcohol and particularly beer intake may increase lung cancer risk after controlling for cigarette smoking. Although the evidence is not conclusive, it warrants additional consideration of alcohol as a risk factor in lung cancer etiology, independent of cigarette smoking. Recommendations for future studies are provided.

Diet and alcohol consumption and lung cancer risk in the New York State Cohort (United States)

The relationship between diet and alcohol and lung cancer was evaluated among participants of the New York State Cohort (United States), comprising 27,544 men (395 cases) and 20,456 women (130 cases) who completed a brief mailed questionnaire in 1980. Participants were followed up through 1987 with the assistance of the New York State Department of Health's Vital Statistics Section and Cancer Registry. Among men, inverse relationships with vitamin C, folate, and carotenoids, and positive associations with total fat, monounsaturated and saturated fat were observed after adjusting for age, education, cigarettes/day, years smoking, and total energy intake. The relationships observed with folate and saturated fat were stronger for heavy smokers. Also, the effect of folate, total fat, and monounsaturated fat seemed to be limited to squamous cell carcinomas. We found no indication that cholesterol or polyunsaturated fat was associated with lung cancer. Diet did not appear to exert a major role on lung cancer risk among women. Although diet modification should never be considered a substitute for smoking cessation, its role as an additional strategy in lung cancer prevention deserves attention.

Alcohol consumption and lung cancer in white males.

Experimental and epidemiologic investigations in alcoholic and nonalcoholic populations have suggested a role of alcohol in lung carcinogenesis. The association between alcohol consumption and lung cancer was investigated among 280 White males with histologically confirmed, primary lung cancer and 564 White male controls, participants in the Western New York Diet Study (United States). Among heavy smokers (over 40 pack-years), total alcohol consumption was associated with an increased risk of lung cancer with adjustment for age, years of education, pack-years of cigarette smoking, and intake of carotenoids and fat. In this group, the odds ratio for drinkers of more than 24 drinks per month was 1.6 compared with those who drank less. Drinkers of more than 12 beers per month were 1.6 times more likely to develop lung cancer than nondrinkers of beer after controlling for age, years of education, and cigarette smoking (95 percent confidence interval = 1.0-2.4, P for trend = 0.003). Occupational and dietary factors did not seem to explain these findings. Although cigarette smoking is the major cause of lung cancer, the role of alcohol, independent or in interaction with cigarette smoking, deserves further investigation.