Mental health and diet quality after primary treatment for ovarian cancer.

AIMS: To investigate anxiety and depression after primary treatment for ovarian cancer in relation to diet quality and intake. METHODS: In a cohort of women with ovarian cancer in Australia, levels of anxiety and depression (normal, subclinical, and clinical) were assessed using the Hospital Anxiety and Depression Scale at 9 months post-diagnosis. Dietary intake was assessed using a validated food frequency questionnaire at 12 months post-diagnosis and scored using the Healthy Eating Index 2015. Multinomial logistic regression and bivariate analyses were used to investigate relationships between levels of anxiety and depression and subsequent diet quality and intake of food groups. RESULTS: Of 595 women, anxiety and depression were identified among 128 (21%) and 80 (13%) women, respectively. Compared to women without anxiety or depression, women with subclinical anxiety (odds ratio = 0.49, 95% confidence interval: 0.25-0.98) and those with clinical depression (odds ratio = 0.25, 95% confidence interval: 0.07-0.93) were less likely to score in the highest quartile for diet quality. Separate adjustment for age, education, employment, disease stage, body mass index, and smoking status did not attenuate these associations. In bivariate analyses, women with subclinical anxiety were more likely to report higher intakes of sweet foods. Those with clinical depression were more likely to report lower intakes of orange vegetables and wholegrains, higher intakes of sweetened beverages, and not consume alcohol or soya foods. CONCLUSIONS: Anxiety or depression after primary treatment for ovarian cancer may be associated with poorer diet quality. Efforts to improve diet quality post-treatment should consider support for mental health.

Folate Intake and Ovarian Cancer Risk among Women with Endometriosis: A Case-Control Study from the Ovarian Cancer Association Consortium.

BACKGROUND: Although folate intake has not been associated with an increased risk of ovarian cancer overall, studies of other cancer types have suggested that high folate intake may promote carcinogenesis in precancerous lesions. Women with endometriosis (a potential precancerous lesion) have an increased risk of developing ovarian cancer; however, whether high folate intake increases risk in this group is unknown. METHODS: We conducted a pooled analysis of six case-control studies from the Ovarian Cancer Association Consortium to investigate the association between folate intake and risk of ovarian cancer among women with and without self-reported endometriosis. We included 570 cases/558 controls with and 5,171/7,559 without endometriosis. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals for the association between folate intake (dietary, supplemental, and total) and ovarian cancer risk. Finally, we used Mendelian randomization (MR) to evaluate our results using genetic markers as a proxy for folate status. RESULTS: Higher dietary folate intake was associated with an increased risk of ovarian cancer for women with endometriosis [OR, 1.37 (1.01-1.86)] but not for women without endometriosis. There was no association between supplemental folate intake and ovarian cancer risk for women with or without endometriosis. A similar pattern was seen using MR. CONCLUSIONS: High dietary folate intake may be associated with an increased risk of ovarian cancer among women with endometriosis. IMPACT: Women with endometriosis with high folate diets may be at increased risk of ovarian cancer. Further research is needed on the potential cancer-promoting effects of folate in this group.

Association of Protein Intake with Recurrence and Survival Following Primary Treatment of Ovarian Cancer.

BACKGROUND: Malnutrition is common during treatment of ovarian cancer, and 1 in 3 patients report multiple symptoms affecting food intake after primary treatment. Little is known about diet posttreatment in relation to ovarian cancer survival; however, general recommendations for cancer survivors are to maintain a higher level of protein intake to support recovery and minimize nutritional deficits. OBJECTIVES: To investigate whether intake of protein and protein food sources following primary treatment of ovarian cancer is associated with recurrence and survival. METHODS: Intake levels of protein and protein food groups were calculated from dietary data collected ∼12 mo postdiagnosis using a validated FFQ in an Australian cohort of women with invasive epithelial ovarian cancer. Disease recurrence and survival status were abstracted from medical records (median 4.9 y follow-up). Cox proportional hazards regression was used to calculate adjusted HRs and 95% CIs for protein intake and progression-free and overall survival. RESULTS: Among 591 women who were progression-free at 12 mo follow-up, 329 (56%) subsequently experienced cancer recurrence and 231 (39%) died. A higher level of protein intake was associated with better progression-free survival (>1-1.5 compared with ≤1 g/kg body weight, HRadjusted: 0.69, 95% CI: 0.48, 1.00; >1.5 compared with ≤1 g/kg, HRadjusted: 0.61, 95% CI: 0.41, 0.90; >20% compared with ≤20% total EI from protein, HRadjusted: 0.77, 95% CI: 0.61, 0.96). There was no evidence for better progression-free survival with any particular protein food sources. There was a suggestion of better overall survival among those with higher total intakes of animal-based protein foods, particularly dairy products (HR: 0.71; 95% CI: 0.51, 0.99 for highest compared with lowest tertiles of total dairy intake). CONCLUSIONS: After primary treatment of ovarian cancer, a higher level of protein intake may benefit progression-free survival. Ovarian cancer survivors should avoid dietary practices that limit intake of protein-rich foods.

Dietary omega-3 fatty acids and endometrial cancer risk in the Epidemiology of Endometrial Cancer Consortium: An individual-participant meta-analysis.

BACKGROUND: Limited data from prospective studies suggest that higher dietary intake of long-chain omega-3 polyunsaturated fatty acids (LCn3PUFA), which hold anti-inflammatory properties, may reduce endometrial cancer risk; particularly among certain subgroups characterized by body mass and tumor pathology. MATERIALS AND METHODS: Data from 12 prospective cohort studies participating in the Epidemiology of Endometrial Cancer Consortium were harmonized as nested case-control studies, including 7268 endometrial cancer cases and 26,133 controls. Habitual diet was assessed by food frequency questionnaire, from which fatty acid intakes were estimated. Two-stage individual-participant data mixed effects meta-analysis estimated adjusted odds ratios (OR) and 95% confidence intervals (CI) through logistic regression for associations between study-specific energy-adjusted quartiles of LCn3PUFA and endometrial cancer risk. RESULTS: Women with the highest versus lowest estimated dietary intakes of docosahexaenoic acid, the most abundant LCn3PUFA in diet, had a 9% increased endometrial cancer risk (Quartile 4 vs. Quartile 1: OR 1.09, 95% CI: 1.01-1.19; P trend = 0.04). Similar elevated risks were observed for the summary measure of total LCn3PUFA (OR 1.07, 95% CI: 0.99-1.16; P trend = 0.06). Stratified by body mass index, higher intakes of LCn3PUFA were associated with 12-19% increased endometrial cancer risk among overweight/obese women and no increased risk among normal-weight women. Higher associations appeared restricted to White women. The results did not differ by cancer grade. CONCLUSION: Higher dietary intakes of LCn3PUFA are unlikely to reduce endometrial cancer incidence; rather, they may be associated with small to moderate increases in risk in some subgroups of women, particularly overweight/obese women.

Coffee consumption and risk of endometrial cancer: a pooled analysis of individual participant data in the Epidemiology of Endometrial Cancer Consortium (E2C2).

BACKGROUND: Epidemiologic studies suggest that coffee consumption may be inversely associated with risk of endometrial cancer (EC), the most common gynecological malignancy in developed countries. Furthermore, coffee consumption may lower circulating concentrations of estrogen and insulin, hormones implicated in endometrial carcinogenesis. Antioxidants and other chemopreventive compounds in coffee may have anticarcinogenic effects. Based on available meta-analyses, the World Cancer Research Fund (WCRF) concluded that consumption of coffee probably protects against EC. OBJECTIVES: Our main aim was to examine the association between coffee consumption and EC risk by combining individual-level data in a pooled analysis. We also sought to evaluate potential effect modification by other risk factors for EC. METHODS: We combined individual-level data from 19 epidemiologic studies (6 cohort, 13 case-control) of 12,159 EC cases and 27,479 controls from the Epidemiology of Endometrial Cancer Consortium (E2C2). Logistic regression was used to calculate ORs and their corresponding 95% CIs. All models were adjusted for potential confounders including age, race, BMI, smoking status, diabetes status, study design, and study site. RESULTS: Coffee drinkers had a lower risk of EC than non-coffee drinkers (multiadjusted OR: 0.87; 95% CI: 0.79, 0.95). There was a dose-response relation between higher coffee consumption and lower risk of EC: compared with non-coffee drinkers, the adjusted pooled ORs for those who drank 1, 2-3, and >4 cups/d were 0.90 (95% CI: 0.82, 1.00), 0.86 (95% CI: 0.78, 0.95), and 0.76 (95% CI: 0.66, 0.87), respectively (P-trend < 0.001). The inverse association between coffee consumption and EC risk was stronger in participants with BMI > 25 kg/m2. CONCLUSIONS: The results of the largest analysis to date pooling individual-level data further support the potentially beneficial health effects of coffee consumption in relation to EC, especially among females with higher BMI.

Dietitian encounters after treatment for ovarian cancer.

BACKGROUND: After ovarian cancer treatment, women report health issues that may be amenable to change with dietary support. The present study investigated how many women encounter a dietitian post-treatment and the factors associated with dietitian service use. METHODS: We used data from a cohort of women with invasive epithelial ovarian cancer to identify socio-economic, clinical and personal factors associated with dietitian encounter after treatment completion. Data were collected at regular intervals using validated questionnaires up to 4 years post-treatment completion. Logistic regression (LR) and generalised linear mixed models (GLMM) were used to calculate adjusted odds ratios (OR) and 95% confidence intervals (CI) to assess factors associated with dietitian encounter at any time-point post-treatment (LR), as well as in the 3 months prior to a follow-up questionnaire (GLMM) to assess time-varying factors. RESULTS: Of 819 women, 97 (12%) reported seeing a dietitian post-treatment. Factors associated with dietitian encounter were being overweight (ORLR  = 1.7, CI = 1.1-2.8), having poorer self-rated health (ORLR  = 2.5, CI = 1.2-5.2; ORGLMM  = 2.3, CI = 1.2-4.4) or poorer diet quality (ORLR  = 0.5, CI = 0.2-1.0) pre-diagnosis, treatment within the public health system (ORGLMM  = 1.8, CI = 1.2-2.7), previous support from dietetic (ORLR  = 3.1, CI = 1.8-5.4; ORGLMM  = 2.8, CI = 1.8-4.2) or other allied health services (ORLR  = 2.0, CI = 1.2-3.2; ORGLMM  = 3.7, CI = 2.4-5.5), and having progressive disease at follow-up (ORGLMM  = 2.2, CI = 1.4-3.3). Most women (86%) with ≥ 3 moderate-to-severe nutrition impact symptoms did not report a dietitian encounter post-treatment. CONCLUSIONS: Few women encounter a dietitian post-treatment for ovarian cancer, including those with multiple nutrition impact symptoms. Further work is needed to engage those likely to benefit from dietitian support but less likely to seek or receive it.

Pre- and Post-Diagnosis Diet Quality and Ovarian Cancer Survival.

BACKGROUND: Prior studies evaluating diet quality in relation to ovarian cancer survival are sparse, and to date none have assessed diet quality or diet-quality change after diagnosis. METHODS: In the prospective Ovarian cancer Prognosis And Lifestyle (OPAL) study, diet-quality scores were calculated using data from food frequency questionnaires completed pre-diagnosis (n = 650) and 12 months' post-diagnosis (n = 503). We used Cox proportional hazard models to estimate adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the association between diet quality and survival. RESULTS: During the median follow-up of 4.4 years, 278 women died from ovarian cancer. There was no evidence of an association between diet quality pre- or post-diagnosis and progression-free, overall, or ovarian cancer-specific survival. No survival advantage was observed for women who had either improved their diet quality or who consumed a high-quality diet both before and 12 months after diagnosis. CONCLUSIONS: Higher pre- and post-diagnosis diet quality was not associated with better survival outcomes in this cohort of women with ovarian cancer. IMPACT: Diet quality is important for a range of health outcomes but may not improve survival after a diagnosis of ovarian cancer.

A healthy lifestyle and survival among women with ovarian cancer.

Ovarian cancer has a poor survival rate and, understandably, women often want to know whether there is anything they can do to improve their prognosis. Our goal was to investigate the association between a healthy lifestyle prediagnosis and postdiagnosis and survival in a cohort of Australian women with invasive epithelial ovarian cancer. We calculated a healthy lifestyle index (HLI) based on women's self-reported smoking status, height, weight, physical activity, diet and alcohol consumption before diagnosis (n = 678) and after completing primary treatment (n = 512). Clinical data and vital status for each woman were ascertained through medical records. Cox proportional hazards regression was conducted to calculate hazard ratios (HR) and 95% confidence interval (CI) for all-cause mortality. There was a suggestive association between a more healthy lifestyle before diagnosis and better survival (HR 0.79, 95% CI: 0.59-1.04), however, the association was stronger for lifestyle after diagnosis, with women in the highest tertile having significantly better survival than women in the lowest tertile (HR 0.61, 95% CI: 0.40-0.93; P-trend = .02). Current smoking, particularly postdiagnosis, was associated with higher mortality (HR 1.68, 95% CI: 1.17-2.42; HR 2.82, 95% CI: 1.29-6.14, for prediagnosis and postdiagnosis smoking, respectively), but women who quit after diagnosis had survival outcomes similar to nonsmokers (HR 0.99, 95% CI: 0.57-1.72). Higher physical activity after diagnosis was associated with better survival (HR 0.60, 95% CI: 0.39-0.92; P-trend = .02). A healthy lifestyle after diagnosis, in particular not smoking and being physically active, may help women with ovarian cancer improve their prognosis.

Pre-diagnosis diet and survival after a diagnosis of ovarian cancer.

BACKGROUND: The relationship between diet and survival after ovarian cancer diagnosis is unclear as a result of a limited number of studies and inconsistent findings. METHODS: We examined the association between pre-diagnostic diet and overall survival in a population-based cohort (n=811) of Australian women diagnosed with invasive epithelial ovarian cancer between 2002 and 2005. Diet was measured by validated food frequency questionnaire. Deaths were ascertained up to 31 August 2014 via medical record review and Australian National Death Index linkage. We conducted Cox proportional hazards regression analysis, controlling for diagnosis age, tumour stage, grade and subtype, residual disease, smoking status, body mass index, physical activity, marital status, and energy intake. RESULTS: We observed improved survival with highest compared with lowest quartile of fibre intake (hazard ratio (HR)=0.69, 95% CI: 0.53-0.90, P-trend=0.002). There was a suggestion of better survival for women with highest compared with lowest intake category of green leafy vegetables (HR=0.79, 95% CI: 0.62-0.99), fish (HR=0.74, 95% CI: 0.57-0.95), poly- to mono-unsaturated fat ratio (HR=0.76, 95% CI: 0.59-0.98), and worse survival with higher glycaemic index (HR=1.28, 95% CI: 1.01-1.65, P-trend=0.03). CONCLUSIONS: The associations we observed between healthy components of diet pre-diagnosis and ovarian cancer survival raise the possibility that dietary choices after diagnosis may improve survival.

Dietary patterns and weight change: 15-year longitudinal study in Australian adults.

BACKGROUND: Dietary intake is one of the most modifiable risk factors associated with obesity. However, data on the relationship between dietary patterns and long-term weight change are limited. PURPOSE: We therefore investigated the association between dietary patterns and 15-year weight change in a sample of 1186 Australian adults (1992-2007). METHODS: We measured body weight and collected data on socio-demographic and lifestyle characteristics in 1992 and 2007. Applying principal component analysis to 38 food groups from a food frequency questionnaire collected at baseline, we identified two dietary patterns: 'meat-and-fat' and 'fruit-and-vegetable.' Using generalized estimating equations, multivariable regression models, stratified by sex, were adjusted for concurrent changes in socio-demographic and lifestyle variables. RESULTS: The average increase in body weight of men in the highest tertile of the meat-and-fat pattern was more than twice that of men in the lowest tertile; mean weight change (95 % CI): 4.8 (-0.1, 9.7) kg versus 2.3 (-2.6, 7.1) kg, P-for-trend = 0.02. In contrast, average weight gain of men in the highest tertile of the fruit-and-vegetable pattern was only about half that of men in the lowest tertile; mean weight change (95 % CI): 2.9 (-2.0, 7.8) kg versus 5.4 (-1.5, 10.4) kg, P-for-trend = 0.02. Among women, dietary patterns were not related to weight change. CONCLUSIONS: These dietary patterns predict change in body weight in men, but not in women. In this cohort, a dietary pattern high in fruit and vegetables was related to less weight gain in men than a dietary pattern high in meat and fat.

Cancers in Australia in 2010 attributable to inadequate consumption of fruit, non-starchy vegetables and dietary fibre.

OBJECTIVES: To estimate the number and proportion of cancers occurring in Australia in 2010 attributable to consumption deficits in fruit, non-starchy vegetables and dietary fibre. METHODS: We estimated the population attributable fraction (PAF) for cancers causally associated with inadequate intake of fruit and non-starchy vegetables (oral cavity, pharynx, oesophageal squamous cell carcinoma, stomach, larynx); inadequate intake of fruit (lung); and insufficient intake of fibre (colorectum). We used standard formulae incorporating prevalence of exposure (1995 National Nutrition Survey) and relative risks from independent studies. RESULTS: Overall, 1,555 (1.4% of all) and 311 (0.3% of all) cancers were attributable to inadequate intakes of fruit and non-starchy vegetables, respectively. A further 2,609 colorectal cancers (18% of colorectal) were attributable to insufficient fibre intake. If Australians increased their fibre intake by eating the recommended daily intakes of fruit and vegetables, an estimated 1,293 (8.8%) colorectal cancers could be prevented. CONCLUSIONS: One in six colorectal cancer cases was attributable to inadequate intake of dietary fibre and about 1,800 cancers at other sites were attributable to insufficient fruit and non-starchy vegetable consumption. IMPLICATIONS: Increasing the proportion of Australians who consume the recommended intake of fruit, vegetables and fibre could prevent up to 4% of all cancers.

Cancers in Australia in 2010 attributable to the consumption of red and processed meat.

OBJECTIVES: To estimate the proportion and numbers of cancers in Australia in 2010 attributable to consuming red/processed meat. METHODS: We estimated the population attributable fraction (PAF) for cancers causally associated with red/processed meat consumption (colon, rectum) using standard formulae incorporating prevalence of consumption (1995 National Nutrition Survey), relative risks associated with consumption and cancer incidence. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that might have occurred under two hypothetical interventions whereby Australian adults reduced their consumption of red/processed meat from prevailing levels to ≤100 g or ≤65 g per day, respectively. RESULTS: An estimated 2,614 cases (18%) of colorectal cancer occurring in Australians in 2010 were attributable to red/processed meat consumption (16% of colon cancers; 23% of rectal cancers). We estimated that if all Australian adults had consumed ≤65 g/day or ≤100 g/day of red/processed meat, then the incidence of colorectal cancer would have been 5.4% (798 cancers) or 1.4% (204 cancers) lower, respectively. CONCLUSIONS: About one in six colorectal cancers in Australians in 2010 were attributable to red/processed meat consumption. IMPLICATIONS: Reducing red/processed meat intake may reduce colorectal cancer incidence, but must be balanced against nutritional benefits of modest lean meat consumption.

Cancers in Australia in 2010 attributable to modifiable factors: introduction and overview.

OBJECTIVE: To describe the approach underpinning a national project to estimate the numbers and proportions of cancers occurring in Australia in 2010 that are attributable to modifiable causal factors. METHODS: We estimated the population attributable fraction (PAF) (or prevented fraction) of cancers associated with exposure to causal (or preventive) factors using standard formulae. Where possible, we also estimated the potential impact on cancer incidence resulting from changes in prevalence of exposure. Analyses were restricted to factors declared causal by international agencies: tobacco smoke; alcohol; solar radiation; infectious agents; obesity; insufficient physical activity; insufficient intakes of fruits, vegetables and fibre; red and processed meat; menopausal hormone therapy (MHT); oral contraceptive pill (OCP); and insufficient breast feeding. Separately, we estimated numbers of cancers prevented by: aspirin; sunscreen; MHT; and OCP use. We discuss assumptions pertaining to latent periods between exposure and cancer onset, choices of prevalence data and risk estimates, and approaches to sensitivity analyses. RESULTS: Numbers and population attributable fractions of cancer are presented in accompanying papers. CONCLUSIONS: This is the first systematic assessment of population attributable fractions of cancer in Australia.

Cancers in Australia in 2010 attributable to modifiable factors: summary and conclusions.

OBJECTIVE: To estimate the numbers and proportions of cancers occurring in Australia in 2010 attributable to modifiable causal factors. METHODS: We estimated the population attributable fraction (PAF) of cancers associated with exposure to 13 causal factors using standard formulae incorporating exposure prevalence and relative risk data. We also calculated the potential impact of changing exposure to some factors. RESULTS: A total of 32% of all cancers diagnosed in Australia in 2010 (excluding keratinocyte cancers) were attributable to the 13 factors assessed (men 33%; women 31%). Leading factors were tobacco smoke (PAF all cancers: 13.4%), solar radiation (6.2%), inadequate diet (6.1%) and overweight/obesity (3.4%). Factors conferring highest PAFs differed by sex: highest PAFs for men were tobacco smoke (15.8%), solar radiation (7.1%) and alcohol (3.0%); while highest PAFs for women were tobacco smoke (10.1%), solar radiation (5.0%) and overweight/obesity (4.5%). Sites with the highest counts of potentially preventable cancers were lung (8,569), colorectal (7,404), melanoma of the skin (7,220) and breast (3,233). CONCLUSIONS: At least one in three cancers in Australia is attributable to exposure to known modifiable factors. IMPLICATIONS: Up to 37,000 cancers could be prevented in Australia each year if the population avoided exposure to 13 common factors known or strongly suspected to cause cancer.

Circulating 25-hydroxyvitamin D and survival in women with ovarian cancer.

BACKGROUND: Vitamin D status might be associated with cancer survival. Survival after ovarian cancer is poor, but the association with vitamin D has rarely been examined. OBJECTIVE: We evaluated the association between serum 25-hydroxyvitamin D [25(OH)D], a marker of vitamin D status, and ovarian cancer survival. DESIGN: Participants were women with invasive ovarian cancer diagnosed between 2002 and 2005 who participated in the Australian Ovarian Cancer Study. Serum samples, collected at diagnosis (n = 670) or after completion of primary treatment and before recurrence (n = 336), were assayed for 25(OH)D. Sociodemographic, dietary, and lifestyle data came from questionnaires self-completed at recruitment, and clinical and survival data were from medical records, supplemented by linkage to the Australian National Death Index (October 2011). Cox proportional hazards regression was used to estimate HRs and 95% CIs for the association between circulating 25(OH)D and survival. RESULTS: Overall, 59% of the women died during follow-up, with 95% of deaths resulting from ovarian cancer. Circulating 25(OH)D concentrations (mean: 44 nmol/L) were significantly associated with age, state of residence, season of blood collection, and body mass index but not with tumor histology, stage or grade, or comorbidities. Higher 25(OH)D concentrations at diagnosis were significantly associated with longer survival (adjusted HR: 0.93; 95% CI: 0.88, 0.99 per 10 nmol/L), but there was no significant association with progression-free survival or for 25(OH)D measured after primary treatment. CONCLUSIONS: In our cohort, higher serum 25(OH)D concentrations at diagnosis were associated with longer survival among women with ovarian cancer. If confirmed in other studies, this suggests that vitamin D status at diagnosis may be an independent predictor of prognosis. Furthermore, if the association is found to be causal, improving vitamin D status may improve ovarian cancer survival rates.

Aspirin, nonaspirin nonsteroidal anti-inflammatory drugs, acetaminophen and ovarian cancer survival.

Aspirin and nonaspirin nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to decrease tumor progression in pre-clinical models of ovarian cancer, however the influence of these drugs on survival in women following a diagnosis of ovarian cancer is unknown. We included 1305 Australian women diagnosed with incident invasive epithelial ovarian cancer, recruited into a population-based case-control study. Use of aspirin, nonaspirin NSAIDs and acetaminophen in the 5 years preceding ovarian cancer diagnosis was assessed from self-reports. Deaths were ascertained up to October 2011 via linkage with the Australian National Death Index. Cox proportional hazards regression models were used to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CI). During a mean follow-up time of 4.9 years (SD 2.8 years), there were 834 deaths, of which 779 (93% of deaths) were from ovarian cancer. We found uniformly inverse, but non-significant, HRs for ever use in the last five years of aspirin, nonaspirin NSAIDs and acetaminophen compared with no use (adjusted HRs 0.92 [95% CI 0.81-1.06], 0.91 [95% CI 0.80-1.05] and 0.91 [95% CI 0.69-1.20], respectively). There was no evidence of any dose response trends. The results remained unchanged when we limited the outcome to ovarian cancer mortality. Associations did not differ by histologic subtype, age at diagnosis or stage. Given current interest in the role of aspirin and nonaspirin NSAIDs in cancer survival these results are noteworthy given they are the first to investigate these associations in women with ovarian cancer. Our results provide no strong evidence that pre-diagnostic use of aspirin or nonaspirin NSAIDs are associated with improved survival in women with ovarian cancer.

A case-control study of glycemic index, glycemic load and dietary fiber intake and risk of adenocarcinomas and squamous cell carcinomas of the esophagus: the Australian Cancer Study.

BACKGROUND: Glycemic index (GI) and glycemic load (GL) have been investigated as etiologic factors for some cancers, but epidemiological data on possible associations between dietary carbohydrate intake and esophageal cancer are scant. This study examined the association between GI, GL, and other dietary carbohydrate components and risk of adenocarcinomas and squamous cell carcinoma of the esophagus accounting for established risk factors. METHODS: We analyzed data from a population-based Australian case-control study (2002-05) comprising 299 adenocarcinoma (EAC), 337 gastro-esophageal junction adenocarcinoma (EGJAC), 245 squamous cell carcinoma (ESCC), and 1507 controls sampled from a population registry. Dietary information was obtained using a 135-item food frequency questionnaire (FFQ); GI and GL were derived from an Australian GI database. Multivariable logistic regression models were used to derive odds ratios (ORs). RESULTS: All three case groups tended to have a lower intake of fiber, and significantly higher intake of fat, total energy, and alcohol (ESCC only) compared to controls. GI was unrelated to all histological types. Higher GL was not associated with risk of EAC and EGJAC, but was inversely associated with risk of ESCC (adjusted model, p(trend) = 0.006), specifically among men where we observed a 58% reduced risk of ESCC in the highest versus the lowest quartile. Increased intake of total carbohydrates and starch was related to similarly large risk reductions of ESCC. Fiber intake was strongly and inversely associated with risk of EAC, EGJAC and ESCC (all p(trend) ≤ 0.001), indicating risk reductions of 28%-37% per 10 g/day. CONCLUSIONS: This study suggests a reduced risk of esophageal SCC with higher GL level particularly in men, but provides no evidence for the role of GI in the development of esophageal cancer. In addition, increased fiber intake appears to be associated with lower risk of all histological types of esophageal cancer.

Dietary phyto-oestrogens and the risk of ovarian and endometrial cancers: findings from two Australian case-control studies.

Phyto-oestrogens have been suggested to have a protective effect on hormone-sensitive cancers. However, few studies have investigated the association between dietary phyto-oestrogens and gynaecological cancers. In the present study, we analysed data from two population-based case-control studies of ovarian (1366 cases and 1414 controls) and endometrial (1288 cases and 1435 controls) cancers. Dietary intake information was obtained using a 135-item FFQ, and phyto-oestrogen intake was estimated using published food composition databases. Unconditional logistic regression was used to estimate adjusted OR and 95% CI. In multivariable analyses, there was a suggestive pattern of inverse associations between increasing intakes of total phyto-oestrogens, isoflavones and enterolignans and the risk of ovarian cancer. However, the results only reached statistical significance for the lignan compounds matairesinol and lariciresinol, where the OR for the highest v. the lowest intake category was 0.72 (95% CI 0.54, 0.96; P for trend = 0.02) for matairesinol and 0.72 (95% CI 0.55, 0.96; P for trend = 0.03) for lariciresinol. When the risk of ovarian cancer was assessed by subtype, there was an indication that increasing intakes of phyto-oestrogens may be associated with a decreased risk of mucinous (cases n 158) ovarian tumours (OR for the highest v. the lowest intake category: 0.47 (95% CI 0.24, 0.93); P for trend = 0.04). However, there were no significant associations with other histological subtypes. In contrast, dietary phyto-oestrogens (total or any subclass) were unrelated to the risk of endometrial cancer cases overall or by subtype.

Higher glycemic index and glycemic load diet is associated with increased risk of esophageal squamous cell carcinoma: a case-control study.

Several studies have indicated the association between intake of foods high in dietary glycemic index (GI) and glycemic load (GL) with an increased risk of digestive tract cancers. We hypothesized that GI and GL may be associated with risk of esophageal squamous cell carcinoma (ESCC) in a high-risk population in Iran. In total, we interviewed 47 cases with incident of ESCC and 96 frequency-matched hospital controls, then calculated the average dietary GI and GL via a validated food frequency questionnaire. Dietary GL was calculated as a function of GI, carbohydrate content, and frequency of intake of certain foods. Dietary GI and GL levels were significantly higher among the ESCC cases compared with the controls (P < .05). After adjustment for potential confounders, those in the highest tertile of dietary GI had 2.95 times higher risk of ESCC compared with those in the lowest (95% confidence interval, 1.68-3.35; P for trend = .002). In addition, being in the highest tertile of dietary GL was positively associated with an ESCC risk (odds ratio, 3.49; 95% confidence interval, 2.98-4.41; P for trend = .001). Findings of the present study indicate that diets with high GI and GL might have potentially unfavorable effects on ESCC risk and suggest a possible role for excess circulating insulin and related insulin-like growth factor 1 in esophageal cancer development.

Vitamin D intake in Australian adults and the modeled effects of milk and breakfast cereal fortification.

OBJECTIVE: Vitamin D intake from foods or supplements is a safe and attractive means to improve vitamin D status of populations. The aim of this study was to help identify population subgroups that would benefit most from efforts to increase intake. To do so, we investigated which personal characteristics are associated with vitamin D intake in an Australian population and modeled possible effects of expanded food fortification practices. METHODS: We investigated vitamin D intake in a population-based random sample of 785 adults, using a validated food frequency questionnaire, and assessed associations with personal and behavioral characteristics. We identified vitamin D food sources and modeled the hypothetical effects of blanket fortification of milk and breakfast cereals. RESULTS: Average total vitamin D intake was 4.4 (±4.0) µg/g and below adequate intake for most participants in all age and sex subgroups. Higher intake was associated with being female, having a serious medical condition, energy intake below the median, and vitamin D supplement use (all P < 0.05). The "meat, fish, and eggs" food group contributed most to total vitamin D intake (51%), followed by dairy products and related foods (43%). If all milk and breakfast cereals were to be fortified with vitamin D, the average intake of vitamin D from foods would increase from 3.6 (±2.4) µg/d to 6.3 (±3.2) µg/d, with similar increases in all age and sex subgroups. CONCLUSIONS: Vitamin D intake in Australia is generally below recommended levels, and few personal characteristics help to identify subgroups with low intake. Blanket vitamin D fortification of milk and breakfast cereals would substantially increase average vitamin D intake in Australian adults of all ages.