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The associations of body mass index (BMI) and other anthropometric measurements with lung cancer were examined in 348,108 participants in the European Investigation Into Cancer and Nutrition (EPIC) between 1992 and 2010. The study population included 2,400 case patients with incident lung cancer, and the average length of follow-up was 11 years. Hazard ratios were calculated using Cox proportional hazard models in which we modeled smoking variables with cubic splines. Overall, there was a significant inverse association between BMI (weight (kg)/height (m)(2)) and the risk of lung cancer after adjustment for smoking and other confounders (for BMI of 30.0-34.9 versus 18.5-25.0, hazard ratio = 0.72, 95% confidence interval: 0.62, 0.84). The strength of the association declined with increasing follow-up time. Conversely, after adjustment for BMI, waist circumference and waist-to-height ratio were significantly positively associated with lung cancer risk (for the highest category of waist circumference vs. the lowest, hazard ratio = 1.25, 95% confidence interval: 1.05, 1.50). Given the decline of the inverse association between BMI and lung cancer over time, the association is likely at least partly due to weight loss resulting from preclinical lung cancer that was present at baseline. Residual confounding by smoking could also have influenced our findings., (© The Author 2016. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Whether risk factors for epithelial ovarian cancer (EOC) differ by subtype (i.e., dualistic pathway of carcinogenesis, histologic subtype) is not well understood; however, data to date suggest risk factor differences. We examined associations between reproductive and hormone-related risk factors for EOC by subtype in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Among 334,126 women with data on reproductive and hormone-related risk factors (follow-up: 1992-2010), 1,245 incident cases of EOC with known histology and invasiveness were identified. Data on tumor histology, grade, and invasiveness, were available from cancer registries and pathology record review. We observed significant heterogeneity by the dualistic model (i.e., type I [low grade serous or endometrioid, mucinous, clear cell, malignant Brenner] vs. type II [high grade serous or endometrioid]) for full-term pregnancy (phet  = 0.02). Full-term pregnancy was more strongly inversely associated with type I than type II tumors (ever vs. never: type I: relative risk (RR) 0.47 [95% confidence interval (CI): 0.33-0.69]; type II, RR: 0.81 [0.61-1.06]). We observed no significant differences in risk in analyses by major histologic subtypes of invasive EOC (serous, mucinous, endometrioid, clear cell). None of the investigated factors were associated with borderline tumors. Established protective factors, including duration of oral contraceptive use and full term pregnancy, were consistently inversely associated with risk across histologic subtypes (e.g., ever full-term pregnancy: serous, RR: 0.73 [0.58-0.92]; mucinous, RR: 0.53 [0.30-0.95]; endometrioid, RR: 0.65 [0.40-1.06]; clear cell, RR: 0.34 [0.18-0.64]; phet  = 0.16). These results suggest limited heterogeneity between reproductive and hormone-related risk factors and EOC subtypes., (© 2015 UICC.)

Intake of dairy products has been associated with risk of some cancers, but findings are often inconsistent and information on hepatocellular carcinoma (HCC) risk is limited, particularly from prospective settings. The aim of our study was to investigate the association between consumption of total and specific dairy products (milk/cheese/yogurt) and their components (calcium/vitamin D/fats/protein), with first incident HCC (N(cases) = 191) in the European Prospective Investigation into Cancer and Nutrition cohort, including a nested case-control subset (N(cases) = 122) with the assessment of hepatitis B virus/hepatitis C virus infections status, liver damage and circulating insulin-like growth factor (IGF)-I levels. For cohort analyses, multivariable-adjusted Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI). For nested case-control analyses, conditional logistic regression was used to calculate odds ratios and 95% CI. A total of 477,206 participants were followed-up for an average of 11 years (person-years follow-up = 5,415,385). In the cohort study, a significant positive HCC risk association was observed for total dairy products (highest vs. lowest tertile, HR = 1.66, 95% CI: 1.13-2.43; p(trend) = 0.012), milk (HR = 1.51, 95% CI: 1.02-2.24; p(trend) = 0.049), and cheese (HR = 1.56, 95% CI: 1.02-2.38; p(trend) = 0.101), but not yogurt (HR = 0.94, 95% CI: 0.65-1.35). Dietary calcium, vitamin D, fat and protein from dairy sources were associated with increased HCC risk, whereas the same nutrients from nondairy sources showed inverse or null associations. In the nested case-control study, similar results were observed among hepatitis-free individuals. Results from this large prospective cohort study suggest that higher consumption of dairy products, particularly milk and cheese, may be associated with increased HCC risk. Validation of these findings in other populations is necessary. Potential biologic mechanisms require further exploration., (© 2014 UICC.)

Several prospective studies have shown a moderate positive association between increasing circulating insulin-like growth factor-I (IGF-I) levels and colorectal cancer risk. However, the associations were often statistically nonsignificant, and the relationship of cancer risk with IGF-I's major binding protein, IGFBP-3, showed major discrepancies between studies. We investigated the association of colorectal cancer risk with serum IGF-I, total and intact IGFBP-3, in a case-control study nested within the EPIC cohort (1,121 cases of colorectal cancer and 1,121 matched controls). Conditional logistic regression was used to adjust for possible confounders. Our present study results were combined in a meta-analysis with those from 9 previous prospective studies to examine the overall evidence for a relationship of prediagnostic serum IGF-I with colorectal cancer risk. In the EPIC study, serum concentrations of IGF-I and IGFBP-3 showed no associations with risk of colorectal cancer overall. Only in subgroup analyses did our study show moderate positive associations of IGF-I levels with risk, either among younger participants only (and only for colon cancer) or among participants whose milk intakes were in the lowest tertile of the population distribution (RR for an increase of 100 ng/ml = 1.43 [95% CI = 1.13-1.93]). Nevertheless, in the meta-analysis a modest positive association remained between serum IGF-I and colorectal cancer risk overall (RR = 1.07 [1.01-1.14] for 1 standard deviation increase in IGF-I). Overall, data from our present study and previous prospective studies combined indicate a relatively modest association of colorectal cancer risk with serum IGF-I.

Objective: This cross-sectional study aims to analyse the relationship between sedentary behaviour and breast cancer (BC) risk from a social perspective. Methods: Women aged 45–70 who participated in the Valencia Region Breast Cancer Screening Programme (2018–2019) were included, with a total of 121,359 women analysed, including 506 with cancer and 120,853 without cancer. The response variable was BC (screen-detected) and the main explanatory variable was sedentary behaviour (≤2 / >2-≤3 / >3-≤5 / >5 hours/day, h/d). Nested logistic regression models (M) were estimated: M1: sedentary behaviour adjusted for age and family history of BC; M2: M1 + hormonal/reproductive variables (menopausal status, number of pregnancies, hormone replacement therapy; in addition, months of breastfeeding was added for a subsample of women with one or more live births); M3: M2 + lifestyle variables (body mass index, smoking habits); M4: M3 + socioeconomic variables (educational level, occupation); Final model: M4 + gender variables (childcare responsibilities, family size). Interaction between sedentary behaviour and educational level was analysed in the Final model. Moreover, for the whole sample, postmenopausal women and HR+ BC, the Final model was stratified by educational level. Results: Sedentary behaviour was associated with an increased risk of BC with a nearly statistically significant effect in the Final model (>2-≤3 h/d: OR = 1.22 (0.93–1.61); >3-≤5 h/d: OR = 1.14 (0.86–1.52); >5: OR = 1.19 (0.89–1.60)). For women with a low educational level, sitting more than 2 h/d was associated with an increased risk of BC in the whole sample (>2-≤3 h/d OR = 1.93 (1.19–3.21); in postmenopausal women (>2-≤3 h/d, OR = 2.12 (1.18–2.96), >5h/d OR = 1.75 (1.01–3.11)) and in HR+ BC (>2-≤3h/d, OR = 2.15 (1.22–3.99)). Similar results were observed for women with one or more live births. Conclusions Sitting >2 h/d is associated with BC risk in women with low educational level, especially in postmenopausal women and those with live births. [ABSTRACT FROM AUTHOR]

Objective: Previous studies have indicated a potential correlation between cheese intake and risk of various diseases. However, establishing a causal relationship is challenging. To address this, we employed Mendelian randomization (MR) to simulate randomized trial groups and to investigate whether there is a causal link between cheese intake and the risk of gastroesophageal reflux disease (GERD) and Barrett's esophagus., Methods: We conducted a multivariable MR analysis using individual-level data on GERD and Barrett's esophagus from the published datasets. Univariable and multivariable MR investigations were carried out to explore and substantiate the causal association between genetically predicted cheese intake and esophageal diseases. Additionally, a network MR analysis was executed to identify potential intermediate variables., Results: Based on the primary causal effects model using MR analyses with the inverse-variance weighted (IVW) method, the genetically predicted that cheese intake demonstrated a protective factor of GERD (OR = 0.356; 95% CI 0.256-0.495; P = 8.22E-10) and Barrett's esophagus (OR = 0.223; 95% CI 0.114-0.437; P = 1.19E-5). These effects remained consistent after adjusting for potential confounders such as tobacco smoking (GERD: OR = 0.440; 95% CI 0.347 - 0.558; P = 1.17E-11; Barrett's esophagus: OR = 0.263; 95% CI 0.160 - 0.432; P = 1.33E-7) and BMI (GERD: OR = 0.515; 95% CI 0.424 - 0.626; P = 2.49E-11; Barrett's esophagus: OR = 0.402; 95% CI 0.243 - 0.664; P = 3.72E-4). Furthermore, the network MR showed that BMI mediated 28.10% and 27.50% of the causal effect of cheese intake on GERD and Barrett's esophagus, respectively, with statistically significant mediation effects., Conclusion: The multivariable MR analysis conducted in this study revealed a reverse causal relationship between cheese intake and GERD and Barrett's esophagus. Furthermore, BMI was potential mediating factor of the cheese intake effects on GERD and Barrett's esophagus. This finding provides causal evidence for the potential protective role of cheese intake in the prevention of esophageal diseases. The mediating effect of BMI suggests that dietary interventions combined with weight management may help reduce the risk of these diseases., Competing Interests: Declarations. Competing Interests: All authors declare no conflicts of interests. Ethics approval: There are no patients involved in our study design, recruitment or research conduction, and thus, there is no need for ethical approval., (© 2024. Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: Circulating IGF-1 concentrations have been associated with higher cancer risk, particularly prostate, breast and colorectal cancer. There is evidence from observational and intervention studies that milk and dairy products intake is associated with higher IGF-1 concentrations, but results were not always consistent. The purpose of this study was to examine the relationship between dairy intake and circulating IGF-1 concentrations in participants of the Second Bavarian Food Consumption Survey, thereby providing data for a German population for the first time. Methods: In this cross-sectional study of 526 men and women aged 18–80 years, in contrast to most previous investigations, dietary intake was assessed with a more detailed instrument than food frequency questionnaires (FFQs), i.e., by three 24-h dietary recalls conducted on random days close in time to the blood collection. Circulating IGF-1 concentrations were measured in blood samples. Multivariable linear regression models were used to examine the association of dairy intake with IGF-1 concentrations. Results: Each 400 g increment in daily dairy intake was associated with 16.8 µg/L (95% CI 6.9, 26.7) higher IGF-1 concentrations. Each 200 g increment in milk per day was associated with 10.0 µg/L (95% CI 4.2, 15.8) higher IGF-1. In contrast, we observed no association between cheese or yogurt intake and IGF-1 concentrations. Conclusions: Our findings are in line with most previous investigations and support the hypothesis that dairy and milk intake are associated with higher IGF-1 concentrations. [ABSTRACT FROM AUTHOR]

Non-functioning pituitary adenomas (NFPAs) are locally invasive with high morbidity. The objective of this study was to diagnose important genes and pathways related to the invasiveness of NFPAs and gain more insights into the underlying molecular mechanisms of NFPAs. The gene expression profiles of GSE51618 were downloaded from the Gene Expression Omnibus database with 4 non-invasive NFPA samples, 3 invasive NFPA samples, and 3 normal pituitary gland samples. Differentially expressed genes (DEGs) are screened between invasive NFPA samples and normal pituitary gland samples, followed by pathway and ontology (GO) enrichment analyses. Subsequently, a protein–protein interaction (PPI) network was constructed and analyzed for these DEGs, and module analysis was performed. In addition, a target gene–miRNA network and target gene–TF (transcription factor) network were analyzed for these DEGs. A total of 879 DEGs were obtained. Among them, 439 genes were upregulated and 440 genes were downregulated. Pathway enrichment analysis indicated that the upregulated genes were significantly enriched in cysteine biosynthesis/homocysteine degradation (trans-sulfuration) and PI3K-Akt signaling pathway, while the downregulated genes were mainly associated with docosahexaenoate biosynthesis III (mammals) and chemokine signaling pathway. GO enrichment analysis indicated that the upregulated genes were significantly enriched in animal organ morphogenesis, extracellular matrix, and hormone activity, while the downregulated genes were mainly associated with leukocyte chemotaxis, dendrites, and RAGE receptor binding. Subsequently, ESR1, SOX2, TTN, GFAP, WIF1, TTR, XIST, SPAG5, PPBP, AR, IL1R2, and HIST1H1C were diagnosed as the top hub genes in the upregulated and downregulated PPI networks and modules. In addition, HS3ST1, GPC4, CCND2, and SCD were diagnosed as the top hub genes in the upregulated and downregulated target gene–miRNA networks, while CISH, ISLR, UBE2E3, and CCNG2 were diagnosed as the top hub genes in the upregulated and downregulated target gene–TF networks. The new important DEGs and pathways diagnosed in this study may serve key roles in the invasiveness of NFPAs and indicate more molecular targets for the treatment of NFPAs. [ABSTRACT FROM AUTHOR]

Purpose of the Review: To summarize the current evidence on the most important dietary and lifestyle factors in colorectal carcinogenesis during different stages of a lifetime with special emphasis on studies investigating exposure during childhood, adolescence, and young adulthood.Recent Findings: A number of studies showed that independent of adult obesity, higher body fatness during childhood, adolescence, and young adulthood is associated with risk of colorectal cancer later in life. In one large cohort study, the Nurses’ Health Study II, adherence to a western pattern diet was associated with higher risk of advanced adenoma. The current evidence relating consumption of individual foods and nutrients as well as physical activity during early life to colorectal cancer is sparse and less consistent, at least in part due to limitations in study design, such as sample size, limited data on potential confounders or lack of a validated dietary assessment instrument.Summary: As colorectal carcinogenesis is a long process and can take up to several decades to develop, early life risk factors may also be etiologically relevant. The recent rise in early-onset colorectal cancer incidence and mortality in the USA, i.e., in individuals younger than 55 years at diagnosis, strongly supports that early life risk factors may influence colorectal carcinogenesis. Considering that the majority of colorectal cancers are preventable, there is an urgent need for well-designed investigations on the role of diet and lifestyle factors throughout the life course and risk of colorectal cancers. [ABSTRACT FROM AUTHOR]

Aim: This study conducts a systematic review and meta-analysis to assess the association between dairy consumption and hepatocellular carcinoma (HCC) risk. Subjects and methods: The association between consumption of overall dairy, specific dairy products (such as milk, cheese, butter, yoghurt, condensed milk, whey, casein, lactose) and HCC risk has not been assessed before. This association between dairy consumption and HCC risk has been reported in several epidemiological studies, but results were controversial and inconsistent. The PubMed, EMBASE and Cochrane databases were searched for relevant studies published up to September 20, 2015. The relative risks (RRs) and odds ratios (ORs) with 95% confidence intervals (CIs) for dairy consumption associated with HCC risk were extracted from each included cohort as well as case-control study. In our study, the pooled RR was obtained using the random-effects model. Heterogeneity was evaluated by Q and I statistics. Results: A total number of 1,084,666 participants and 2041 HCC patients from three cohort studies and five case-control studies were included in this meta-analysis. The pooled RR of dairy was 1.38 (95% CI: 1.00-1.91, p = 0.00) in all studies. The pooled RR of milk, yoghurt, and cheese was 1.13 (95% CI: 0.67-1.88, p = 0.00), 0.40 (95% CI: 0.14-1.14, p = 0.00) and 1.45 (95% CI: 1.02-2.07, p = 0.80), respectively. Conclusions: This meta-analysis indicates that consumption of overall dairy may be associated with increased HCC risk and a risk factor involved in the etiology of HCC. [ABSTRACT FROM AUTHOR]

Higher body fatness is not only associated with a higher risk of hypertension, type 2 diabetes, and coronary heart disease but also with certain types of cancer. The scope of this review is to summarize the epidemiological evidence for an association between body fatness and specific types of cancer and to outline the mediating role of obesity-related biomarkers in this context. Epidemiological studies have gathered convincing evidence that greater body fatness is associated with a higher risk of colorectal cancer, postmenopausal breast cancer, endometrial cancer, esophageal adenocarcinoma, renal cell carcinoma, and pancreatic cancer. Further, evidence for an association between higher body fatness and higher risk of ovarian cancer, advanced prostate cancer, and hepatocellular carcinoma is growing. Abdominal obesity is an independent risk factor for colorectal cancer beyond general obesity, whereas an independent role is less clear for other obesity-related cancer types. Epidemiological biomarker studies have shown that the positive association between body fatness and risk of cancer may be partly explained by hyperinsulinemia and altered concentrations in adipokines and sex-steroid hormones. In addition, obesity-associated low-grade inflammation plays a role in colorectal carcinogenesis. While epidemiology has contributed substantially to the understanding of the role of higher body fatness and related metabolic alterations in the development of cancer, further epidemiological biomarker studies are necessary to elucidate the complex interrelations between mediating pathways as well as to study novel pathways. Knowledge resulting from this research may help identify an obesity phenotype that is particularly strongly associated with cancer risk and thus pave the way for targeted prevention of cancer morbidity and mortality. [ABSTRACT FROM AUTHOR]

Cancer is the most widely recognized reason for human deaths globally. Conventional anticancer therapies, including chemotherapy and radiation, are very costly and induce severe side effects on the individual. The discovery of natural anticancer compounds like peptides may thus be a better alternative for cancer prevention and management. The anticancer peptides also exist in the amino acid chain of milk proteins and can be generated during proteolytic activities such as gastrointestinal digestion or food processing including fermentation. This paper presents an exhaustive overview of the contemporary literature on antitumor activities of peptides released from milk proteins. In addition, caseins and whey proteins have been evaluated for anticancer potential using the AntiCP database, a web-based prediction server. Proline and lysine, respectively, dominate at various positions in anticancer peptides obtained from caseins and whey proteins. The remarkable number of potential anticancer peptides revealed milk proteins as favorable candidates for the development of anticancer agents or milk and milk products for reduction of cancer risks. Moreover, anticancer peptides liberated from milk proteins can be identified from fermented dairy products. Although current findings of correlation between dairy food intakes and cancer risks lack consistency, dairy-derived peptides show promise as candidates for cancer therapy. This critical review supports the notion that milk proteins are not only a nutritious part of a normal daily diet but also have potential for prevention and/or management of cancer. [ABSTRACT FROM AUTHOR]

Background: Mammographic density represents epithelial and stromal proliferation, while insulin-like growth factor (IGF)-1, insulin-like growth factor-binding protein-3, growth hormone (GH), and estrogen may influence cellular proliferation. However, whether these growth factors independently, or in combination with estrogen, influence mammographic density in premenopausal women remains unclear. Materials and methods: Growth factors were assessed in 202 ovulating premenopausal women participating in the Energy Balance and Breast Cancer Aspects-I study. Estrogen was assessed in serum, and daily in saliva, throughout a menstrual cycle. Computer-assisted mammographic density (Madena) was obtained from digitized mammograms (days 7-12 of the menstrual cycle). Associations between growth factors, estrogen, and mammographic density were studied in regression models. Results: Women with a mean age of 30.7 years had a mean percent mammographic density of 29.8 %. Among women in the strata (above median split) of IGF-1 (>25 nmol/l) or GH (>0.80 mlU/l), we observed that an increase in salivary 17β-estradiol was associated with a higher odds for having higher percent mammographic density (>28.5 %). The odds ratios (ORs) per standard deviation increase in 17β-estradiol were 1.81 [95 % confidence interval (CI) 1.08-3.03] in the high IGF-1 stratum and 2.08 (95 % CI 1.10-3.94) in the high GH stratum. Furthermore, women in these strata of growth factors (above median) who had an overall average 17β-estradiol above median (>16.8 pmol/l) had higher ORs for having higher percent mammographic density (>28.5 %): IGF-1 4.13 (95 % CI 1.33-12.83) and GH 4.17 (95 % CI 1.41-12.28). Conclusion: Growth factors, in combination with cycling estrogen, were associated with percent mammographic density, and may be of potential clinical relevance. [ABSTRACT FROM AUTHOR]

Purpose: The purposes of this study are to examine (1) the feasibility and efficacy of two different home-based exercise protocols on the level of physical activity (PA), and (2) the effect of increased PA via home-based exercise program on biomarkers of colorectal cancer. Methods: Seventeen patients (age 55.18 ± 13.3 years) with stage II-III colorectal cancer completed the 12-week home-based exercise program. Subjects were randomized into either casually intervened home-based exercise group (CIHE) or intensely intervened home-based exercise group (IIHE). The primary outcome was the level of PA. Furthermore, insulin, homeostasis model assessment of insulin resistance, insulin-like growth factor axis, and adipocytokines were measured. Results: Both CIHE and IIHE program significantly increased the level of PA at 12 weeks compared to its level at baseline (CIHE, 10.00 ± 8.49 vs. 46.07 ± 45.59; IIHE, 12.08 ± 11.04 vs. 35.42 ± 27.42 MET hours per week). Since there was no difference in PA change between groups ( p = 0.511), the data was combined in analyzing the effects of increased PA on biomarkers. Increase in PA significantly reduced insulin (6.66 ± 4.58 vs. 4.86 ± 3.48 μU/ml, p = 0.006), HOMA-IR (1.66 ± 1.23 vs. 1.25 ± 1.04, p = 0.017), and tumor necrosis alpha-α (TNF-α 4.85 ± 7.88 vs. 2.95 ± 5.38 pg/ml, p = 0.004), and significantly increased IGF-1 (135.39 ± 60.15 vs. 159.53 ng/ml, p = 0.007), IGF binding protein (IGFBP)-3 (2.67 ± 1.48 vs. 3.48 ± 1.00 ng/ml, p = 0.013), and adiponectin (6.73 ± 3.07 vs. 7.54 ± 3.96 μg/ml, p = 0.015). Conclusion: CIHE program was as effective as IIHE program in increasing the level of PA, and the increase in PA resulted in significant change in HOMA-IR, IGF-1 axis, TNF-α, and adiponectin levels in stage II-III colorectal cancer survivors. [ABSTRACT FROM AUTHOR]

Background: Insulin, glucose, and other insulin-related proteins that mediate insulin signaling are associated with colorectal neoplasia risk, but associations with common genetic variation in insulin axis genes are less clear. In this study, we used a comprehensive tag single-nucleotide polymorphisms (SNPs) approach to define genetic variation in six insulin axis genes ( IGF1, IGF2, IGFBP1, IGFBP3, IRS1, and IRS2) and three genes associated with estrogen signaling ( ESR1, ESR2, and PGR). Methods: We assessed associations between SNPs and distal colorectal adenoma (CRA) risk in a case-control study of 1,351 subjects. Cases were individuals with one or more adenomas diagnosed during sigmoidoscopy, and controls were individuals with no adenomas at the sigmoidoscopy exam. We used unconditional logistic regression assuming an additive model to assess SNP-specific risks adjusting for multiple comparisons with P. Results: Distal adenoma risk was significantly increased for one SNP in IGF2 [per minor allele OR = 1.41; 95 % confidence interval (CI) = 1.16, 1.67; P = 0.005] and decreased for an ESR2 SNP (per minor allele OR = 0.78; 95 % CI = 0.66, 0.91; P = 0.041). There was no statistically significant heterogeneity of these associations by race, sex, BMI, physical activity, or, in women, hormone replacement therapy use. Risk estimates did not differ in the colon versus rectum or for smaller (<1 cm) versus larger ( >1 cm) adenomas. Conclusions: These data suggest that selected genetic variability in IGF2 and ESR2 may be modifiers of CRA risk. [ABSTRACT FROM AUTHOR]

Background:Insulin-like growth factors (IGFs) and their binding proteins (BPs) regulate cell differentiation, proliferation and apoptosis, and may have a role in the aetiology of various cancers. Information on their role in pancreatic cancer is limited and was examined here in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition.Methods:Serum concentrations of IGF-I and IGFBP-3 were measured using enzyme-linked immunosorbent assays in 422 cases and 422 controls matched on age, sex, study centre, recruitment date, and time since last meal. Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) adjusted for confounding variables.Results:Neither circulating levels of IGF-I (OR=1.21, 95% CI 0.75-1.93 for top vs bottom quartile, P-trend 0.301), IGFBP-3 (OR=1.00, 95% CI 0.66-1.51, P-trend 0.79), nor the molar IGF-I/IGFBP-3 ratio, an indicator of free IGF-I level (OR=1.22, 95% CI 0.75-1.97, P-trend 0.27), were statistically significantly associated with the risk of pancreatic cancer. In a cross-classification, however, a high concentration of IGF-I with concurrently low levels of IGFBP-3 was related to an increased risk of pancreatic cancer (OR=1.72, 95% CI 1.05-2.83; P-interaction=0.154).Conclusion:On the basis of these results, circulating levels of components of the IGF axis do not appear to be the risk factors for pancreatic cancer. However, on the basis of the results of a subanalysis, it cannot be excluded that a relatively large amount of IGF-1 together with very low levels of IGFBP-3 might still be associated with an increase in pancreatic cancer risk. [ABSTRACT FROM AUTHOR]

Background: Protein needs for athletes are likely higher than those for the general population. However, athletes may perceive their protein needs to be excessively high. The purpose of this research was to compare collegiate athletes' perceived protein needs and measured protein intake to the recommended protein intake (RDI) for healthy adults (i.e. 0.8 g/kg/d) and to the maximum beneficial level for strength-trained athletes (i.e. 2.0 g/kg/day). Methods: Perceived protein needs were quantified in 42 strength-trained collegiate male athletes by using a survey that asked the athletes to provide their perception about protein needs in specific quantitative terms (i.e. g/ kg/d). Perceived protein needs were also determined by having the athletes select a daylong menu that they perceived to have adequate protein content from a collection of 5 isoenergetic menus, which differed in terms of protein content. Actual protein intake was quantified using 3-day food records and nutrient analysis. Single sample t-tests were used to compare protein intake and perceived protein needs to 0.8 g/kg/day and 2.0 g/kg/day. Results: When asked to provide, in quantitative terms, protein needs for athletes, 67% of the athletes indicated "do not know." Of the remaining 33% of athletes, all gave values greater than 2.0 g/kg/d (mean 21.5 ± 11.2 g/kg/d, p = 0.14 vs. 2.0 g/kg/d). Based on the menu selection method for determining perceived protein needs, the athletes indicated that their protein needs were 2.4 ± 0.2 g/kg/d, which was greater than the RDI for protein (p < 0.0001) and tended to be greater than the maximally beneficial protein intake of 2.0 g/kg/d (p = 0.13). Measured protein intake was 2.0 ± 0.1 g/kg/d, which was greater than the RDI (p < 0.0001) but not different from the maximally beneficial protein intake of 2.0 g/kg/d (p = 0.84). Conclusions: Male collegiate athletes recognize that their protein needs are higher than that of the general population and consume significantly more protein than recommended in the RDI. However, it also appears that athletes are not aware of objective recommendations for protein intake and may perceive their needs to be excessively high. This study highlights the need for nutrition education in collegiate athletes, in particular nutrition education on macronutrient distribution and protein needs. [ABSTRACT FROM AUTHOR]