Andalusian School of Public Health

Polyphenols represent the largest and most diverse class of dietary antioxidants. Epidemiological evidence linking specific (poly)phenol classes, such as flavonoids and lignans, to breast cancer (BC) risk remains limited and largely inconclusive in prospective studies. The aim of this study is to examine the association between the intake of total (poly)phenols-and its classes and subclasses-and BC risk-overall and by subtypes (estrogen, progesterone, and human epidermal growth factor receptor 2 (HER2))-in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. The EPIC cohort includes 257,960 adult women from seven European countries. During a mean follow-up of 14 years, there were 10,722 incident overall BC cases. Associations were computed using Cox regression models adjusted for potential confounders. No significant associations were found between total (poly)phenol intake and overall BC risk (HRQ5 vs. Q1 = 1.02; 95% CI: 0.95-1.11). In addition, null associations were mostly found between classes and subclasses of (poly)phenols and BC subtypes. After stratifying by menopausal status, no significant associations were observed. In conclusion, this study found no evidence of associations between the intake of any class or subclass of (poly)phenols and BC risk in the European population.

Pleural mesothelioma (PM) is a rare, asbestos-linked cancer with a long asymptomatic latency, delaying diagnosis and limiting treatment options. Identifying blood‐based biomarkers that signal disease before symptoms onset could improve surveillance of at‐risk individuals. In our work, we conducted a prospective proteomic study of pre-diagnostic serum from 21 PM cases (< 5 years before diagnosis) and 21 asbestos‐exposed controls in the EPIC cohort using SWATH‐MS, followed by ELISA validation. Findings were tested in an independent MoMar cohort of 32 pre‐diagnostic plasma samples (< 1 year before diagnosis) and 32 matched controls. SWATH-MS identified 12 differentially expressed proteins (nominal p < 0.05, fold change > 1.3 or < 0.75). Transferrin and complement C4A were elevated, while beta‐2‐microglobulin and dermcidin were reduced in pre‐diagnostic cases. ELISA confirmed a borderline significant rise in beta‐2‐microglobulin within two years of diagnosis in EPIC. Calretinin and mesothelin were also detected in both cohorts, with the five‐marker panel achieving an AUC of 0.91 (p = 0.001) in MoMar but not reaching significance in EPIC (AUC = 0.88, p = 0.17). Integrating novel proteomic biomarker candidates with established markers enhances early PM detection in high-risk populations. Larger, multi‐cohort validation is warranted to refine this biomarker panel for clinical surveillance.

ABSTRACT This systematic review of prospective studies examined whether psychological stress—conceptualised as cumulative stressful life events or perceived stress—is associated with cancer incidence. It was pre-registered in PROSPERO (IDCRD42020175681) and conducted following PRISMA guidelines. Methodological quality was assessed using the NIH Tool for Observational Studies, and the certainty of evidence was assessed using the GRADE tool. Hazard ratios were synthesised using random-effects meta-analyses. Nineteen studies were included, evaluating the effect of stressful life events (k=6) and/or perceived stress (k=15) on overall (k=3), breast (k=10), prostate (k=3), colorectal (k=2) and endometrial (k=1) cancer. Neither stressful life events nor perceived stress was consistently associated with cancer risk. Conflicting results emerged for perceived stress, including both protective and detrimental effects, particularly for breast and colorectal cancer. Most studies employed non-validated stress measures (k=12), assessed stress only once (k=17), and did not examine its impact comprehensively (k=11). The certainty of evidence was graded as very low. This review found no consistent evidence linking psychological stress to cancer risk. More high-quality prospective studies using comprehensive and validated measures of psychological stress and exploring potential moderators can help advance knowledge on the role of psychological stress in cancer incidence.

BackgroundAlcohol consumption has been described to exhibit a J-shaped relationship with dementia risk, but previous observations may be partly biased due to “sick-quitters” and competing risks of death.ObjectiveTo examine the association between baseline and lifetime alcohol consumption and the risk of dementia and subtypes in a large Mediterranean cohort, accounting for lifetime drinking patterns, potential confounding, and competing risks of death.MethodsProspective study of 30,211 participants, 29–69 years at recruitment (1992–1996), from the EPIC-Spain dementia cohort. Alcohol intake was assessed using a validated dietary history and retrospective questionnaires covering ages 20, 30, and 40 years. Dementia cases (n = 1,114) were ascertained through linkage with healthcare and mortality databases and individual medical record review over a mean follow-up of 22.8 years. Multivariate competing risk models were used to estimate sub-hazard ratios (sHRs) for dementia by categories of baseline and lifetime alcohol consumption, using lifetime abstainers as the reference group.ResultsMean lifetime alcohol consumption was 41.9 and 4.4 g/d in men and women, respectively. No significant associations were found between baseline or lifetime alcohol consumption and risk of overall dementia (sHRcurrentvs.never = 0.96, 95% CI: 0.82, 1.13; sHRevervs.never = 0.96, 95% CI: 0.82, 1.11), Alzheimer's disease, or non-Alzheimer subtypes. These null findings remained consistent across strata of sex, BMI or smoking categories, and by beverage type. Sensitivity analyses excluding mis-reporters of energy intake or low-quality diagnoses yielded similar results.ConclusionsIn this large prospective cohort with over 1,100 dementia cases and long-term follow-up, alcohol consumption was not significantly associated with dementia risk. These findings challenge the notion of a protective effect of moderate drinking and warrant continued investigation using methodologically rigorous approaches to clarify the role of alcohol dose, timing, and pattern on dementia risk.