{"title":"Dietary carotenoids and breast cancer risk: evidence from a large population-based incident case-control study.","authors":"Bahar Darouei, Torsten Bohn, Farhad Vahid, Reza Amani-Beni, Shaghayegh Haghjooy Javanmard, Kazem Zendehdel, Ibrahim Abdollahpour","doi":"10.1186/s12986-025-01007-x","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Although mechanistic studies suggest protective roles for carotenoids against breast cancer (BC), human studies yield inconsistent findings. Few have comprehensively evaluated dietary intake of individual and grouped carotenoids in relation to BC risk.</p><p><strong>Methods: </strong>This population-based case-control study recruited 600 patients with newly diagnosed BC and 600 healthy controls. Dietary carotenoid intake was assessed using a validated 168-item food frequency questionnaire. The intake levels of α-carotene, β-carotene, β-cryptoxanthin, lutein/zeaxanthin, lycopene, astaxanthin, phytoene, phytofluene, neoxanthin, violaxanthin, and total carotenoids were categorized into quartiles. Logistic regression models were employed to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for BC risk, controlling for potential confounders.</p><p><strong>Results: </strong>Higher intake of lycopene, phytoene, phytofluene, total non-provitamin A and provitamin A, β-carotene, lutein/zeaxanthin, as well as total carotenoids was significantly associated with reduced BC risk Lycopene showed the strongest inverse association (Q4 vs. Q1: OR = 0.23; 95% CI: 0.14-0.37). Total provitamin A (Q4 OR = 0.46; 95% CI: 0.29-0.75) and total non-provitamin A carotenoids (Q4 OR = 0.25; 95% CI: 0.15-0.41) also showed strong protective associations. Total carotenoid (Q4 OR = 0.34, 95% CI: 0.20-0.56, p < 0.001) intake also showed inverse associations across all quartiles. Conversely, α-carotene, β-cryptoxanthin, astaxanthin, neoxanthin, and violaxanthin displayed weaker or inconsistent associations.</p><p><strong>Conclusion: </strong>These findings support an inverse association between dietary intake of specific carotenoids, particularly lycopene, lutein/zeaxanthin, and colorless carotenoids (phytoene and phytofluene) and BC risk. Promoting a carotenoid-rich diet may represent a feasible strategy for BC prevention.</p>","PeriodicalId":19196,"journal":{"name":"Nutrition & Metabolism","volume":"22 1","pages":"107"},"PeriodicalIF":4.1000,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12487211/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nutrition & Metabolism","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12986-025-01007-x","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NUTRITION & DIETETICS","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Although mechanistic studies suggest protective roles for carotenoids against breast cancer (BC), human studies yield inconsistent findings. Few have comprehensively evaluated dietary intake of individual and grouped carotenoids in relation to BC risk.
Methods: This population-based case-control study recruited 600 patients with newly diagnosed BC and 600 healthy controls. Dietary carotenoid intake was assessed using a validated 168-item food frequency questionnaire. The intake levels of α-carotene, β-carotene, β-cryptoxanthin, lutein/zeaxanthin, lycopene, astaxanthin, phytoene, phytofluene, neoxanthin, violaxanthin, and total carotenoids were categorized into quartiles. Logistic regression models were employed to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for BC risk, controlling for potential confounders.
Results: Higher intake of lycopene, phytoene, phytofluene, total non-provitamin A and provitamin A, β-carotene, lutein/zeaxanthin, as well as total carotenoids was significantly associated with reduced BC risk Lycopene showed the strongest inverse association (Q4 vs. Q1: OR = 0.23; 95% CI: 0.14-0.37). Total provitamin A (Q4 OR = 0.46; 95% CI: 0.29-0.75) and total non-provitamin A carotenoids (Q4 OR = 0.25; 95% CI: 0.15-0.41) also showed strong protective associations. Total carotenoid (Q4 OR = 0.34, 95% CI: 0.20-0.56, p < 0.001) intake also showed inverse associations across all quartiles. Conversely, α-carotene, β-cryptoxanthin, astaxanthin, neoxanthin, and violaxanthin displayed weaker or inconsistent associations.
Conclusion: These findings support an inverse association between dietary intake of specific carotenoids, particularly lycopene, lutein/zeaxanthin, and colorless carotenoids (phytoene and phytofluene) and BC risk. Promoting a carotenoid-rich diet may represent a feasible strategy for BC prevention.
期刊介绍:
Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects.
The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases.
Key areas we wish to encourage submissions from include:
-how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes;
-the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components;
-how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved;
-how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.