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Integrating Biobanking Into Conservation Practice: The Development and Impact of the EAZA Biobank.

Zoological biobanks are becoming essential tools in conservation, offering a means to preserve genetic material and support in situ population management amid accelerating biodiversity loss. With rapid advances in genomics, cryopreservation, and assisted reproduction technologies, biobanks enable a proactive approach to providing insurance against genetic erosion and facilitating future research, supplementation, and genetic rescue. However, to be effective, zoological biobanks must be purposefully designed, strategically integrated into conservation frameworks such as the Convention on Biological Diversity (CBD) Kunming-Montreal Global Biodiversity Framework (KMGBF), and regularly evaluated for coverage and impact. Using the EAZA Biobank as an example, we outline the structure, development, and collaborative foundations that have enabled its rapid growth, built on community support and conservation impact. Leveraging EAZA's institutional network and data-sharing platforms such as ZIMS, the Biobank employs a decentralized, four-hub model of zoological institutions storing samples. A gap analysis, integrating threat status, breeding programs, genomic data repositories, and phylogenetic diversity, highlights current sampling strengths and deficiencies and guides future collection priorities. The integration of specimen-specific genomic data and the EAZA Biobank Cryonetwork of institutions with expertise in storing and generating gametes and cell lines will expand the Biobank's role in population management and conservation. Zoological biobanks must now evolve alongside advances in biotechnology and genomics. Sample collection strategies should serve conservation needs and anticipate future applications in genomics, cryobiology, and conservation medicine, linking biospecimens with the wealth of data generated from them. This approach should be scalable beyond EAZA, forming the foundation of a global standardized biobanking framework. Ultimately, zoological biobanks are not merely repositories of the past-they are essential infrastructures shaping the future potential of species conservation.

EAZA

Benchmarking large language models for extracting biobank-derived insights into health and disease.

Biobank-scale datasets such as the UK Biobank have become foundational resources for advancing biomedical discovery. Yet the complexity and heterogeneity of these resources, spanning genomics, imaging, clinical records, and metadata, pose substantial barriers to access and interpretation. Large Language Models (LLMs) offer a promising avenue for making such datasets more navigable through natural language interfaces. However, the extent to which current general-purpose LLMs can retrieve and synthesize biobank-specific insights has not yet been systematically evaluated. In this study, we present a reproducible, multi-metric evaluation framework to benchmark the capabilities of leading LLMs. We evaluated six leading large language models: Gemini 3 Pro, Claude Opus 4.5, Claude Sonnet 4.5, GPT-5.2, Mistral Large 2, and DeepSeek V3, on four benchmark tasks designed to assess biobank-related knowledge retrieval. We evaluate model performance across six dimensions (semantic accuracy, factual correctness, domain knowledge, reasoning quality, response depth, and biobank specificity) and assessed output consistency using curated UK Biobank references and a robust random baseline. All models outperformed the baseline by 2&#xd7; to 3&#xd7;&#x2009;, with strong statistical separation (p&#x2009;<&#x2009;0.001), confirming meaningful biobank-specific knowledge retrieval. Gemini 3 Pro achieved the highest overall accuracy across tasks such as keyword synthesis, institution recognition, and topic inference, while Claude Sonnet 4.5 demonstrated the most uniform performance across evaluation dimensions. Our benchmark provides a rigorous framework for evaluating LLMs in biomedical settings. Using the UK Biobank as a real-world testbed, we highlight both the capabilities and limitations of current models, measuring their capacity to recall structured biomedical knowledge consistent with authoritative biobank metadata.

Large Language Models

Quantifying and improving rheumatoid arthritis algorithm performance in biobank settings.

OBJECTIVE: To quantify and improve the performance of standard rheumatoid arthritis (RA) algorithms in a biobank setting. METHODS: This retrospective cohort study within the Mayo Clinic (MC) Biobank and MC Tapestry Study identified RA cases by presence of at least two RA codes OR positive anti-cyclic citrullinated peptide antibodies (CCP) plus disease-modifying anti-rheumatic drug (DMARD) prescription as of 7/18/2022. Rheumatology physicians manually verified all RA cases using RA criteria and/or rheumatology physician diagnosis plus DMARD use. All other biobank participants served as non-RA controls. We defined seropositivity as rheumatoid factor and/or anti-CCP positivity. We assessed rules-based and Electronic Medical Records and Genomics (eMERGE) RA algorithms using positive predictive value (PPV). Finally, we developed a novel RA algorithm using a LASSO-based machine learning approach with five-fold cross validation. RESULTS: We identified 1,316 confirmed RA cases (968 MC Biobank, 348 Tapestry, 70 % seropositive) and 82,123 non-RA controls (mean age 65, 61 % female). The PPV of 3 RA codes was 43 %, codes plus DMARD was 54 %, and codes plus DMARD plus seropositivity was 85 %. The PPV of eMERGE was 77 %. Available in the MC Biobank, self-reported RA (PPV 10 %) only minimally improved algorithm performance (PPV from 83 % to 85 %), whereas family history of RA (PPV 3 %) worsened performance. At 90 % PPV, the novel RA algorithm incorporating key variables such as anti-CCP and DMARD use increased sensitivity by 4-11 % compared to eMERGE. CONCLUSION: Rules-based and eMERGE RA algorithms had worse performance in biobank than administrative settings. Our novel RA algorithm outperformed these standard algorithms.

Humans

Using Large Genomic Biobanks to Generate Insights into Genetic Kidney Disease.

Chronic kidney disease (CKD) affects approximately 9% of the global population, leading to increased risks of end-stage kidney disease (ESKD), cardiovascular disease (CVD), and mortality. Patients with CKD are a huge burden on health care resources globally. CKD is a complex condition influenced by a combination of genetic, environmental, and traditional risk factors. Family studies have suggested heritability rates for CKD ranging from 30% to 75%, and large genomic biobank studies have proven essential in identifying genes with substantial effects on CKD risk and in capturing cumulative genetic risk through polygenic risk scores. These biobanks are crucial for discovering new genes associated with kidney health and disease, and their growing size enhances the power to detect novel genetic associations. Integrating multi-omics technologies such as transcriptomics, metabolomics, and proteomics further enriches our understanding of CKD, while advanced computational tools continue to expand our insights into genetic data. Polygenic risk scores, derived from hundreds of genetic variants with small effect sizes, can help identify individuals at high risk of CKD. Genomic biobanks offer valuable opportunities for early identification and personalized treatment of monogenic kidney disorders, such as autosomal dominant polycystic kidney disease and Alport syndrome. These biobanks help fill knowledge gaps, particularly in individuals with milder or asymptomatic presentations who are often underrepresented in traditional studies. Expanding genomic biobank efforts globally, especially in diverse populations, is vital to enhancing our understanding of the genetic underpinnings of kidney disease. This review highlights the significant contributions of genomic biobanks to advancing our comprehension of the genetics of CKD.

Humans

Underrepresented voices in a Colorado Biobank: Perspectives from focus groups on motivations, return of results, and data sharing.

Most participants in large cohorts, such as biobanks, are of European descent. This lack of representation has been an ongoing challenge in genomic research. Understanding the perspectives on genomics research and participation in biobanks of historically underrepresented populations could provide insight into ways to better engage with these groups. We conducted a series of virtual and in-person focus groups with individuals who self-identified as American Indian or Alaska Native (AI/AN), African American/Black (AA/B), or Hispanic/Latino (H/L) and who were enrolled in the Colorado Center for Personalized Medicine (CCPM) biobank. The focus group discussions were centered on participant experiences, including but not limited to their motivations, return of results, and data sharing. There was a total of 23 participants across the six focus groups. The majority of participants identified as AI/AN (60.9%), followed by H/L (39.1%), and AA/B (21.7%); many participants identified with multiple race/ethnicities. The motivations for participating in the biobank included the potential to advance science and health, the potential for return of results, to learn more about one's ancestry, and a few indicated that they were interested in helping the biobank be more representative of all populations. Notably, many expressed positive feedback of the focus groups and felt that their views were valued, illustrating the importance of community-centered work. Our findings can be used to guide recruitment and engagement of biobank participants, especially from diverse backgrounds, contributing to enhanced partnerships advancing knowledge and healthcare.

biobank

The Biobank Rare Variant consortium powers the discovery of rare genetic associations through global collaboration.

Rare coding variants can have large effects on disease risk and provide direct routes from human genetics to disease mechanisms and therapeutic targets, but their discovery is constrained by sample size, particularly for low-prevalence diseases. Here we establish the Biobank Rare Variant Analysis (BRaVa) consortium, a global rare variant association resource that integrates sequencing and linked health-record data from ten biobanks and cohorts comprising over 1.2 million individuals across diverse ancestries. We performed gene-based meta-analyses of rare coding variation across 33 clinical endpoints and 11 quantitative traits. Aggregating evidence across biobanks and ancestries identified 514 gene-trait associations, including 31 not previously reported in prior studies or curated association resources following systematic literature review. Notably, 36.1% of gene-level associations were undetectable in any individual biobank, and 91 emerged only through cross-ancestry meta-analysis, demonstrating that federated integration enables discovery beyond the reach of single cohorts. Similar gains were observed at the variant level, where 25.0% of phenotype-locus associations were detectable only through meta-analysis. Effect size estimates were correlated across ancestries with concordant directions of effect, supporting the generalizability of rare variant associations. The identified signals implicate pathways involved in transcriptional and epigenetic regulation, metabolism, vascular and epithelial biology, and immune function, highlighting rare coding variation as an engine for biological discovery across medical record phenotypes. For example, damaging variation in ANKRD12 implicates inflammatory transcriptional dysregulation in asthma and chronic obstructive pulmonary disease, and ultra-rare predicted loss-of-function variants in NAA15 link protein acetylation processes to type 2 diabetes risk. BRaVa establishes a scalable framework and freely available community resource for rare variant meta-analysis across global biobanks. Public release of gene- and variant-level association summary statistics provides a reference map of rare coding variant associations to support disease gene discovery, biological interpretation, and therapeutic target prioritization as sequencing-linked health-record resources continue to expand.

Journal Article

CLINICAL AND COGNITIVE PHENOTYPING OF COPY NUMBER VARIANTS ASSOCIATED WITH NEURODEVELOPMENTAL DISORDERS FROM A MULTI-ANCESTRY BIOBANK.

Clinical biobanks with electronic health records (EHRs) linked to genotype data continue to expand yielding an opportunity to further characterize disease-relevant genomic risk factors, yet few recall-by-genotype studies from biobanks have been published to date. For example, copy number variants (CNVs) that significantly increase risk for multiple neurodevelopmental disorders (NDDs) and negatively affect neurocognition, may present in up to 2% of population cohorts, with public health implications for ascertaining NDD CNV carriers. From BioMe, a multi-ancestry biobank derived from the Mount Sinai healthcare system (New York, NY), 892 adult participants were recontacted for deep phenotyping, including 335 NDD CNV carriers as well as comparators, 217 individuals with schizophrenia and 340 controls. Clinical and cognitive assessments were administered to each participant. There was no disclosure of genetic information. Eight percent of recontacted biobank participants completed the study (30 NDD CNV carriers across 15 unique loci, 20 schizophrenia and 23 controls). The study sample had a mean age of 48.8 (10.2) years, was 66% female and of diverse ancestry, 36% African, 34% Hispanic, and 26% European. Overall, 70% of 30 NDD-CNV carriers harbored at least one neuropsychiatric or developmental phenotype, including 40% with mood or anxiety disorders. Further, 22 NDD CNV carriers were significantly impaired compared to controls on digit span backwards (Beta=-1.76, FDR=0.04) and digit span sequencing (Beta=-2.01, FDR=0.04), but higher performing than schizophrenia on verbal learning (Beta=4.5, FDR=0.05). Thirty NDD CNV carriers were successfully recruited from a multi-ancestry biobank, as well as healthy controls and low-functioning individuals with schizophrenia. Deep phenotyping corroborated past reports, while also identifying discordance with EHRs. Future recall-by-genotype studies may further benchmark the study design and elucidate feasibility.

Biobank

The importance of family-based sampling for biobanks.

Biobanks aim to improve our understanding of health and disease by collecting and analysing diverse biological and phenotypic information in large samples. So far, biobanks have largely pursued a population-based sampling strategy, where the individual is the unit of sampling, and familial relatedness occurs sporadically and by chance. This strategy has been remarkably efficient and successful, leading to thousands of scientific discoveries across multiple research domains, and plans for the next wave of biobanks are underway. In this Perspective, we discuss the strengths and limitations of a complementary sampling strategy for future biobanks based on oversampling of close genetic relatives. Such family-based samples facilitate research that clarifies causal relationships between putative risk factors and outcomes, particularly in estimates of genetic effects, because they enable analyses that reduce or eliminate confounding due to familial and demographic factors. Family-based biobank samples would also shed new light on fundamental questions across multiple fields that are often difficult to explore in population-based samples. Despite the potential for higher costs and greater analytical complexity, the many advantages of family-based samples should often outweigh their potential challenges.

Humans

The phenotype-genotype reference map: Improving biobank data science through replication.

Population-scale biobanks linked to electronic health record data provide vast opportunities to extend our knowledge of human genetics and discover new phenotype-genotype associations. Given their dense phenotype data, biobanks can also facilitate replication studies on a phenome-wide scale. Here, we introduce the phenotype-genotype reference map (PGRM), a set of 5,879 genetic associations from 523 GWAS publications that can be used for high-throughput replication experiments. PGRM phenotypes are standardized as phecodes, ensuring interoperability between biobanks. We applied the PGRM to five ancestry-specific cohorts from four independent biobanks and found evidence of robust replications across a wide array of phenotypes. We show how the PGRM can be used to detect data corruption and to empirically assess parameters for phenome-wide studies. Finally, we use the PGRM to explore factors associated with replicability of GWAS results.

Humans

Streamlining large-scale genomic data management: Insights from the UK Biobank whole-genome sequencing data.

Biobank-scale whole-genome sequencing (WGS) studies are increasingly pivotal in unraveling the genetic bases of diverse health outcomes. However, managing and analyzing these datasets' sheer volume and complexity presents significant challenges. We highlight the annotated genomic data structure (aGDS) format, substantially reducing the WGS data file size while enabling seamless integration of genomic and functional information for comprehensive WGS analyses. The aGDS format yielded 23 chromosome-specific files for the UK Biobank 500k WGS dataset, occupying only 1.10 tebibytes of storage. We develop the vcf2agds toolkit that streamlines the conversion of WGS data from VCF to aGDS format. Additionally, the STAARpipeline equipped with the aGDS files enabled scalable, comprehensive, and functionally informed WGS analysis, facilitating the detection of common and rare coding and noncoding phenotype-genotype associations. Overall, the vcf2agds toolkit and STAARpipeline provide a streamlined solution that facilitates efficient data management and analysis of biobank-scale WGS data across hundreds of thousands of samples.

Humans

Biobank-wide association scan identifies risk factors for late-onset Alzheimer's disease and endophenotypes.

Rich data from large biobanks, coupled with increasingly accessible association statistics from genome-wide association studies (GWAS), provide great opportunities to dissect the complex relationships among human traits and diseases. We introduce BADGERS, a powerful method to perform polygenic score-based biobank-wide association scans. Compared to traditional approaches, BADGERS uses GWAS summary statistics as input and does not require multiple traits to be measured in the same cohort. We applied BADGERS to two independent datasets for late-onset Alzheimer's disease (AD; n=61,212). Among 1738 traits in the UK biobank, we identified 48 significant associations for AD. Family history, high cholesterol, and numerous traits related to intelligence and education showed strong and independent associations with AD. Furthermore, we identified 41 significant associations for a variety of AD endophenotypes. While family history and high cholesterol were strongly associated with AD subgroups and pathologies, only intelligence and education-related traits predicted pre-clinical cognitive phenotypes. These results provide novel insights into the distinct biological processes underlying various risk factors for AD.

Alzheimer Disease

Recall-by-genotype of neurodevelopmental disorder copy number variants in a multi-ancestry, healthcare-system biobank.

Clinical biobanks linking electronic health records (EHRs) with genotype data enable the study of genomic risk factors in real-world populations. However, recall-by-genotype (RbG) of psychiatric risk variants in diverse healthcare-system biobanks remains scarce. Leveraging BioMe, a multi-ancestry biobank within the Mount Sinai Health System, we recalled carriers of rare copy number variants (CNVs) that confer increased risk for neurodevelopmental disorders (NDDs) to establish empirical benchmarks for RbG implementation. We recontacted 892 participants: 335 NDD CNV carriers, 217 individuals with schizophrenia without NDD CNVs, and 340 neurotypical controls without NDD CNVs. Participants completed clinical and cognitive assessments. Overall, 18% of recontacted participants responded to recruitment, and 8% completed the study: 30 NDD CNV carriers, 20 individuals with schizophrenia, and 23 controls. The mean age was 48.8 years, 66% were female, and self-reported ancestry was 37% African, 34% Hispanic, and 26% European. Seventy percent of NDD CNV carriers had at least one neuropsychiatric or developmental condition, including mood or anxiety disorders (40%). Among 22 NDD CNV carriers at loci implicated in impaired cognition, performance was lower than controls on Digit Span Backward (&#x3b2;&#x2009;=&#x2009;-1.76, FDR&#x2009;=&#x2009;0.04) and Digit Span Sequencing (&#x3b2;&#x2009;=&#x2009;-2.01, FDR&#x2009;=&#x2009;0.04). NDD CNV carriers also outperformed the schizophrenia group on verbal learning (&#x3b2;&#x2009;=&#x2009;4.5, FDR&#x2009;=&#x2009;0.05). Recall of individuals-including those with psychiatric illness-yielded phenotypes not captured in EHRs and provides empirical benchmarks relevant to RbG implementation and precision psychiatry in diverse healthcare systems.

Journal Article

An Annotated Biobank of Triple-Negative Breast Cancer Patient-Derived Xenografts Features Treatment-Na&#xef;ve and Longitudinal Samples during Neoadjuvant Chemotherapy.

UNLABELLED: Triple-negative breast cancer (TNBC) that fails to respond to neoadjuvant chemotherapy (NACT) can be lethal. Developing effective strategies to eradicate chemoresistant disease requires experimental models that recapitulate the heterogeneity characteristic of TNBC. To that end, we established a biobank of 92 orthotopic patient-derived xenograft (PDX) models of TNBC from the tumors of 75 patients enrolled in A Robust TNBC Evaluation fraMework to Improve Survival clinical trial (ARTEMIS, NCT02276443), including 12 longitudinal sets generated from serial patient biopsies collected throughout NACT treatment and from metastatic disease. Models were established from both chemosensitive and chemoresistant tumors, and nearly 30% of the PDX models were capable of metastasizing to the lungs. Comprehensive molecular profiling demonstrated conservation of genomes and transcriptomes between patient and corresponding PDX tumors, with representation of all major transcriptional subtypes. Transcriptional changes observed in the longitudinal PDX models highlighted dysregulation in pathways associated with DNA integrity, extracellular matrix interactions, the ubiquitin-proteasome system, epigenetics, and inflammatory signaling. These alterations revealed a complex network of adaptations associated with chemoresistance. Overall, this PDX biobank provides a valuable tool for tackling the most pressing issues facing the clinical management of TNBC. SIGNIFICANCE: The development of a patient-derived xenograft biobank that comprehensively captures the genomic and transcriptional diversity of triple-negative breast cancer promises to be a robust resource to investigate and overcome chemoresistance and metastasis.

Animals

PMBB Geno-Pheno Toolkit: A suite of scalable, reproducible pipelines for cross-biobank association analyses.

Electronic health record (EHR)-linked biobanks generate unprecedented genomic and phenotypic datasets, but their scientific utility is constrained by data fragmentation across institutional silos and incompatible computing infrastructures, forcing researchers to rewrite ad-hoc scripts for each new environment. We present the PMBB Geno-Pheno Toolkit, a suite of modular Nextflow pipelines for biobank-scale association analyses. This note focuses on the toolkit's SAIGE family of pipelines - supporting genome-wide (GWAS), exome-wide (ExWAS), and phenome-wide (PheWAS) association testing - together with the companion GWAMA and ExWAS meta-analysis pipelines that enable cross-biobank replication. All components are containerized (Docker/Apptainer) and orchestrated with Nextflow, allowing the same workflows to run unmodified on local HPC clusters, cloud platforms, and the All of Us Research Workbench. Complementary toolkit pipelines for PLINK-based GWAS, polygenic scoring, LD-based clumping, and phenotype harmonization are also available and briefly noted.

Journal Article

Whole-genome sequencing of 490,640 UK Biobank participants.

Whole-genome sequencing provides an unbiased and complete view of the human genome and enables the discovery of genetic variation without the technical limitations of other genotyping technologies. Here we report on whole-genome sequencing of 490,640 UK Biobank participants, building on previous genotyping effort1. This advance deepens our understanding of how genetics associates with disease biology and further enhances the value of this open resource for the study of human biology and health. Coupling this dataset with rich phenotypic data, we surveyed within- and cross-ancestry genomic associations and identified novel genetic and clinical insights. Although most associations with disease traits were primarily observed in individuals of European ancestries, strong or novel signals were also identified in individuals of African and Asian ancestries. With the improved ability to accurately genotype structural variants and exonic variation in both coding and UTR sequences, we strengthened and revealed novel insights relative to whole-exome sequencing2,3 analyses. This dataset, representing a large collection of whole-genome sequencing&#xa0;data that is available to the UK Biobank research community, will enable advances of our understanding of the human genome, facilitate the discovery of diagnostics and&#xa0;therapeutics with higher efficacy and improved safety profile, and enable precision medicine strategies with the potential to improve global health.

Humans

Genome-wide association, polygenic risk scores, and machine learning for chronic post-surgical pain risk stratification: A UK biobank study.

Chronic post-surgical pain is a prevalent and debilitating complication following surgery, representing a clinical challenge. Despite the established heritability of pain phenotypes, large-scale genetic studies remain limited. This study aimed to identify genetic variants associated with chronic post-surgical pain, develop polygenic risk scores, and integrate these with clinical features for risk prediction. UK Biobank data from 47,836 participants (2490 cases and 45,346 controls) were split into training (80%; n = 38,268) and validation (20%; n = 9568) sets prior to analysis. A genome-wide association study was conducted on the training set only, across 19 million variants, and polygenic risk scores were constructed and integrated with clinical features in a logistic regression framework. Two close, rare, imputed signals crossed the genome-wide significance threshold but lacked local linkage-disequilibrium support, while 220 variants crossed the suggestive threshold. In the held-out validation set, cases had higher mean polygenic risk scores than controls (0.138 vs. -0.021; Cohen's d = 0.16, p < 0.001). A logistic regression model integrating clinical features and polygenic risk scores achieved an area under the curve of 0.639 (95% CI: 0.583-0.693), higher than models using either feature set alone. The polygenic risk score for chronic post-surgical pain was among the most important predictors. Risk stratification revealed the top quartile had 3.84-fold higher odds of chronic post-surgical pain than the bottom quartile (95% CI: 2.00-7.37). These findings suggest a possible modest genetic contribution to chronic post-surgical pain. Polygenic risk scores may complement clinical factors in surgical risk stratification. PERSPECTIVE: Chronic post-surgical pain may have a modest genetic contribution. This UK Biobank study identified over 220 variants at suggestive significance and constructed a polygenic risk score that was significantly elevated in cases. A combined clinical-genomic model achieved a 3.84-fold difference in odds across predicted-risk quartiles.

Chronic post-surgical pain

A genome-wide association study of stroke risk in Asian statin users: evidence from KoGES and UK Biobank.

BACKGROUND: Despite proven efficacy of statins in stroke prevention, genetic factors may influence individual stroke risk among statin users. With increasing precision medicine approaches and growing evidence of population-specific genetic variations, identifying genetic markers that predict stroke risk in statin-treated Asian populations has become critically important for personalized cardiovascular prevention strategies. METHODS: We conducted a genome-wide association study of 1,678 participants using lipid-lowering agents in the Korean Genome and Epidemiology Study (KoGES) cohort. Significant findings were replicated in 2,170 Asian participants on statins from the UK Biobank using an additive genetic model adjusted for relevant covariates. RESULTS: In the discovery analysis, 83 single nucleotide polymorphisms were suggestively associated with stroke (p&#x2009;<1.0&#x2009;&#xd7;&#x2009;10-5). Among these, 21 SNPs in the CDH13 gene were associated with increased stroke risk. The lead SNP, rs7201829, was significantly replicated in the UK Biobank (odds ratio: 2.29, p&#x2009;=&#x2009;2.39&#x2009;&#xd7;&#x2009;10-5). CONCLUSIONS: This study identified CDH13 as a significant genetic marker associated with stroke risk among Asian statin users. These findings provide the first genome-wide evidence for genetic determinants of stroke susceptibility during statin therapy, supporting the development of personalized prevention strategies in Asian populations.

Aged

Diet Changes and Colorectal Cancer Risk in the UK Biobank.

BACKGROUND: Modifying dietary behaviors into healthier habits may attenuate the risk of colorectal cancer. This study aimed to investigate the association between dietary changes and the risk of colorectal cancer. METHODS: Following dietary recommendations for red and processed meat, fruit and vegetables, and alcohol consumption, we classified 50,640 participants into poor and good adherence groups in the UK Biobank. Changes in dietary habits were defined as stable poor, poor to good, good to poor, and stable to good adherences. A Cox proportional hazard model was used to examine the association between dietary changes and colorectal cancer risk. RESULTS: Women were more likely to follow dietary recommendations than men. After a median of 3.3 years from the latest follow-up, 8,328 (16.4%) participants followed an improved dietary habit and 5,808 (11.5%) participants had a worsened diet. Compared with men who stably consumed fruit and vegetables <5 servings/day, those who increased their consumption to &#x2265;5 servings/day were related to colorectal cancer risk reduction [HR: 0.24 (0.09-0.63)]. However, the beneficial associations of increased fruit and vegetable consumption were not statistically significant in women [HR: 0.41 (0.11-1.56)]. CONCLUSIONS: Our findings support the evidence that increasing fruit and vegetable intake could serve as a beneficial strategy to mitigate colorectal cancer risk in men. IMPACT: Participants from the UK Biobank significantly changed their adherence to dietary recommendations during the follow-up. Increasing fruit and vegetable consumption was inversely associated with colorectal cancer risk among men.

Humans