rs117619191 - CEP164

Magnitude 2.2 · 2 studies on file

Reported associations

  • Genetics of 35 blood and urine biomarkers in the UK Biobank - Unknown journal (n.d.) · Unknown authors · PubMed 33462484

    ABSTRACT: Clinical laboratory tests are a critical component of the continuum of care. We evaluate the genetic basis of 35 blood and urine laboratory measurements in the UK Biobank (n=363,228 individuals). We identify 1,857 loci associated with at least one trait, containing 3,374 fine-mapped associations, and additional sets of large-effect (> 0.1 sd) protein-altering, HLA, and copy-number variant associations. Through Mendelian Randomization analysis, we discover 51 causal relationships, including previously known agonistic effects of urate on gout and cystatin C on stroke. Finally, we develop polygenic risk scores for each biomarker and built 'multi-PRS' models for diseases using 35 PRSs simultaneously, which improved chronic kidney disease, type 2 diabetes, gout, and alcoholic cirr

  • Blood metabolic biomarkers and colorectal cancer risk: results from large prospective cohort and Mendelian randomisation analyses - Unknown journal (n.d.) · Unknown authors · PubMed 40307439

    ABSTRACT: Background Emerging evidence suggests metabolic dysregulation may contribute to colorectal cancer (CRC) aetiology. We aimed to identify pre-diagnostic metabolic biomarkers for CRC risk in 230,420 UK Biobank participants. Methods Nuclear magnetic resonance spectroscopy was used to quantify 249 metabolic biomarkers in plasma samples collected at baseline. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals (CIs) for associations of metabolic biomarkers with CRC risk after adjusting for potential confounders. To infer the potential causality of biomarkers that were associated with CRC independent of the others, we performed genome-wide association analyses among 199,732 UK Biobank participants of European ancestry to identify biomarker-as


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Lifestyle context

Concrete actions anchored to the cited research. We do not prescribe, we describe.

Diet

  • refined carbohydrates and added sugars High

    Refined carbohydrates and added sugars elevate triglyceride levels; minimizing these is standard management for genetically elevated triglycerides

    Prioritize whole grains, legumes, fruits, vegetables; limit refined grains and sugary drinks

Discuss with your doctor

  • triglyceride management plan High

    Genetic predisposition to elevated triglycerides warrants individualized clinical management based on current levels and cardiovascular risk factors

    Discuss genetic findings and management strategy at next visit

Exercise

  • aerobic exercise High

    Regular aerobic exercise is a primary intervention for reducing triglyceride levels in individuals with genetic predisposition

    150 minutes moderate-intensity aerobic exercise per week, or 75 minutes vigorous-intensity

Screening

  • serum triglyceride levels High

    rs117619191 C allele is associated with genetically elevated triglyceride levels, increasing cardiovascular risk

    Annual lipid panel including fasting triglycerides