Expressive

rs11901649 - APOB

Magnitude 2.2 · 4 studies on file

Reported associations

  • Gastroesophageal reflux GWAS identifies risk loci that also associate with subsequent severe esophageal diseases - Unknown journal (n.d.) · Unknown authors · PubMed 31527586

    ABSTRACT: Gastroesophageal reflux disease (GERD) is caused by gastric acid entering the esophagus. GERD has high prevalence and is the major risk factor for Barrett's esophagus (BE) and esophageal adenocarcinoma (EA). We conduct a large GERD GWAS meta-analysis (80,265 cases, 305,011 controls), identifying 25 independent genome-wide significant loci for GERD. Several of the implicated genes are existing or putative drug targets. Loci discovery is greatest with a broad GERD definition (including cases defined by self-report or medication data). Further, 91% of the GERD risk-increasing alleles also increase BE and/or EA risk, greatly expanding gene discovery for these traits. Our results map genes for GERD and related traits and uncover potential new drug targets for these conditions. Gastr

  • A Genome-Wide Association Study of Genetic Variants of Apolipoprotein A1 Levels and Their Association with Vitamin D in Korean Cohorts - Unknown journal (n.d.) · Unknown authors · PubMed 36140721

    ABSTRACT: Dyslipidemia is an important independent risk factor for cardiovascular disease (CVD). Specifically, apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), and the ApoB/A1 ratio have been linked to CVD. We conducted a genome-wide association study meta-analysis of two Korean cohorts containing a total of 12,924 patients to identify novel single nucleotide polymorphisms (SNPs) associated with ApoA1 and ApoB levels and the ApoB/A1 ratio. Additionally, an expression quantitative trait locus (eQTL) and differentially expressed genes (DEGs) analysis were performed. The statistically significant eQTL, DEG, and Gene Ontology (GO) results were used to explore the predicted interaction networks and retrieve the interacting genes and proteins. We identified three novel SNPs (rs11066280, p = 3

  • GWAS and multi-omics integrative analysis reveal novel loci and their molecular mechanisms for circulating fatty acids - Unknown journal (n.d.) · Unknown authors · PubMed 40545721

    ABSTRACT: Summary Previous genome-wide association studies (GWAS) have identified genetic loci associated with the circulating levels of fatty acids (FAs), but the biological mechanisms of these genetic associations remain largely unexplored. Here, we conducted GWAS to identify additional genetic loci for 19 circulating FA traits in UK Biobank participants of European ancestry (n = 239,268) and five other ancestries (n = 508-4,663). We leveraged the GWAS findings to characterize genetic correlations and colocalized regions among FAs, explore sex differences, examine FA loci influenced by lipoprotein metabolism, and apply statistical fine-mapping to pinpoint putative causal variants. We integrated GWAS signals with multi-omics quantitative trait loci (QTL) to reveal intermediate molecular

  • A genetic map of human metabolism across the allele frequency spectrum - Unknown journal (n.d.) · Unknown authors · PubMed 41044249

    ABSTRACT: Genetic studies of human metabolism have been limited in scale and allelic breadth. Here we provide a data-driven map of the genetic regulation of circulating small molecules and lipoprotein characteristics (249 traits) measured using proton nuclear magnetic resonance spectroscopy across the allele frequency spectrum in ~450,000 individuals. Trans-ancestral meta-analyses identify 29,824 locus-metabolite associations mapping to 753 regions with effects largely consistent between men and women and large ancestral groups represented in UK Biobank. We observe and classify extreme genetic pleiotropy, identify regulators of lipid metabolism, and assign effector genes at >100 loci through rare-to-common allelic series. We propose roles for genes less established in metabolic control (

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Lifestyle context

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

Bloodwork

  • apolipoprotein B, lipid profile High

    rs11901649 increases APOB expression, elevating apolipoprotein B levels which directly increase atherosclerosis risk

    Check ApoB, total cholesterol, LDL, HDL; annual screening typical

Diet

  • saturated fat Moderate

    Elevated ApoB from this variant can be partially managed through reduction of dietary saturated fat, which decreases LDL cholesterol production

    Limit saturated fat to less than 7% of total daily calories

  • soluble fiber Moderate

    Soluble fiber reduces cholesterol absorption and promotes LDL excretion, counteracting ApoB elevation from this genetic variant

    Target 10-25 grams per day from oats, beans, apples, citrus

Discuss with your doctor

  • GERD susceptibility and Barrett's esophagus screening High

    rs11901649 increases GERD risk and is associated with Barrett's esophagus and esophageal adenocarcinoma development

    Inform doctor of genetic GERD susceptibility; ask about Barrett's screening if chronic GERD develops

  • apolipoprotein B elevation and cardiovascular risk High

    rs11901649-associated ApoB elevation is an independent cardiovascular disease risk factor; doctor may recommend preventive therapy

    Bring ApoB results to doctor; ask about cardiovascular risk assessment and preventive options

Lifestyle

  • GERD triggers and risk behaviors High

    This variant increases baseline GERD risk; lifestyle modifications reduce reflux frequency and protect esophageal epithelium

    Avoid eating 2-3 hours before bed; limit alcohol and acidic foods; maintain healthy weight

Screening

  • gastroesophageal reflux disease symptoms High

    rs11901649 increases gastroesophageal reflux disease susceptibility and progression to Barrett's esophagus, warranting symptom surveillance

    Track reflux frequency and severity; report changes to doctor