Publications by authors named "Humaira Rasheed"

Background: Our goal was to identify genetic and modifiable risk factors for upper urinary tract infections (UTIs).

Methods: We used data from UK Biobank, the Trøndelag Health Study, and the Michigan Genomics Initiative to conduct genome-wide association studies and sex-stratified analyses on upper UTI. Mendelian randomization (MR) analyses were conducted to examine potential causal relationships between cardiometabolic risk factors and upper UTIs.

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  • Trace elements play a crucial role in human health but can also be toxic; their absorption and effects are influenced by genetics, but this area is still under-researched.
  • This study conducted genome-wide analysis on 57 trace elements using blood samples from Scandinavian individuals, identifying 11 new genetic locations linked to the levels of specific elements such as arsenic, zinc, and selenium.
  • The findings suggest some trace elements may have weak to moderate health impacts, with notable indications of increased zinc potentially being harmful and linked to prostate cancer, though more validation is required.
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Heart failure (HF) causes substantial morbidity and mortality but its pathobiology is incompletely understood. The proteome is a promising intermediate phenotype for discovery of novel mechanisms. We measured 4877 plasma proteins in 13,900 HF-free individuals across three analysis sets with diverse age, geography, and HF ascertainment to identify circulating proteins and protein networks associated with HF development.

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Aims: A low resting heart rate (RHR) implies a more efficient heart function and a lower risk of cardiovascular disease. However, observational studies have reported a U-shaped association between RHR and atrial fibrillation (AF). In contrast, Mendelian randomization (MR) studies have found an inverse causal association between RHR and AF.

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Background: Previous Mendelian randomization (MR) studies using population samples (population MR) have provided evidence for beneficial effects of educational attainment on health outcomes in adulthood. However, estimates from these studies may have been susceptible to bias from population stratification, assortative mating and indirect genetic effects due to unadjusted parental genotypes. MR using genetic association estimates derived from within-sibship models (within-sibship MR) can avoid these potential biases because genetic differences between siblings are due to random segregation at meiosis.

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Objective: In this study, we aimed to establish the causal effects of lowering sclerostin, target of the antiosteoporosis drug romosozumab, on atherosclerosis and its risk factors.

Methods: A genome-wide association study meta-analysis was performed of circulating sclerostin levels in 33,961 European individuals. Mendelian randomization (MR) was used to predict the causal effects of sclerostin lowering on 15 atherosclerosis-related diseases and risk factors.

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Background: Preeclampsia is a leading cause of maternal morbidity, and dyslipidemia has been associated with preeclampsia in observational studies. We use Mendelian randomization analyses to estimate the association between lipid levels, their pharmacological targets, and the risk of preeclampsia in 4 ancestry groups.

Methods: We extracted uncorrelated (<0.

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The Trøndelag Health Study (HUNT) is a population-based cohort of ∼229,000 individuals recruited in four waves beginning in 1984 in Trøndelag County, Norway. Approximately 88,000 of these individuals have available genetic data from array genotyping. HUNT participants were recruited during four community-based recruitment waves and provided information on health-related behaviors, self-reported diagnoses, family history of disease, and underwent physical examinations.

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  • Researchers studied the genetic connections to blood fats using data from 1.6 million people from different backgrounds to understand why certain fats are higher or lower in the body.
  • They looked at special genes and how they interact in the liver and fat cells, finding that the liver plays a big part in controlling fat levels.
  • Two specific genes, CREBRF and RRBP1, were highlighted as important in understanding how our bodies manage fats due to strong supporting evidence.
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  • The study investigates the genetic factors contributing to the decline in estimated glomerular filtration rate (eGFR), a key indicator of kidney function, by analyzing data from 62 longitudinal studies involving over 343,000 participants.
  • Twelve significant genetic variants related to eGFR decline were identified, with most showing interaction effects based on age, which highlights how genetic influences on kidney function change as individuals get older.
  • The findings emphasize that individuals with certain genetic profiles face higher risks for kidney failure and acute kidney injury, providing valuable insights that could aid in drug development and strategies for managing kidney health.
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  • Reduced glomerular filtration rate (GFR) is a precursor to kidney failure, influenced by factors like genetics and diabetes (DM), but the interaction between these factors is not well understood.
  • A large-scale genome-wide association study (GWAS) analyzed eGFR across almost 1.5 million individuals, revealing distinct genetic loci that differ between those with and without diabetes.
  • The findings identified potential new targets for drug development aimed at protecting kidney function, highlighting that many drug interventions could be effective for both diabetic and non-diabetic populations.
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Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes.

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Background: Taller people have a lower risk of coronary heart disease but a higher risk of many cancers. Mendelian randomization (MR) studies in unrelated individuals (population MR) have suggested that these relationships are potentially causal. However, population MR studies are sensitive to demography (population stratification, assortative mating) and familial (indirect genetic) effects.

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  • - This study explored the links between 45 risk factors and chronic kidney disease (CKD) in Europeans and 17 in East Asians using genetic data to test for causal relationships.
  • Eight risk factors were identified as having a causal effect on CKD in Europeans, with body mass index (BMI), hypertension, and type 2 diabetes being notable, while only three risk factors had similar evidence in East Asians.
  • The findings suggest specific risk factors like high BMI can increase the risk of CKD, emphasizing the need for targeted interventions to address these prevalent health issues across different ancestries.
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Increased blood lipid levels are heritable risk factors of cardiovascular disease with varied prevalence worldwide owing to different dietary patterns and medication use. Despite advances in prevention and treatment, in particular through reducing low-density lipoprotein cholesterol levels, heart disease remains the leading cause of death worldwide. Genome-wideassociation studies (GWAS) of blood lipid levels have led to important biological and clinical insights, as well as new drug targets, for cardiovascular disease.

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  • Lower respiratory tract infections (LRTIs) are significant health issues, and this study aimed to uncover genetic factors and risks linked to them using data from large health studies.
  • A genome-wide association study identified the 15q25.1 genetic locus as significantly associated with LRTI susceptibility, showing a protective effect for smokers but not non-smokers.
  • Key lifestyle factors like high body mass index, smoking, and elevated blood pressure were found to increase the risk of developing LRTIs, suggesting that addressing these factors could help reduce their impact.
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Genes underneath signals from genome-wide association studies (GWAS) for kidney function are promising targets for functional studies, but prioritizing variants and genes is challenging. By GWAS meta-analysis for creatinine-based estimated glomerular filtration rate (eGFR) from the Chronic Kidney Disease Genetics Consortium and UK Biobank (n = 1,201,909), we expand the number of eGFRcrea loci (424 loci, 201 novel; 9.8% eGFRcrea variance explained by 634 independent signal variants).

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Background: The causal nature of the observed associations between serum lipids and apolipoproteins and kidney function are unclear.

Methods: Using two-sample and multivariable Mendelian randomization (MR), we examined the causal effects of serum lipids and apolipoproteins on kidney function, indicated by the glomerular-filtration rate estimated using creatinine (eGFRcrea) or cystatin C (eGFRcys) and the urinary albumin-to-creatinine ratio (UACR). We obtained lipid- and apolipoprotein-associated genetic variants from the Global Lipids Genetics Consortium (n = 331 368) and UK Biobank (n = 441 016), respectively, and kidney-function markers from the Trøndelag Health Study (HUNT; n = 69 736) and UK Biobank (n = 464 207).

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