The role of linoleic acid in asthma and inflammatory markers: a Mendelian randomization study
Zhao JV, Schooling CM
The American journal of clinical nutrition · 20 citas
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Cómo se estudió
- Diseño
- Estudio de casos y controles (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2019-06-05 · Am J Clin Nutr · vol. 110 · número 3 · págs. 685–690
- Editorial
- Elsevier BV
- Citado
- 29 citas · más que el 88% de estudios similares · 2.3× el promedio de su campo
- Referencias
- 51 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Asthma and respiratory diseases · Fatty Acid Research and Health · Genetic Associations and Epidemiology
- Palabras clave
- linoleic acid, asthma, omega-6 fatty acids, eosinophil count, neutrophil count, monocyte count, genetic variants, reverse causality, dietary fatty acids
- MeSH
- humans, asthma, genetic predisposition to disease, inflammation, linoleic acid, multivariate analysis, case-control studies, polymorphism, single nucleotide, genome-wide association study, united kingdom
2 autores
- Jie V. Zhao🇭🇰University of Hong Kong
- Catherine Mary Schooling🇺🇸🇭🇰 · autor de correspondenciaCity University of New York; University of Hong Kong
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Asthma is a common respiratory disease, possibly caused by autoimmunity. Linoleic acid (LA), the main n-6 (ω-6) PUFA from widely used vegetable oils, is thought to suppress immune responses that might have benefits for asthma. However, this question has not been examined in randomized controlled trials.
Objectives
To obtain unconfounded estimates, we assessed how genetically predicted LA affected asthma using 2-sample Mendelian randomization. We also examined its role in white blood cell traits (eosinophil, neutrophil, and low monocyte counts) identified as potential causal factors in asthma.
Methods
We used 18 uncorrelated, genome-wide significant genetic variants to predict LA, which we applied to a large genetic case (n = 19,954)-control (n = 107,715) study of asthma, to the UK Biobank (408,961 people of European ancestry with 26,332 asthma cases), and for white blood cell traits to the UK Biobank. We also repeated the analysis on asthma using 29 replicated, functionally relevant genetic variants. In addition, we examined the role of asthma in LA to assess reverse causality.
Results
Genetically predicted LA was associated with lower risk of asthma (OR: 0.89 per SD increase in LA; 95% CI: 0.85, 0.93), with no association of asthma with LA. Genetically predicted LA was associated with lower eosinophil count (-0.03; 95% CI: -0.061, -0.004) and lower neutrophil count (-0.04; 95% CI: -0.057, -0.023). These estimates were robust to different selections of genetic variants and sensitivity analyses.
Conclusions
LA might protect against asthma possibly via white blood cell traits, with relevance to the identification of effective new interventions for asthma.
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