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Associations of Observational and Genetically Determined Caffeine Intake With Coronary Artery Disease and Diabetes Mellitus

Said MA, van de Vegte YJ, Verweij N, van der Harst P

Journal of the American Heart Association · 45 citas

Cómo se estudió

Diseño
Estudio de cohortes (clasificado por nuestro filtro de IA)
Estudiado en
Personas
Resultado principal
Eventos clínicos como enfermedad o muerte

Quién lo pagó

Financiación
Financiación independiente
Universidad u hospital
Rijksuniversiteit Groningen
Gobierno
Nederlandse Organisatie voor Wetenschappelijk Onderzoek
Universidad u hospital
Universitair Medisch Centrum Groningen
Universidad u hospital
Center for Information Technology
Gobierno
Dutch Research Council (NWO)
Subvenciones
Nederlandse Organisatie voor Wetenschappelijk Onderzoek (016.186.125)

Según 5 financiadores declarados y la declaración de financiación del texto completo.

Publicación

Publicado
2020-12-08 · J Am Heart Assoc · vol. 9 · número 24 · pág. e016808
Editorial
Wiley
Citado
51 citas · más que el 92% de estudios similares · 3.0× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
49 trabajos
Acceso
Acceso abierto (revista) · CC-BY-NC-ND
Áreas de investigación
Coffee research and impacts · Obesity, Physical Activity, Diet · Eating Disorders and Behaviors
Palabras clave
Mendelian randomization, Medicine, Observational study, Caffeine, Coronary artery disease, Hazard ratio, Internal medicine, Diabetes mellitus, Type 2 Diabetes Mellitus, Disease, Endocrinology, Confidence interval, Genetics, Gene, Genotype, Biology
MeSH
humans, diabetes mellitus, type 2, caffeine, proportional hazards models, risk factors, risk reduction behavior, causality, coffee, tea, aged, middle aged, female, male, coronary artery disease, genetic variation, genome-wide association study, mendelian randomization analysis

4 autores

  • M. Abdullah Said🇳🇱University Medical Center Groningen; University of Groningen
  • Yordi J. van de Vegte🇳🇱University Medical Center Groningen; University of Groningen
  • Niek Verweij🇳🇱University Medical Center Groningen; University of Groningen
  • Pim van der Harst🇳🇱🇩🇪University Medical Center Groningen; University of Groningen; Heidelberg University; University Hospital Heidelberg; University Medical Center Utrecht; Netherlands Heart Institute

Resumen

El texto original del estudio, en el idioma en que se publicó.

Background Caffeine is the most widely consumed psychostimulant and is associated with lower risk of coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM). However, whether these associations are causal remains unknown. This study aimed to identify genetic variants associated with caffeine intake, and to investigate evidence for causal links with CAD or T2DM. In addition, we aimed to replicate previous observational findings. Methods and Results Observational associations were tested within UK Biobank using Cox regression analyses. Moderate observational caffeine intakes from coffee or tea were associated with lower risks of CAD or T2DM, with the lowest risks at intakes of 121 to 180 mg/day from coffee for CAD (hazard ratio [HR], 0.77 [95% CI, 0.73-0.82; P-16]), and 301 to 360 mg/day for T2DM (HR, 0.76 [95% CI, 0.67-0.86]; P=1.57×10-5). Next, genome-wide association studies were performed on self-reported caffeine intake from coffee, tea, or both in 407 072 UK Biobank participants. These analyses identified 51 novel genetic variants associated with caffeine intake at P-8. These loci were enriched for central nervous system genes. However, in contrast to the observational analyses, 2-sample Mendelian randomization analyses using the identified loci in independent disease-specific cohorts yielded no evidence for causal links between genetically determined caffeine intake and the development of CAD or T2DM. Conclusions Mendelian randomization analyses indicate genetically determined higher caffeine intake might not protect against CAD or T2DM, despite protective associations in observational analyses.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY-NC-ND).

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