The effect of daily caffeine use on cerebral blood flow: How much caffeine can we tolerate?
Addicott MA, Yang LL, Peiffer AM, Burnett LR, Burdette JH, Chen MY, Hayasaka S, Kraft RA, Maldjian JA, Laurienti PJ
Human brain mapping · 150 citas
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institutes of Health
- Gobierno
- National Institute on Drug Abuse
- Gobierno
- National Institute of Neurological Disorders and Stroke
- Gobierno
- National Institute of Biomedical Imaging and Bioengineering
- Gobierno
- National Center for Research Resources
- Gobierno
- NIBIB NIH HHS
- Gobierno
- NIDA NIH HHS
- Gobierno
- NCRR NIH HHS
- Gobierno
- NINDS NIH HHS
- Subvenciones
- National Institute of Biomedical Imaging and Bioengineering (EB03880); National Institute of Neurological Disorders and Stroke (NS 042568); National Institute of Neurological Disorders and Stroke (K08NS042568); National Institute of Biomedical Imaging and Bioengineering (R01 EB004673); National Center for Research Resources (M0-1RR 007122); National Institute on Drug Abuse (DA024950); National Institute of Biomedical Imaging and Bioengineering (EB004673); National Center for Research Resources (RR 07122); National Institute on Drug Abuse (F31 DA024950); National Institute of Biomedical Imaging and Bioengineering (R01 EB003880)
Según 9 financiadores declarados.
Publicación
- Publicado
- 2009-02-13 · Hum Brain Mapp · vol. 30 · número 10 · págs. 3102–3114
- Editorial
- Wiley
- Citado
- 208 citas · más que el 96% de estudios similares · 5.3× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 69 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Coffee research and impacts · Migraine and Headache Studies · Adenosine and Purinergic Signaling
- Palabras clave
- caffeine, cerebral blood flow, adenosine receptors, cerebral vasoconstriction, gray matter perfusion, caffeine tolerance, caffeine withdrawal
- MeSH
- brain, saliva, humans, caffeine, central nervous system stimulants, imaging, three-dimensional, echo-planar imaging, brain mapping, administration, oral, analysis of variance, retrospective studies, double-blind method, cerebrovascular circulation, dose-response relationship, drug, adolescent, adult, middle aged, female, male, statistics as topic, young adult
10 autores
- Merideth A. Addicott🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Lucie L. Yang🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Ann M. Peiffer🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Luke Burnett🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Jonathan H. Burdette🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Michael Y. Chen🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Satoru Hayasaka🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Robert Kraft🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Joseph A. Maldjian🇺🇸Wake Forest University Health Sciences; Wake Forest University
- Paul J. Laurienti🇺🇸Wake Forest University Health Sciences; Wake Forest University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Caffeine is a commonly used neurostimulant that also produces cerebral vasoconstriction by antagonizing adenosine receptors. Chronic caffeine use results in an adaptation of the vascular adenosine receptor system presumably to compensate for the vasoconstrictive effects of caffeine. We investigated the effects of caffeine on cerebral blood flow (CBF) in increasing levels of chronic caffeine use. Low (mean = 45 mg/day), moderate (mean = 405 mg/day), and high (mean = 950 mg/day) caffeine users underwent quantitative perfusion magnetic resonance imaging on four separate occasions: twice in a caffeine abstinent state (abstained state) and twice in a caffeinated state following their normal caffeine use (native state). In each state, there were two drug conditions: participants received either caffeine (250 mg) or placebo. Gray matter CBF was tested with repeated-measures analysis of variance using caffeine use as a between-subjects factor, and correlational analyses were conducted between CBF and caffeine use. Caffeine reduced CBF by an average of 27% across both caffeine states. In the abstained placebo condition, moderate and high users had similarly greater CBF than low users; but in the native placebo condition, the high users had a trend towards less CBF than the low and moderate users. Our results suggest a limited ability of the cerebrovascular adenosine system to compensate for high amounts of daily caffeine use.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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