Acute Caffeine Intake Does Not Modulate Active or Reactive Inhibition in Non-Clinical Young Adults, and ADHD Symptoms Do Not Moderate Its Effects
Altınok A
Human psychopharmacology · 0 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
Según la declaración de financiación del texto completo.
Publicación
- Publicado
- 2026-10-04 · Hum Psychopharmacol · vol. 41 · número 6 · pág. e70067
- Editorial
- Wiley
- Citado
- 0 citas · más que el 82% de estudios similares · 0.0× el promedio de su campo
- Referencias
- 21 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY
- Áreas de investigación
- Coffee research and impacts · Attention Deficit Hyperactivity Disorder · Neural and Behavioral Psychology Studies
- Palabras clave
- inhibitory control, active inhibition, reactive inhibition, ADHD symptoms, go/no-go task, flanker task, young adults, Bayes factor, null hypothesis testing, cognitive performance
- MeSH
- humans, caffeine, central nervous system stimulants, severity of illness index, cross-over studies, double-blind method, reactive inhibition, reaction time, attention deficit disorder with hyperactivity, adolescent, adult, female, male, young adult, inhibition, psychological, cognitive enhancement
1 autor
- Ahmet Altınok🇳🇱🇹🇷 · autor de correspondenciaUniversity of Groningen; Pamukkale University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Caffeine is consumed for its presumed cognitive benefits, yet controlled studies have repeatedly failed to find effects on inhibitory control. Cross-sectional work suggests that people with elevated attention-deficit/hyperactivity disorder (ADHD) symptoms may benefit from chronic, moderate caffeine consumption, but whether acute intake improves cognition in proportion to symptom severity has not been tested experimentally.
Aims
We tested whether 250 mg of caffeine improves active inhibition (withholding a prepared response) and reactive inhibition (resolving response conflict), and whether ADHD symptom severity moderates these effects.
Methods
In a preregistered, randomised, double-blind, placebo-controlled crossover trial, a nonclinical sample of 36 young adults received 250 mg of caffeine or placebo in counterbalanced order, with testing 45 min after ingestion. Active inhibition was assessed with a Go/No-Go task (204 trials), reactive inhibition with an arrow flanker task (200 trials) and symptoms with the Adult ADHD Self-Report Scale. Mixed-effects models included treatment, symptom severity, their interaction and ten covariates; Bayes factors quantified evidence for the null.
Results
Both tasks produced their benchmark effects (dz = 1.24 and 1.09) and all indices were reliable (split-half r = 0.73-0.98). Caffeine affected neither commission errors (BF01 = 4.98), response criterion (5.14), Go reaction time (2.83), reaction time variability (4.35), flanker reaction time (5.49) nor flanker accuracy (5.09). ADHD symptoms moderated no effect (15 preregistered tests; smallest p = 0.514), yet predicted performance itself (flanker accuracy r = -0.42), indicating that the null is not due to an insensitive measure.
Conclusions
Caffeine produced no acute benefit for either form of inhibition, and ADHD symptoms did not moderate its effects. Bayes factors supported the absence rather than the nondetection of these effects, arguing against an acute improvement of inhibitory control that scales with ADHD symptom severity in nonclinical young adults. Whether this also holds for chronic consumption or for adults with diagnosed ADHD remains to be tested.
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