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Updated: Mar 13, 2026

Measuring Delay Discounting in Humans Using an Adjusting Amount Task
Published on: January 9, 2016
Attention-Deficit/Hyperactivity Disorder and Monetary Delay Discounting: A Meta-Analysis of Case-Control Studies
Jacob N S Jackson1, James MacKillop2
1Peter Boris Centre for Addictions Research, McMaster University/St. Joseph's Healthcare Hamilton, Hamilton, Ontario, Canada.
Background:
A growing number of studies have investigated delay discounting, a behavioral economic index of impulsivity, and its relevance to attention deficit hyperactivity disorder (ADHD), but with mixed findings. The current meta-analysis synthesizes the literature on the relationship between monetary delay discounting and ADHD in studies using case-control designs. Specifically, the objectives were: 1) to characterize the aggregated differences in monetary delay discounting between individuals with ADHD (cases) and controls in studies using categorical case-control designs; 2) to examine potential differences based on sample age (<18 vs. >18), reward outcome (real vs. hypothetical), and prevalence of conduct disorder and oppositional defiant disorder in the sample; and 3) to evaluate potential small-study (publication) bias in the literature.
Methods:
From 567 candidate articles, 21 independent investigations yielded 25 case-control comparisons (total N=3,913). Random effects meta-analysis was conducted using Cohen's d as the common effect size. Publication bias was evaluated using fail-safe N, Begg-Mazumdar and Egger tests, and metaregression of publication year and effect size.
Results:
Across studies, a statistically significant difference of medium magnitude effect size was present for the case-control comparisons (d=0.43; p < 10-15). No significant differences based on sample age, reward outcome, or comorbid status was detected. Minimal heterogeneity and evidence of publication bias was present.
Conclusions:
These findings provide robust evidence that delay discounting is significantly elevated among individuals with ADHD compared to controls. Gaps in the literature and the importance of characterizing the neural and genetic bases of this relationship are discussed.
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