Energetic insufficiency in neurons due to inadequate lactate supply is implicated in several neuropathologies, including attention-deficit/hyperactivity disorder (ADHD). By formalizing the mechanism and implications of such constraints on function, the behavioral Neuroenergetics Theory (NeT) predicts the results of many neuropsychological tasks involving individuals with ADHD and kindred dysfunctions, and entails many novel predictions. The associated diffusion model predicts that response times will follow a mixture of Wald distributions from the attentive state, and ex-Wald distributions after attentional lapses. It is inferred from the model that ADHD participants can bring only 75–85% of the neurocognitive energy to bear on tasks, and allocate only about 85% of the cognitive resources of comparison groups. Parameters derived from the model in specific tasks predict performance in other tasks, and in clinical conditions often associated with ADHD. The primary action of therapeutic stimulants is to increase norepinephrine in active regions of the brain. This activates glial adrenoceptors, increasing the release of lactate from astrocytes to fuel depleted neurons. The theory is aligned with other approaches and integrated with more general theories of ADHD. Therapeutic implications are explored.