What’s the Deal With Dopamine and ADHD?

This is part 4 of a 5-part series on modern perspectives on ADHD. Part 3, "Is ADHD Really a Disorder?" is available here.

If a distinct population of individuals have something we describe as ADHD, there should be clear biological markers for it. While structural differences have been found in the ADHD brain—including corpus callosum, cerebellum, and basal ganglia reduced white matter volumes¹—one integral part of the story appears to lie with our neurotransmitters.

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Dopamine Signalling and ADHD

Of particular interest in the ADHD brain is dopamine. Dopamine is a signalling molecule (neurotransmitter) released when we’re stimulated by something interesting or rewarding. Dopamine is also required for control of our executive functions (thoughts, feelings, and behaviours). You could think of it like we earn dopamine through rewarding activity and spend it immediately to operate our executive functions.

When we’re adequately stimulated and our brain detects enough dopamine, we feel satisfied and content with staying focused, calm, and still; when we’re inadequately stimulated and dopamine signals are low, we feel dissatisfied and will start searching for stimulation. This could involve moving our "attentional spotlight" around, focusing on objects in our surroundings or imagination, or we might start physically moving around or fidgeting, and we might feel generally bored, irritable, or stressed.

ADHD Brain Differences

One hypothesis has been that ADHDers have a "dopamine deficit." However, research suggests it’s less about dopamine levels and more about dopamine signal strength arising from dopamine receptor variation within the ADHD brain². These neural differences are why we refer to ADHDers as neurodiverse when compared to the majority of individuals, who we can think of as being neurotypical.

ADHDers are more likely to have variant dopamine receptor alleles (genetic code for a particular gene)³. ADHDers are more likely to have seven instead of four repeats to a 48 base pair sequence encoding their D4 dopamine receptor. Additionally, they’re more likely to have a 148 base pair sequence instead of the typical 136 base pair sequence encoding their D5 dopamine receptor. These differences produce receptors that have lower dopamine binding affinity, making it more difficult for the receptors to detect—or "hear"—dopamine.

The D4 and D5 receptors primarily reside in the prefrontal and anterior cingulate cortices—brain regions responsible for executive functions including attention, error detection, decision-making, impulse control, and emotional regulation. Furthermore, one variant of the D2 dopamine receptor gene found more commonly in ADHDers is implicated in lower dopamine receptor expression in the striatum³, a brain region responsible for bodily movement and motivation.

As there are multiple genes implicated in ADHD, ADHD presents with different subtypes and severity. Some genetic differences, such as the D2 receptor variation, may lead to more physical hyperactivity, and others to more cognitive hyperactivity. Also, the more of these differences an individual has, the more severe their presentation is likely to be.

Dopamine and ADHD Stimulation Needs

The results indicate that those with variant dopamine receptor genes require more novel and stimulating engagement with the world to maintain the same dopamine signal as neurotypicals. That is, they require more stimulation to remain focused, calm, and still.

For ADHDers who have these genetic differences, the need for adequate stimulation is met much less often, so they’re seen more often in an emotionally heightened, unfocused, and hyperactive state. Furthermore, these individuals will compensate for this low dopamine signal through enhanced activity with their mind and body to increase their dopamine signal levels.

The idea that there’s something particular about ADHD biology might suggest its associated difficulties are something we have to entirely accept. However, there are many ways to manage ADHD difficulties. I’ll cover this in the next and last post in this series on ADHD.