Earlier I was intentionally simplifying things.
You’re right that the old “simple chemical imbalance” explanation of ADHD is outdated. But completely discarding biology in response goes too far in the other direction. ADHD is a neurodevelopmental disorder involving dysregulation across multiple systems. It isn’t just a neutral difference in brain wiring.
Dopamine and norepinephrine still matter here. The fact that stimulant and non-stimulant medications targeting these systems consistently reduce symptoms is not a coincidence. That clinical effectiveness reflects real underlying biology, even if no single neurotransmitter abnormality fully explains ADHD on its own.
In medicine and psychology, we don’t define disorders based on imaging findings. We define them based on persistent impairment and dysfunction, and ADHD clearly meets that bar. That’s why it has a diagnosis in the DSM. The impairments are real, measurable, and reproducible.
It’s also true that structural and functional differences in areas like the prefrontal cortex, basal ganglia, and limbic system tend to be subtle and overlap with neurotypical populations. But subtle doesn’t mean irrelevant. These differences are consistently linked to problems with executive function, reward processing, impulse control, and emotional regulation. More importantly, they show up in real-world outcomes: academic difficulties, unstable employment, higher injury rates, and increased risk of comorbid psychiatric conditions.
The idea that ADHD is primarily an evolutionary adaptation rather than a disorder is, at this point, speculative. Models like the “hunter versus farmer” hypothesis haven’t been supported by evolutionary genetics or population-level data. Current evidence doesn’t show clear positive selection for ADHD-associated alleles, and some data actually suggest reduced reproductive fitness over time. There’s a meaningful difference between metaphors that help people feel better about themselves and explanations that are supported by solid evidence.
Acknowledging strengths commonly seen in people with ADHD—creativity, energy, novel problem-solving—is important and appropriate. But recognizing strengths doesn’t cancel out pathology. Many medical and neurodevelopmental conditions come with areas of resilience or advantage. That doesn’t turn them into adaptations instead of disorders.
ADHD is considered a disorder because, across cultures and contexts, it reliably causes clinically significant impairment without treatment or accommodation. Minimizing that reality in the name of reducing stigma ends up doing people with ADHD a disservice.
ADHD is a legitimate disorder with real, measurable impairments. At the same time, people with ADHD are not broken, deficient, or without meaningful strengths. Both of those things can be true at once.
Earlier I was intentionally simplifying things. You’re right that the old “simple chemical imbalance” explanation of ADHD is outdated. But completely discarding biology in response goes too far in the other direction. ADHD is a neurodevelopmental disorder involving dysregulation across multiple systems. It isn’t just a neutral difference in brain wiring.
Dopamine and norepinephrine still matter here. The fact that stimulant and non-stimulant medications targeting these systems consistently reduce symptoms is not a coincidence. That clinical effectiveness reflects real underlying biology, even if no single neurotransmitter abnormality fully explains ADHD on its own. In medicine and psychology, we don’t define disorders based on imaging findings. We define them based on persistent impairment and dysfunction, and ADHD clearly meets that bar. That’s why it has a diagnosis in the DSM. The impairments are real, measurable, and reproducible.
It’s also true that structural and functional differences in areas like the prefrontal cortex, basal ganglia, and limbic system tend to be subtle and overlap with neurotypical populations. But subtle doesn’t mean irrelevant. These differences are consistently linked to problems with executive function, reward processing, impulse control, and emotional regulation. More importantly, they show up in real-world outcomes: academic difficulties, unstable employment, higher injury rates, and increased risk of comorbid psychiatric conditions.
The idea that ADHD is primarily an evolutionary adaptation rather than a disorder is, at this point, speculative. Models like the “hunter versus farmer” hypothesis haven’t been supported by evolutionary genetics or population-level data. Current evidence doesn’t show clear positive selection for ADHD-associated alleles, and some data actually suggest reduced reproductive fitness over time. There’s a meaningful difference between metaphors that help people feel better about themselves and explanations that are supported by solid evidence.
Acknowledging strengths commonly seen in people with ADHD—creativity, energy, novel problem-solving—is important and appropriate. But recognizing strengths doesn’t cancel out pathology. Many medical and neurodevelopmental conditions come with areas of resilience or advantage. That doesn’t turn them into adaptations instead of disorders.
ADHD is considered a disorder because, across cultures and contexts, it reliably causes clinically significant impairment without treatment or accommodation. Minimizing that reality in the name of reducing stigma ends up doing people with ADHD a disservice. ADHD is a legitimate disorder with real, measurable impairments. At the same time, people with ADHD are not broken, deficient, or without meaningful strengths. Both of those things can be true at once.