There is no single cause that explains ADHD.
Shared influences, many small effects
Shared influences, many small effects
Instead, many small ingredients shape inattention and hyperactivity in everyone.
Here are some risk factors scientists have found.
Very early birth
Lead exposure in childhood
Extreme lack of care early in life
Many DNA variants can influence inattention and hyperactivity.
Many different variants can contribute.
Let’s illustrate how different influences can combine in three people.
Most common DNA variants linked to ADHD each have only a tiny effect.
Several influences can combine with an ordinary level of inattention and hyperactivity.
For some people, the combined effects contribute to difficulties that seriously disrupt daily life.
Some influences are still unknown.
These difficulties can lead someone to seek help and an ADHD assessment.
ADHD has many contributing causes. Many of the same influences also shape inattention and hyperactivity across the whole population.
What the examples mean
A risk factor is linked to a higher chance of an outcome. It does not tell us what will happen to one person. People with similar ADHD traits can have different histories.
Shared influences across the continuum
Research supports substantial overlap in the genetic influences on ADHD diagnoses and ADHD traits in the wider population. This does not mean that every influence is identical for everyone.
Many small genetic effects
Most common DNA differences associated with ADHD have very small individual effects. Many can contribute together. Some rare genetic variants have larger effects.
The DNA numbers identify illustrative variants, not named genes or a complete list. People differ in which variants they carry. Having a risk-associated variant does not mean that someone will have ADHD.
The deprivation example refers to extreme lack of early care studied in institutions. It does not mean ordinary differences in parenting cause ADHD.
How the illustration was drawn
The three people and their combinations of influences are fictional. The icons, stack heights, and dashed lines are illustrative, not measured effects or a way to calculate a diagnosis. The drawing highlights influences associated with greater difficulties; other influences can reduce difficulties, and effects depend on the person and their circumstances. The diagnostic threshold line is not a universal boundary: clinical assessment considers symptoms, their history, and impairment across settings.