When someone asks what causes ADHD? the honest answer is: no single thing. ADHD is one of the most studied neurodevelopmental conditions in psychiatry, and decades of research converge on one point — it is multifactorial. Three forces interact: genetics, brain neurobiology, and environment. Understanding each one changes how we think about ADHD — and about ourselves.
1. Genetic factors: the foundation (70–80% heritable)
ADHD is one of the most heritable psychiatric conditions known. Twin studies consistently put heritability at around 70–80%, meaning the largest single driver is genetic (Faraone et al., 2021). But there is no single "ADHD gene." ADHD is polygenic: hundreds of common variants each contribute a tiny fraction of risk, most of them touching dopamine signalling pathways — DRD4, DRD5, DAT1. A smaller number of people carry rare copy-number variants (CNVs) with larger individual effects.
This polygenic nature explains why ADHD runs in families without following a simple inheritance pattern — and why no genetic test can reliably diagnose it on its own.
2. Brain neurobiology: how genes play out
Genes do not cause ADHD directly — they shape how the brain develops and functions. Research consistently points to the fronto-striatal circuit: the network linking the prefrontal cortex (executive control), basal ganglia (habit and reward), and connected structures. In ADHD, this network is characterised by four overlapping features:
- Neurotransmitter imbalance — dopamine and noradrenaline signal with lower efficiency in key circuits, affecting motivation, reward timing, and impulse control.
- Neuroinflammation — emerging evidence links low-grade neuroinflammation to ADHD in a subset of individuals (Leffa et al., 2018).
- Circadian system imbalance — many people with ADHD have disrupted circadian rhythms, contributing to sleep-onset delay and fatigue-driven inattention.
- Altered neural development — differences in cortical maturation trajectories and subcortical volumes, observed at group level in the ENIGMA study (Hoogman et al., 2017).
These are not fixed deficits — they are differences in neural tuning that interact with demands and context.
3. Environmental influences: what shapes expression
Even with a high genetic load, the environment modulates how ADHD manifests. Prenatal and early-life factors that increase risk include:
- Maternal stress during pregnancy — chronic stress alters foetal cortisol exposure and brain development trajectories
- Toxin exposure — lead, organophosphates and air pollution are associated with increased ADHD risk
- Prematurity and low birth weight — disrupts the final stages of cortical maturation
- Iron deficiency — iron is critical for dopamine synthesis; early deficiency affects dopaminergic pathways
- Psychological adversity — early trauma and chronic stress can amplify existing genetic vulnerability
None of these factors cause ADHD on their own — but each one influences how genetic risk is expressed.
"Genes load the gun, environment pulls the trigger"
This phrase from behavioural genetics captures the relationship well. Someone may carry variants associated with ADHD without ever meeting diagnostic criteria — or those same variants may express fully when combined with environmental stressors. ADHD is best understood as a threshold condition: when enough genetic and environmental factors converge, the brain tips into a pattern of attention regulation that differs significantly from the statistical norm.
Why this matters — from blame to precision
Understanding ADHD as multifactorial does something important: it removes blame. The person who cannot start a task is not lazy — their fronto-striatal circuit is genuinely less efficient at translating intention into action without sufficient dopamine signal. The parent wondering whether they caused their child's ADHD needs to know that genetics plays the dominant role.
It also points toward more precise, individualised support. Someone whose ADHD involves significant circadian disruption may benefit from chronotherapy alongside stimulants. Someone with iron deficiency may respond differently to medication. The diagram below (adapted from NeuroSci, 2025) shows how these three forces combine into symptoms, comorbid conditions, and finally treatment targets — each layer building on the one before it.
Curious about your own profile?
Our free ADHD screening test (ASRS-v1.1) takes about 5 minutes and gives an instant result. If you have raw DNA data from 23andMe, AncestryDNA or MyHeritage, our Free DNA Neuro Analyzer can look for dopamine-related markers in your file. Neither replaces a clinical evaluation, but together they can be meaningful first steps toward understanding how your brain works.
References: Faraone SV et al. (2021). The World Federation of ADHD International Consensus Statement. Neurosci Biobehav Rev. | Hoogman M et al. (2017). Subcortical brain volume differences in participants with ADHD. Lancet Psychiatry. | Leffa DT et al. (2018). A systematic review on the relationship between neuroinflammation and ADHD. Front Psychiatry. | Thapar A & Cooper M (2016). ADHD. Lancet. | NeuroSci. (2025). ADHD multifactorial model.