A post going around this week shows a neuron with dozens of gene names pinned to it: on the axon, in the sending terminal, in the receiving one. The caption says the genes linked to ADHD fall into six biological pathways, and that every one of them ends up regulating dopamine. Unlike many viral neuroscience graphics, this one comes from a real, peer-reviewed source: a 2022 review in Frontiers in Molecular Neuroscience by Kessi and colleagues. Here is what it says, in plain language, and what it does not say.
First, the Number Everyone Quotes
ADHD runs in families. The review puts heritability at 0.76 for childhood ADHD, which means that about three quarters of the differences between children, in whether they have ADHD or not, track with genetic differences. It is one of the most heritable conditions in psychiatry, in the same range as height. Twin studies, not gene lists, are where that number comes from; we go through 37 of them in our article on ADHD, genetics and childhood trauma.
Heritable does not mean determined. The same review calls the cause of ADHD "multifactorial" and lists the environmental factors with the best evidence: nicotine and alcohol during pregnancy, lead and manganese exposure, iron and zinc deficiencies, and maltreatment. Genes and environment interact throughout development. A child does not inherit ADHD the way one inherits eye colour; they inherit a large number of small tilts.
Six Pathways, One Destination
What makes this review useful is that it sorts the candidate genes by the chemical system they belong to. Six systems come up.
1. Dopamine. The classic pathway: DRD1, DRD2 and DRD4 (receptors), DAT1 (the transporter that recycles dopamine). This is where stimulant medication acts, and it is the part of the story most people already know. We covered these genes one by one in ADHD genes and dopamine.
2. Serotonin. TPH2 (the enzyme that makes serotonin), the receptors HTR1A, HTR1B and HTR2A, and the transporter SLC6A4. Serotonin shapes impulsivity and mood, which is one reason ADHD so often travels with anxiety and depression.
3. Noradrenaline. DBH (the enzyme that turns dopamine into noradrenaline), the transporter NET1, and the receptors ADRA2A and ADRA2C. This is the pathway targeted by non-stimulant medications such as atomoxetine and guanfacine, and it matters for alertness and working memory.
4. Acetylcholine. Two nicotinic receptor genes, CHRNA4 and CHRNA7. Acetylcholine tunes attention and the filtering of distractions, and it is the system nicotine acts on, which may be part of why smoking rates are higher in ADHD.
5. Glutamate. The metabotropic receptors GRM1, GRM5, GRM7 and GRM8. Glutamate is the brain's main accelerator signal; these receptors keep it in check and have been found mutated in several ADHD cohorts.
6. GABA. GAD1, the enzyme that makes GABA, the brain's main brake. If glutamate is the accelerator, this is the pedal that stops the car, and we looked at the imaging evidence in ADHD and GABA.
The review also cites genes that do not sit in one pathway: ADGRL3 (a receptor involved in wiring neurons together, repeatedly linked to ADHD severity and stimulant response), SNAP25 and STX1A (the machinery that releases neurotransmitter from the sending terminal), MAOA (an enzyme that breaks down dopamine, serotonin and noradrenaline) and BDNF (a growth factor for neurons).
Why Every Road Leads to Dopamine
The sentence from the review that the viral post paraphrases is this one, from the legend of its figure: "All of the genes have a significant role in regulating dopamine neurotransmission directly or indirectly." That is the real message, and it is more subtle than "ADHD is low dopamine". Serotonin, noradrenaline, acetylcholine, glutamate and GABA neurons all synapse onto, or are wired in loops with, the dopamine circuits that run from the midbrain to the striatum and the prefrontal cortex. A variant in a serotonin receptor can change how much dopamine gets released two synapses away. Dopamine is not the whole story; it is where the stories converge.
Two cautions the review itself makes. Most of these associations come from candidate-gene studies, which test a gene chosen in advance and are prone to false positives. And each variant has a tiny effect on its own. Modern genome-wide studies find dozens of regions across the genome, each shifting risk by a fraction of a percent. Nobody has "the ADHD gene", because there is no such thing.
What a DNA File Can and Cannot Tell You
If you have a raw file from 23andMe, AncestryDNA or a similar service, it contains a handful of the variants discussed above. Our free DNA neuro analyzer reads it in your browser (nothing is uploaded) and flags, among others, COMT rs4680 (dopamine breakdown in the prefrontal cortex), DRD2, HTR2A, TPH2, ADGRL3 and several loci from the large ADHD genome-wide studies such as FOXP2, DUSP6 and SORCS3.
What it will tell you is which common variants you carry and what the research associates them with. What it cannot tell you is whether you have ADHD. Carrying a "risk" variant in DRD4 changes your odds by a few percent; not carrying it does not rule anything out. Genetic predisposition is a slope, not a verdict, which is also why the viral "genetics of ADHD wheel" that pairs each gene with a supplement does not hold up, and why DNA-based nutrient testing for ADHD has no trial support.
What Actually Answers the Question
If the question is "do I have ADHD?", the tool with real evidence behind it is not a DNA file but a validated screening questionnaire followed by a clinical evaluation. The ASRS-v1.1, the World Health Organization's adult screener, takes about ten minutes, is free here, and gives you a score you can bring to a professional. The genetics explain why ADHD exists and why it clusters in families. They do not replace the conversation with someone who can assess you.
So the viral post is right on the substance: many genes, six systems, one convergence point. Just read the fine print. "Shaped by genetics and the world around a child" is the honest version, and it is the one the review actually wrote.
Source: Kessi M, Duan H, Xiong J, et al. Attention-deficit/hyperactive disorder updates. Frontiers in Molecular Neuroscience, 2022;15:925049. Open access. Gene lists and quotations are taken from the review; interpretations in plain language are ours. This article is educational and is not a diagnosis.