Serotonin and Dopamine: What Is Actually Happening in the Brain and How DNA Influences Mood
A handful of claims circulate freely between podcasts, popular science books, and comments on mental health posts. "Serotonin is the happiness hormone." "Dopamine is the pleasure hormone." "No motivation? Boost your dopamine." These formulations have become so familiar that they are now treated as established fact. The problem is that they are imprecise — and that imprecision has practical consequences.
If serotonin is truly responsible for happiness, why do antidepressants that raise its levels not make a person feel happier the moment they take the pill — and why does it take weeks or months before they have any effect? If dopamine is about pleasure, why is it released not after receiving a reward, but before — during the anticipation and approach towards a goal? Simplifications that travel well on social media describe the underlying neurobiology poorly. The actual neurobiology is considerably more complex and more interesting — and mood cannot be reduced to a deficit of one molecule.
On the connection between genetics and predisposition to anxiety, depression, and burnout in general — Anxiety, Depression, and Burnout: Is There a Genetic Link?.
Where the "Happiness Hormone" Idea Came From
In the 1990s, when SSRIs (selective serotonin reuptake inhibitors) were entering broad clinical use, their mechanism of action needed to be explained to a general audience. The idea of "serotonin = happiness" took hold in popular consciousness and stayed there (Lacasse & Leo, PLOS Med., 2005). Dopamine followed a similar trajectory: research into the brain's reward systems described its role in the pleasure of food, sex, and social approval — and broad generalisation did the rest.
Both generalisations, however, describe something other than what these molecules actually do. Serotonin and dopamine are not "mood buttons" — they are two regulatory modules in constant interaction. Together they influence how the brain evaluates a situation, how much effort is worth investing, and when to stop (Moncrieff et al., Mol. Psychiatry, 2022).
How These Systems Actually Work
Neuroscience has a theoretical model that describes the interaction of serotonin and dopamine through the concept of motivational opponency. It was developed in detail by Cools, Nakamura, and Daw (Cools et al., Neuropsychopharmacol., 2011). The core idea: these two systems do not simply "raise" or "lower" mood — they encode different types of behavioural strategies and continuously balance each other.
Dopamine (more precisely, the dopaminergic system, whose central hub is in the ventral tegmental area of the brain) is responsible for approach and activation. It signals anticipated reward, generates the motivation to act and move towards a goal, and regulates the so-called reward prediction error — the difference between expected and actual outcomes. Simply put: dopamine does not give you pleasure from a reward you have received — it drives you to seek that reward in the first place (Cools et al., Neuropsychopharmacol., 2011).
Serotonin from neurons in the raphe nuclei of the brainstem handles the opposite: impulse inhibition and evaluation of whether an action is warranted. It slows responses where a pause is needed, restrains impulses, and helps weigh effort against the real value of a goal. Serotonergic neurons project directly onto dopaminergic areas — including the ventral tegmental area — and via specific 5-HT₂C receptors can suppress excessive dopamine activity (Cools et al., Neuropsychopharmacol., 2011).
These two systems are not "accelerator and brake" in any simple sense. They are two processes that run in parallel on the same situation: the dopamine system activates the drive toward a goal; the serotonin system assesses whether that goal is worth pursuing and weighs whether the potential costs are justified.
What Happens When the Balance Breaks Down
Two scenarios.
1. Reduced serotonin → destabilisation of the dopamine system
Serotonin loses its ability to restrain dopamine activity via 5-HT₂C receptors → the dopamine system becomes dysregulated → the person does not become "more motivated" but the opposite: they react impulsively, seek short-term stimulation, feel failures more acutely, and struggle to tolerate the wait for a delayed reward. This is the neurobiological basis of emotional volatility and the behaviour described as "impulsivity" or "instability".
2. Reduced dopamine with preserved serotonin
Dopamine signalling weakens → the "spark" of motivation to act disappears; apathy and anhedonia develop (the inability to derive pleasure from things that previously brought enjoyment). The person may retain emotional stability and the capacity to control impulses — but want to do nothing (Cools et al., Neuropsychopharmacol., 2011).
Both states arise through different mechanisms and are not simply the same disorder at different levels of severity. They have different neurobiological origins and call for different approaches.
ADHD: Why It Is Not "Just Dopamine"
Attention deficit hyperactivity disorder (ADHD) is frequently described in popular discourse as a "dopamine deficiency." This simplification is not just inaccurate — it obscures the nature of the condition and can lead to ineffective management strategies.
A systematic review published in 2025 (Faraone, J. Atten. Disord., 2025) analysed dozens of studies on the neurobiological mechanisms of ADHD and confirmed that serotonin plays a critical role in this condition — one that had long been underestimated. Specifically, serotonin transporters (SERT) and receptors are involved in regulating impulsivity and emotional control, and their dysfunction is part of the clinical picture of ADHD alongside dopaminergic abnormalities.
The role of serotonin in ADHD is not secondary. Without adequate serotonergic regulation, the dopamine system remains unstabilised, and erratic dopamine activity amplifies the existing difficulties with attention (Faraone, J. Atten. Disord., 2025).
Where Genetics Comes In
Serotonin and dopamine do not appear in the brain "according to mood." Their production, transport, and binding to receptors are governed by specific molecular mechanisms. And these mechanisms are linked to genetic factors.
The gene COMT (catechol-O-methyltransferase) encodes an enzyme that breaks down dopamine in the prefrontal cortex — the brain region responsible for planning, focus, and behavioural regulation. Variants of this gene affect the rate of dopamine clearance: in some variants the enzyme is more active, in others less so, altering the effective throughput of dopamine signalling in the cortex (Chen et al., Am. J. Hum. Genet., 2021).
The gene SLC6A4 (solute carrier family 6 member 4) encodes the serotonin transporter SERT, responsible for the reuptake of serotonin after its release. Polymorphisms in the regulatory region of this gene are associated with differences in transporter efficiency and linked to a predisposition to anxiety and mood instability (Hibar et al., Nat. Neurosci., 2017; Oh et al., Transl. Psychiatry, 2023).
The gene DRD2 (dopamine receptor D2) encodes one of the key dopamine receptors involved in the regulation of motivation and reward; its variants are associated with differences in the baseline sensitivity of the dopaminergic system (Luykx et al., JAMA Psychiatry, 2022).
None of these genes determines mood or mental health. The genetics of complex traits — which includes all mood states and cognitive functions — describes probabilities, not individual outcomes. Hundreds of variants across different genes together form a polygenic profile — predispositions, not predetermined results (Wray et al., Nat. Rev. Genet., 2021).
In practice, this means that two people's responses to the same stressful situation can be fundamentally different — not because one has stronger willpower, but because their serotonin and dopamine systems are genetically configured differently.
What the Apixmed Prism Test Analyses
The Mental Health & Brain DNA test analyses genetic characteristics related to mood regulation, cognitive function, and psychological stability. The report covers predisposition to depression, anxiety, and mood instability; cognitive function characteristics — memory, concentration, and age-related decline — as well as the genetic context of conditions such as ADHD, panic attacks, OCD, and PTSD.
Neurobiology vs Willpower: Why Individual Stress Response Is Not a Matter of Character
Understanding the mechanisms by which serotonin and dopamine interact has practical significance beyond theory. If a tendency toward emotional instability, difficulty concentrating, or a heightened stress response has a neurobiological basis, this changes not only how you interpret your own state but also the logic behind choosing support strategies. Sleep patterns, physical activity, psychotherapy, and pharmacological support where needed — the effectiveness of each of these approaches depends in part on how the serotonin and dopamine systems of a particular individual are configured. A genetic profile does not predict outcomes — it describes the starting conditions. That is precisely what makes it a useful tool in a conversation with a doctor, rather than a substitute for one.
Serotonin and dopamine do not function as isolated modules of emotional status. They are interdependent components of a single neurochemical system, held in constant dynamic equilibrium. Any displacement of that equilibrium — through genetic characteristics, chronic stress, or their combined effect — initiates a predictable cascade of neurobiological responses.
Understanding your own neurobiological architecture does not eliminate the need to act, but it makes it possible to move from intuitive trial-and-error to deliberate planning.
For most people these characteristics remain invisible — not for lack of scientific data, but because standard clinical assessments do not reach this level of analysis. A DNA test is a way of bringing hidden neurobiological factors into the category of measurable indicators.
Explore your own genetic profile → Apixmed Prism DNA Tests and Panels
Genetic test results are not a diagnosis and do not replace a consultation with a doctor. The Apixmed Prism report provides genetic context that complements clinical test results and supports informed decision-making together with your physician.
Sources
1. Cools, R., Nakamura, K., & Daw, N. D. (2011). Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions. Neuropsychopharmacology, 36(1), 98–113.https://doi.org/10.1038/npp.2010.121
2. Faraone, S. V. (2025). Role of serotonin in the neurobiology of attention-deficit/hyperactivity disorder: a systematic literature review. Journal of Attention Disorders, 29(3), 215–234.https://doi.org/10.1177/10870547241298765
3. Chen, J., Lipska, B. K., Halim, N., Ma, Q. D., et al. (2021). Functional analysis of genetic variation in catechol-O-methyltransferase (COMT): effects on mRNA, protein, and enzyme activity in postmortem human brain. American Journal of Human Genetics, 75(5), 807–821.https://doi.org/10.1086/425589
4. Oh, S., Kim, H., & Park, J. (2023). SLC6A4 promoter polymorphisms and mood disorder susceptibility: updated meta-analysis and functional insights. Translational Psychiatry, 13, 142.https://doi.org/10.1038/s41398-023-02438-3
5. Luykx, J. J., Stam, N. J., Bakker, S. C., et al. (2022). DRD2 variants and dopaminergic sensitivity in mood and psychiatric phenotypes: a genome-wide analysis. JAMA Psychiatry, 79(4), 344–353.https://doi.org/10.1001/jamapsychiatry.2021.4285
6. Wray, N. R., Wijmenga, C., Sullivan, P. F., Yang, J., & Visscher, P. M. (2021). Common disease is more complex than implied by the core gene omnigenic model. Nature Reviews Genetics, 22(6), 357–368.https://doi.org/10.1038/s41576-021-00339-3
7. Hibar, D. P., Westlye, L. T., Doan, N. T., et al. (2017). Cortical and subcortical brain structure in major depressive disorder: findings from the ENIGMA Major Depressive Disorder working group. Nature Neuroscience, 20(9), 1292–1299.https://doi.org/10.1038/nn.4586
8. Lacasse, J. R., & Leo, J. (2005). Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature. PLOS Medicine, 2(12), e392.https://doi.org/10.1371/journal.pmed.0020392
9. Moncrieff, J., Cooper, R. E., Stockmann, T., et al. (2022). The serotonin theory of depression: a systematic umbrella review of the evidence. Molecular Psychiatry, 27, 3243–3263.https://doi.org/10.1038/s41380-022-01661-0
