What Actually Causes ADHD?
Photo by Lacie Slezak on Unsplash.
Why it’s time to move beyond the dopamine deficit model.
Attention Deficit Hyperactivity Disorder (ADHD) is widely misunderstood. Its name implies that it’s a disorder when, in fact, it’s more accurate to understand it as a neurodevelopmental condition. It’s a natural variation in brain wiring that affects attention, self-regulation, and executive function. Recognising it as part of neurodiversity helps reduce stigma and shift the focus from deficits to differences. We don’t all think in the same way, nor should we.
While ADHD has traditionally been linked to dopamine dysregulation, the idea of a simple "dopamine deficit" is, quite frankly, overly reductive. The current research highlights a complex interplay of genetics, neurobiology, and environmental factors that contribute to ADHD characteristics. Genetic variants influence ADHD traits, while brain imaging studies reveal structural and functional differences in regions like the prefrontal cortex and basal ganglia, which regulate attention and impulse control. Beyond biology, environmental factors—including childhood experiences, stress, diet, and social interactions—also shape how ADHD symptoms manifest.
It’s also worth understanding that ADHD as a diagnosis is based purely on a pattern of symptoms – there’s no biomarker or physical measure that contributes to diagnosis. Nor does diagnosis necessarily seek to explain why a person exhibits ADHD characteristics. This seems illogical to me as you wouldn’t administer the same medication for two different conditions with similar symptoms in other circumstances. For instance, adrenal fatigue and hypothyroidism present in very similar ways, and while both are endocrine disorders, they’re treated very differently.
As such, I believe it’s important to take a more nuanced approach to working with ADHD that takes what’s driving symptoms into account. This holistic perspective moves away from a one-size-fits-all approach, paving the way for more personalised strategies that address the unique interactions between genetic, neurobiological, and environmental influences that each individual is subject to.
Let’s take a look at what’s currently understood about ADHD - and then what I’m proposing.
Competing Theories of ADHD
Several theories have been proposed to explain the neurodevelopmental condition of ADHD. While each offers insights into different aspects of the condition, none fully encapsulate its complexity. Let's examine these theories and their strengths and limitations.
1. Dopamine Deficit Theory
This longstanding theory posits that ADHD results from low dopamine levels, impairing attention, motivation, and impulse control. We know that stimulant medications that boost dopamine improve symptoms in some individuals but not in everyone. This model is overly simplistic. ADHD involves dopamine dysregulation rather than a mere deficit, and it fails to account for genetic, environmental, and neurobiological variations.
In addition, ADHD isn’t always linked (biologically) to low dopamine. For example, the COMT gene regulates dopamine metabolism in the prefrontal cortex (PFC), crucial for attention and impulse control. The Val158Met polymorphism affects enzyme activity. The Val variant leads to faster dopamine breakdown, while the Met variant leads to slower dopamine breakdown. Interestingly, evidence suggests that the Met allele may have a stronger association with ADHD traits and that carriers may be more sensitive to adverse early childhood experiences. So ADHD traits in this instance are not necessarily the product of a deficit of dopamine but rather, a (relative) excess, which likely influences receptor sensitivity.
Likewise, SNAP25 is a crucial component of synaptic vesicle fusion, facilitating neurotransmitter release at synapses. It plays a key role in synaptic plasticity, which affects learning, memory, and cognitive flexibility. Variants in SNAP25 have been linked to reduced efficiency in neurotransmitter release, particularly in brain regions involved in attention and executive function. This dysregulation of synaptic transmission may contribute to difficulties with sustained attention, working memory, and impulse control. It’s important to note, though, that these variants don’t necessarily just impact dopamine systems – they can impact other neurotransmitter systems within the brain as well.
2. Cognitive Dysregulation Theory
ADHD is also described as an executive function disorder, affecting working memory, impulse control, and cognitive flexibility. This makes perfect sense in the context of some genetic variants like DRD4. It’s 7-repeat allele is linkedto reduced receptor sensitivity to dopamine, meaning dopamine is less effective at activating reward-related pathways. This diminished signalling contributes to increased novelty-seeking and impulsivity, traits commonly seen in ADHD.
Similarly, variations in the DRD5 gene influence dopamine signalling and attention regulation. The DRD5 gene encodes the dopamine D5 receptor, which plays a role in modulating dopamine levels in brain regions involved in attention and cognitive function. Certain variants in DRD5 have been associated with altered receptor expression and reduced dopamine efficiency, which may contribute to attention deficits in individuals with ADHD.
While this theory aligns with observed difficulties in ADHD, it does not fully explain hyperfocus or the underlying neurobiological mechanisms that contribute to executive dysfunction.
3. Default Mode Network (DMN) Dysregulation
The DMN, active during rest and mind-wandering, appears overactive in ADHD, leading to difficulty switching to task-focused states. DAT1 encodes the dopamine transporter (DAT), which is responsible for reuptaking dopamine from the synaptic cleft back into presynaptic neurons, regulating dopamine availability. The 10-repeat allele of DAT1 has been linked to increased dopamine reuptake, which reduces extracellular dopamine levels, particularly in regions like the striatum and prefrontal cortex—both critical components of the DMN. This decreased dopamine availability is thought to contribute to ADHD symptoms by impairing reward processing, executive function, and response inhibition.
This explains distractibility and time-blindness in some people but does not fully address hyperactivity (which some people experience more than others) or the ability to hyper-focus (which others with ADHD may also experience).
4. Environmental Sensitivity Hypothesis
Some argue ADHD traits were once adaptive in novelty-seeking, fast-paced environments, but that they’re less well-suited to today’s environment. For instance, many people with ADHD thrive in settings that require innovation, adaptability, and intense bursts of focus. One study found that ADHD symptoms were context-dependent in their 125 subjects and that ADHD traits were strengths in the right context. We need to understand that being different is not the same as being dysfunctional.
Yet, while this perspective helps destigmatise ADHD, it overlooks the neurobiological underpinnings and challenges posed by modern circumstances, like overly structured settings or settings in which stress or trauma may also be factors.
5. The Trauma Perspective
Chronic stress and trauma can alter brain function and gene expression, influencing ADHD symptoms through epigenetic mechanisms. Research shows that early-life stress affects dopamine receptor density and cortisol regulation, impairing executive function and worsening ADHD symptoms. These kinds of Adverse childhood experiences (ACEs) can lead to lasting changes in gene expression, particularly in stress-response and neurotransmitter systems. These modifications may exacerbate ADHD or increase susceptibility in genetically predisposed individuals
6. Nutrition and Biochemistry
ADHD can begin before birth, as prenatal and early-life environments shape brain development. For example, maternal stress, which results in elevated cortisol during pregnancy, can alter foetal brain structures, particularly in areas governing attention, memory, and impulse control. Toxins like lead, nicotine, and alcohol can also disrupt neurotransmitter systems, impair cognitive development, and heighten ADHD susceptibility. Maternal smoking, for instance, is linked to increased ADHD development. Meanwhile, low prenatal vitamin D has been linked to neurodevelopmental changes associated with ADHD.
The gut microbiome, essential for overall health, is also increasingly linked to ADHD via its role in neurotransmitter production, inflammation, and immune function. Imbalanced gut bacteria can disrupt dopamine and serotonin levels, impairing attention and mood regulation. Dysbiosis also triggers systemic inflammation, which can affect brain function. Probiotics, prebiotics, and dietary interventions are being explored to restore gut balance and improve ADHD symptoms, offering promising adjuncts to conventional treatments.
Why We Need a Unified Perspective
Each theory contributes valuable insights but none fully explain ADHD. Dopamine dysregulation, cognitive dysfunction, neural network imbalances, and environmental influences all interact, making ADHD a complex, multifactorial condition. Future research should focus on integrating these perspectives to refine treatment approaches. For example, we can think of genetics as being predisposing to ADHD characteristics – but your genes still aren’t a surefire way of knowing you’ll have ADHD. Meanwhile, you might grow up in a household where you feel threatened or your needs aren’t met, yet you still may never exhibit symptoms of ADHD. On top of this, these symptoms may come and go. Some days can be more of a struggle than others. And maybe your ADHD symptoms don’t cause you any problems at all, but give you certain advantages depending on your setting.
Which brings us to a strengths-based perspective. Rather than solely focusing on the deficits associated with ADHD, I think it’s high time that the traits commonly seen in individuals with ADHD—such as creativity, resilience, high energy, and hyperfocus—be seen as the assets they are. What I propose is that we develop an appreciation of our differences and learn to leverage them through targeted lifestyle changes that address how psychosocial, neurological, and biological contexts contribute to your unique experience.
Thus, while each of the leading theories of ADHD offers valuable insights into different aspects of the condition, they all have limitations. A more holistic view is needed—one that incorporates genetics, neurobiology, and environmental factors to understand the full complexity of ADHD.