When I tell people I work with ADHD through an attachment lens, I often get a version of the same question: “But isn’t ADHD neurological? Aren’t we talking about dopamine and brain chemistry?” The answer is yes — and that’s exactly why attachment matters. Understanding the neuroscience doesn’t contradict the attachment framework; it explains how attachment does its work. It reveals the biological pathways through which early relationship becomes brain structure, through which emotional experience shapes neurochemistry, through which the quality of connection determines the capacity for attention.

The attachment framework I’ve described isn’t just psychological theory — it’s grounded in neurobiology.(For the full exploration of how ADHD runs in families through relational patterns, see “Three Generations of ADHD”.) Recent research reveals the specific mechanisms through which secure attachment literally builds the brain circuitry required for attention, impulse control, and emotional regulation. Understanding these mechanisms helps explain why ADHD emerges for some people during periods of disrupted attachment bonds, and why relational repair can transform symptoms.

The Dopamine Connection

Andrew Huberman, neuroscientist at Stanford, describes ADHD through what’s called the “low dopamine hypothesis”: individuals with ADHD have insufficient dopamine signalling in the prefrontal cortex, leading to unnecessary neural firing unrelated to the task at hand. This creates the scattered attention, impulsivity, and difficulty with sustained focus that defines the ADHD experience.

But here’s what the purely genetic model misses: dopamine systems don’t develop in isolation. They’re profoundly shaped by early relational experience.

Research by Allan Schore and others demonstrates that, during infancy, the mother’s emotionally expressive face generates high levels of dopaminergic-driven arousal in the infant’s developing brain. Dopamine neurons in the ventral tegmental area respond to these “ethologically salient” stimuli — the technical term for what happens when a baby locks eyes with their caregiver — by shifting from steady baseline firing to rapid “burst firing.” This phasic dopamine release doesn’t just feel good; it literally shapes the developing architecture of the prefrontal cortex.

The attuned caregiver’s face becomes the infant’s first and most powerful source of dopamine regulation. Through thousands of interactions — eye contact, facial expressions, vocal tone, touch — the caregiver’s nervous system teaches the infant’s nervous system how to modulate arousal, sustain attention, and regulate emotion. These aren’t just psychological experiences. They’re neurobiological events that determine how dopamine circuits wire themselves during critical developmental windows.

Attachment Builds Executive Function

The prefrontal cortex — the brain region governing attention, impulse control, working memory, and decision-making — develops more slowly than any other brain region. It doesn’t fully mature until the mid-twenties. Throughout this extended developmental period, the prefrontal cortex requires external regulation from caregivers to organise itself properly.

Recent research published inNature Communications Psychology reveals the precise mechanisms: Oxytocin released during attuned caregiver-infant interactions increases dopaminergic activity in pathways leading directly to the prefrontal cortex. This oxytocin-dopamine crosstalk, as researchers call it, doesn’t just create temporary good feelings. It reorganises neural networks, strengthens synaptic connections, and literally builds the circuitry required for executive function.

Secure attachment, from this neurobiological perspective, is the developmental scaffold that allows dopamine systems to wire properly. When an infant experiences consistent, attuned caregiving, several crucial things happen:

First, dopamine circuits learn proper regulation. The prefrontal cortex develops the capacity to maintain optimal dopamine levels — not too high, not too low, but in the precise range required for sustained attention and impulse control.

Second, default-mode and task-related neural networks learn to coordinate. Huberman describes how in ADHD, these two networks fire simultaneously rather than in opposition. The default network (mind-wandering, internal focus) should quiet when the task network (external focus, goal-directed behaviour) activates. Secure attachment during development teaches these networks to work together properly.

Third, the prefrontal cortex develops robust connections to subcortical regions. Attention isn’t just a cortical function — it requires coordination between the prefrontal cortex and deeper brain structures involved in arousal, motivation, and reward. Secure attachment builds these connections through repeated experiences of co-regulation.

Why Orchid Children Are More Vulnerable

This is where the orchid-dandelion framework gains additional precision. Research on prefrontal cortex development reveals that dopamine has an “inverted U” dose-response curve: too little dopamine impairs executive function, but so does too much. The optimal level sits in a narrow range.

Orchid children, with their heightened sensitivity, appear to have dopamine systems that require more precise calibration. Their systems are more reactive to both positive and negative experiences, meaning they need more consistent, attuned co-regulation to develop stable dopamine functioning.

Dandelion children have dopamine systems with wider tolerance ranges. They can develop adequate executive function across a broader spectrum of caregiving styles. Not because their brains are “better,” but because their neurochemistry is less sensitive to environmental variation.

This explains why the same parenting that works fine for one sibling leaves another struggling. It’s not that parents are failing — it’s that different nervous systems require different levels of regulatory support to develop properly.

The Critical Windows

Most ADHD research emphasises the strong genetic component, but genetics alone can’t explain the full picture. What research on attachment and brain development reveals is that there are critical windows when dopamine systems are particularly plastic — particularly responsive to environmental input.

The first two years of life represent the most sensitive period for right-brain development, including the orbitofrontal cortex regions that regulate emotion and attention. During this window, the infant’s brain grows faster than at any other time in life, creating massive numbers of synaptic connections that will later be pruned based on experience.

But development doesn’t stop there. The prefrontal cortex continues maturing through adolescence and into the mid-twenties. This means attachment ruptures during these later periods can still significantly impact dopamine regulation and executive function development.

This is exactly what happened in my own story: functioning adequately until age 21, when my parents’ separation occurred during a critical window of prefrontal cortex maturation. My developing executive function circuits lost the external regulatory support they still needed, and my dopamine systems — already on the sensitive end of the spectrum — couldn’t maintain proper regulation independently.(For the full personal narrative of why my ADHD didn’t appear until age 21, see my blog post.)

The Mechanism Behind Intergenerational Transmission

Understanding the neurobiology also clarifies how ADHD patterns transmit across generations. It’s not just that parents pass down genes for ADHD. They pass down their own dopamine regulation patterns through the way they attune (or don’t attune) to their children.

A parent whose own dopamine system is dysregulated — perhaps because they didn’t receive sufficient attachment attunement in their development — cannot easily provide the consistent, attuned co-regulation their child’s developing dopamine system requires. Not because they don’t love their child or aren’t trying, but because their own neurobiology limits what their nervous system can offer.

The grandmother whose dopamine system adapted to wartime stress couldn’t provide the relaxed, playful attunement required for optimal dopamine development in her daughter. Her daughter, growing up with compromised dopamine regulation, couldn’t provide it to her son. Three generations of dopamine dysregulation, transmitted not through genes but through the neurobiology of relationship.(To see how this pattern played out across three generations in my own family, read my personal story.)

Why This Changes Everything

Understanding the neuroscience doesn’t diminish the psychological or relational aspects of ADHD — it strengthens them. When we see that secure attachment literally builds the brain circuitry required for attention and self-regulation, the attachment framework stops being “soft” psychology and becomes hard neuroscience.

This also explains why medication alone often isn’t enough. Stimulant medications like Adderall and Ritalin increase dopamine availability, which can temporarily improve focus. But they don’t build the underlying circuitry that secure attachment creates. They don’t teach the prefrontal cortex how to maintain optimal dopamine levels independently. They don’t repair the developmental gaps left by insufficient co-regulation.

What does build that circuitry? The same thing that would have built it in the first place: consistent, attuned relationship. Somatic therapy. Attachment repair. Co-regulation from someone whose nervous system can hold steady when yours is dysregulated. These aren’t just nice ideas — they’re neurobiological interventions that can literally rewire dopamine circuits and strengthen prefrontal cortex functioning.

Research demonstrates that neural plasticity continues throughout life. The brain isn’t fixed. Dopamine systems remain responsive to environmental input — including relational input — long after the initial critical periods close. This is why attachment repair in adulthood works. The mechanisms that built the brain in the first place remain available for rebuilding.

Bridging Neuroscience and Experience

When Huberman describes how dopamine coordinates default-mode and task-related networks, he’s describing the same phenomenon Gordon Neufeld and Gabor Maté identify from an attachment perspective. When Allan Schore maps how caregiver attunement shapes right-brain dopamine development, he’s providing the neurobiological substrate for what attachment theory has described relationally.

The neuroscience doesn’t replace the attachment framework — it explains how attachment does its work. It reveals the biological pathways through which relationship becomes brain structure, through which emotional experience shapes neurochemistry, through which the quality of early connection determines the capacity for later attention.

For orchid children, this understanding is crucial. Their ADHD isn’t evidence of a broken brain that needs fixing. It’s evidence of a sensitive dopamine system that didn’t receive the precise calibration it required during critical developmental windows. The same sensitivity that makes them vulnerable also makes them capable of extraordinary focus, creativity, and depth — when their relational environment provides adequate support.(Learn more about our ADHD family support approach.)

The question isn’t “what’s wrong with this brain?” The question is “what did this particular nervous system need that it didn’t receive, and how can we provide it now?”

The neuroscience gives us the answer: consistent, attuned relationship that teaches dopamine systems how to regulate properly. Not as a metaphor, but as a biological intervention that rewires neural circuits and rebuilds what insufficient attachment left undeveloped.

This is why healing is possible. This is why ADHD symptoms can transform through relational work. Not because we’re thinking differently about the problem, but because we’re actually changing the brain.

References

Feldman, R. (2017). The neurobiology of human attachments. Trends in Cognitive Sciences, 21(2), 80–99.

Huberman, A. (2021). ADHD & how anyone can improve their focus. Huberman Lab Podcast.

Luo, L., et al. (2024). The neurobiological mechanisms underlying the effects of attachment on mental and physical health.Nature Communications Psychology, 2, 158.

Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. W. W. Norton & Company.

Schore, A. N. (2001). Effects of a secure attachment relationship on right brain development, affect regulation, and infant mental health. Infant Mental Health Journal, 22(1–2), 7–66.

Schore, A. N. (2003). Affect regulation and the repair of the self. W. W. Norton & Company.

Volkow, N. D., et al. (2021). The dopamine hypothesis of ADHD. Nature Neuropsychopharmacology, 46(2), 310–320.

About the Author:Ariel-Paul Saunders is a Registered Therapeutic Counsellor (RTC) in Nelson, BC, specializing in attachment-based ADHD support for families and adults. Through Securely Thriving, Ari integrates somatic therapy, attachment theory, and current neuroscience research from Andrew Huberman, Allan Schore, Ruth Feldman, and others to help families understand ADHD as a relational and neurobiological adaptation rather than a fixed genetic disorder.

Resources:

• Download the free guide: “Securely Connected: Foundations for Supporting Children with ADHD”

• Learn about ADHD family support services

• Explore somatic therapy

• Join the Thriving Together 8-week parent series

• Book a free consultation for 1:1 support