Causes of ADHD and How Common Is It?

ADHD is one of the most heritable mental health conditions. It is extremely common in families of patients with ADHD, to the point where it is rare to find family members without ADHD or at least traits.

Because of under-recognition, many parents or siblings remain undiagnosed. Instead, they may show patterns such as erratic job histories, repeated business ventures, substance misuse, or anger problems. These are often labelled as Depression or Anxiety personality disorder or rapid cycling Bipolar when the underlying ADHD is missed.

• During pregnancy: infections, or exposure to alcohol or drugs, can cause brain changes linked to ADHD.
• Birth complications: low birth weight, prematurity, or traumatic deliveries increase risk.
• Childhood brain injury: head injuries can also result in ADHD-like changes.

In recent decades there has been more understanding of the impact of environment. There is extremely complex interaction between genetics and environment in how eventually ADHD develops. There are a few studies which have suggested that significant early life trauma / deprivation of children in care can also result in ADHD but there is overwhelming consensus that ADHD is still predominantly a genetic/ biological disorder.

ADHD is not caused on it’s own by:

• Poor parenting
• Trauma or abuse in later life
• Diet
• Substance use
• Sleep problems

These can worsen symptoms or mimic ADHD like symptoms, but they do not produce the brain changes that define the condition. For example, poor diet or trauma may lead to distractibility or emotional instability, and also lead to more comorbidities but they so not cause ADHD itself.

Research shows that ADHD brains differ from non-ADHD brains in the way areas of the brain connect and communicate. These are called Neuronal pathways or circuits. The main problems involve neurotransmitters — especially dopamine and noradrenaline.

Affected circuits/ networks include:

• • Dorsal Frontostriatal Circuit: Connects the dorsolateral PFC with the striatum, crucial for cognitive control and working memory.
• • Orbitofronto-Striatal Circuit: Links the orbitofrontal cortex to the striatum, regulating motivation, reward processing, and impulsivity.
• • Fronto-Cerebellar Circuit: Involves the PFC and cerebellum, responsible for timing, motor control, and cognitive pacing.
• • Default Mode Network (DMN): A set of brain regions that is active when the brain is at rest; in ADHD, this network fails to deactivate properly during tasks, leading to inattention.
• • Mesocorticolimbic Circuit: Involves dopamine pathways related to reward and emotional regulation.

As it is obvious most of these are directly or indirectly coordinated through the frontal lobe/ prefrontal cortex.

Because these changes occur at the level of circuits and neuronal pathways, brain scans cannot yet be used for an individual diagnosis. Imaging shows consistent differences at a group level but lacks the precision for clinical use.

• Children: Around 5–7% of school-age children are estimated to have ADHD. The male-to-female ratio is about 4:1 in childhood, as boys are more likely to be diagnosed. Girls often present differently (for example with inattentive symptoms rather than overt hyperactivity), which can lead to underdiagnosis.
• Adults: The ratio becomes much more equal in adulthood, partly because diagnostic recognition improves and ADHD in women is more frequently identified. Overall, 2–4% of adults meet criteria. About 60–70% of children continue to have ADHD into adulthood, while the remainder may still struggle with low self-esteem and confidence.
• Mental health clinics: 30–40% of patients are estimated to have ADHD.
• Substance misuse services: Around 50 % of patients have ADHD.
• Prisons and forensic hospitals: Up to 50 % of inmates or forensic patients meet ADHD criteria.

ADHD may remain hidden when protective factors are present, such as stable family environments, intelligence, physical activity, or flexible occupations.

ADHD often becomes more visible during life transitions, when compensatory strategies no longer work. Common triggers include:

• Increased academic pressure in higher studies.
• Changes in work demands, such as moving into administrative or sedentary roles, promotions to supervisory/managerial positions with more paperwork, or a shift from flexible/shift work to rigid daytime hours.
• Loss of exercise routines, for example after injury or during late adolescence when sports and activity levels reduce.
• Worsening substance misuse, often becoming clearer in university or early adulthood.
• Parenting young children, where added stress, lack of sleep, and the demands of caregiving brings ADHD difficulties into focus and compensatory strategies stop working. In addition, children may also have ADHD traits, increasing family stress.
• Relationship breakdowns, which may result from stress, rejection sensitivity, or the loss of a partner who previously provided practical and administrative support.
• Job loss or unemployment, where procrastination and disorganisation can no longer be masked.

At these points, ADHD symptoms often intensify and individuals are more likely to seek help.