Attention deficit hyperactivity disorder (ADHD) causes symptoms that can disrupt a patient’s life. For example, the patient can have problems sustaining attention during a task, staying still or controlling impulses. These symptoms can affect how a child performs in school and how an adult does at work.

Over the years, the number of ADHD cases has increased. The Centers for Disease Control and Prevention (CDC) states that between 1997 and 2006, the number of ADHD cases increased by about three percent a year. But why? It may be due to a genetic link that affects neurotransmitter levels in patients. The Mayo Clinic states that in 25 percent of children with ADHD, they have another relative with the disorder. Researchers have looked into the exact genes linked to ADHD, and other factors that trigger the disorder.

Neurotransmitter Difference in the Three Subtypes of ADHD

Attention deficit hyperactivity disorder has three subtypes, which vary by the presentation of symptoms. With predominantly inattentive ADHD, the patient has six or more symptoms that fall into the inattentive category. The patient may also have hyperactivity and impulsive symptoms, but five or less of them to be diagnosed with this subtype of ADHD. The same is with the predominantly hyperactivity-impulsive subtype of ADHD: the patient has six or more hyperactivity and impulsive symptoms; if the patient has inattention symptoms as well, she must have five or less symptoms. With the combined ADHD subtype, the patient has six or more symptoms of both inattention and hyperactivity/impulsiveness.

One explanation for the three subtypes of attention deficit disorder is that patients have different levels of neurotransmitters, which alter their behavior. In particular, ADHD patients have variations on the transporter genes for these neurotransmitters. For example, patients with predominantly inattentive ADHD had changes to their norepinephrine transporter gene, which affects norepinephrine levels in their brains. Patients with predominantly hyperactivity-impulsive ADHD had changes to their dopamine transport gene, thus affecting dopamine levels in the brain. Medications on the market for ADHD target these particular neurotransmitters. Stimulants such as Ritalin and Adderall increase dopamine by blocking its transporter; nonstimulants, such as Strattera, also increase norepinephrine by blocking its transporter. However, patients with combined ADHD have altered transporter genes for a different neurotransmitter. Vanderbilt University Medical Center notes that combined ADHD patients have an altered choline transporter gene. Choline, the precursor to acetylcholine, also influences neural communication, like norepinephrine and dopamine. However, no medications for ADHD currently on the market target this neurotransmitter.

Serotonergic System and ADHD

Another gene linked to attention deficit disorder is 5HTTLPR, a serotonin transporter gene. Molly Nikolas et al. note that dopamine and norepinephrine are associated with reward processing, but not the emotional dysregulation seen in ADHD. Serotonin, however, is related to impulse control and aggression. The researchers found that two variants of 5HTTLPR, the “short” allelic variant and the “long” allelic variant, have been linked to ADHD and to disorders that often occur along with attention deficit disorder, such as conduct disorder and mood problems. These 5HTTLPR alleles result in either low or high serotonin transporter activity.

The authors point out that genetics are not the only factor in the onset of ADHD: the family environment, such as emotional stress and conflict between the parents, also contributes. As part of the study, the participants filled out the Children’s Perception of Inter-parental Conflict scale, which rated conflict between the parents. The participants answered if they lived with both biological parents, one parent and another adult, or one parent and had contact with the other parent. The authors found that children who did not have ADHD were more likely to live with both biological parents than children with ADHD. This trend led the authors to hypothesize that the ADHD children saw more marital conflict, resulting in the children reporting higher levels of self-blame.

A correlation was found between the 5HTTLPR and self-blame, especially with the “short” and “long” 5HTTLPR alleles. The combination of the genes and self-blame resulted in hyperactivity and impulsiveness symptoms, but not inattention or cognitive problems. However, the authors found that if participants had intermediate activity genotypes, meaning that they did not have either high or low serotonin output, they “appeared to be immune to whatever effects self-blame was having on hyperactivity/impulsivity.”

Knowing which neurotransmitters cause ADHD in a patient can help find the right medication to manage symptoms. However, genetics are not the only factor involved in the onset of ADHD. The environment that the patient is growing up in has an impact on the display of symptoms, and how he deals with self-image.