AD / HD For Dummies
Book image
Explore Book Buy On Amazon

Although the exact cause of AD/HD is still unknown, there is no shortage of research into the biology of AD/HD. This research fits into four broad categories: genetic, anatomical, functional, and chemical.


AD/HD runs in families — so much so that when diagnosing the condition, an AD/HD professional's first step may be to look at the person's family to see if anyone else has it. The precise genetic factor has yet to be confirmed, but recent research has identified a couple of genes that may contribute to AD/HD.

Many studies have examined AD/HD from a genetic perspective. These include studies that look at adoptive versus biological parents, the prevalence of AD/HD in families, twins' tendency to share AD/HD, and specific genes associated with AD/HD. Here's a short sampling of some of these areas of investigation:

  • A study conducted by Dr. Florence Levy of the University of New South Wales, Australia showed that if one identical twin has AD/HD, 81 percent of the time the other one will as well. By contrast, only 29 percent of paternal twins share AD/HD. Because identical twins share the exact same DNA, this strongly suggests a genetic component to AD/HD.
  • Several studies by Dr. Joseph Biederman and his colleagues at the Massachusetts General Hospital have shown that AD/HD runs in families. In one study, Dr. Biederman and his colleagues found that first-degree relatives (parents or siblings) of someone with AD/HD have a five times greater chance of also having AD/HD than someone who has no close relatives with the condition.
  • Studies by Dr. Dennis Cantwell on adopted children with the hyperactive/impulsive type of AD/HD found that these children resemble their biological parents more than their adoptive parents in their hyperactivity. His studies suggest that the environment in which children grow up has less impact on the development of AD/HD than their genes.
  • In a 1991 study, David Comings and his colleagues suggested that a mutation in the dopamine D2 receptor gene is connected to AD/HD. Research is underway now that is exploring several dopamine genes as possible links to AD/HD. A few researchers have suggested that two genes in particular — DAT1 and DRD4 — are the culprits. In fact, a recent study by researchers at the University of California, Irvine, suggests that the DRD4 7R gene may be associated with several AD/HD traits, such as novelty-seeking, increased aggression, and perseverance.


Researchers have conducted a few studies into the size and shape of the brains of people with AD/HD compared to people without it. A lot of conflicting data exists in this area, but a couple basic ideas have been suggested:

  • One study suggested that the size of the corpus collosum (a bundle of nerves that ties the hemispheres of the brain together) is different in some people with AD/HD than in some people without it. Other researchers have suggested that this part of the brain operates differently in people with AD/HD than in others, so this observation may have some validity.
  • Some research has indicated that asymmetry in the basal ganglia (a set of nuclei deep in the brain that are involved in regulation and control of the motor system) may be indicative of AD/HD.

While anatomical research continues, most of the AD/HD research being done right now focuses on differences in brain activity between the AD/HD and non-AD/HD populations.


The brains of people with AD/HD seem to function differently than the brains of people without it. This area of research is buzzing right now, not only because it helps explain the cause of AD/HD, but also because these studies use relatively new technologies for imaging. Here's a sampling:

  • A study by Alan Zemetkin, MD, using PET scans on adults with AD/HD discovered that when the subjects concentrated, the level of activity in the front part of the brain (the frontal lobe) decreased from its level at rest. People without AD/HD have an opposite response — an increase in activity in the frontal lobe when they concentrate. This study is generally credited with showing that AD/HD is a biologically based condition.
  • Dr. Joel Lubar at the University of Tennessee conducted several studies using quantitative electroencephalogram (EEG). The studies showed that when people with AD/HD concentrate, there is an increase in theta activity (slow brainwaves) in the frontal lobe of the brain. This finding corresponds to a lower level of activity in the region.
  • Dr. Daniel G. Amen conducted extensive testing at his clinic using Single Photon Emission Computed Tomography (SPECT) technology. He observed several variations in brain activity in people with AD/HD and has suggested that AD/HD is actually several different conditions, each with a different brain activity signature. According to his research, the areas affected by AD/HD include:

Frontal lobe: Dr. Amen found a decrease in activity in this area when people with AD/HD are asked to concentrate. This corresponds with research done by Drs. Lubar and Zemetkin.

Limbic system: The limbic system is located deep inside the center of the brain and is often involved with the way we feel and express our emotions. Dr. Amen's research found that some people with AD/HD have heightened limbic activity in addition to the decreased frontal lobe activity. This corresponds with a perspective put forth by researcher Paul Wender suggesting that the limbic system is at the center of the problems in AD/HD.

Parietal lobe: Located toward the back of the brain, this section is also referred to as the sensory cortex. Dr. Amen suggests that certain people with AD/HD have more activity in this area than other people.

  • Dr. Robert Chabot and his colleagues at New York University found that 11 different patterns of QEEG (quantitative electroencephalogram — a device that measures surface brain wave activity and compares it to normal measurements found in a database) are associated with people diagnosed with AD/HD. They also found that some of these people could be predicted to respond well to certain medications and poorly to others.


For information to pass from one part of the brain to another requires the action of neurotransmitters — chemicals within the brain. A neurotransmitter is a small chemical messenger that allows one neuron (nerve) to communicate with another. When the upstream neuron gets excited and wants to pass on information to the downstream neuron, it releases the neurotransmitter molecules into a closed connection (like an airlock in a submarine or a space ship) called a synapse. The neurotransmitter then crosses the space to the downstream neuron's membrane and binds to specific receptors that cause an effect inside the receiving nerve.

One way to think about AD/HD is that it is a problem of balance between the activities of norepinephrine and dopamine two different neurotransmitters. When you have too much norepinephrine working, you are agitated, and you can pay attention only to things that may be threats or targets of opportunity (the "fight or flight" mechanism is very active). When you have more dopamine dominance, you tend to get stuck on repetitive activities, and you don't get bored doing the same things over and over. AD/HD is associated with having too much norepinephrine.

About This Article

This article is from the book:

About the book authors:

Jeff Strong is the Founder and President of REI Institute, which focuses on neuro-developmental disabilities. Michael O. Flanagan, MD, is a neuropsychiatrist in private practice in New Mexico.

This article can be found in the category: