3	What Causes ADHD?

ADHD has multiple causes. Our knowledge of these causes and of how they influence the brain and behavior has increased dramatically over the past 30 years and especially the last decade. Just as important, we have learned that other things once thought to cause ADHD do not. This chapter reviews the chief causes of ADHD and debunks some widely disseminated myths.

As you read, keep in mind how difficult it is to produce direct and incontrovertible scientific proof that anything causes a problem with human behavior. The experiments required to give direct, conclusive evidence that, for example, ADHD is caused by damage to the frontal part of a child’s brain during its development are simply unthinkable because they are unethical and inhumane. Scientists are not going to damage children’s brains in various controlled ways and amounts just to see what happens. So behavioral scientists who wish to study the biological causes of ADHD are often left searching for information that is less direct than this but highly suggestive of a cause. As a parent attempting to keep abreast of the research, then, it is extremely important for you to understand the possible sources of information and their relative reliability.

One such source is studies that show a consistent relationship between a potential causal agent and ADHD or the behavior problems characteristic of it. For instance, smoking by a mother during pregnancy is associated with an increased risk of hyperactivity and inattention in the offspring of that pregnancy. The fact that two events or conditions occur together, however, does not prove that one causes the other. It is merely suggestive.

Another source is studies of accidents of nature involving the cause in which we are interested. For example, when interested in the role of brain injury in ADHD, we may study children who have suffered diseases that attack the brain or children who have had clear-cut head trauma or other neurological injuries. This type of evidence is somewhat stronger because we can see that an accident (a brain injury) changed something in a child (the child shows the behaviors of ADHD), but it still is not definitive proof that brain injury causes ADHD. Other factors associated with the process of being injured may be the real culprits, and we must remember that most children with ADHD have no evidence of a brain injury.

A third source of evidence comes from studies in which the causal agent is given directly to some animals but not to others in a true experimental test of that cause. To see if exposure of a fetus to alcohol during pregnancy causes hyperactivity, scientists give large doses of alcohol to some pregnant animals, such as mice, rats, or primates, and not to others. They then study the behavior of the animals born of those pregnancies to see how the offspring in these two groups may differ. The scientists may also sacrifice the animals and directly inspect the brain tissue for signs of abnormal development caused by the alcohol. Although such experiments prove more directly that some agent causes hyperactivity or ADHD in the animals, such conclusions cannot be generalized perfectly to humans. The brains of animals (especially primates) and humans are more similar than different, but they are not identical. So it is likely but not certain that what causes hyperactivity in animals may well cause it or ADHD in humans.

More recently, a fourth line of evidence has come from new technologies that allow scientists to gain an image of the structure and even the activity or functioning of the brains of children and adults with ADHD and compare it to those of people without the disorder. Such research often shows that certain areas of the brain in people with ADHD are a different size or have a different level of activity when engaged than is seen in others.

With few exceptions—such as direct tests of whether certain foods or chemicals in our diet may cause ADHD—behavioral scientists have had to depend on indirect evidence to show that any particular factor is a cause of ADHD. It is usually the combination of various lines of evidence such as the types discussed above that is taken to be sound proof that some toxin, agent, or event may cause ADHD. Scientists must consider the totality or weight of the evidence and whether it is logically consistent. They must consider all possible explanations for their findings and justify their conclusions to other scientists. This need to convince the widest possible audience of scientists working in the same field through objective evidence, logical explanation, and public debate is the basis of the scientific method. Through this method, evidence has been mounting that ADHD is the result of abnormalities in brain development and functioning and that these abnormalities are related more to neurological and hereditary factors than to social ones.

THE CAUSES: CURRENT EVIDENCE

We now have extensive scientific research in hundreds of published studies on the causes of ADHD that it originates mainly in problems in the brain—resulting from either brain injuries or abnormal brain development. I begin this section by discussing the research pertaining to brain injuries. Since relatively few children with ADHD have been found to have actual brain injuries, however, I concentrate here on abnormal brain development. I first review the neurological findings regarding deficiencies in brain chemicals, lowered activity in certain brain regions, and structural immaturities or reductions in the size of the brain (smaller brain regions in five areas related to executive functioning). I then consider studies seeking to determine the causes of these abnormalities, which have centered on two groups of factors: (1) environmental agents, such as fetal exposure to alcohol and tobacco, and early exposure to high levels of lead; and (2) heredity (especially, in recent years, molecular genetics).

Research on Brain Injuries and ADHD

For almost 200 years, since Drs. Melchior Adam Weikard in Germany and Alexander Crichton of Scotland first wrote on the causes of attention disorders, scientists have suspected that what we now call ADHD is caused by some injury to the brain. They noticed striking similarities in behavior problems between children with ADHD and people who had suffered damage by injuries to the front part of the brain, just behind the forehead, known as the prefrontal region. This brain region is one of the most proportionately large in humans compared to other animals and is believed to be responsible for executive functioning and self-regulation, as discussed in Chapter 2—inhibiting behavior, sustaining attention, employing self-control, and planning for the future.

Research in neurology and neuropsychology is replete with case reports and studies of larger groups of patients who have experienced injury to the prefrontal part of the brain as a consequence of trauma, brain tumors, strokes, diseases, or penetrating wounds (such as gunshot wounds). Earlier in this century, this research convinced scientists that injuries to the brain from infections such as encephalitis and meningitis, trauma such as that caused by a fall or a blow to the head, or complications of pregnancy or delivery were the chief causes of ADHD symptoms. More than 35 years ago, however, scientists realized that most children with ADHD had no history of obvious or significant brain injuries from these sources. At most, perhaps 5–10% of children were likely to have developed ADHD from some sort of brain damage, by which I mean destruction of normal brain tissue. As discussed later in this chapter, children with ADHD tend to have had more pregnancy or birth complications than children without ADHD, but evidence that those complications have caused brain injury that in turn has caused ADHD is inconclusive.

Experiments with animals have served as a second line of research, producing evidence that ADHD may arise from brain injuries. There are many such studies, and they are quite consistent in their results. In these studies, primates such as chimpanzees are trained to perform certain psychological tests; then the scientists disable the prefrontal region of their brains through surgery or other means, and the tests are repeated. The animals’ natural behavior in their environment may also be observed. These studies have shown consistently that the primates’ behavior patterns are quite similar or even identical to those seen in children with ADHD when these prefrontal brain regions are altered: the animals become more hyperactive, less able to pay attention for long periods of time, and more impulsive on the psychological tests. They are also less able to inhibit their behavior or delay their responding to events created in the experiments. These animals often develop significant problems in their social behavior with other animals as well. The studies also show that injuries created elsewhere in the brain do not produce these patterns of ADHD-like behavior. So the frontal area of the brain can be implicated in producing symptoms of ADHD in primates. Fewer than 10% of children with ADHD can be shown to have suffered brain injuries, however, so something must be disrupting the development or functioning of this part of the brain even if no tissue damage is evident.

Abnormal Brain Development in ADHD: Neurological Findings

The Structure of the Brain

Numerous studies attest to the involvement of the brain in ADHD. Consider that by 2007 Dr. Eve Valera at Massachusetts General Hospital and her colleagues were able to review and combine more than 21 studies that had been published to that date on the brain structure of individuals with ADHD (total of 565) compared to typical people of the same age (total of 583). This review concluded that at least five brain regions were significantly smaller in those with ADHD than in the control people: (1) the cerebellum, a very old structure lying at the back of the head and base of the skull; (2) the front part of the corpus callosum (the splenium), which is a large bundle of nerve fibers that connects the right and left hemispheres, allowing cross-communication between them; (3) the right side of the caudate nucleus, one of several structures forming the basal ganglia and the center of the brain; (4) the right hemisphere of the brain more generally; and (5) the frontal regions of the brain.

In 2011, yet another review was published, involving 14 separate studies measuring the gray matter volume of the brain. The review, called a meta-analysis, was done by an international team of scientists led by Dr. Tomohiro Nakao and combined and reanalyzed the data from all of these separate studies. They showed unequivocally that the brain volume of those with ADHD is significantly smaller and that the greatest size reduction was in the caudate region (part of the basal ganglia, as noted above). They also found that these differences in brain volume improved with age and with the length of time children had been taking stimulant medication (implying that taking medication does not harm brain development and may facilitate maturation in brain size). Further evidence for these conclusions has been found in other recent studies.

Among the largest, most unusual, and most fascinating studies of brain volume in children with ADHD published after this large literature review in 2007 was done by Dr. Philip Shaw and colleagues working at the NIMH in Bethesda, Maryland, in collaboration with researchers at Montreal Children’s Hospital in Canada. These investigators initially compared the brain sizes and cortical structure of 223 children with ADHD and approximately the same number of normal children. They then repeated the scans on these groups of children every few years for up to 10 years. This allowed them to compare the pattern of growth or maturation of the brain between these two groups. They found that, on average, the children with ADHD were 2 to 3 years behind in their brain maturation, particularly in regions in the frontal lobes, but that brain size appeared to finally reach that of the normal children by their late teenage years. Note that while brain volume in children with ADHD may eventually become normal, this does not mean that brain functioning in these regions is necessarily becoming normal.

In general, the studies in this area of research have found that the prefrontal region, especially on the right side, several structures in the basal ganglia (the striatum and the globus pallidus), the midline anterior cingulate cortex (found at the midline of the prefrontal lobes), and the central area in the cerebellum, again, more on the right side, were significantly smaller and/or less active in children with ADHD than in normal children. These five brain regions are usually involved during tasks requiring inhibition, holding information in mind to guide behavior (known as working memory), and other executive functions. All of these results have led scientists to the conclusion that ADHD arises from delayed or impaired maturation of these regions that are significantly smaller, less mature, and less active than is typical of normal or non-ADHD individuals (prefrontal lobes, anterior cingulate cortex, caudate/striatum, cerebellum, and corpus callosum).

Brain Chemistry

Some scientists have suggested that certain neurotransmitters are deficient in those with ADHD. These are chemicals in the brain that permit nerve cells to transmit information to other nerve cells. Support for this idea comes from several sources:

1. Stimulant and nonstimulant drugs that are known to affect neurotransmitters (see Chapter 18) temporarily improve the behavior of children with ADHD.

2. Studies with animals suggest that these drugs increase the amount of the neurotransmitters, typically dopamine and norepinephrine, in the brain. These stimulants and nonstimulants produce significant improvements in the behavior of those with ADHD. This implies that the drugs are increasing the amount of these two chemicals in the brain, and so these two chemicals may be less plentiful in the brains of those with ADHD.

3. When the brain pathways that are rich in these neurotransmitters, such as dopamine, are selectively destroyed by a particular chemical in young animals, such as rats and dogs, these animals become quite hyperactive as they mature. Such studies have also found that this hyperactivity can be reduced by giving stimulant medications to these animals—the same stimulant medicines used to treat children with ADHD.

4. Some studies have taken samples of spinal fluid from children with ADHD to see if it contains more or less of certain chemicals related to those in the brain. These studies have indicated the possibility that a lower amount of certain neurotransmitters, again like dopamine, may be related to ADHD. Evidence from other studies, however, using blood and urine samples, has not always agreed.

More recently, scientists have conducted hundreds of studies using various methods to identify particular genes that may be involved in ADHD. At least four genes that regulate dopamine have already been identified as having such an association. One is involved in the removal of dopamine from the synapse (the tiny gap between neurons) and is called the dopamine transporter mechanism. Another two are involved in determining the sensitivity of neurons to dopamine itself, and the fourth is involved in converting dopamine to another chemical transmitter called norepinephrine. (Note: Other genes have been identified that affect brain growth, how nerve cells migrate during development to arrive at their normal sites, and the way in which nerve cells connect to each other.) Children or adults with ADHD have been found to have different versions of these genes that affect these neurotransmitters from people without the disorder, suggesting that they are involved in the development of ADHD. Undoubtedly more genes will be found to be related to ADHD in the future (see “Heredity and ADHD,” below).

What evidence there is seems to point to at least one possible problem in how much dopamine (and possibly norepinephrine) is produced or released in the brains of those with ADHD or how sensitive those brain areas are to this chemical when it is released during nerve activation. This evidence suggests that abnormalities in certain brain chemicals are likely to be involved in causing ADHD.

Brain Activity

Many studies to date have measured brain activity or functioning in people with ADHD and have found it to be lower in the prefrontal area of these people’s brains than it is for people without ADHD.

Lower Electrical Activity. Dr. Sandra Loo and I reviewed a large number of studies in 2005 that compared the brain electrical activity of children with ADHD to that of children without ADHD using a device known as an electroencephalograph (EEG). Some of the studies we reviewed examined the children with ADHD while they were sitting at rest, and some studies did so also while the children were performing certain mental tasks. The totality of evidence we reviewed shows that the brain electrical activity of children with ADHD is less than that seen in children without ADHD, particularly over the frontal area. The research to date shows that children with ADHD have an increased amount of slow-wave brain activity that is often associated with immaturity of the brain, drowsiness, and lack of concentration while having smaller degrees of fast brain-wave activity that is typically associated with focused concentration and sustained attention. Our conclusions have been strengthened by additional studies published since our review was done, making these findings some of the most reliable or robust in research on brain activity in ADHD.

Nearly 40 years ago, in 1973, in one of the first studies of brain electrical activity in ADHD, Drs. Monte Buchsbaum and Paul Wender, then at the NIMH, measured EEG activity in response to repeated stimulation in 24 children with ADHD and 24 normal children. The pattern they found in the children with ADHD was typical of younger children without ADHD; their responses reflected a less mature pattern of brain electrical activity. These researchers also found that giving stimulant medication to the children with ADHD reduced these differences. These findings have been replicated numerous times by other scientists such as Dr. Rafael Klorman working at the University of Rochester (New York). We now know for certain that this problem of brain underreactivity to stimulation is reasonably typical of children with ADHD. The results tell us that the problem here is not at the initial level of perception or in detecting the stimulus but at the level where the prefrontal lobes of the brain would enhance attention to that stimulus. This enhancing effect seems to be less in those with ADHD. Although children with ADHD show less activation in certain types of EEG activity, this does not automatically mean that training them to increase this activity is an effective therapy (see sidebar Can EEG Biofeedback or Neurofeedback Help Treat ADHD?).

Less Blood Flow. The more active certain brain regions are, the more blood they require. By measuring blood flow to various brain regions, one can therefore gain an idea of just how active those regions are. For instance, as long ago as 1984 Drs. Hans Lou, Leif Henriksen, and Peter Bruhn, working at the Kennedy Institute in Denmark, published a study comparing the blood flow in the brains of 11 children with ADHD (some of whom also had a learning disability) to the blood flow seen in nine children without ADHD. They found the children with ADHD had less blood flow to the frontal area and also in the caudate nucleus—an important structure in the pathway between the most frontal portion of the brain and the structures in the middle of the brain known as the basal ganglia. The caudate nucleus is made up of several bundles of nerve fibers, one region of which is known as the striatum. This region is important in inhibiting behavior and sustaining attention. In another study, these scientists compared the blood flow of nine children with ADHD to that of 15 children without ADHD and obtained similar results. In a third study, the same researchers and their colleagues compared 19 young patients with ADHD to nine children without ADHD. Again, the results showed decreased blood flow to the frontal brain areas, and especially to the striatum region of the caudate nucleus. When stimulant medication like that used to treat ADHD was given to these patients, the blood flow to these underactive areas increased to near-normal levels. These findings have been replicated by other scientists since then and lend further support to the idea that abnormal brain activity in particular brain regions is associated with ADHD.

Lower Brain Activity on PET and fMRI Scans. Another approach to studying brain activity besides using blood flow relies on the amount of oxygen that is being used in various brain regions or on other tracers injected into the bloodstream and monitored as they enter the brain. The first evidence that a problem existed in the brain activity of adults with ADHD came from a study done more than 20 years ago, in 1990, by Dr. Alan Zametkin and his colleagues at the NIMH. In this study, the brain activity of 25 adults with ADHD was compared to that of 50 adults without ADHD using a very sensitive procedure known as a positron emission tomography, or PET, scan. In this procedure radioactive glucose, the sugar used as fuel by nerve cells in the brain, is injected into the bloodstream. A PET scan device then takes pictures of the brain as it uses this glucose. Dr. Zametkin and colleagues found that adults with ADHD had less brain activity, particularly in the frontal area. The low level of activity was temporarily corrected when the adults took stimulant drugs like those commonly used clinically to treat children with ADHD. Dr. Zametkin repeated this study with 20 adolescents with ADHD and again found reduced activity in the frontal region, more on the left side than on the right side. The results were especially obvious for teenage girls with the disorder compared to girls without ADHD and less so for the teenage boys with ADHD relative to boys without it. Since then, many other studies using this and other neuroimaging technologies have found similar results, all implying that underfunctioning and even underdevelopment of certain brain regions contributes to ADHD.

Another way to study brain activity is through functional magnetic resonance imaging, or fMRI. Like PET, the devices and procedures involved in fMRI can show how well or poorly different brain regions are activating, typically in response to some mental task the individual must perform while in the scanner. Many studies using this technology have also demonstrated that various regions of the brain in those with ADHD are not functioning normally or optimally relative to the brains of people without the disorder. Most of these studies were reviewed in 2007 by Dr. Yannis Paloyelis and colleagues at the Institute of Psychiatry in London, who commented that all studies using fMRI had found differences in the brain activity between cases having ADHD and typical individuals of the same age. Again, much of this reduced activity appears to be occurring in one or more of the five brain regions discussed above.

Comparing Brain Activity in ADHD and Other Psychiatric Disorders. In a study using similar brain-imaging techniques, Dr. Karl Sieg and colleagues at the University of Kansas reported as early as 1995 that they had also found significantly reduced brain metabolic activity in the frontal regions of 10 patients with ADHD, compared to six patients with other psychiatric disorders but not ADHD. This study is important because it provided some evidence that the reduced frontal brain activity is specific to patients with ADHD and does not just accompany any psychiatric disorder. Many other studies since then have supported such distinctions between brain structure and functioning in ADHD in comparison to other disorders, such as studies in the past decade by Dr. Joseph Biederman and colleagues (see above) that compared cases of bipolar disorder with those having ADHD or those having conduct disorder to those with ADHD that showed different brain regions associated with these various disorders. For instance, a study in 2009 by Dr. Katya Rubia and colleagues, then at the Institute of Psychiatry in London, found reductions in brain activity in those with ADHD and also patterns of underactivation that were distinct from those patterns seen in patients with conduct disorder.

Can EEG Biofeedback or Neurofeedback Help Treat ADHD?

If children with ADHD have low brain electrical activity, teaching them how to increase it might help them alleviate their ADHD symptoms. Over 30 years ago scientists began to test that theory using EEG biofeedback, and to this day some dramatic claims have been made for this kind of treatment. You may have seen advertisements stating that EEG biofeedback is an effective alternative to medication; that it results in permanent changes in the brain physiology underlying ADHD; that it improves IQ, social skills, and even learning disabilities; and that such improvements can last into adulthood in up to 80% of all treated cases. Those are fantastic claims for any treatment. How much of this should you believe?

Only some of it and only then with much greater caution. The term biofeedback means that a child is given back biological information about her brain activity through electrodes placed near the scalp that detect brain waves and a computer that classifies them. Over a great number of sessions, typically 40–80 sessions over 3–10 months or longer—at a cost of several thousand dollars ($100+ per session)—the child supposedly learns to improve her brain activity. She does this through mental exercises and some form of signal from the biofeedback equipment that she has been successful at increasing the desired brain activity related to sustained attention and decreasing the undesired activity associated with daydreaming or distraction. She is then rewarded as well for doing so. The result, supposedly, is that the child’s inattention, hyperactivity, and impulsivity will then also improve.

Unfortunately, to date there have been only a few well-controlled studies, and they are contradictory in their results. Therefore, the evidence is mixed on the effectiveness of EEG biofeedback for children with ADHD, as reported in a 2012 review by Dr. Nicholas Lofthouse and colleagues.

Many of the studies that have been published by proponents of the treatment have not used sound scientific methods that would allow us to draw any straightforward conclusions from their results, even though they claim to have found this treatment to be effective. They do not clarify whether the biofeedback training or the academic tutoring and rewards program that accompanied it were responsible for the improved school and home behavior observed. So although we cannot rule out the possibility that EEG biofeedback training might be of some benefit, we cannot consider it a well-established and effective treatment at this time.

Furthermore, a child and family could receive 12 years of stimulant medication, 3 years of weekly group parent training, nearly 3 years of twice-monthly classroom consultations by a clinical psychologist, or almost 2 years of twice-weekly educational tutoring for the cost of 6 months of this treatment, based on current average charges. Which choice would you make for your child? My advice is to try the most effective and scientifically based treatments first (medication, behavior management techniques, classroom accommodations, etc.) and only after them, if more improvement is desirable, should you try neurofeedback and only then if you have sufficient expendable income to cover the cost of treatment.

Conclusions

In summary, the scientific findings from many lines of scientific research to date clearly indicate that at least five interconnected areas of the brain are involved in ADHD, especially that area in the very front part of the brain, known as the prefrontal region. This region connects to an area at the midline of the prefrontal lobes called the anterior cingulate cortex. This region is connected to the amygdala and limbic system, which are very old brain structures that govern our emotions. This pathway has come to be known as the “hot” executive circuit because of its role in the “top-down” executive control of our primary emotions. The prefrontal lobes also send connections through a pathway of nerve fibers into a structure called the caudate nucleus (which is part of the striatum). This pathway is known as the “what” or “cold” executive circuit because it is responsible for how well what information we are holding in mind is likely to guide our actual behavior. The prefrontal lobes also send connections farther back into an area at the back part of the brain known as the cerebellum. This path has been called the “when” executive circuit because it appears to be involved in the timing and timeliness of our thoughts and especially the actions guided by our thoughts. Substantial evidence now exists to show that these three executive circuits may be responsible for the development of ADHD. Variation among people with ADHD in how poorly each of these circuits is functioning probably helps to explain some of the individual differences we see in the types of symptoms people with ADHD may express.

As I have described earlier, these brain areas are those that create our executive functions or abilities. They help us inhibit our behavior, be aware of ourselves and our actions, contemplate the past and future, sustain our attention and actions toward our goals and the future, and inhibit responding to distractions when we are pursuing tasks and our goals. They also let us inhibit and control our emotions and motivation, as well as help us use language (rules or instructions) to control our behavior and plan for the future. These scientific findings are very consistent with my view that a problem with executive functioning or self-control is the hallmark of ADHD and that this arises from abnormal levels of activity in the regions of the brain responsible for these human abilities.

How is it, many parents still ask, that children with ADHD, who are more active and energetic than children without ADHD, could have brains that are less active? Remember that the areas of the brain that are not as active as they should be are the parts that inhibit behavior, delay responding to situations, and permit us to think about our potential actions and consequences before we respond—the executive brain. The less active these inhibitory and executive centers are, the less “top-down” self-control a child will be able to demonstrate.

Some Causes of Abnormal Brain Development

We now know that certain brain chemicals seem to be altered, and that certain brain regions are underactive and underdeveloped, in people with ADHD. We still need to discover why. Among the possible explanations, two stand out from the evidence available: hazardous agents and events that affect early brain development and genetics of the brain.

Environmental Agents

Substances Consumed during Pregnancy. Nicotine from cigarette smoking and alcohol from drinking during pregnancy have been shown to cause significant abnormalities in the development of several of these brain regions, such as the caudate nucleus and the prefrontal regions of the brain. Nearly 40 years ago, in 1975, a study showed that the mothers of 20 hyperactive children had consumed more than twice as many cigarettes per day during pregnancy as mothers of 20 reading-disabled and 20 control children.

A much larger 1992 study found that direct exposure to cigarette smoke during pregnancy or indirect exposure after pregnancy increased the odds of behavior problems in the children of these pregnancies. The combination of exposure both during and after pregnancy created the greatest likelihood that the children of that pregnancy would have significant behavior problems. Subsequently, in 1996, Dr. Sharon Milberger and her colleagues, then at Massachusetts General Hospital and Harvard Medical School, found a significant relationship between the quantity of cigarettes smoked during pregnancy and the risk for ADHD in the children of those pregnancies, even after the researchers controlled for the family history of ADHD that might have existed. Many other studies done since then have found this link between maternal smoking during pregnancy and risk for ADHD in the offspring of that pregnancy. Thus, substantial scientific evidence suggests that exposure to cigarette smoke is related to a higher risk for behavior problems similar to those in ADHD. Mothers who smoke at least 10 cigarettes per day or more during their pregnancies increase the risk of ADHD in their children by 2.5 times the risk seen in the nonsmoking population.

Research indicates that children born to alcoholic mothers are more likely to have problems with hyperactivity and inattention and even clinical ADHD. Many studies support this association. The amount of alcohol consumed by their mothers when pregnant appears to be related directly to the degree of risk for inattention and hyperactivity in their children at ages 4–7. The risk of having a child with ADHD increases 2.5 times for women who drink during pregnancy over women who do not.

Keep in mind, however, that all of these studies merely provide evidence of an association between these substances and ADHD, and associations can be misleading. Again, however, Dr. Milberger and colleagues did control for family history in their research on smoking and ADHD, and so we can have more confidence in the possibility that smoking during pregnancy is probably related to ADHD.

Similarly, we know that adults with ADHD drink more alcohol than others whether they are pregnant or not. We also know that ADHD is highly likely to be inherited (as discussed below). Therefore it may very well be genetics alone and in interaction with the alcohol or tobacco smoking that caused ADHD in the children in these studies. Research by Dr. Rosalind Neuman and colleagues found persuasive evidence of just such gene × toxin interactions that showed that each increased the risk of having ADHD but that in combination the risk genes for ADHD and maternal smoking made the risk to the children for developing ADHD markedly worse.

Supporting a direct causal connection between these toxins consumed by mothers during pregnancy and ADHD symptoms, animal studies have shown fairly conclusively that tobacco smoking and alcohol cause abnormal development of certain brain regions and that these abnormalities lead to increased hyperactive, impulsive, and inattentive behavior. So perhaps the most significant conclusion is that a mother may increase the risk of ADHD in her child by smoking or drinking during pregnancy, and this risk may be increased further if the mother herself also has ADHD.

Exposure to Lead. As discussed by Dr. Joel Nigg of the Oregon Health Sciences University in his 2006 book What Causes ADHD?, there is some scientific evidence that high levels of lead in the bodies of young children may be associated with a higher risk for hyperactive and inattentive behavior. This relationship seems to exist especially when the lead exposure occurs between 12 and 36 months of age. The relationship is rather weak, although it is found consistently in many studies. For instance, on a scale of 1–100, the relationship between body lead and hyperactivity rates only 6–15. But even at high levels of exposure, a 1979 study found that fewer than 36% of children with elevated lead levels were rated by teachers as inattentive, distractible, impulsive, and hyperactive. High levels of lead in the body may well cause some cases of ADHD because animal and human studies do show that lead exposure at moderate to high levels injures brain tissue. So lead is a toxin to the brain, just as alcohol and tobacco are; it may therefore be viewed as a potential cause of inattention, hyperactivity, or even full-fledged ADHD in some cases. But like the other toxins discussed above, consuming it does not guarantee that a child is automatically going to develop ADHD as a consequence.

Heredity and ADHD

Only a minority of children (25–35%) appear to have acquired their ADHD as a consequence of toxins or other hazardous events that may have disrupted early brain development, according to Dr. Joel Nigg in his 2006 book What Causes ADHD? What else could be causing the altered brain chemistry, brain underactivity, and smaller brain regions? One highly likely reason has been found in the substantial research on the role of genetics and heredity in ADHD—for one thing, the disorder clearly runs in families. For many years we’ve had evidence that the biological relatives of children with ADHD have more types of psychological problems—particularly depression, alcoholism, conduct problems or antisocial behavior, as well as hyperactivity/ADHD—than relatives of children who do not have ADHD. Such a family contribution to ADHD was evident as long as 40 years ago in initial studies on the families of hyperactive children conducted by Drs. James Morrison and Mark Stewart, then at the University of Iowa Medical School, as well as Dr. Dennis Cantwell and colleagues at the University of California, Los Angeles, Neuropsychiatric Institute. Such research strongly supports the idea that a genetic predisposition contributes substantially to this disorder.

Family Studies. Clearer and stronger evidence that ADHD may be inherited comes from studies that directly evaluate all members of an immediate family for ADHD and determine the risk to other family members if one of them is diagnosed with ADHD. As an example, consider the large study by Drs. Joseph Biederman, Stephen Faraone, and their associates at Massachusetts General Hospital. Published in 1990, the study evaluated the 457 first-degree relatives (mothers, fathers, and siblings) of 75 children with ADHD and compared their results to their evaluation of the family members of 26 control children (that is, children with no psychiatric disorders) and 26 children with psychiatric disorders other than ADHD. They found that over 25% of the first-degree relatives in the families of children with ADHD also had ADHD, whereas this rate was only about 5% in each of the other groups. This 5% is what you would expect by chance to find in any sample of children, since it is the prevalence of the disorder in the population at large. Notice that if a child has ADHD, then, there is a five times greater increase in the risk to other members in that family. Many other subsequent studies have found similar results.

Twin Studies. Research using twins is even more persuasive. Scientists have found that if one twin has symptoms of ADHD, the risk that the other will have the disorder is as high as 75–90%. This risk is two to three times greater than the risk to one sibling if another one has the disorder (25–35%) and 9–15 times greater than the risk seen in the general population of children (5–8%). For example, consider the results of a study published in 1992 by Dr. Jacquelyn Gillis and associates at the University of Colorado. They found that 79% of identical twins both had ADHD when one of the twins had already been diagnosed. For fraternal twins the figure was only 32%, but that is still 6–10 times greater than that seen among unrelated children, where the prevalence of ADHD at the time was only 3–5%.

Besides comparing the risk between two identical twins if one has the disorder, scientists can also study large samples of identical twins compared to nonidentical or fraternal twins and mathematically compute the degree to which differences among all of the people in the sample are a result of differences in their genetic makeup. More than 40 very large studies of twins have been done in various countries to date. They have been able to determine that differences in genetic makeup explain between 55 and 97% of the differences among people in their level of symptoms of ADHD, with an average of about 78% of such individual differences being due to genetics.

These studies can also determine the extent to which unique environmental events or factors contribute to variation in ADHD traits in the population. Such events are called “unique” because they happen to just that child (and not others in the family)—such as toxins like lead poisoning, maternal infections that occurred during just that pregnancy, maternal use of tobacco or alcohol that occurred in just that pregnancy, that child being born highly premature, or other complications occurring during that pregnancy and birth. Such unique hazardous biological events seem to explain only between 6 and 15% of the differences among people in level of ADHD traits. This clearly supports a very large role for heredity in the expression of ADHD. Yet it also supports the discussion above that a small degree of ADHD can arise from nongenetic sources, like brain injuries or maternal alcohol and tobacco consumption during that child’s pregnancy.

Twin studies can also be used to calculate the amount of variation in ADHD traits among people that arise from shared environmental events or factors. These are things that all children in a family are likely to have experienced, such as a similar diet, amount of exposure to TV and video games, problems in parenting, psychological difficulties in one or both parents, the neighborhood in which they are all being raised, and so on. What is so surprising and important in these studies is that they have consistently shown that these shared or within-family events do not explain much if any of the variation in ADHD traits among children. This is why we can now safely conclude that bad parenting or other things occurring in a family to which all of their children are exposed does not contribute to causing ADHD. Besides the strong genetic contribution to ADHD found in all of these studies, this finding of little or no role for the within-family environment in ADHD is one of the most reliable findings in scientific research on ADHD to date.

What Exactly Is Inherited? The specific factors inherited in ADHD probably include a tendency toward problems in the development of the prefrontal cortex of the brain, the caudate nucleus, and the other brain regions discussed above. Scientists are now carrying out studies that evaluate all members of a family that include a child with ADHD and are scanning the entire human genome (all active gene sites in humans) to determine just how many genes are involved in the disorder and their locations. Subsequent research can then investigate the nature of the genes located at these sites and help us begin to understand how that gene functions in the human brain (build nerve cells, help with their normal migration, support the cells, determine their sensitivity to neurotransmitters, create the neurotransmitter chemical itself, etc.). So far 22–40 or more sites have been identified in these initial genome scans. The genes at some of these sites are already known, while others remain to be identified.

Suffice it to say here that this is one of the most exciting and most rapidly developing areas of research in ADHD at this time. What all this means is that ADHD is caused by multiple genes. Each gene makes a relatively small contribution to the risk for having the disorder. But a child who gets enough of those ADHD-risk genes will manifest symptoms severe enough to be diagnosed with the disorder. Family members that have fewer numbers of these genes may show a few and milder symptoms of the disorder but not enough to be diagnosed with it or to be necessarily impaired by it. They show what researchers call the “family phenotype” of the disorder even if they don’t show the full spectrum or severity of the disorder itself. We are also learning that the genes that may be involved in causing ADHD are really not an abnormal one or a “disease” gene. Typical people without ADHD are likely to have this gene. But the version of the gene related to ADHD may be different in some way, typically being unusually longer or shorter than that seen in people without the disorder.

For instance, a number of studies have confirmed that at least two genes involved in the neurotransmitter dopamine mentioned earlier may be related to ADHD. One of these, called the DRD4, is related to the personality dimension known as novelty seeking. Children and adults with ADHD are more likely to have a longer version of this gene. The gene may make their dopamine nerve cells in the brain less sensitive to normal amounts of dopamine. They require more of it than other people to make the cells activate. This effect on the nerve cells may make them more likely to seek out novelty because it stimulates their brain and especially the release of dopamine. They are therefore said to have novelty seeking in their personality. That is, they exhibit more sensation-seeking behavior, risk taking, impulsiveness, and restless behavior than is typical for the normal population.

A second gene, the DAT1 gene, also has a longer form that is more commonly associated with ADHD than would be expected to occur in the general population. This gene may help to regulate dopamine activity in the brain by influencing how quickly dopamine is removed from the synapse, the small gap between neurons (see “Brain Chemistry,” above). Besides these two genes, at least seven others have been identified as likely risk genes for the disorder. And as the genome scans found above, ADHD results from even more genes than these nine. Be sure to watch for news reports about new scientific discoveries related to the genetics of ADHD.

Is ADHD Simply an Extreme Form of a Normal Human Trait? The genetic explanation of ADHD has an important implication that can easily go overlooked: ADHD may simply represent an extreme form of a normal human trait and not a grossly pathological condition in most cases. As we have just seen, which of us end up with ADHD seems to be determined much more by genetics than by environmental factors. In that sense, ADHD may be viewed in the same way as height, weight, intelligence, or reading ability, to name a few traits that are dimensional (people vary in degree) and that are largely (but not wholly) genetically determined: the trait of executive functioning and the self-control related to it represents a dimension or continuum of a human ability, and we differ in how much of it we inherit, just as we differ in how much height, weight, intelligence, or reading ability we inherit. What is considered “abnormal” for any trait is simply a reflection of where we draw a line on the continuum. When people fall near the extreme lower end of the continuum for a dimensional trait like ADHD and that deficiency results in their suffering impairment in their major life activities (social relations, education, work, etc.), we label them as having a disorder. Such labels make it appear that the disorder is like some category that some people fall into while most do not. It can obscure the fact that those with ADHD fall along a dimension of normal abilities differing only from typical people as a matter of degree, not as being a different kind of person. The difference here is a quantitative one, not a qualitative one. To put it another way, we all have a degree of this ADHD trait because we all have executive functioning and self-regulation. Those who are diagnosed with ADHD simply represent the extreme lower end of the dimension(s) related to self-regulation and executive functioning.

Understanding that ADHD is just an extreme form of a trait we all possess and that it is something people “come by naturally” should help everyone view ADHD from a kinder perspective, I hope. Your child was born with this problem; it is through no fault of his own that he lies at that position on the continuum. Likewise, you should neither assign blame to yourself nor accept it from others.

THE MYTHS: WHAT DOES NOT CAUSE ADHD

No doubt you’ve encountered claims that factors other than those just discussed cause ADHD. Some of these were originally founded in sound hypotheses but have since been disproven. Others are sheer falsehoods; there is not now and never has been any scientific support for them. As we continue to make conclusive findings about ADHD, let us hope that quackery surrounding the subject will greatly diminish if not vanish altogether. In the meantime, use what you know about the scientific method to sort fact from fiction.

It’s Probably Not Something They Ate

In the 1970s and early 1980s, it was very popular to view ADHD as resulting from chemical food additives. This theory stemmed mainly from the widespread media attention given to Dr. Benjamin Feingold’s claim that over half of all hyperactive children got that way from eating foods that contained additives and preservatives. Most of the substantial amount of research done over the next decade was simply unable to support Feingold’s claim. In fact, only a very small number (5% or fewer) of children, mainly preschoolers, showed a slight increase in activity or inattentiveness when consuming these substances. No evidence has ever been provided that normal children develop ADHD by consuming such substances or that children with ADHD are made considerably worse by eating them. In 1983, Drs. Kenneth Kavale and Steven Forness of the University of California–Riverside published a review of 23 studies investigating the Feingold diet. They concluded that diet modification was not effective for treating hyperactivity.

Despite that view being shared by many scientists studying ADHD, the popular media continued to tout this now unfounded belief. In 1986, in fact, Ann Landers published and personally supported a letter from a parent making such an erroneous claim and directing parents to write to the Feingold Association of the United States (Worcester Telegram and Gazette, September 19, 1986). Unfortunately for parents who may have read such nonsense and taken the advice, nothing could be further from the truth. More recently, scientific interest in this theory has diminished greatly, and so has that of the general public.

“Is it sugar that causes ADHD, as I so often hear?”

However, in its place, the public then adopted a popular view that sugar causes ADHD. So widely accepted was this idea that in January 1987 it was paired as the correct response to the statement “The major cause of hyperactivity in North America” on the popular television game show Jeopardy. Not a single scientific study has been provided by proponents to support these claims. Since 1987 a number of scientific studies of sugar have been conducted, and these have generally proven negative. As an example, a study published in 1988 by Dr. Lee Rosen of Colorado State University and colleagues showed that even when given a beverage with the equivalent of two candy bars’ worth of sugar, normal preschool- and elementary school-age children may have slightly increased their activity level, but not so as to be detectable by their teachers or the experimenters throughout the school day. No effect of sugar was found on the academic work of the children. Only the girls showed a slight decrease in their attention and learning on one of the psychological tests done within 20–30 minutes after they had the drink, but this was a very small change and not noted on any of the teacher ratings or observations. No child developed the disorder of ADHD. The conclusion of the authors was that sugar does not cause clinically significant or dramatic changes in children’s behavior, much less the clinical disorder of ADHD.

Drs. Mark Wolraich, Richard Milich, Phyllis Stumbo, and Frederick Schultz at the University of Iowa Hospital School then conducted two studies of hyperactive children published in 1985. They intensively studied 16 boys in each study who were admitted to the hospital school for 3 days, during which the sugar content of their diet was directly manipulated. To keep the children and other staff from knowing what days the sugar was in the diet, the investigators used aspartame (Nutrasweet) as a placebo. These scientists took 37 different measures of behavior and learning and found no significant effects of sugar on either behavior or learning. In 1986, Drs. Richard Milich, Mark Wolraich, and Scott Lindgren published a review of all of the research conducted up to that time on the adverse effects of sugar on children’s behavior. They concluded that “most studies have failed to find any effects associated with sugar ingestion, and the few studies that have found effects have been as likely to find sugar improving behavior as making it worse” (p. 493).

How could this be the case when nearly half of the parents and teachers queried in one of these studies stated that their children appeared to them to be quite sugar-sensitive? One answer has been known to psychological research for decades, and that is the power of psychological suggestion. To evaluate this possibility, Drs. Daniel Hoover and Richard Milich at the University of Kentucky published a study in 1994 using 31 boys ages 5–7 whose mothers reported them to be behaviorally “sugar-sensitive.” When each mother and child came to the clinic, the mother had been told that on the day of the appointment their child would be given either sugar or aspartame (as a placebo, again) in Kool-Aid. Actually, though, none of the children were given any sugar in their drink. On the morning of the appointment, half of the mothers were told their children were getting sugar and the other half that the children were getting aspartame. The mothers and children were then observed interacting during a period when they played freely and then during a period when they performed work together. The mothers also rated their children’s behavior at the end of these periods. Direct measures of the children’s activity level were also taken. The scientists found that the mothers who had been told their children received sugar rated their children as being more hyperactive than the mothers who were told the truth (that aspartame was given). The mothers who thought their children received sugar also were more critical of their children’s activities, maintained closer physical proximity to their children (hovering), and talked more frequently to their children than the mothers who knew the children had aspartame. This study clearly shows that what parents believe about a dietary cause of hyperactivity (in this case, sugar) not only can bias their reports but also can change the way the parents treat their children. This study is worth keeping in mind the next time someone tells you that something children eat makes them hyperactive or causes ADHD. But despite research over the past 25 years showing no significant link between sugar and ADHD, it still remains today as one possible cause of ADHD in the minds of some in the general public.

“I saw a doctor on a talk show who said that food allergies cause ADHD. Can you test my son for that? If not, where can I go to have him tested?”

Over the years other unsubstantiated claims have been made about the influence of diet on ADHD. Almost 40 years ago, several professionals claimed that large doses of vitamins, particularly vitamins B₃, C, and pyridoxine, would be of benefit to severely mentally ill patients. Nearly 20 years later, another professional published statements that hyperactive and children with learning disabilities could benefit from so-called megavitamin therapy or orthomolecular psychiatry. None of these claims has been verified by scientifically rigorous research. In fact, one reasonably well-done study found that the behavior of children with ADHD actually became worse on the megavitamin treatment program. Similar claims have been made for large doses of minerals. There is no evidence that megadoses of vitamins or minerals can help children with ADHD, or that vitamin or mineral deficiencies in any way cause the disorder. Parents should also be aware that large doses of vitamins (especially fat-soluble vitamins) and minerals can actually be harmful to children.

You may also have read (or seen on TV talk shows) that allergies to substances in foods besides the chemical additives targeted by Dr. Feingold can cause ADHD symptoms (and, incidentally, a raft of other symptoms). One very large study conducted in The Netherlands by Dr. Lidy Pelsser and colleagues that was published in 2010 compared a large general population sample of children not receiving a controlled diet and another group that had various substances controlled or eliminated from their diet. It reported that children in the controlled diet improved in their inattention, activity level, and other symptoms of ADHD. These improvements were noted primarily by parents and might well have arisen in part because the parents could tell which children were receiving the controlled diet and which were not. While this study suggests that some children may benefit from removal of certain chemicals, colorings, or flavorings from the food in their diet in improving their behavior, the results of this study go against most other studies recently reviewed by Dr. Joel Nigg and associates that found a much smaller effect of treatment. As always, more and better research is necessary to completely rule in or out the possibility that some children may be adversely affected in their behavior by certain food additives. But the evidence is not compelling to me as of this writing that this is a major cause of ADHD, even though some small effects have been seen in some studies. Also the American Academy of Allergy and Immunology does not advocate investigating allergies when ADHD symptoms appear. Americans have been so fascinated for the last 35 years with how foods affect human health that it should come as no surprise when links between diet and ADHD continue to be proposed, but at this point most such claims cannot be taken seriously.

Are Hormones Involved in ADHD?

A study published in early 1993 (by Dr. Peter Hauser and colleagues) showing a link between low thyroid hormone levels and ADHD received a great deal of publicity from the media. Some stories even claimed that the “gene” for ADHD had been discovered because the gene for thyroid deficiency is known and it was assumed that the two must be related in some way. These hormones, chemicals produced in the thyroid (a gland in the neck), are important in controlling human growth and may have other functions that are not fully understood. A few people may have a rare condition of thyroid deficiency that may be genetically determined. The study found that 70% of children and 50% of adults who were deficient in thyroid hormone had ADHD. Since then this link has been studied in three additional published papers, and none has found any significant link between problems with thyroid hormone functioning and hyperactivity or ADHD. Thus the initial study appears to have been flawed in some way. Children with ADHD should not be routinely tested for thyroid deficiencies, nor should thyroid hormone treatments be considered to hold any promise for the treatment of ADHD at this time.

No other hormones have been shown to have any relationship to ADHD.

Motion Sickness and ADHD

For many years Dr. Harold Levinson of Great Neck, New York, has been garnering media coverage for his theory that ADHD, learning disorders, and other behavioral and emotional problems can occur because of a problem within the vestibular system of the brain, which affects balance, sense of gravity, and head position. This system is located in the inner ear and makes connections with parts of the brain, especially the cerebellum, located at the lower back portion of the skull. Contrary to what most scientists believe, Dr. Levinson claims that this system also regulates our energy levels, so that any impairment in this system can lead to hyperactivity and impulsive behavior. He recommends that children with ADHD or learning disorders take Dramamine or dimenhydrinate (an anti-motion-sickness medicine available over the counter) because it is known to have some effects on the vestibular system. He provides patients with other medicines as well, some of them powerful psychiatric drugs, other vitamin supplements, or herbal extracts.

In their 1994 review of the evidence available on Dr. Levinson’s theory and treatment recommendations, two psychologists, Drs. Barbara Ingersoll and Samuel Goldstein, concluded that the theory is surely inconsistent with what is known about ADHD and the vestibular system and its functions. The vestibular system does not seem to be involved in any way with impulse control, attention span, or regulation of activity level. Dr. Levinson claims to have used this approach to treat thousands of patients with ADHD and learning disorders, with at least 70–80% of patients responding well. Even so, he has never published a well-controlled scientific study on this issue. Thus we have only his word to take on how useful this treatment program is for those with ADHD. As with the dietary treatments discussed earlier, parents should avoid this treatment program and view it as entirely unsubstantiated by legitimate scientific research.

Can Yeasts Cause ADHD?

Dr. William Crook, a pediatrician and allergist from Jackson, Tennessee, has been a vocal proponent of yeasts—particularly those such as Candida albicans that can live in the body—as a major cause of many different learning, behavioral, and emotional problems, especially ADHD. These yeasts are typically kept in check by other bacteria in the body as well as by the body’s immune system. Dr. Crook believes that toxins given off by the yeasts can irritate the brain and nervous system and can weaken the body’s immune system. He recommends that children with ADHD be placed on low-sugar diets, because sugar can stimulate the growth of yeasts. Like Dr. Feingold, he also believes that additives and other chemicals in foods may contribute to a yeast problem in the body, and so these should be eliminated from the diets of ADHD children. He believes that some children may even need to be treated with an antiyeast medication such as nystatin, and that others may need vitamin, mineral, or other dietary supplements to control their behavior problems.

Presently, not a shred of sound scientific evidence supports Dr. Crook’s theory. Given that the American Academy of Allergy and Immunology has found the theory of yeast sensitivity unproven, parents are encouraged to ignore any advice based on it. Certainly Dr. Crook’s recommendations that children take large doses of vitamins and minerals, as noted earlier, can be potentially harmful to children.

Can Bad Parenting or Chaotic Family Life Cause ADHD?

Theories that blame the social environment as the major cause of ADHD have not received much support in the scientific literature. Some writers have claimed that ADHD symptoms such as hyperactive behavior can result from poor parental management of the children; these parents are thought to be too permissive or too disorganized in their parenting or do not provide enough training, structure, or discipline. No studies support this view. Yet even in the January 28, 2012, New York Times an op-ed piece was published by L. Alan Sroufe, PhD, a psychologist at the University of Minnesota, in which a similarly baseless claim was made about parenting causing ADHD. There simply is no evidence available to support such parent bashing in explaining ADHD, while there is much evidence that refutes it, raising questions about the motives of those who would continue to make such outlandish and strongly scientifically contradicted assertions that certain behaviors of parents toward their child can cause ADHD. Earlier in my career, I studied family life and particularly the interactions between parents and their children with ADHD for more than 24 years. My own research did show that the parents of children with ADHD are more likely to give commands to their children, to be more directive and negative toward them, and in some instances to be less attentive and responsive to their children than are parents of children without ADHD. My colleagues and I also have found that the children with ADHD were less compliant with their parents’ commands and directions, were more negative and stubborn, and were less able than children without ADHD to keep complying over time with the parents’ commands. Many other studies have noted these and other differences in the parent–child interactions of families having children with ADHD. Is it the parents’ fault that the children are acting this way, or the children’s fault that the parents are reacting this way?

“My parents think that I spoil my son too much, that I don’t discipline him the way I should, and that this is why he acts this way. How do I convince them he really has a disability?”

To evaluate this question further, we gave stimulant medication (Ritalin) on some weeks and placebos on the other weeks to children with ADHD. Then we observed what happened in mother–child interactions. Neither the mothers nor the children knew which weeks the children were on the real medicine and which weeks they were taking the placebo. We found that when the children were on the real medicine, their behavior toward their mothers was much improved. But we also found that the mothers’ behavior toward the children was improved. It even resembled the behavior of the mothers of children without ADHD. This indicates that much of the negative behavior of the mothers seemed to be in response to the difficult behavior of these children and not the cause of it. After all, by directly changing the ADHD symptoms of the children with medication, we showed that the behavior of their mothers became much more “normal.”

You may also have read claims that a chaotic family life or a “dysfunctional” family can cause ADHD, based on the fact that parents of children with ADHD are somewhat more likely to have psychological problems or even psychiatric disorders. Studies have found that the parents (and immediate relatives) of children with ADHD are more likely to have problems with alcohol and substance abuse, antisocial behavior, and depression, and to have had school problems and hyperactivity when they themselves were children. Parents of children with ADHD also report more stress in their role as parents and more marital or couple problems than other parents. Moreover, the families of children with ADHD move more frequently than families who do not have such children. Such things can easily influence how well a household runs, how organized the parents are in managing their personal and family life, and how well they are able to manage their children. These disruptive influences can also create much more stress for the children than may be experienced in the family life of children without ADHD.

In the minds of many people (including some professionals), this line of reasoning justifies the claim that ADHD can arise out of disorganized, dysfunctional family life. But several lines of reasoning clearly disprove this view. First, the greater problems seen in family members of children with ADHD are easily explained by the hereditary evidence described earlier. We should expect to see more ADHD and its symptoms in the biological parents and family members of children with ADHD, even if the children with ADHD were adopted away at birth; and we do. This explains why the family members of children with ADHD may be having more trouble themselves, may move more often, and may have more marital or couple problems and a higher divorce rate than families without such children. It is not the psychiatric problems of these family members and the resulting “bad” family environment that cause ADHD in the children, but the ADHD risk genes that the parents and children have in common.

Second, later research contradicts this theory. Studies found that these psychiatric problems among the family members of children with ADHD occurred most often in only a subgroup composed of children who also have serious problems with aggressive, defiant, and antisocial behavior. The parents and relatives of this subgroup are the ones who are more likely to have problems with drug and alcohol abuse, depression, and antisocial behavior. Children who have only ADHD, without significant aggressive behavior, do not seem to have these serious problems among relatives any more frequently than do children without ADHD. This tells us that these parent and family problems are linked to the development of aggressive and antisocial behavior in the children and not to the children’s ADHD. In other words, chaotic or dysfunctional family life due to psychological problems in the parents may be contributing directly to children’s risk of having very aggressive and antisocial behavior. Thus, although chaotic family life and parental psychiatric problems are associated with and may well cause serious defiant and aggressive behavior, they are not causative of ADHD.

Finally, there are the findings from my own research that have been replicated since by others: my colleagues and I videotaped interactions between parents and their children with ADHD and compared these to the interactions of children without ADHD and their parents. But we also subdivided the children with ADHD into those who were very oppositional, defiant, and aggressive and those who were not. We discovered that the interactions in the group of children with ADHD who were not aggressive were no different from the interactions of the families of normal children in most respects. It was only in the aggressive group that we found more negative interactions between the parents and their children. Both the aggressive children with ADHD and their parents used more insults, putdowns, and commands with each other. They also were less positive in their interactions than were the other two groups of children (nonaggressive children with ADHD and children without ADHD). These families of aggressive children reported the greatest amount and intensity of conflicts with each other at home. The parents of these aggressive children also reported more personal psychological problems in themselves than did the parents of the other groups of children. This finding is in keeping with the results that parental psychological problems are more common in the families of aggressive children with ADHD. Also, recall the point made earlier that twin studies have found that the home or rearing environment of children does not make a significant contribution to the expression of the disorder.

All of this evidence makes it highly unlikely that any purely social cause, such as “bad parenting” or a disruptive, stressful home life, creates ADHD in the children of such families. Instead, the research suggests that children with ADHD can create stress for their parents and cause some disruption of family life. In cases where poor parenting and disruptive family life have some influence on children, it seems to be one of contributing to aggressive and defiant child behavior, not to ADHD.

Is It Due to Too Much Television?

Some years ago, the syndicated newspaper columnist and family therapist John Rosemond, among others, argued that ADHD resulted primarily from children spending too much time viewing TV—much more than was typical in earlier generations. This idea has some superficial appeal because it is consistent with popular folklore that watching too much TV surely must shorten a person’s attention span. To my knowledge, no scientific studies have ever shown this folklore to be true. While some studies have found that children with ADHD watch more TV than normal children do, such studies do not prove that watching TV causes ADHD. Even these studies have not been consistent in their findings; just as many found no association between TV viewing and ADHD symptoms as have noted such an association. I and other scientists believe that it is more likely that people with ADHD watch more TV because it requires less effort and a shorter attention span than other leisure pursuits, such as reading. For instance, in my own research in which we followed children with ADHD into adulthood, we asked them as adults how they spent their leisure time. We found that the young adults who had ADHD watched more TV, played more video games, talked on the phone more, and went joyriding more often in their cars than the control young adults did, while the latter spent more time reading, studying for work or college, and exercising than the young adults with ADHD. Such studies tell us only what those with ADHD like to do with their spare time, not that the things they do during that time are directly causing their ADHD. But the greatest evidence against Rosemond’s idea comes from twin studies that have found that the rearing environment that twins and siblings share growing up in the same family makes no significant contribution to differences among children in their degree of ADHD symptoms. TV viewing is a part of that shared environment, so these studies indicate that too much TV does not contribute to ADHD.

WHO IS AT RISK FOR DEVELOPING ADHD?

Even before a child is born, certain parental or family characteristics increase the odds that the child will have ADHD. These risk factors may not necessarily directly cause ADHD, but their presence signals that a child born into that family may be more likely to have ADHD than children born into families without those risk factors.

Features of the Parents and Family

As you know, studies tell us that parents who have ADHD are about eight times more likely to have children with ADHD. This is obviously because of the strong hereditary role in the disorder as reported above. In fact, any family history of ADHD increases the odds of a child’s having ADHD. For instance, having a sibling with ADHD increases the likelihood that another child in the family will have ADHD to 25–35% overall. Scientists estimate this risk to be approximately 13–17% for girls and 27–30% for boys, regardless of the gender of the sibling with ADHD. It is not clear why boys have a greater risk of having ADHD than girls within the same family. The reasons may lie in the realm of genetics—we know, for example, that it is possible for a characteristic inherited in the genes of both boys and girls in the same family to become manifest only in the boys. Maleness, you might say, has some greater biological risks associated with it, and ADHD may be one of them. Such sex differences are evident not only in ADHD but also in mental retardation and learning disabilities such as dyslexia (reading disorder). Whatever the explanation, it is not likely to rest on purely social factors, such as differences in the ways in which parents treat boys and girls within the same family.

As seen above, if a child has ADHD, the risk goes up significantly that other family members may also have ADHD. But what if it is the parent who has ADHD? Then the risk to the children of that parent is between 20 and 54%. In other words, a parent with ADHD is 8 to 10 times more likely to have a child with ADHD than a parent who does not have ADHD. This clearly shows how strong the genetic contribution is to the disorder. Other family risk factors associated with the early development and persistence of ADHD are (1) less education of the mother, (2) lower socioeconomic status of the parents, (3) single parenthood, and (4) abandonment of the family by the father. However, these factors produce only a very small elevation in risk for ADHD and obviously do not cause ADHD in the children of such parents. They are simply associated with a greater risk for ADHD, most likely because of some third condition that explains both these risk factors and the ADHD itself—again, possibly due to the shared genetics for the traits of ADHD.

Features of the Pregnancy

Several studies have shown that mothers who experience complications of their pregnancies or deliveries are more likely to have children with ADHD than mothers without such complications are. This is also true for repeated infections experienced by the mother in her pregnancy. The type of complication or infection does not seem to be as important as the total number of such complications. These complications may cause ADHD by interfering with the normal brain development of the fetus, or a third factor may be involved: ADHD in the mother. In this case, the mother’s ADHD would lead to poorer prenatal self-care and thus greater complications; the cause of the child’s ADHD would be genetic inheritance. This is an example of noncausal association, discussed earlier in this chapter.

The fact is that there is little evidence that these complications actually cause ADHD. Even 40 years ago, evidence was accruing that pregnancy and birth complications might contribute some risk to causing ADHD in the offspring of those pregnancies. For instance, in a large study by Dr. Nichols and colleagues known as the Perinatal Collaborative Project, conducted by the federal government in the 1970s, the following complications before or during birth were found to increase (by a small degree) the risk that a child might have symptoms of ADHD: the number of cigarettes smoked by the mother per day, seizures in the mother, the number of times the mother was hospitalized during pregnancy, breathing problems in the child during and after delivery, and the weight and health of the placenta when inspected after delivery. A higher incidence of problems in these areas increased the odds that a child would have symptoms of ADHD; the worse the mother’s problems, the worse the child’s symptoms.

Studies of babies born prematurely and with low birth weights have frequently shown that these infants have a markedly higher likelihood of developing ADHD in later childhood—sometimes five to seven times higher than that of the general childhood population. A study from 20 years ago suggested that this may be due to the fact that such babies have a high risk of having small hemorrhages in their brains. Over 40% of such babies who had these small bleedings in their brain were found to have ADHD (among other developmental and learning problems) later in childhood, whereas those without such bleedings were far less likely to have these problems.

Features of Infancy and the Toddler Years

Scientists have also identified some features in the early development of children that may predict a greater risk for the later appearance of ADHD in those children. Delays in motor development, smaller head size at birth and at 12 months of age, amniotic fluid stained by meconium (material from the intestine of the fetus), signs of nerve damage after birth, breathing problems after birth, and low birth weight were found in the Perinatal Collaborative Project to be related to risk for later hyperactivity. The risk was still quite low, however, even when these signs were present. Children who are less healthy during their infancy or preschool years, and who are slow to develop in motor coordination, have also been found to be at a higher risk for early and persistent ADHD symptoms later in childhood.

Young children who are excessively active as babies may have a higher risk for having ADHD later in childhood. Also, children who attend to objects or toys for short periods of time, who cannot persist as well in pursuing objects in their field of vision, or who show a strong intensity of reaction to being stimulated may be at higher risk for having ADHD. Infants or toddlers who are very demanding of their parents are more likely to display ADHD later on. We do not believe that these features of children or their early development cause the ADHD symptoms to occur later. Instead, many psychologists believe that these are just the early signs of the ADHD itself, which may not be fully formed in its expression at so early an age as infancy or toddlerhood. Very young children display only the behavior that is possible for them to show at that early stage of the brain’s development. The “seeds” of ADHD may be within these children, but will not appear until the stages of development where attention span, inhibition, and the other executive functions that help with self-control over activity and behavior normally emerge. At those points, children with ADHD will fall behind other children.

Features of the Preschool Years

During the preschool years (ages 2–5 years), the development of early and persistent problems with overactivity and with getting along with other children can mark a child as being at risk for ADHD. Also, not surprisingly, young children with excessive inattention and emotional difficulties (such as frequent anger or temper outbursts, or a proneness to becoming easily upset by things) may be more likely to have ADHD as they grow up.

Once again, young children whose early temperament is negative and demanding are more likely to be diagnosed as having ADHD later on. Temperament refers to an early and persistent pattern of personality characteristics, including activity level, intensity or degree of energy in a response, persistence or attention span, being demanding of others, quality of mood (irritability or quickness to anger or display emotion), adaptability or capacity to adjust to change, and rhythmicity or the regularity of sleep–waking periods, eating, and elimination (bowel and bladder control). As predictors, these features appear to be as important in the preschool years as they are in infancy. These characteristics, especially overactivity, high intensity, inattention, negative mood, and low adaptability, have also predicted the continuation of ADHD into later childhood once it develops. Certainly children whose inattentive or hyperactive symptoms are sufficiently severe to get them a diagnosis of ADHD in early childhood are quite likely to continue to receive this diagnosis up to 5–10 years later.

The presence of these personality characteristics early in life is a very strong predictor of later risk for ADHD. For instance, even 30 years ago, in 1990, Dr. Susan Campbell and colleagues at the University of Pittsburgh found evidence of this when they studied 46 children who were reported by their parents to be excessively active, inattentive, and defiant at ages 2–3 years. They also studied 22 children who had no significant behavior problems of this sort. They then followed all of the children until age 6 and reevaluated them. At age 6, approximately 50% of the children with early behavioral problems were still hyperactive or had a formal diagnosis of ADHD, which suggests that children who are hyperactive and difficult to manage at age 2 have at least a 50% chance of being labeled as ADHD or hyperactive by entry into school at age 6.

Still, 50% of the children did not persist in their behavior problems. Dr. Campbell and colleagues found that in cases where this pattern of early hyperactive and defiant behavior was combined with other factors in a child’s life, ADHD was more likely to develop. What were these other features? Among the important ones were the characteristics of the parents’ personality, especially the presence of psychiatric or psychological problems that may have interfered with caregiving and raising the child. Dr. Campbell and colleagues studied this issue and found that a negative, critical, and commanding style of child management by mothers of young children with hyperactivity was likely to predict persistence of those problems into later years. Parents who are very hostile or who are having marital/couple problems may also contribute to the risk for ADHD in preschool children with negative temperament. Thus it appears that child temperament, while an important early risk factor, can be either improved or worsened by the type of home environment parents create and the manner in which they respond to a difficult child. This environment can combine with a child’s early temperament problems to increase the risk for later ADHD. These problems with parents are not necessarily causing the child’s ADHD. It is possible (1) that they may exacerbate it somewhat; or (2) that the parent is simply reacting to a child who has more severe symptoms of ADHD, and it is that severity that determines the persistence of the child’s ADHD over development, and not so much the parents’ behavior. More important, such parenting factors may increase the risk that the child may develop oppositional defiant disorder (discussed in Chapter 1).

I along with Dr. Terri Shelton and other colleagues did a 5-year study of preschool children at risk for ADHD at the University of Massachusetts Medical School in the 1990s. We screened most children from 4½ to 6 years of age entering the public school kindergarten program in Worcester, Massachusetts, for those having high levels of ADHD symptoms and aggressiveness. We then gave these children a thorough psychological evaluation and found that over 65% of them qualified for a diagnosis of ADHD—a figure that changed very little over the next 3 years that we followed and annually reevaluated these children.

Taken together, these research findings suggest that it is possible to identify children at risk for developing an early and persistent pattern of ADHD symptoms prior to their starting kindergarten, and perhaps even as early as 2 or 3 years of age. A combination of child and parental variables seems the most useful guide to making such predictions. The following factors, listed in descending order of importance, would appear to be useful as potential predictors of the early emergence and persistence of ADHD in children:

1. The early emergence of high activity level and demandingness in a child’s infancy or preschool years.

2. Family history of ADHD.

3. Smoking and alcohol consumption by, and poor health of, the mother during pregnancy.

4. A greater-than-normal number of complications during pregnancy (especially premature delivery and/or low birth weight that is associated with bleeding in the brain).

5. Being a single parent and having less education than normal (which may be an indication of possible ADHD symptoms in the parents).

6. Poor health of the infant, and delays in motor and language development.

SUMMARY

To summarize, biological factors (abnormalities in brain development) are most closely associated with and may perhaps be causes of ADHD. Studies so far indicate a very strong genetic contribution to ADHD symptoms—one that is much greater than the contribution of environmental agents or purely social factors. Everything we know points to the idea that children with ADHD have delayed brain development and less brain activity, especially in the prefrontal regions—precisely those brain centers known to be involved in executive functioning and self-control, such as inhibition, persistence toward tasks and goals, resistance to distraction, and control of one’s activity level. The precise cause of this delayed maturation and underactivity is not known but appears to likely be due to genetics: people with ADHD have different versions of genes that build and operate these brain regions, and these variations may be contributing to altered brain development and functioning.

Where purely social factors seem to be important, as in the case of poor child management skills by parents, is in predicting which children may have more aggressive and defiant behavior. Even the existence of this relationship, however, does not mean that how parents are managing a child with ADHD is the cause of the ADHD, only of the defiant and aggressive behavior.

We have much more to learn about ADHD and its potential causes. Nevertheless, great advances have been made in the last decade in understanding the possible causes of ADHD. All of the evidence to date points to genetically based neurological factors as being the most important in explaining the extent of ADHD in the population. A smaller percentage of cases of ADHD appear to be due to acquired injuries to the developing brain, such as through toxins consumed by the mother during pregnancy or child after birth. When we fully comprehend what causes this disorder, perhaps we will also discover how to cure it. In the meantime, the information that is available, along with what we know about the nature of ADHD (see discussion in Chapter 4), has brought us a long way toward successful management of ADHD—the subject of Parts II, III, IV (Chapters 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19).