You may be one of those people who just wants a quick solution to your problem and who would rather eat worms than have to slug through reading about the science behind treatments for ADHD. If you have ADHD, it may be particularly difficult for you to slow down and focus on this material, but it will be worth the effort because a little science can go a long way in helping you to understand the many causes of ADHD and how to use multiple viewpoints and treatments to overcome symptoms. Knowing the science behind the behaviors that drive you and your loved ones crazy can help to reduce guilt, blame, and anger. Also, this knowledge will help you to evaluate new treatments you might hear about or read about on the Internet and to decide if they are really worth trying and are likely to apply to your particular situation. A lot of time, money, and disappointment can be avoided if you know how to assess product claims and even so-called “research evidence” that may be used to boost sales.
We are going to ease you in with an overview—just the most important highlights—to give you a sense of where the science of ADHD is now and where it is going. If this whets your appetite for more, you may continue to feast on the chapters that follow.
Neurotransmitters are the molecules that move between neurons (brain cells) and enable them to communicate and transmit information. These molecules deliver messages by first attaching to receptor sites on the surface of the neurons. Small shifts in the balance of neurotransmitters dancing on receptor sites can make all the difference in how smoothly the mind functions.
The problem with studying neurotransmitters is that there are too many of them and they are everywhere in the nervous system, slipping through cell membranes, hugging and releasing surface receptors, swimming across synaptic clefts, fending off attacks by enzymes, exciting some nerves while squelching others. Tracking these chemical acrobats is like watching a circus with thousands of rings in which the performers keep jumping into each others’ acts. Imagine that you are the catcher swinging on a high trapeze and that just as your flying partner is about to seize your wrists, another aerialist dives from above to snatch your hands away while your partner tumbles helplessly into the net. That’s what it’s like all the time in the wacky world of neurotransmitters. (See Figure 2.1.)
Figure 2.1 Neurotransmitters at a Synapse
Neurotransmitter molecules released from the presynaptic neuron traverse the synaptic cleft, attach to a matching receptor on the postsynaptic neuron and are taken up into the postsynaptic neuron to participate in cell processes.
Another maddening aspect of neurotransmitters is that just when we think we know all of the major players, somebody discovers a new one. Unfortunately, our brains can’t function without the little devils, so we do need to know who they are, what they do, and how to help them work better.
The neurotransmitters involved in ADHD include catecholamines and non-catecholamines. The easiest way to remember the catecholamines is to think of three cats. For definitions of neurotransmitters, see Sidebar 2.1. While each transmitter has many functions throughout the brain, here are some of their major actions that affect ADHD:
Catecholamines
Dopamine—activation for pleasure and reward
Norepinephrine —attention and alertness
Epinephrine—arousal and alertness
Non-catecholamine
neurotransmitters
Serotonin—mood regulation, inhibition of action, and balancing dopamine activity
Gamma-aminobutyric acid (GABA)— calms and quiets the brain
Acetylcholine—learning, memory, and attention
Histamine—learning to inhibit behaviors
Sidebar 2.1.
Neurotransmitter Definitions
Acetylcholine—important for learning and short-term memory. Recent studies indicate that it also has a role in attentional effort (voluntary directing of attention) and the detection of important stimuli (Klinkenberg, Sambeth, & Blokland, 2010). Acetylcholine modulates the allocation of visual attention—for example, the selection of which visual cue to focus on when there are many things going on in the environment (Rokem, Landau, Garg, Prinzmetal, & Silver, 2010; Dalley et al., 2004).
Dopamine—important for activation and processing of reward and pleasure. Its activity is affected by the other neurotransmitters, including serotonin, epinephrine, and GABA.
Epinephrine—involved in arousal and alertness.
Gamma-aminobutyric acid (GABA)—inhibits and reduces excessive activation and is essential for feelings of calmness.
Glutamate—an excitatory transmitter crucial for memory (through long-term potentiation).
Histamine—necessary for learning to inhibit behaviors.
Norepinephrine—essential for attention, alertness, overall arousal, mood, and sexual behavior; it supports and amplifies the effects of serotonin and probably dopamine.
Serotonin—important for the regulation of mood and the inhibition of actions that would cause pain. Insufficient serotonergic* (i.e., involving serotonin) activity is associated with depression. Serotonin affects sleep, cognitive functions, anxiety regulation, and sexual activity, and it balances the activity of dopamine.
Although the DSM diagnostic categories have provided more consistency in the diagnosis of ADHD, they have created a somewhat limited view of the disorder as a collection of observable behaviors, the “core symptoms” of inattention, hyperactivity, and impulsivity. We want to go beyond the DSM-IV surface description of symptoms by delving a little deeper into three areas of dysfunction that are based on neu-rophysiology, neuroanatomy, and genetic research: (1) hypoarousal and impulse control, (2) reward deficiency, and (3) emotional dysregulation. These categories are important because they enrich our understanding of the causes of ADHD behaviors and help us to home in on treatments that may better target the underlying dysfunctions in brain systems. We’re going to use a case example to first give you a sense of the ways in which these categories can be expressed in behaviors and interactions.
Although she had never been formally diagnosed with or treated for ADHD, I suspected that Mrs. L. had this disorder. Despite being highly intelligent, she had dropped out of high school and become the black sheep of her family, the only one without a college education. As a teenager, she drank, experimented with drugs, and had her first child at age 17. Determined to be a good mother, she stopped drinking and began a small landscaping business. By working long hours 7 days a week, she gained customers and soon she had five people working for her. What she lacked in organizational skills, she made up for in energy.
Mrs. L. understood that yelling and arguing with her husband was hurting their relationship and setting a terrible example for their four children, but she was unable to control herself. Any negative comment, such as his complaining about the house clutter, would set her off on a torrent of accusations. In all fairness, hubby was very critical. When her son entered adolescence and began talking back, Mrs. L.’s yelling got out of control. As the family fights escalated and her son became more provocative, Mr. L. began losing control, either becoming physically violent or running out of the house to avoid hitting someone. Mrs. L. came to therapy asking for help with the family turmoil.
Mrs. L. refused to take any prescription medications because, to her, that would confirm that something was wrong with her brain. Her low self-esteem made it even more difficult for her to accept even the idea of medication. One day she brought her 15- year-old son, Lamar, to the office and told him to sit in the waiting room and read a book during her session. Within 5 minutes, we began to hear noises, banging, stomping, and finally knocking on my office door. Lamar stood there grinning, saying, “I’m bored. When will my mother be finished?” I gave Lamar a sketch pad and asked him to stay quietly in the waiting room, reminding him that it would be another 40 minutes. No sooner had I sat down, than the noises began again, thumping and shrieking. The phone rang. The other therapists in my suite were complaining about the noise and the mess in the waiting room. What mess? Opening the door, we saw Lamar laughing and splashing water from the fountain all over the carpet. Mrs. L. let out a grunt of rage through clenched teeth. The Three Faces of ADHD had struck again: hypoarousal with poor impulse control, reward deficiency, and lack of emotional regulation.
ADHD has been called a disorder of hypoarousal, meaning that part of the brain is under-aroused or not active enough (Kuntsi, McLoughlin, & Asherson, 2006). How can we say that the brain is underactive in a person who is overactive and hardly seems to sleep? How can a stimulant calm down a system that seems to be in overdrive? The key to making sense of this puzzle lies in the particular parts of the brain that are under-aroused: brain circuits in the command-and-control centers that are supposed to regulate attention, impulse control, and pleasure-seeking behaviors. When dopamine levels are low, these control circuits are sluggish, slow to respond, and less effective. Stimulants such as methylphenidate (Ritalin) are believed to work in part by increasing neurotransmitter levels, particularly of dopamine and norepinephrine (Kuntsi et al., 2006).
If we think of our impulses as mice scurrying around our emotion centers just waiting for a chance to run amuck, and imagine the neurotransmitters as cats, then we can understand why having drowsy cats doesn’t work very well. Underactive neurotransmitters (sleepy cats), particularly norepinephrine and serotonin, compromise the ability of the brain circuits to control impulsive behavior (trouble-making mice). So, for instance, when Lamar feels an impulse to knock on the door and interrupt his mother’s therapy session, his centers of judgment and control fail to remind him that he should sit quietly and not disturb anyone. In a sense, his inhibitory circuits are asleep at the wheel, failing to put on the behavioral brakes as he careens out of control. Stimulants such as methylphenidate (Ritalin) increase norepinephrine activity in the impulse control circuits. Norepinephrine also enhances the inhibitory effects of serotonin. As a result of the increased norepinephrine, the impulse control centers (combined with serotonin inhibition) are better able to maintain more appropriate behavior. Furthermore, by increasing levels of norepinephrine, stimulants improve arousal and alertness. We tend to be less alert when norepinephrine levels are low. Alertness is a necessary part of paying attention.
Complementary treatments, such as stimulating herbs and mind–body practices, can also improve hypoarousal and the balance of neurotransmitters (more on that topic later).
Many people with ADHD complain of feeling bored, just like Lamar sitting in the waiting room. How did he get so bored so quickly? Why couldn’t he read a book or draw pictures? He didn’t feel like reading or drawing. These activities did not give him pleasure or satisfaction. Reward deficiency syndrome (RDS) is a condition in which the person is unable to experience pleasure or a sense of reward in ordinary activities that others enjoy. This inability is thought to be due to dysfunction in the neurotransmitter systems involved in feelings of reward, such as pleasure, excitement, and satisfaction. As a result, there is a tendency to feel bored, restless, impatient, and a need to stir up trouble or provoke intense emotional reactions.
In order to have fun, Lamar needed to do something more exciting or dangerous, something that would get him into trouble—better yet, something that would get everyone upset and angry. His mother would be embarrassed. Maybe everyone would start yelling. For Lamar, that would be exciting enough to stimulate his pleasure centers. That would really be fun.
The problem is that without the usual everyday “feel good” experiences, people with reward deficiency syndrome tend to feel bored, unhappy, discontented. They are prone to engage in activities that will stimulate their system intensely enough to produce some pleasurable experiences. This puts them at increased risk for engaging in dangerous, addictive, impulsive, or compulsive behaviors. Reward deficiency syndrome can be found in people being treated for substance abuse and addictions. Studies are also finding that a subset of people with ADHD may also have genetic variants that lead to imbalances in the neurotransmitter systems in brain areas involved in reward processing.
Dopamine plays the largest role in reward processing. The release and activity of dopamine is affected by other neurotransmitters such as serotonin, norepinephrine, and gamma-aminobutyric acid (GABA). GABA, in particular, controls or inhibits the amount of dopamine released in brain reward areas. If there is too little dopamine reaching the reward centers, then it is more difficult for the person to experience pleasure (Blum et al., 2008). For example, increasing dopamine levels improves the ability to enjoy social rewards such as praise and approval. It is easier to teach a child appropriate behavior when the child is able to enjoy pleasing his or her parent or teacher.
The identification of gene variants that affect dopamine is consistent with the idea that inheritance of ADHD is polygenetic (i.e., involves multiple genes). Specific gene variants that have been linked to ADHD include the dopamine receptor gene DRD4, a transporter gene (DAT1), and a B-hydroxylase gene (DBH). In one study, the number of variants in genes affecting dopamine correlated with the severity of ADHD symptoms. In other words, people with three gene variants had more severe ADHD than those with two, and people with two gene variants had worse ADHD than those with only one.
The ability of stimulants such as methylphenidate (Ritalin) and Dexedrine to improve symptoms of ADHD has been attributed in part to their increasing the level of dopamine in synapses (the spaces between neurons) in the frontal lobes. In Chapter 3 you will find a discussion of an herb that has been shown to increase levels of dopamine. This may be an alternative way to enhance feelings of pleasure and well-being without needing excessive stimulation.
Many people with ADHD complain of feeling bored, just like Lamar. Why did he get bored so quickly? Why couldn’t he just sit quietly reading a book or drawing pictures like most boys his age? Being unable to enjoy quiet pleasures left him feeling unsatisfied. In an attempt to have fun, Lamar tried more exciting activities, doing things he knew were wrong and that would put him in danger of getting into trouble. Better yet, he did things that would get everyone angry and upset to create more excitement and stimulate his sluggish pleasure centers.
Recognizing problems in reward processing can help us understand some of the behaviors that occur in ADHD and thereby help us develop more effective treatment approaches. For example, it is known that many children with ADHD respond differently to rewards than other children, and they cannot tolerate the usual delays involved in being rewarded for finishing or accomplishing something. In general, children with ADHD prefer small immediate rewards rather than larger delayed rewards. Therefore, if rewards are being used as part of a behavioral treatment plan, they should be structured in a way that will elicit responses more effectively in these children. See the Resources section at the end of Chapter 1 for help with specific behavior management strategies.
Helping children and adolescents learn how to enjoy healthy activities may also reduce their risk-taking behaviors. Teaching mind–body practices that induce feelings of well-being can compensate for symptoms of reward deficiency syndrome; Chapter 5 describes some of these techniques.
One of the more recent concepts in understanding ADHD is that of deficient emotional self-regulation (DESR). Deficient emotional self-regulation can be seen as a politically correct way of describing people who tend to lose control of their emotional reactions so frequently and to such an extent that this lack of self-control causes significant problems in their academic, professional, and personal lives. Deficient emotional self-regulation may contribute to the following problems:
• Inability to inhibit inappropriate behavior associated with strong emotions.
• Inability to self-soothe physiological responses aroused by strong emotions (e.g., once the person becomes upset, it is very difficult for him or her to calm down); this includes physiological responses such as adrenaline release, heart pounding, rapid breathing, shaking, or muscle tensing.
• Inability to refocus attention.
• Inability to organize coordinated behaviors to accomplish a goal.
People with ADHD are often impaired in their ability to control their emotions, particularly frustration, impatience, and anger. Lapses in inhibition of these emotions result in emotional impulsivity—that is, rapid negative reactions (e.g., anger) and responses (e.g., shouting, hitting, or attacking). This response pattern erupted over and over again whenever Mrs. L. felt insulted or unappreciated. Her anger rushed in, her control circuits failed, and within seconds she was yelling uncontrollably. She was at the mercy of her hurt and angry feelings, unable to soothe or calm herself.
Russell Barkley explains the relationship between emotional impulsivity and emotional self-regulation in this way: “One cannot self-soothe or otherwise moderate one’s initial emotional reactions to events if one has not first inhibited the impulsive expression of those initial reactions. EI [emotional impulsivity], therefore, will interfere with subsequent efforts to engage in emotional self-regulation” (p. 6). Dr. Barkley recommends including emotional impulsivity–deficient emotional self-regulation (EI-DESR) as a core symptom of ADHD because it is an underlying factor in low frustration tolerance, impatience, quickness to anger, and easy excitability to emotional reactions. EI-DESR contributes to serious impairments in social interactions, work, driving, marriage/cohabitation, and parenting (Barkley, 2009).
Understanding emotional self-regulation is central to dealing with ADHD. In Chapters 5 and 6 we focus on mind–body treatments and neurostimulatory techniques that can improve emotional self-regulation, which is critical for controlling anxiety, over-reactivity, anger, aggression, and other impulsive behaviors.
At the moment, and as noted above, ADHD is divided into three subtypes based on symptom clusters:
1. Predominantly hyperactive/impulsive
2. Predominantly inattentive
3. Combined hyperactive/impulsive and inattentive
In the not-too-distant future, however, genetic research is going to change the way we diagnose and treat ADHD. In fact, the change has already begun. The various symptoms seen among the subtypes of ADHD may reflect differences in the absolute and relative levels of neurotransmitters. There are genes within our DNA that code for the manufacturing of not only neurotransmitters, but also substances that affect their transportation and how they function. For example, genetic variants (polymorphisms) can affect the levels of the major catecholamines—norepinephrine and dopamine. Looking at the ADHD subtypes and genetic variants may ultimately help us design more effective treatments (Blum et al., 2008). Let’s look into our crystal microscope to see what the polymorphisms are telling us about the future of ADHD treatment.
“Eenie, meenie, chili beanie! The spirits are about to speak”
—Rocky & Bullwinkle, 1961
Polymorphisms are found in specific genes. To get a clearer picture of polymorphism codings, imagine a gene that is capable of designing a shoe. We’ll call it gene SH1. This gene comes in different forms, or polymorphisms, which can produce different styles of shoes. So, the polymorphism SH1B produces blue shoes, and the polymorphism SH1R makes red shoes. To be more specific, SH1B2 makes blue shoes with 2-inch heels, whereas SH1B6 makes blue shoes with 6-inch heels. SH1B6L makes leather blue shoes with 6-inch heels, and SH1B6S makes blue suede shoes with 6-inch heels. Transfer this concept into thinking about your genetic code, and you can see how scientists create code names for polymorphisms based on the specific traits or actions they produce. For example, just for fun, let’s decipher a gene:
• DR is a dopamine receptor.
• DRD4 is the gene that codes for the D4 type of dopamine receptor.
Are they friendly spirits? —Rocky & Bullwinkle, 1961
Polymorphisms of the genes that affect dopamine levels have been found in ADHD, especially in the hyperactive/impulsive subtype. Similarly, variants in genes that affect norepinephrine have been identified in the inattentive subtype of ADHD. In addition, polymorphisms in genes involved in cholinergic transmission have been noted in ADHD with both inattention and hyperactivity/impulsivity.
Each gene is a segment of DNA that carries the code for a specific trait. Chromosomes come in pairs, and each pair of chromosomes is a double helix that contains pairs of matched genes, one set from each parent. Different genes code for at least five types of dopamine receptors: D1, D2, D3, D4, and D5.
The DRD4 gene is located on the 11th human chromosome in a segment called 11p15.5. DRD4 contains the code for making the dopamine receptor D4. During dopaminergic transmission, the neurotransmitter dopamine attaches to and activates the D4 receptors on the nerve cell membranes. One polymorphism of the “DRD4 long” variant, with 7-repeat (7R) base pairs, has been linked to ADHD. The 7R polymorphism reacts less strongly to dopamine molecules. This means that the neurons in people with the 7R variant are not as easily activated when dopamine attaches to their receptors as in people without the 7R variant. The dopamine transmission is less in these individuals, and this decrease could contribute to symptoms of ADHD. (See Figure 2.2.)
How did the DRD4 7R long variant evolve? The 7R allele appeared about 40,000 years ago (Chen, Burton, Greenberger, & Dmitrieva, 1999), and it occurred more frequently in populations who migrated long distances in the past 1,000–30,000 years. In short, nomadic populations had higher frequencies of 7R alleles than sedentary ones. In two studies scientists found that people whose personality testing showed them to be exploratory and excitable—two hallmarks of novelty-seeking behavior—also possessed a 7R version of DRD4 compared with those who are more reserved and reflective (Ebstein et al., 1996; Benjamin et al., 1996).
In the section on reward deficiency syndrome we discussed evidence for the link between polymorphisms in the dopamine receptor (DRD4) and dopamine transporter (DAT1) genes and the severity of ADHD symptoms. Because these genes have been identified as playing a role in ADHD, they are considered to be candidates for research directed toward creating new treatments (Stergiakouli & Thaper, 2010). The race is on to discover treatments that could correct, modify, or compensate for the effects of polymorphisms. However, these dopamine polymorphisms account for only a small portion of the genetic effects on ADHD symptoms. So far, other genomic studies have not been able to demonstrate more significant effects for specific polymorphisms, perhaps because of confounding factors such as environmental, dietary, and psychosocial effects.
Figure 2.2
The role of food additives in ADHD has been hotly contested since 1975 when Benjamin Feingold, M.D., popularized the notion that artificial food colors, flavors, and preservatives caused hyperactivity and learning disabilities (Feingold, 1975). These issues are discussed in greater detail in Chapter 4. Over the past 35 years, studies have yielded inconsistent results. Now geneticists are figuring out why.
At the University of Southamptom School of Medicine in Hampshire, England, Dr. Jim Stevenson and colleagues (2010) discovered a connection between the effects of food additives and histamine degradation gene polymorphisms on ADHD symptoms in children. An enzyme produced by the histamine degradation gene is responsible for breaking down histamine molecules. Certain variants in the histamine degradation gene result in diminished capacity to degrade histamine molecules. If a child has an allergic reaction to food additives, histamine may be released. Normally, the excess histamine is degraded. However, if the child has certain polymorphisms, then there is less capacity to degrade the histamine such that it accumulates and interferes with neurotransmission. This could result in increased symptoms of ADHD. In a well designed study of 153 children ages 3 and 4 and 144 children ages 8 and 9, researchers simply rubbed a small swab on the inside of each child’s cheek to obtain a sample of tissue for genetic testing. Children who had the histamine degradation polymorphisms of HNMT showed greater overall hyperactivity and were more vulnerable to the effects of food additives on their behavior. The fact that in some children food additives exacerbate ADHD symptoms, whereas in others they do not, could be explained by these polymorphisms. Although the scientists caution that more studies are needed to confirm these findings, nevertheless, this is a milestone in the quest for new ways to determine who is more likely to benefit from specific treatment approaches.
Q: What does histamine have to do with food additives and ADHD?
A: Histamine may be the missing link in our understanding of why some food additives exacerbate ADHD symptoms in some people but not in others. Histamine receptors are found throughout the brains of mammals (including humans). When it was discovered that causing histamine levels to rise in mice adversely affected their ability to learn to inhibit certain behaviors and increased their hyperactivity, the histamine neurotransmitter system became a new candidate for ADHD researchers. Histamine is more commonly known for its role in allergic reactions. When allergens provoke basophil cells to release histamine, it can produce a skin rash. Certain food additives, such as Azo dyes (i.e., dyes with a particular synthetic chemical structure), can cause histamine release. This can occur even in the absence of a skin rash. In people with certain polymorphisms of the histamine degradation gene (HNMT), there is a reduced capacity to degrade and clear histamine out of the cells. So, if such a person eats something that causes histamine release, such as food containing an Azo coloring, then he or she will not be able to clear the histamine as rapidly. The histamine will accumulate and could then increase hyperactivity and interfere with the person’s ability to inhibit behaviors. This was the hypothesis that was tested by Dr. Stevenson’s group. Although their study does not absolutely prove this theory, it certainly provides strong support for pursuing this line of research.
Q: How can I use this information now?
A: We can do what the researchers did. Although we cannot yet get cheek swabs to identify histamine receptor polymorphisms, we can still use this information. In their study, they gave a standardized test to assess the level of ADHD symptoms (the Abbreviated ADHD Rating Scale–IV) before and after a 6-week period of eliminating the following artificial colors and preservatives in the children’s diets:
• Tartrazine (Yellow 5)
• Sunset yellow (Yellow 6)
• Quinoline yellow, carmosine (Red 3)
• Allura red AC (Red 40)
• Ponceau 4R
• A preservative called sodium benzoate
It should be possible for you to get a standard ADHD symptom test, eliminate or reduce as much as possible (does not have to be 100%) the same food colorings for 6 weeks, and then repeat the testing. In addition to the testing, you and your family may observe changes. If you see significant improvements in ADHD symptoms, then it is possible that you have a histamine receptor polymorphism and that you would continue to benefit by restricting your consumption of foods containing color additives. On the other hand, if you don’t notice much change, then this approach is not worth pursuing unless you wish to reduce artificial additives for general health reasons. In Chapter 4 we go into more detail on the effects of food and dietary treatments on symptoms of ADHD.
Q: What do you see in the future regarding the use of genetics to identify and treat ADHD?
A: Someday, you will be able to get a cheek swab to check for polymorphisms related to ADHD. Then, based on the profile of your particular polymorphisms, you will be able to select from a menu of treatment options those that are most likely to be beneficial for you.
When we read about scientific studies, it is important to assess the quality of the evidence. There are many ways to do a scientific study. Although there is no guarantee that the results of any one study will stand the test of time, some methods are believed to produce more solid, significant, and higher-quality evidence than others. In general, studies with larger numbers of participants and those that use a randomized, double-blind, placebo-controlled design are considered to be more convincing than smaller studies that do not use a control group, randomization, or double-blind conditions. In a randomized study, participants are randomly assigned to different groups. In a double-blind study, the participants do not know which group they are in (treatment vs. control group), and the researchers who administer the tests do not know which group participants are in. Placebo-controlled studies use an identical placebo tablet (a tablet that has no biological effect—a “sugar pill”) for the control group to compare their response with the group given a tablet with the active ingredient being tested. Although these methods reduce the potential for bias, they do not guarantee accurate results. Treatments that are supported by more than one study and by studies of better design are considered to have a more solid evidence base.
Q: Why aren’t there more randomized, double-blind, placebo-controlled studies of non-drug treatments for ADHD?
A: It is very costly to do randomized, double-blind, placebo-controlled studies. The pharmaceutical industry is able to finance studies of prescription medications because they can make a good profit through high drug prices. In contrast, small herbal companies and businesses developing alternative treatments find it extremely difficult to raise enough money to do such studies. Although there are some grants for CAM research, they are often for small amounts of money, and the granting agencies tend to fund the same old familiar herbs rather than the “new kids” on the block.
Q: If there are fewer studies, how do you decide that a non-drug treatment is worth trying?
A: We wrote this book to help you, your doctor, and your other health care providers make those decisions. Also, we have tried many of these treatments in our practices over the years. This book emphasizes treatments we have used successfully in our patients and which are supported by credible scientific evidence. When we describe the studies, we will indicate the study methods, the limitations of the study, and the rationale for our recommendations.
Now that you understand more about the underlying causes of ADHD, we can explore some non-drug treatments that can help reduce symptoms and improve the quality of every day of your life. The next chapters introduce you to nutrients, herbs, mind–body practices, and brain stimulation methods. For some people these approaches will make it possible to reduce the amount of prescription medication needed, whereas for others these treatments will build on the benefits of medication, leading to even more improvements in attention, mood, productivity, relationships, and enjoyment of life.
*-ergic—Adding the suffix -ergic to a neurotransmitter name means activated by, or involving, that transmitter. For example, cholinergic transmission is the activation of a sequence of nerves that utilizes choline (from acetylcholine). Similarly, dopaminergic refers to nerve cells that contain dopamine, substances that cause nerves to release dopamine, or nerve cells that respond to dopamine.
