Examining the Reality of ADD/ADHD
Examining the Reality of ADD/ADHD
by Meghan Hamilton
For a large majority of individuals outside the medical or psychological community, Attention Deficit Hyperactivity Disorder remains as a disorder which is often misunderstood due to a lack of proper education. While only four to six percent of the U.S. population has been diagnosed with this disorder, it is described as "the current diagnostic label for one of the most prevalent developmental disorders of childhood" (West, Houghton, Douglas, 2002). Through the thorough examination of current research in its attempt to further define the misconceptions, causes, symptoms, and treatment of Attention Deficit Hyperactivity Disorder, society may begin to better appreciate this disorder for its frustrating symptoms and begin to positively interact with diagnosed individuals to understand the reality of their disabilities.
Attention Deficit Hyperactivity Disorder is a disorder caused by a difference in brain chemistry that results in abnormal behavior. The research of Dr. Peter Jaska suggests most behaviors indicating ADHD appear before age 7 and continue for at least six months. The most common features influencing a diagnosis of ADHD include: distractibility, impulsivity, and hyperactivity. Examples of such behavior are indicated by poor sustained attention on tasks, delay of gratification, and physical restlessness. While theoretically almost everyone experiences these symptoms from time to time, an individual is only considered to have ADHD if these behaviors create a serious handicap in at least two aspects of their life (Amen, 2001). Perhaps one of the most confusing aspects of this disorder for the general public comes in understanding the difference between Attention Deficit Hyperactivity Disorder from Attention Deficit Disorder. ADHD is the official diagnosis of the disorder that can be broken down into different subtypes. Most commonly, these subtypes include the Predominantly Inattentive Type, Predominantly Hyperactive-Impulsive Type, and the Combined Type which exhibits symptoms from both categories (DuPaul, 2003). ADD is generally used as a term to associate all types of ADHD, especially in media presentations. Whether a study or doctor uses ADD or ADHD, both refer to a serious disorder with significant obstacles for diagnosed individuals.
The irregular and commonly uncontrollable behavior associated with this disorder are defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, as "often fails to give close attention to details or makes careless mistakes; often has difficulty sustaining attention on tasks, often does not seem to listen when spoken to directly, losing or forgetting important things; feels restless". With a malfunctioning system, physiological differences in the brain often create frustration for individuals who cannot act in "normal" ways. For those who do not understand the disorder, it may be difficult to understand the actual inability to control certain brain functions that result in undesirable behaviors.
As easy as it may be to address the restlessness and inattentiveness as merely bad manners, existing differences in brain chemistry create very different resulting actions; "several areas of the brain are affected by the disorder, including the frontal lobes, inhibitory mechanisms of the cortex, limbic system, and reticular activating system"(Jenzen, 1995). While research is still being developed to discover causes and better define the specific malfunctions in these systems, the resultant symptoms of ADHD can cautiously be traced to the functions of localized areas: the frontal lobes are involved in focusing attention on certain tasks, maintaining concentration, making good decisions, remembering learned information, and behaving appropriately; inhibitory mechanisms of the cortex function as control factors for hyperactivity, restraining anger and interruptions, and aids in inhibiting impulsive behavior; the limbic system acts as a control tower for our emotions and, when functioning normally, maintains levels of energy, sleep routines, and the ability to cope with stress. Because "70% of the brain functions to inhibit the other 30% of the brain" (Jenzen, 1995) and ADHD may affect one or all of these areas, individuals diagnosed with this disorder no longer contain the ability to regulate their behavior in the same manner as individuals without the disorder.
Interestingly, other unexplainable findings differentiate an ADHD brain from a normal brain. One researcher found that the right hemispheres of ADHD diagnosed boys were "on average 5.2% smaller when compared with a control group of non ADHD boys" (Castellanos, 1996). Another study also found that ADD subjects had significantly higher theta amplitudes sustained for longer periods of time and also discovered, "significant differences in the ratios of theta and beta waves" (Jenzen, 1995). This study implies that individuals diagnosed with ADHD show excessively slow brainwave activity when compared to non-diagnosed individuals and that perhaps this slower activity results in a decreased ability of self-regulation and control. This information has important implications for current theories of attention. Hillyard (1973) used dichotic listening tasks and ERP tests to discover an increased NI wave at 90ms, indicating that attention acts like a spotlight to amplify information for greater sensory and associated cortex registration. It would be interesting to determine if individuals with ADHD amplify this wave in the same manner as non diagnosed individuals. Other studies did not test this particular wave but showed differences in brain activity during vigilance tests which suggested under-responsiveness to stimuli.
Another author explained the frustrating effects of ADD and the resultant slow processing between and lack of neural connections when trying to process information: "It will be like a pipe that is too small to handle a large volume of water. It will take in some, but the rest will be stopped and won't go down the pipe rapidly. Learning will take place, but the time that it takes to process information will be slowed significantly" (Jaska, 1998). With differences in the number of brain cells, the size of brain cells, and the number of connections between brain cells, any deficiencies in these areas are easily identified in timed tasks: even when a child may know the material in great detail, it will take time for the individual to process the question and recall the answer.
In a study conducted by Burgess JR, (2000), a subgroup of ADHD subjects with an EFA deficiency was found to have significantly lower proportions of plasma and the fatty acids arachidonic acid and docosahexaenoic acid. The study also showed that with lower levels of these acids, ADHD subjects experienced significantly more behavioral problems than those with higher proportions of the acids. Current studies continue to examine reasons for these lower levels of fatty acids and to explain why this altered metabolism results in ADHD behavioral characteristics. It will be important to further explore this relationship to discover implications it may have. DHA is essential for the maintenance of normal brain function in adults, and a "plentiful DHA diet improves learning ability, whereas deficiencies cause deficits in learning" (Horrocks, 1999). While individuals with ADHD already contain low levels of this acid, they may be at risk for even greater deficiencies of this fatty acid due to improper nutrition that may be associated with the appetite suppressant characteristic of Adderal XR. Long term affects of stimulant medication include the possibility of a loss in weight and height suppression, and has proven to be dose-related (Root and Resnick 2003). Many therapists must continuously monitor height and weight of patients, as stimulants are frequently used well into adolescence and adulthood (Root 2003). As individuals with ADHD may have lower fatty acid levels have and associated greater behavioral problems they may be more likely to be prescribed medication to alleviate symptoms; however, as medicated individuals no longer have the desire to consume large amount of calories, skipping meals or indulging only in snack food will result in an increased lack of necessary levels of DHA, which present in fish, meat, and eggs, and may increase the symptom complex of the behavioral disorders they are attempting to treat.
Because past research has identified the associated brain structures affected by ADHD, it would seem simple to find what causes these malfunctions and treat this disease. However, despite many theories, researchers still have not identified an exact cause of ADHD, as the brain remains to be an organ that holds many mysteries difficult to define. Recent research has shown that ADHD may have a genetic link, (Reuters, 2001) and that an alteration in the dopamine receptor gene DRD4 can contribute to the disorder. Statistically, chances of an individual having ADHD increases if a family member has been diagnosed. The study claimed "if one person in a family has been diagnosed with ADHD, there is a 25% to 35% probability that any other family member also has ADHD, compared to a 4% to 6% probability for someone in the general population" (Reuters, 2001). Despite historical theories about the causes of ADHD, Scientists at the National Institute of Health (1998) have disproved poor parenting or teaching, family problems, too much television, or food allergies. The only theory that appeared to have any validity was the influence of too much sugar, where scientists found that about 5% of ADHD children were hyperactive or inattentive as a result of refined sugar and food additives" (Klein & Mannuzza, 1998). Another undocumented theory came from the idea that ADHD was caused by minor head injuries or damages to the brain, as ADHD was referred as "minimal brain damage" or "minimal brain dysfunction". However, one study (Castellaneous, 1996) proved the vast majority of people with ADHD involved in the studies had no past experience or evidence of a head injury. This last misconception may have come from two possible correlations between ADHD and injury. The first comes from a study that found 7-11 year old boys who watched video simulations of rough play. While both ADHD and non ADHD boys were able to identify the hazards in the simulation, ADHD boys "anticipated less severe consequences following risky behavior and reported fewer methods of preventing injury...resulting in an increased injury liability with ADHD boys" (Farmer & Peterson, 1995). Perhaps this increased injury liability and its increased probability of brain damage through injury was too hastily associated as the cause of ADHD in earlier studies. The second comes from a study that claimed children diagnosed with ADHD were more likely to have been a victim of past trauma. However, the study was careful to indicate that "ADHD alone was not associated with trauma exposure" (Ford, Rascusin, Davis, Ellis, Thomas, Rogers, Reiser, Schiffman, Sengupta, 1999).
Treatment for ADHD can involve behavioral therapy, yet often includes medication as a means of improving attention and reducing hyperactive symptoms, allowing a diagnosed individual to calm down and learn new behavior techniques. The effects of stimulant medication suggest that the neurotransmitters dopamine, norepenephrine, epinephrine, and serotonin may be involved. Specifically, evidence suggests a deficiency in dopamine and neuroepinephrine (Aman 1998). While it may seem oxymoronic, individuals diagnosed with ADHD actually have a lack of stimulant and symptoms associated with the disorder appear to be a form of overcompensation. To fix this deficit, medications such as Adderal XR offer a stimulant to reduce hyperactive symptoms. The effects of stimulant medication is apparent in the high corresponding rates of teens who self medicate through stimulant drugs, such as nicotine and other psychoactive drugs (meth-amphetamines) as they work as agonists for dopamine and neuroepeniphrine. ADHD teens often show a correlation of adolescent delinquency, and while this may be the result of poor social skills, perhaps the relationship to drug use may actually be a form of self-medication for the disorder, especially in lower SES where diagnosis and medication is often less accessible/affordable. While stimulant medication is the primary medical treatment for the disorder, as with most psychoactive-related drugs researchers only primarily know that they work, not how they work. Adderal XR was actually a diet suppressor that was discovered to improve attention processes, which was later tested and applied to ADHD. Because neurotransmitters function throughout the brain and have complex processes, it is difficult to specifically determine the answer.
The disorders and personal struggles created through these physical malfunctions create multiple consequences in social settings. Individuals uneducated about the disease might easily criticize behaviors of ADHD as merely being unmotivated. In fact, past studies have shown that "poor response inhibition actually manifests a disinclination to invest effort or reflects a motivational deficit" (Oosterlaan, 1998). In reality, individuals with ADHD do not have the same motivational drive and do not utilize the same effort to perform at optimum levels compared to non ADHD individuals. In social situations of job and school settings, individuals diagnosed with ADHD are often mistakenly seen as being careless or having a bad attitude when they do not apply themselves or show genuine effort.
Perhaps the most enlightening information of the social conflicts from ADHD comes from a study by Gerdes, (2003) examining the relationship between boys with ADHD and their parents. The study found that mothers and fathers of ADHD boys perceived the relationship with their son as significantly more negative than parents of the non ADHD boys. These parents also practiced more control and structure, were more power assertive and demanding, and responded less positively than the control parents. Through the continued negative interactions with their children, parents of ADHD boys started to perceive their relationship more negatively. Ironically, the ADHD boys did not differ from the control boys in their perception of the relationship with the parents. The author of the study described how the ADHD boys positively inflated their perceptions, "as providing support for a positive illusory bias in the social self perceptions of ADHD children" (Gerdes, 2003). Another study also emphasized inflated self perceptions of ADHD individuals when asked to assess social competence. ADHD participants in the study felt they were less skilled at self-regulating social behavior, but claimed they had a greater sensitivity to the violation of social rules when compared to non ADHD participants (Friedman, 2003). However, the study proved that the ADHD individuals were less accurate than the controls in identifying correct facial emotion. Interestingly, the ADHD participants also showed little awareness that they were misinterpreting the emotions of others and particularly recognized contempt and disgust. Perhaps the sensitive perception of negative emotions exhibited in ADHD is a result of an environment displaying these emotions in times of frustration. While some studies suggest this personal bias is intentional as a source of personal protection and a means of coping with negative experiences (Gerdes 2003), it shows the reality of how detrimental these biases can be in social interactions when ADHD individuals fail to recognize when things are not going well (Friedman, 2003). The study also explained that ADHD adults often reacted with surprise when they realized what they had perceived as a good relationship was seen as a negative interaction by others. These studies offer insight for the possible increased frustration and stress that may cause a greater strain on relationships for individuals with ADHD and may indicate that some of the negative perceptions others may attributed to the automatic assumption of conflict when working with someone who is "labeled" with the disorder.
Unfortunately, the study mentioned above and numerous others assessing the implications of ADHD have only involved male subjects, and though the disorder occurs more frequently in boys, more research is necessary to explore the extent of ADHD in females. In Kathleen Nadeau's recent book, Is Your Daughter A Daydreamer, Tomboy, or "Chatty Kathy"? She may have Undiagnosed Attention Deficit Disorder, she explains, "only a few of girls who show symptoms like ADHD boys are sent for assessment". Girls who remain undiagnosed with the disorder are often seen as ditzy, spacey, or non-academic, and girls who are highly intelligent with ADHD usually are never noticed as having a disorder. Ironically, because girls are more likely to please their parents or teachers and have higher expectations to be polite, respectful, and cooperative when compared to boys, their ADHD symptoms are only seen as undisciplined actions and they are often never considered as having a disorder. With further research, perhaps parents and teachers will gain enough education to abandon their engendered social norms, begin to recognize true symptoms of ADHD in young girls, and offer more opportunities through awareness to seek treatment.
Though the diagnosis of ADHD usually occurs in childhood, problems still persist in adulthood, which can cause serious problems for college students. In a study assessing the performance of college students with ADHD, they had significantly more problems with mental restlessness and that these students "may be at risk for low academic achievement and other related problems" (Weyandt, 2003). While these college students may seem to be struggling compared to their fellow students, they are fortunate to have found the social support in reaching their academic goals. As many as "35% of people with ADHD never finish high school, 52% of untreated teens and adults abuse drugs and alcohol, and 43% of boys will be arrested for a felony by age 16 and parents of ADHD divorce three times more often" (Amen, 2001). Another study claims adolescents with ADHD are more likely to engage in substance use (Burke, Loeber, Lahey 2001), as ADHD adolescents see "trouble making" peers more fun be with or gravitate to deviant groups through rejection of their peers (Bagwell, Molina, Pelham 2001).Though our society has made some advancements in recognizing this disorder such as Federal Legislation recognizing ADHD as a disability in both the Americans with Disabilities Act and the Individuals with Disabilities Education act and allowing ADHD individuals to receive reasonable accommodations at school and the workplace, these statistics stand as evidence for the need of continued research to understand, treat , and greater address the social consequences of this disorder.
Progress in ADHD treatment seems to increase as research in brain function and chemistry makes advancements. Original therapeutic activities revolved around outside intervention to help individuals learn coping skills and adaptive behaviors. According to one study the most effective treatment involves a combination of medication and therapy (Jaska 1998). Medication is used to help in chemical reactions in the brain to normalize activity, such as stimulant medications Ritalin, Dexedrine, and Adderall. However, medications may cause certain side affects, and finding the best medication may be a matter of individual experimentation. While researchers may understand how medication changes brain chemistry, they don't necessarily know why they alleviate symptoms of ADHD. The area of pharmacology as it relates to ADHD allows for advancement in research as we continue to learn more about the brain.
ADHD is becoming more predominant in today's society, yet still has many aspects that remain unknown. Continued research in understanding the causes and treatments for ADHD will allow society, doctors, and diagnosed individuals to become more educated about this disorder and begin to truly understand the reality of ADHD.
Aman, Christine J.; Roberts, Ralph J.; Pennington, Bruce F. (1998) A Neuropsychological Examination of the Underlying Deficit in Attention Deficit Hyperactivity Disorder: Frontal lobe versus right parietal lobe theories. Development Psychology. Vol. 34.5, 956-969
Amen, Daniel G. (2001) Healing ADD: The Breakthrough Program that Allows you to see and Heal the six types of ADD. New York, NY; G.P. Putnam and Sons. Pp xvii.
Bagwell, C.; Molina B.S.; Pelham, W.E.; Hoza, B. (2001). Attention-Deficit Hyperactivity Disorder and problems in peer relations: Predictions from childhood to adolescence. Journal of the American Academy of Child and Adolescent Psychiatry. 40, 1285-1292.
Baving, Lioba (1999). Atypical Brain Activation in ADHD: Preschool and Elementary School Boys and Girls. Retrieved Mar 1, 2004 from http://www.findarticles.com
Brown, Ronald T. La Rosa, Angela; Recent developments in the pharmacotherapy of ADHD. Professional Psychology: Research and Practice. 71.1, 327-393.
Burke, J.D., Loeber, R &Lahey, BB. (2001) Which aspects of ADHD are associated with tobacco use in early adolescence? Journal of Psychology and Psychiatry. 42, 492-502.
Castellanos, F.X. (1996) Toward a pathophysiology of Attention Deficit Hyperactivity Disorder. Clinical Pediatrics, 36, 381-393.
DuPaul, George J. (2003). Assessment of ADHD Symptoms. Psychological Assessment. 15.1, 115-117.
Faraone, Stephen V.; Monuteaux, Michael C.; Biederman, Joseph; Cohan, Sharon L.; Mick, Erick; (2003). Does parental ADHD bias maternal reports of ADHD symptoms in children? Journal of Consulting and Clinical Psychology. Vol 71.1, 168-175.
Farmer, Janet E.; Peterson, Lizette.; (1995). Injury of Risk factors in children with Attention Deficit Hyperactivity Disorder. Health Psychology. Vol 14.4 325-332/
Freidman S.; Rapport L. (2003). Aspects of social and emotional competence in adult ADHD. Neuropsychology, 17, 50-58.
Ford, Julian D.; Racusin, Robert; Davis, William B.; Ellis, Cynthia G.; Thomas, Julie; Rogers, Karen; Reiser, Jessica; Schiffman, Jill; Sengupta, Anjana; (1999). Trauma exposure among children with oppositional defiant disorder and Attention Deficit Hyperactivity Disorder. Journal of Consulting and Clinical Psychology. Vol 67.5 786-89.
Gerdes, Alyson C. (2003). ADHD boy's relationships with their mothers and fathers: Child, mother and father perceptions. Development and Psychopathology. 15, 363-384.
Hillyard, S.A., Hink, R.F., Schwent, V.L., Picton, T.W. (1973). Electrical signs of selective attention in the human brain. Science. 182: 77-180.
Hinshaw, Stephen P. (2002). Preadolescent girls with ADHD: Background characteristics, comorbidity, cognitive and social functioning, and parenting practices. Journal of Consulting and Clinical Psychology. 70.5, 1086-1098.
Jenzen, Troy, (1995). Differences in baseline EEG measures for ADD and normally achieving preadolescent males. Biofeedback and Self Regulation, 20.1, 56-82.
Klein, R.G. & Mannuzza, S. (1998). Hyperactive boys almost grown up: Methylphenidate effects on ultimate height. Archives of General Psychiatry. 45, 1131-134.
Mason, W & Windle, M. (2002). Reciprocal relations between adolescent substance use and delinquency: a longitudinal latent variable analysis. Journal of Abnormal Psychology. 111, 63-67.
Nadeau, Kathleen G. (1997). Is Your Daughter a Daydreamer, Tomboy, or "Chatty Kathy"? She May Have Undiagnosed ADD. New York, NY. Advantage Books, 16.
Oosterlaan, Jaap. (1998). Effects of reward and response cost on response inhibition in ADHD disruptive, anxious, and normal children. Neuropsychology, 41, 112.
Root, Richard W.; Resnick, Robert J.; (2003). An update on the diagnosis and treatment of ADHD in children. Professional Psychology: Research and Practice. 34.1, 34-41.
West, J.; Houghton, S.; Douglas, G.; (2002). Response inhibition, memory, and attention in boys with ADHD. Journal of Learning Disabilities. 36.4, 533-551.
Weyandt, Lisa L. (2003). The internal restlessness scale: Performance of college students with and without ADD. Journal of Learning Disabilities. 36.4, 382-390.
Zucker, R.A. & Gomber, E.S.L. (1986) Etiology of alcoholism reconsidered: the case of biopsychoscial process. American Psychologist, 41, 1285-1292.