Genetic Explanations of Attention-Deficit Hyperactivity Disorder - Essay Example

Are Genetic Explanations of ADHD Faulty? Introduction: The U.S. Surgeon General has defined attention-deficit hyperactivity disorder (ADHD) as “ a metabolic form of encephalopathy, impairing release and homeostasis of neurological chemicals, and reducing the function of the limbic system. Yet, research has indicated that in all likelihood it is the frontal lobes, their connections to the basal ganglia and the central aspects of the cerebellum that are involved in ADHD. It is also likely that a region in the middle or medial aspects of the frontal lobe, known as the anterior cingulated. The Diagnostic and Statistical Manual of Mental Disorders -IV-TR defines ADHD as a developmental disorder that occurs in childhood, invariably prior to the age of seven, and is characterized by “developmentally inappropriate levels of inattention and/or hyperactive-impulsive behavior”, which causes impairment to one or more than one of major life activities, like family, peer, educational, occupational, social or adpative funtioning. This lack of a single acceptable definition provides indication of the division of the interpretation of the evidence available on ADHD, and is acceptable as knowledge. Children with ADHD display inattentiveness, impulsive behavior, and restlessness. They find it difficult to maintain attention in particular to activities that do not appeal to them or is non-rewarding. This behavior is often combined with the problem of responding to distractions that make it difficult to focus on tasks at hand. Adults with ADHD often have difficulty with time management, procrastination, organization, risk taking, careless behavior, and distractible and impulsive behavior, which leads to poor structuring of their lives, and inability to plan and execute complex daily tasks. (Attention-deficit hyperactivity disorder). The Genetic Explanation Controversy: The original manner in which children with ADHD was looked at was to treat them as children with learning difficulties, and that provide them with special education as a means to make them all right. Thus making it essentially an issue of nurture. Present day psychologists tend to question this understanding of ADHD, and have brought a new perspective of ADHD from the nature angle, in the form of a biological or neurochemical problem, as an explanation for ADHD. Support for this comes from psychologists, who believe that the mind and body are more closely intertwined than was earlier believed, and that the body could cause problems of the mind. These beliefs are founded or the findings that Downs syndrome and cancer could have a genetic basis. Extending this to possibility to ADHD was natural process, and as a result came the possibility of a genetic explanation to ADHD. In essence the arguments against the genetic explanation for ADHD arises from the traditional concept of ADHD as a nurture issue that makes the environment of the child the essential cause for ADHD, and does not accept the genetic explanation of ADHD from evidence that research has provided on the grounds that these research findings are flawed because of improper modalities in the conduct of the research. Arguments in favor of the genetic explanation are founded in the evidence of such research. In rejecting the genetic explanation of ADHD, Dr. Jay Joseph cites that it is not possible to distinguish between genetic and environmental components through family studies. In addition twin studies surmise that the environmental factors are the same for both fraternal and identical twins, and this is not true. Research into the genetic cause for ADHD through twin studies is flawed, and inconclusive. He goes on to add that genetic factors as a cause for ADHD is not supported, and that emphasis of future research into ADHD should be on the psychosocial cause or the environment. (Joseph, J., 2000). Dr. Stephen V. Faroane and Dr. Joseph Biederman have opposed this view of Dr. Jay Joseph. They argue in favor of the genetic explanation of ADHD, on the grounds that family studies have shown that ADHD runs in families and unequal environments need not necessarily mean that identical twins are prone to more trait-relevant environmental factors than is the case with fraternal twins. In addition they claim that the minor methodological flaws of research into genetic does not call for their rejection, but only affects the strength of the conclusions that are drawn from them. They also claim that the genetic theories give the most parsimonious explanation. (Faroane, V.S., & Biederman, J., 2000). There are a number of study reports that indicate that ADHD is highly heritable. This perspective does not only rely on twin studies, but also on adoption and molecular genetic studies, giving it added value. In addition studies have indicated that obstetric complications and psychosocial factors pose predisposing risks for the development of ADHD. Evidence from animal and human studies have suggested that dysregualtion of the frontal-subcortical-cerebellar catecholaminergic circuits in the pathway may be responsible for the pathophysiology of ADHD. The possibility of abnormal dopamine transporter causing impaired neurotransmission has come from molecular imaging studies. Over the last ten years studies have established the safety and effectiveness of non-stimulant and long acting drugs formulations using methylphenidate and amfetamine. These findings suggest the validity of genetic explanation of ADHD. Even so the psychosocial role in ADHD is not ruled out with findings that suggest that it may be appropriate to use psychosocial treatments along with the use of drugs. (Biederman, J., & Faraone, V.S., 2005). Most of the twin studies on ADHD that have found strong links to genetic influences on ADHD, and unique environmental influences have used DSM ADHD symptoms that were collected over the telephone by interviewing the mothers of children. To make these findings more conclusive a study was conducted to test the genetic architecture of ADHD by using the ADHD index from Conner’s Rating Scales-Revised from information gathered through interviews of 1,595 seven year old twin pairs in the Netherlands. Rates of ADHD were calculated by using Conner’s gender-and age –specific cutoff points. The prevalence rate was found to be in the region of four percent from the reports of the mothers, and this was in keeping with findings of other studies. Genetic analyses generated a model that gave genetic dominance at forty-eight percent, additive genetic factors at thirty percent, and environmental factors at twenty two percent. These results were consistent with the earlier research findings the predominant influences on ADHD are genetic factors that are both dominant and additive. The finding of this study reinforces the earlier studies using DSM ADHD symptoms, and rules out any arguments against any perspectives of shortcomings in the DSM ADHD symptoms. (Hudziak, J.J., et al., 2005). Many studies have established the role of genetics and non-shared environmental factors in the cause of in ADHD. A better understanding of the role of non-shared environmental factors that cause ADHD would provide stronger validity of the claim to non-shared environmental factors. Some of the factors that have been attributed as causes for ADHD have been pregnancy, labor/delivery and neonatal complications. It is necessary to separate the shared and non-shared nature of these factors to establish the role of non-shared environmental factors on ADHD. In a study that was planned and executed with this objective, it was found that children with ADHD had significantly elevated rates of neonatal complications in comparison to their siblings that had remained unaffected. In addition it was found that neonatal complications in children with ADHD were associated with worse Child Behavior Checklist, and poorer performance with regard to Continuous Performance Test. This study enables the understanding that neonatal complications create higher rates of ADHD, and that these neonatal complications are a non-shared environmental risk that could be pathogenic in children that have ADHD. (Amor, L. B., et al., 2005). The exposure of the fetus to toxic substances and psychological trauma may have a role to play in ADHD. Studies have shown that fetal exposure to nicotine, by the mothers smoking during pregnancy result in hyperactivity in childhood. (Kotima, A.J., et al., 2003). In addition with hereditary factors playing a role in ADHD, marital discord, and alcohol and substance abuse among the parents poses additional risk for ADHD in their children. (Adler, L., et al., 2005). To further differentiate the role of genetics and environment in ADHD it would be useful to examine the genetic and environmental correlation among the ratings of Conduct Disorder (CD) and Oppositional-Defiant Disorder (ODD), and the pattern of genetic and environmental correlation between CD, ODD, and ADHD. In a study that was conducted with this objective it was found that genetic correlation with respect to inattention, impulsivity, and hyperactivity was large, but did not come up to unity. There was hardly any evidence to support symptoms of CD and ODD were genetically independent. There was no evidence with regard to rater contrast effects, or of shared family environmental influences in twin resemblance for ODD and CD. (Eaves, L., et al., 2000) The role of the genetic factor as a cause for ADHD gets enhanced as more and more evidence is collected with respect to the need to consider ADHD as a neuro-biological disorder. (Valera, M.E., & Seidman, L., 2006). Skepticism persists in the role of the gene factor in criminal behavior, and one of the main arguments against the role of the gene factor in criminal behavior is that if that were true, a candidate gene should have been identified for it by now. Such an argument cannot exist in the case of the gene factor as a cause for ADHD, as a candidate gene has been identified. Molecular genetic studies have provided evidence for the candidate gene. The candidate gene or genes are the genes influencing the functioning of the dopamine system, with particular reference to the dopamine receptor D4 gene known as DRD4. (Stevenson, J., et al., 2005). Dopamine occurs naturally in the brain, and is a neurotransmitter that sends signals. The release of dopamine happens during an action potential in the pre-synaptic neuron. The quantum of dopamine released is proportional to the firing of the neuron. In the post-synaptic neuron there are many dopamine receptors that take up the dopamine. In case too much of dopamine is released special dopamine transporter proteins become active, and to deactivate, and recycle the dopamine. Proper functioning of the dopamine receptors and transporters is essential for maintaining neurotransmitter homeostasis. It is in this role that the dopamine receptor D4 gene comes into play in ADHD. Dopamine has a strong affect by its presence and signaling in four areas of the brain. These four areas are the frontal lobe, the cortex, the forebrain gray and white matter, which make up the limbic system, and the Reticular Activating system of the brain, which is the converging point for all signals from the external world and the internal environment. Dopamine is known to have an influence on behavior through the mechanism known as the reward pathway. Thus dopamine with its influence on behavior is present in the vital areas of the brain. The dopamine receptor gene with its influence on the uptake of dopamine thus is identified as the gene that is the likely cause for ADHD. (Gulick, E.) The very large numbers of people that exhibit ADHD suggests that if ADHD is hereditary. it should have been a part of human beings for a very long time. This is difficult to test. There is a theory that suggests that the behavior seen in individuals with ADHD may be a trait that is not appreciated as modern man evolved, but it would have been a useful behavior for ancient man. During evolution based on Darwin’s theory of evolution, this gene has survived in humankind and presents itself, through behavior known as ADHD. (Shelley-Tremblay, Rosen, J.F., & Lee, A., 1996.) Conclusion: The controversy on the genetic explanation of ADHD will continue as long as science does not come up with irrefutable proof that genes have a very important role to play in ADHD. Literary References Attention-deficit hyperactivity disorder. Retrieved April 28, 2006, from Wikepedia, Web site: http://en.wikipedia.org/wiki/ADHD. Adler, L., et al. (2005). Medical Crossfire: Assessing Treatment Options in Adult ADHD. Retrieved April 28, 2006, from, Medscape. Website: http://www.medscape.com/viewprogram/4810. Amor, L. B., et al. (2005). Perinatal complications in children with attention-deficit hyperactivity disorder and their unaffected siblings. Journal of Psychiatry $ Neuroscience, 30(2), 120-126. Biederman, J., & Faraone, V.S. (2005). Attention-deficit hyperactivity disorder. The Lancet, 366(9481), 237-248. Eaves, L., et al., (2000). Genetic and Environmental Causes of Covariation in Interview Assessments of Disruptive Behavior in Child and Adolescent Twins. Behavior Genetics, 30(4), 320-334. Faroane, V.S., & Biederman, J. (2000). Nature, Nurture, and Attention Deficit Hyperactivity Disorder. Development Review, 20 (4). Gulick, E. The Familial Inheritance of ADHD: Are Dopamine Receptor and Transporter Genes Responsible. Retrieved April 28, 2006. Web site: http://www.stfrancis.edu/srsymposium/projects/biol/egulick_biol.pdf. Hudziak, J.J., et al. (2005). The Genetic and Environmental Contributions to Attention Deficit Hyperactivity Disorder as Measured by the Conners Rating Scales-Revised. The American Journal of Psychiatry, 162(9), 1614-1621. Joseph, J. (2000). Not in Their Genes: A Critical View of the Genetics of Attention-Deficit Hyperactivity Disorder. Development Review, 20 ( 4). Kotima, A.J., et al., (2003). Maternal Smoking and Hyperactivity in 8-Year-Old Children. Journal of the American Academy of Child & Adolescent Psychiatry, 42(7), 826-833. Shelley-Tremblay, Rosen, J.F., & Lee, A. (1996). Attention deficit hyperactivity disorder: An evolutionary perspective. New York, 157(4), 443. Stevenson, J., et al.(2005). Characterizing the ADHD phenotype for genetic studies. Developmental Science, 8(2), 115-121. Valera, M.E., & Seidman, L., (2006). Neurobiology of Attention-Deficit/Hyperactivity Disorder in Preschoolers. Infants $ Young Children, 19(2), 94-108. Read More