ADHD: A Dialogue With a Non-Believer, part three
It was with some interest that I read the article What You Should Know About Attention Deficit Disorder by Edward W. after having it handed to me by a member of our church. There were elements of the article that were insightful, helpful, and needed to be said in a public forum, especially the discussion of the moral and spiritual dimensions of behavior. For this part of the article I applaud Mr. W.
However, Mr. W's discussion on the physiological/biological aspects of ADD ADHD was lacking to the point of being misleading to the readers. I am sure that Mr. Welch had no intention of misleading any readers, as that would hardly reflect the "biblical guidelines with which to understand ADD" that he seeks to communicate. Therefore, for the sake of clarifying some details, may I present the following evidence. Perhaps in the near future you would run an article that would present some of this information to your readers, so that they have an accurate understanding of the disorder.
We continue the dialogue here in part three.
"The popular assumption is that there is an underlying biological cause for the behaviors, but the assumption is unfounded. Although there are dozens of biological theories to explain ADD, there are presently no physical markers for it; there are no medical tests that detect its presence. Food additives, birth and delivery problems, inner ear problems, and brain differences are only a few of the theories that are? unsupported by evidence."
There are, in fact, biological causes for the behaviors.
Now, what are the "behaviors" that we are talking about? The "behaviors" of the diagnostic criteria. We are not talking about behaviors with a moral basis such as hitting your sister. We are talking about the specific behaviors of the DSM-IV diagnostic criteria for ADHD.
"Although there are dozens of biological theories to explain ADD, there are presently no physical markers for it;?"
Just because there are dozens of theories, most of which will prove to be wrong and go away, does not mean that one (or more) of the theories are not accurate descriptions of reality. In fact, research shows that there are several "physical markers" of ADHD.
Here are a few articles, both from peer reviewed journals and from the media discussing peer reviewed journal articles, that might be of interest to your readers. They are just 15 studies or articles about the various biological underpinnings of ADHD. It is certainly not a comprehensive list, as there have probably been more than 200 similar studies published in the past ten years alone. These are just the studies that I looked up last weekend for another project and already had in my word processor:
Brain Scan Found Effective in Diagnosing Attention Disorder
Brain scans have identified a clear-cut chemical abnormality in people with attention deficit-hyperactivity disorder, a problem that makes life difficult for an estimated 3 to 5 percent of US schoolchildren, scientists say.. It could be a first step toward a long-sought objective test for ADHD, say researchers at Harvard Medical School and Massachusetts General Hospital.
Two neuropsychological measures of executive functions--Six Elements Tests (SET) and Hayling Sentence Completion Test (HSCT)-were administered to 110 adolescents, aged 12-15 years. Participants comprised four groups: Attention Deficit Hyperactivity Disorder (ADHD) only (n = 35). ADHD and Oppositional Defiant Disorder/Conduct Disorder (ODD/CD) (n = 38), ODD/CD only (n = 11), and a normal community control group (n = 26). Results indicated that adolescents with ADHD performed significantly worse on both the SET and HSCT than those without ADHD, whether or not they also had ODD/CD. The adolescents with ADHD and with comorbid ADHD and ODD/CD were significantly more impaired in their ability to generate strategies and to monitor their ongoing behavior compared with age-matched controls and adolescents with ODD/CD only. It is argued that among adolescents with clinically significant levels of externalizing behavior problems, executive function deficits are specific to those with ADHD. The findings support the sensitivity of these two relatively new tests of executive functions and their ecological validity in tapping into everyday situations, which are potentially problematic for individuals with ADHD.
Executive functions and developmental psychopathology.
In this paper, we consider the domain of executive functions (EFs) and their possible role in developmental psychopathologies. We first consider general theoretical and measurement issues involved in studying EFs and then review studies of EFs in four developmental psychopathologies: attention deficit hyperactivity disorder (ADHD), conduct disorder (CD), autism, and Tourette syndrome (TS). Our review reveals that EF deficits are consistently found in both ADHD and autism but not in CD (without ADHD) or in TS. Moreover, both the severity and profile of EF deficits appears to differ across ADHD and autism. Molar EF deficits are more severe in the latter than the former. In the few studies of more specific EF tasks, there are impairments in motor inhibition in ADHD but not in autism, whereas there are impairments in verbal working memory in autism but not ADHD. We close with a discussion of implications for future research.
Brain Differences in Attention Deficit Disorder
Scientists have strong new evidence that attention deficit disorder (ADD)--a condition in which children are hyperactive and have difficulty concentrating--stems from an abnormality in the brain. According to a report in today's Proceedings of the National Academy of Sciences, children with ADD have elevated nerve firing in a brain region involved in motor activity. In addition, the researchers found, Ritalin--the drug most commonly prescribed for the disorder--triggers a surprisingly different biochemical response in the brains of children with ADD than in those without the condition.
Binding characteristics of tritiated imipramine on blood platelets were determined in daytime hospitalized prepubertal children who had mixed diagnoses of conduct disorder (CD) plus attention deficit disorder hyperactivity (ADDH) and in inpatient adolescents who had a history of aggressive behavior. The number of (3H)-imipramine maximal binding sites (Bmax) was significantly lower in the prepubertal patient group of CD plus ADDH; the dissociation constant (Kd) was not significantly different. There were significant negative correlations between Bmax and the Externalizing or Aggressive factors of the Child Behavior Checklist when the CD plus ADDH prepubertal patients were combined with their matched controls and within the adolescent inpatient group. We propose that a decreased platelet imipramine binding Bmax value, as an index of disturbed presynaptic serotonergic activity, is not specific to depression and may be used as a biologic marker for the lack of behavioral constraint in heterogeneous. populations of psychiatric patients.
Neuropsychiatric and neuropsychological evaluations were performed in a pilot study of adolescents with DSM-III-R disruptive behavior disorders, including conduct disorder (CD) and attention-deficit hyperactivity disorder (ADHD). The following comparisons were made: 1) CD comorbid with ADHD vs. CD only; 2) all subjects with ADHD vs. all non-ADHD; and 3) all subjects with CD vs. all non-CD. The CD + ADHD group had increased left-sided soft signs compared with the CD group. CD + ADHD subjects significantly underperformed CD subjects on several executive functioning measures, with no differences on Verbal IQ subtests. Results are discrepant with previous findings of deficient verbal functioning in delinquent populations.
Epidemiology: In a large sample from the U.S. population, the prevalence of ADHD (male: female ratio) in school-age children was 6.7 percent (5.1:1). Depending on the use of adaptive functioning ratings to define definite maladjustment, prevalence estimates of 6.6 percent and 9.5 percent
Family Studies: Several studies demonstrate that ADHD aggregates in families [13-15]. The rates in probands' sibs in three older studies [16-18] ranged from 17 percent to 41 percent, with respective rates in controls' sibs ranging from zero to 8 percent [16, 17]. Rates of childhood ADHD in parents of hyperactive probands in several older studies ranged from 15 percent to 44 percent for fathers and 4 percent to 38 percent for mothers [19-22], although one study found no evidence of an increased rate of childhood ADHD in parents of ADHD probands
Twin Studies: Two small twin studies found that 4 of 4  and 3 of 3  MZ twins were concordant for ADHD. A larger twin study  reported respective MZ and dizygotic (DZ) probandwise concordance rates of 51 percent and 33 percent, with a heritability estimate of 64 percent.
Adoption Studies: Increased rates of hyperactivity or a history of hyperactivity have been found among both adopted-away sibs of children with ADHD  and the biological parents of hyperactive boys compared with controls [21, 44, 45].
Mode of Inheritance: Deutsch and colleagues found limited evidence in a small sample  for an incompletely penetrant autosomal dominant single major locus transmission. A segregation analysis of a different data set  also resulted in statistical evidence -- including estimates of transmission parameters that were not significantly different from Mendelian expectations -- for an incompletely penetrant dominant or additive autosomal single major locus . Low penetrance estimates predicted that only 46 percent of boys and 31 percent of girls with the ADHD gene would develop the disorder.
Molecular Genetic Studies: A population-based association study reported evidence of an association between ADHD and an allele at the dopamine D2 receptor gene on 11q (p = 0.0003) , but this finding has not been replicated and was most likely an artifact of population stratification. The Tranmission Disequilibrium Test (TDT)  was used in a family-based association study to identify an association between ADHD and a specific allele at the dopamine transporter locus on 5p (p = 0.006) . Another population-based association study found an association between ADHD and an allele at the dopamine D4 receptor on 11p (p = 0.01) .
Neurophysiological correlates of Attention Deficit Disorder with and without Hyperactivity (ADD/HD) and effects of methylphenidate are explored using electroencephalographic (EEG) and auditory eventrelated potentials (ERPs). In the first of four studies, a database of ADD/HD individuals of varying ages and matched adolescent/adult controls is presented. Study 2 compares controls and age-matched children with ADD, and children with ADHD on and off methylphenidate. Study 3 examines habituation of the auditory ERPs of controls and children with ADHD both on and off methylphenidate. The relationship between successful neurofeedback training and EEG changes is presented in Study 4. Overall, these studies support a neurologic basis for ADD/HD and raise questions regarding the role of methylphenidate in modulating cortical processing.
Three well known tests (WISC-R, WRMT-R, WRAT-R) were administered to all subjects prior to the main part of the study, a series of cognitive tests performed while connected to a 19 lead EEG cap. Findings:
The most consistent finding was that ADD subjects have significantly higher theta amplitudes (p < .05) for all sites at both baseline and while performing cognitive tasks.
Need I go on? I have more!
This is the end to part three of this discussion. You can learn more about Attention Deficit Hyperactivity Disorder by visiting the ADHD Information Library's family of web sites.
Douglas Cowan, Psy.D., is a family therapist who has been working with ADHD children and their families since 1986. He is the clinical director of the ADHD Information Library's family of seven web sites, including http://www.newideas.net, helping over 350,000 parents and teachers learn more about ADHD each year. Dr. Cowan also serves on the Medical Advisory Board of VAXA International of Tampa, FL., is President of the Board of Directors for KAXL 88.3 FM in central California, and is President of NewIdeas.net Incorporated.
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