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Attention deficit hyperactivity disorder controversies

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PET scans show which parts of the brain are being used at a particular moment. In this example, the parts of the brain being used by someone diagnosed with ADHD is compared to the brain activity of a person not diagnosed with ADHD when both have been assigned a task requiring attention. The controversial part of this picture is that it is often used as a dramatic representation of differences in the ADHD brain whereas it might merely illustrate the fact that the ADHD person is not doing the assigned task, hardly unexpected from someone with ADHD

The psychiatric diagnosis of Attention-deficit hyperactivity disorder (ADHD) has attracted an assortment of critical positions that individually challenge the ontology or preconceptions of the diagnosis as it is defined in the DSM IV-TR. Among the criticisms are disagreements over the cause of ADHD, differences over research methodologies, and skepticism toward its classification as a mental disorder. Critics also express concerns over the effects of diagnosis on the mental state of patients and the effects of the medication available for the condition. Further, some critics suspect ulterior motives of the medical industry, which both authorizes the psychiatric definitions of mental disorders and promotes the use of pharmaceutical drugs for their treatment.

The ADHD diagnosis identifies characteristics such as hyperactivity, forgetfulness, mood swings, poor impulse control, and distractibility, as symptoms of a neurological pathology. But critics point out that the etiology of this mental disorder is not yet well defined by neurology, genetics, or biology.

Status as a disorder

Many critics of the diagnosis of ADHD do not agree that it should be classified as a disorder, but rather that it should only be considered a difference in methods of thought and mental organisation, more akin to being shorter than average than to other disorders. Arguments for this position include:

Utility of hyperfocus

The ADHD diagnosis provides symptoms of attention deficit, but identifies only chronic forms of distraction. What may be mistaken for distraction, however, may be a focused mental state. Hyperfocus is a term given to extended or increased attention to a subject. While hyperfocus is known to be useful for discerning details and thinking abstractly, it is sometimes taken as a symptom of attention deficit.

Debate about criteria

Critics of the ADHD diagnosis suggest that the diagnostic criteria are sufficiently general or vague to allow virtually any child with persistent unwanted behaviors to be classified as having ADHD of one type or another.

A number of critics have wondered why the number of children diagnosed with ADHD in the U.S. and UK has grown so dramatically over a short period of time. However, doctors often claim that improving methods of diagnosis and greater awareness are probably in part, if not mostly the reason for this increase.[citation needed]

Also, much of the research about ADHD actually contradicts facts asserted by the mainstream psychiatric establishment. The brain scans that lead this article supposedly show the difference between an "ADHD" and "Normal" brain, yet Zametkin later admitted that differences in sampling led to any discovered differences in the 1990 study.[citation needed] There are massive ambigiutities still in the science and NIMH does not widely release their data for re-analysis by other researchers who may be critical of the concept of ADHD[citation needed], which is exactly the opposite of the ideal scientific method.

While a believer that ADHD is a biological condition, it is noteworthy that Xavier Castellanos M.D., head of ADHD research at the National Institute of Mental Health (NIMH) (interviewed October 10, 2000 on Frontline) was very explicit about biological knowledge. When Frontline asked him how ADHD works on the brain, he replied:

"We don't yet know what's going on in ADHD." [1]

Despite the repeated references to the genetics of ADHD being unequivocal, according to Joseph Glenmullen, M.D., clinical instructor in psychiatry at Harvard Medical School, "no claim of a gene for a psychiatric condition has stood the test of time, in spite of popular misinformation."[1]

Sub-clinical ADHD

Another source of skepticism towards making the diagnosis of "ADHD or not ADHD" may arise from the rising diagnosis of subclinical forms of ADHD. So called 'Shadow-syndromes' or 'sub-syndromes' stand for weaker forms of ADHD and are described in various degrees by John J. Ratey and Catherine Johnson on their book Shadow Syndromes: The Mild Forms of Major Mental Disorders That Sabotage Us.

Another explanation comes from a common misconception of the symptoms that leads to an incorrect diagnosis. For example, an employee of a school might think that a student has ADHD simply because the child cannot be controlled in the classroom. A teacher may think a student whom they cannot control has ADHD, but in reality the problem may be a lack of discipline. The same teacher might not notice a child who forgets their papers, stares (entranced) at the carpet for long periods of time, or shows many of the recognized symptoms.

However, the results achieved in clinical tests with medication and anecdotal evidence of parents, teachers, and both child and adult sufferers has been taken as proof that there is both a condition and successful treatment options for most people who meet the criteria for a diagnosis. But critics point out that neurological differences exist among individuals just as with any human trait, such as eye color or height; and that stimulants have an effect on anyone, not just those diagnosed with ADHD. [citation needed]

Etiology of syndrome

A further problem is that ADD and ADHD are syndromes, associations of symptoms. There is no well established cause for the condition. This means that it may actually be a blanket term covering a multitude of conditions with a variety of causes (although this is true of many physical and mental illnesses). In fact, genome scans have identified several gene alleles which are prevalent among individuals diagnosed with ADHD, but no single allele can account for all cases, and not all cases have been explained genetically.[citation needed]

Confusion may also arise from the fact that ADD/ADHD symptoms vary with each individual, and some mimic those of other causes. A known fact is that, as the body (and brain) matures and grows, the symptoms and adaptability of the individual also change. Many individuals diagnosed with ADD/ADHD successfully develop coping skills, while others may never do so.[citation needed]

There are numerous, often contradictory, claims that the brain is physically different in children with ADHD. However, even if this eventually is confirmed, by no means does it establish that the condition is biological. Behavior can cause changes to the structure of the brain. For example, learning Braille causes enlargement of the part of the motor cortex that controls finger movements.[2] After they have passed their licensing exam, London taxi drivers have been found to have a significantly enlarged hippocampus compared to non-taxi drivers[3][4]. Patients abused during their childhood with post traumatic stress disorder will have a flattened out hippocampus.[5] Professional musicians have brains that are different from non-musicians.[6] Monks who meditate show measurable differences in their prefrontal lobes.)[7][8][9] So diminished concerted effort when confronted with tasks thought to be drudgery (homework, paying attention to teachers, and the like) even if not caused by differences in the brain, could have brain changing effects.

Views from neurodiversity

Another view is that while there does exist a phenotype that corresponds roughly to the ADHD diagnostic criteria, this phenotype should not necessarily be described as a pathology. Some psychiatrists have argued that ADHD may represent an evolutionary advantage [citation needed]. There are many phenotypes considered normal-variant, which have liabilities, and perhaps some advantages as well, such as homosexuality and left-handedness. In other words, ADHD may be better seen as a form of neurodiversity.

Questions about the falsifiability of the disorder

Critics have noted that the hypothesis "ADHD exists as an objective disorder" is unscientific, and point out that people generally assume that something is scientific just because it sounds scientific [10]. In other words, ADHD does not have good Popperian criteria for falsifiability. To be falsifiable, there would need to be a possible empirical observation which could show that the hypothesis is false.

Opposing theories (e.g. "ADHD exists only as a social construct") may be falsifiable and thus scientific. That is, it could be shown that ADHD exists as an objective entity by finding an objective characteristic which separates all diagnosable individuals from all undiagnosable ones. In contrast, to prove that ADHD does not exist as an objective entity, it would need to be shown that said objective characteristic does not exist. This task, which consists of proving a negative, is clearly not feasible.

A further issue is that even if a sharp objective difference is found between ADHD and non-ADHD groups, this does not prove that the difference constitutes a pathology. Behavior that is considered normal-variant (e.g. homosexuality, left-handedness, giftedness, being asleep, tired, etc.) likely has a neurochemical or neuroanatomical basis as well.

Genetic basis of hyperactivity

See genetic disease for a full discussion of the mechanics of defective genes.

Evidence suggests that hyperactivity has a strong heritable component[2]. Candidate genes include dopamine transporter (DAT), dopamine receptor D4 (DRD4), dopamine beta-hydroxylase (DBH), monoamine oxidase A (MAOA), catecholamine-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytriptamine 2A receptor (5-HT2A), and 5-hydroxytriptamine 1B receptor (5-HT1B).

Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17.[3] If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a "genetic disease" and is better viewed as a complex interaction among genetic and environmental factors. As the authors of a review of the question have noted, "Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified."[4]

Moreover, studies of genetics and epigenetics show that physical characteristics that are undoubtably heritable, such as eye color or hair color are not carried by single genes, but instead by hosts of genes known as polymorphisms. Two people with the same DNA, such as identical twins, do not always have the same hair color, eye color, height, weight, or other characteristics. A genetic basis for hyperactivity does not prove that one gene, or even one line of descent, is responsible for it.

Nor does a genetic basis for hyperactivity prove that it is a disease. In contrast to mental illnesses, genetic diseases are only known to affect small populations of people. Chromosomes disaffecting health or life expectency are not expressed by everyone with the same DNA, and have only been found in combination with one or more other chromosomes. One reason for this may be that nature selects against genetic abnormalities that do not have any advantage.

Nor does a genetic basis for the characteristic of hyperactivity prove a biological basis of Attention Deficit Hyperactivity Disorder. Particularly, the theory that DNA may contribute a probabalistic susceptibility to mental disorders, often assumed in medical literature, is unproved, and possibly unprovable. Psycholgical diagnoses may well fall into the category of unfounded cultural prejudices, along with racial classifications based on skin color, and religious hatred.

Although many theories exist, there is no definitive biological, neurological, or genetic etiology for "mental illness." The concept of mental illness has been criticized by authors such as Thomas Szasz in The Myth of Mental Illness. Szasz points out that diseases infect tissues, and in some cases perception, but not beliefs. From this perspective, neither belief, nor mental life in general, may have a biological basis.

Advocates of neurodiversity argue that heritable traits with no definitive biological pathology (for example, autism) are natural variations of biology. Additionally, heritable or inheritable behaviors that are often regarded as abnormal, such as hyperactivity, eccentricity, absentmindedness, or homosexuality are not disorders but natural variations of behavior. According to this view, neither hyperactivity nor inattention is a disorder. According to this view, the institutional designation of these characteristics as Attention Deficit Hyperactivity Disorder is an unfounded prejudice akin to social stigmas for red hair or short stature.

Alternative theories concerning origins of the condition

Dr. Mary Megson argued in her presentation to the House Government Reform Committee on Autism and Vaccines (2000) that the apparent increases in both ADHD and autism are a result of the increasing use of vaccines that deplete vitamin A stores, combined with a G-protein defect. This is especially likely in a family where at least one parent suffers night blindness, she claimed. However, no research to substantiate her claims has appeared in any major peer-reviewed medical journal, and the "vaccine-vitamin hypothesis" is not generally accepted.

It has been suggested that the causes of the apparent ADHD epidemic lie in cultural patterns that variously encourage or sanction the use of drugs as a simple and expeditious cure for complex problems that may stem primarily from social and environmental triggers rather than any innate disorder.[citation needed] Some critics assert that many children are diagnosed with ADHD and put on drugs as a substitute for parental attention, causing massive disruption to other individuals and relationships, as well as to environments with dysfunctionally structured relationships such as are manifest in many classrooms.[citation needed] This criticism also includes the use of prescription drugs as a substitute for parental duties such as communication and supervision.[citation needed]

Hunter in a Farmer's Society theory

Proposed by Thom Hartmann, this evolutionary psychology theory holds that ADHD was an adaptive behavior for the "restless" hunter before agriculture became widespread. Scientific concern around Hartmann's theory revolves around the mismatch between the behaviours symptomatic of ADHD, and those he describes as being adaptive for hunters, which better fit a diagnosis of hypomania [5]. A positive feature of the theory is the idea that thinking in terms of attentional 'differences' rather than attentional 'disorders' may direct effort toward utilizing an affected individual's strengths and uniqueness. Conversely, it could also reinforce a person's denial and refusal to seek treatment.

ADHD as a social construct

Following from the Hunter-versus-farmer theory, as with many conditions in the field of psychiatry, ADHD can be explained as a social construct (Timimi, 2002) rather than an objective 'disorder'.

In this view, in societies where passivity and order are highly valued, those on the active end of the active-passive spectrum may be seen as 'problems'. Medically defining their behaviour (by giving a label such as ADHD) serves the purpose of removing blame from those 'causing the problem'. This model would require removing "non-hyperinteractive" forms of attention deficit into a completely distinct diagnosis, much as drapetomania was once considered a valid diagnosis to explain the "irrational urge" of slaves to escape their situation and dysaethesia Aethiopica "explained" a slave's lack of motivation.

Evidence presented against the social constructionist view comes from a number of studies that demonstrate significant differences between ADHD and typical individuals across a wide range of social, psychological, and neurological measures as well as those assessing various areas of functioning in major life activities. More recently, studies have been able to clearly differentiate ADHD from other psychiatric disorders in its symptoms, associated features, life course, comorbidity, and adult outcome adding further evidence to its view as a true disorder.[citation needed]

Invocation of this evidence is seen by proponents of the social construct theory as a misunderstanding, nonetheless. The theory does not state that individuals across a behavioral spectrum are identical neurologically and that their life outcomes are equivalent. It is not surprising for PET scan differences to be found in people at one end of any behavioral spectrum. The theory simply says that the boundary between normal and abnormal is arbitrary and subjective, and hence ADHD does not exist as an objective entity, but only as a 'construct'.

Nor does evidence of successful treatment persuade the social constructionist; for example the American National Institute on Drug Abuse [11] reports that Ritalin is abused by non-ADHD students partly for its ability to increase their attention. Evidence showing that ADHD is associated with certain liabilities does not appear to undermine this view either; normal-variant behavior could have certain liabilities as well, and a life outcome cannot be predicted with certainty for any given diagnosed individual.

Critics of the social constructionist view contend that it presents no evidence in support of its own position. Theories must present their details and mechanisms in as precise a manner as possible so that they are testable and falsifiable, and this theory is said to provide no such details. But proponents of the view disagree that criteria for falsifiability is lacking. One way, for example, is to show that there exists an objective characteristic possessed by virtually all diagnosed individuals which does not exist in any non-diagnosed individual. Current candidates for falsifiability include PET scans, genes, neuroanatomical differences, and life outcomes. However, none of these have been shown to be precise predictors of a diagnosis or lack thereof.[citation needed] Such criteria is generally fulfilled by well-understood medical diseases.[citation needed]

Critics of this view also assert that it is not consistent with known findings. For instance, they claim that ADHD is as frequent in Japan and China as in the US[citation needed], yet in such societies (which favor child obedience and passivity) one would expect higher rates of ADHD if this theory were correct. Of course, this argument falls prey to the same criticism leveled against the Social Constructivist theory in the first place: whether or not the societies of Japan and China value "passivity and obedience" is not experimentally verified; calling them such amounts to stereotyping. Additionally, rates of medical diagnoses in China cannot be a reliable indicator of ADHD prevalence, especially for such non-life-threatening disorders as ADHD, due to the large peasant population in that country who cannot easily seek the services of a trained child psychologist. Timimi's view has been seriously criticized by Russell Barkley and numerous experts in Child and Family Psychology Review (2005). In any case, it has been shown that Chinese and Indonesian clinicians give significantly higher scores for hyperactive-disruptive behaviors than did their Japanese and American colleagues when evaluating the same group of children.[6]

Significant differences in the prevalence of ADHD across different countries have been reported, however (Dwivedi, 2005). Timimi himself cites a range of prevalence that goes from 0.5% to 26% as support for his theory.

Concerns about the impact of labeling

Dr. Thomas Armstrong [12], a prominent critic of ADHD as an objective disorder, has said that the ADHD label is a "tragic decoy" which erodes away the potential to see the best in every child. Armstrong is a proponent of the idea that there are many types of "smarts" and has adopted the term neurodiversity (first used by autistic rights activists) as an alternative, less damaging, label [13].

Thom Hartmann became interested in ADHD when his son was diagnosed; Hartmann has said that the brain disorder label is "a pretty wretched label for any child to have to bear" [14].

Others have expressed concern that the brain disorder label can negatively impact the self-esteem of a child and effectively become a self-fulfilling prophecy mainly through self-doubt.

Concerns about medication

Many parents and professionals have raised questions about the safety of drugs used to treat ADHD, particularly methylphenidate (Ritalin). Despite belief to the contrary, no significant effects have been observed on stature or the emergence of tics [15]. Deaths attributed to methylphenidate are believed to be caused by interactions with other drugs, and are extremely rare. Matthew Smith died at 14 after long-term usage of ritalin. The medical examiner determined that Matthew Smith died from ritalin usage, but medical experts dispute this. The examiner also argued that the likelihood that diabetic children were at higher risk for cardiac problems.[citation needed] The usage of stimulants, which increase pulse rate, in those with heart or hypertension problems might cause serious health issues.[citation needed]

The Pediatric Advisory Committee of the Food and Drug Administration (FDA) released a statement on June 30, 2005 identifying two possible safety concerns regarding Concerta and methylphenidate: Psychiatric adverse events and cardiovascular adverse events [16]. On February 9, 2006 the FDA's advisory panel voted in favor of having Ritalin and other stimulant drugs carry a strong "black box" warning after looking into the deaths of 25 people, including 19 children [17].

A new concern, raised by a small-scale 2005 study, is that methylphenidate might cause chromosome aberrations [18], and suggested that further research is warranted considering the established link between chromosome aberrations and cancer and considering that all the children in this study showed suspicious DNA changes within a very short time. A team from the Food and Drug Administration (FDA), the National Institutes of Health (NIH) and the Environmental Protection Agency (EPA) went to Texas on May 23, 2005 to evaluate the methodology of the study. Dr. David Jacobson-Kram of the FDA said that the study had flaws in its methods but that its results could not be dismissed. Flaws cited are (1) that the study did not include a control group on placebo, and (2) that it is too small. Several research teams will attempt to replicate the study on a larger scale.[citation needed]

Studies on rats have suggested there could be plastic changes in personality and brain functioning after chronic use into adulthood, including changes in sensitivity to reward [19] [20]. But, again, studies in humans are lacking and so such results cannot be automatically extrapolated to humans.

See also

Notes

  1. ^ Glenmullin, Joseph (2000). Prozac Backlash. New York: Simon & Schuster. pp. 192–198.
  2. ^ Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26.
  3. ^ M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine. 6 (1): 1–15.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine. 6 (1): 1–15.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Mota-Castillo, M. (2005). Review of The Edison Gene: ADHD and the Gift of the Hunter Child. Psychiatric Services, 56, 500.
  6. ^ E. M. Mann, Y. Ikeda, C. W. Mueller, A. Takahashi, K. T. Tao, E. Humris, B. L. Li, D. Chin (1992). "Cross-cultural differences in rating hyperactive-disruptive behaviors in children". American Journal of Psychiatry. 149 (11): 1539–1542.{{cite journal}}: CS1 maint: multiple names: authors list (link)

Research News on ADHD from ScienceDaily]