Beyond polemics: science and ethics of ADHD.
ABSTRACT What is attention-deficit hyperactivity disorder (ADHD)? Why are so many children being diagnosed with ADHD and prescribed medication? Are stimulant drugs an effective and safe treatment strategy? This article explores the current state of scientific research into ADHD and the key social and ethical concerns that are emerging from the sharp rise in the number of diagnoses and the use of stimulant drug treatments in children. Collaborations among scientists, social scientists and ethicists are likely to be the most promising route to understanding what ADHD is and what stimulant drugs do.
- Neuroethics 12/2014; 7(3):337-344. · 1.04 Impact Factor
- Neuroethics 12/2014; 7(3):373-375. · 1.04 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: Background Previous research indicates that Attention-deficit hyperactivity disorder (ADHD) is highly associated with Substance Use Disorders (SUD). These studies however, have failed to clarify the nature of the overlap. The main aim was to explore if the overlap between ADHD and SUD could be explained by shared genetic and environmental factors or by harmful effects of ADHD medication. Method Matched cohort design across different levels of family relatedness recorded from 1973 to 2009. By linking longitudinal Swedish national registers, 62,015 ADHD probands and their first and second degree relatives were identified and matched 1:10 with non-ADHD controls and their corresponding relatives. Any record of SUD defined by discharge diagnoses of the International Classification of Diseases and/or a purchase of any drug used in the treatment of SUD. Result First degree relatives of ADHD probands were at elevated risk for SUD (ORSUD1st 2.2 and 1.8) compared to relatives of controls. The corresponding relative risk in second degree relatives was substantially lower (ORSUD2nd 1.4 and 1.4). The familial aggregation patterns remain similar for first degree and second degree relatives after excluding individuals with coexisting disorders such as schizophrenia, bipolar disorder, depression and conduct disorder. Conclusion Our findings suggest that the co-occurrence of ADHD and SUD are due to genetic factors shared between the two disorders, rather than to a general propensity for psychiatric disorders or harmful effects of ADHD medication.Biological Psychiatry 10/2014; · 9.47 Impact Factor
71. Spear, L. P. Alcohol’s effects on adolescents. Alcohol
Res. Health 26, 287–291 (2002).
72. White, A. M. et al. Differential effects of ethanol
on motor coordination in adolescent and adult
rats. Pharmacol. Biochem. Behav. 73, 673–677
73. Doremus, T. L., Brunell, S. C., Varlinskaya, E. I. &
Spear, L. P. Anxiogenic effects during withdrawal from
acute ethanol in adolescent and adult rats. Pharmacol.
Biochem. Behav. 75, 411–418 (2003).
74. Silveri, M. M. & Spear, L. P. The effects of NMDA and
GABAA pharmacological manipulations on ethanol
sensitivity in immature and mature animals. Alcohol.
Clin. Exp. Res. 26, 449–456 (2002).
75. White, A. M. & Swartzwelder, H. S. Hippocampal
function during adolescence: a unique target of
ethanol effects. Ann. NY Acad. Sci. 1021, 206–220
76. Li, Q., Wilson, W. A. & Swartzwelder, H. S. Differential
effect of ethanol on NMDA EPSCs in pyramidal cells in
the posterior cingulate cortex of juvenile and adult
rats. J. Neurophysiol. 87, 705–711 (2002).
77. Brown, S. A. & Tapert, S. F. Adolescence and the
trajectory of alcohol use: basic to clinical studies. Ann.
NY Acad. Sci. 1021, 234–244 (2004).
78. De Bellis, M. D. et al. Hippocampal volume in
adolescent-onset alcohol use disorders. Am. J.
Psychiatry 157, 737–744 (2000).
79. Adriani, W. & Laviola, G. Windows of vulnerability to
psychopathology and therapeutic strategy in the
adolescent rodent model. Behav. Pharmacol. 15,
80. Andersen, S. L. & Teicher, M. H. Stress, sensitive
periods and maturational events in adolescent
depression. Trends Neurosci. 31, 183–191 (2008).
81. Birmaher, B. & Axelson, D. Course and outcome of
bipolar spectrum disorder in children and adolescents:
a review of the existing literature. Dev. Psychopathol.
18, 1023–1035 (2006).
82. Beesdo, K. et al. Incidence of social anxiety disorder
and the consistent risk for secondary depression in the
first three decades of life. Arch. Gen. Psychiatry 64,
83. Reinherz, H. Z., Paradis, A. D., Giaconia, R. M.,
Stashwick, C. K. & Fitzmaurice, G. Childhood and
adolescent predictors of major depression in the
transition to adulthood. Am. J. Psychiatry 160,
84. Blumberg, H. P. et al. Amygdala and hippocampal
volumes in adolescents and adults with bipolar disorder.
Arch. Gen. Psychiatry 60, 1201–1208 (2003).
85. De Bellis, M. D. et al. Brain structures in pediatric
maltreatment-related posttraumatic stress disorder: a
sociodemographically matched study. Biol. Psychiatry
52, 1066–1078 (2002).
86. DelBello, M. P., Zimmerman, M. E., Mills, N. P., Getz,
G. E. & Strakowski, S. M. Magnetic resonance imaging
analysis of amygdala and other subcortical brain
regions in adolescents with bipolar disorder. Bipolar
Disord. 6, 43–52 (2004).
87. Thomas, K. M. et al. Amygdala response to fearful
faces in anxious and depressed children. Arch. Gen.
Psychiatry 58, 1057–1063 (2001).
88. Monk, C. S. et al. Adolescent immaturity in attention-
related brain engagement to emotional facial
expressions. Neuroimage 20, 420–428 (2003).
89. Angold, A. & Costello, E. J. Puberty and depression.
Child Adolesc. Psychiatr. Clin. N. Am. 15, 919–937
90. Hayward, C. & Sanborn, K. Puberty and the
emergence of gender differences in psychopathology.
J. Adolesc. Health 30 (4 Suppl.), 49–58 (2002).
91. Patton, G. C. et al. Menarche and the onset of
depression and anxiety in Victoria, Australia.
J. Epidemiol. Community Health 50, 661–666 (1996).
92. Shen, H. et al. Reversal of neurosteroid effects at
α4β2δ GABAA receptors triggers anxiety at puberty.
Nature Neurosci. 10, 469–477 (2007).
93. Shaw, P. et al. Intellectual ability and cortical
development in children and adolescents. Nature 440,
94. Wallace, G. L. et al. A pediatric twin study of brain
morphometry. J. Child Psychol. Psychiatry 47,
95. Schmitt, J. E. et al. A multivariate analysis of
neuroanatomic relationships in a genetically informative
pediatric sample. Neuroimage 35, 70–82 (2007).
96. Pausova, Z. et al. Genes, maternal smoking, and the
offspring brain and body during adolescence: design
of the Saguenay Youth Study. Hum. Brain Mapp. 28,
97. Sisk, C. L. & Foster, D. L. The neural basis of puberty
and adolescence. Nature Neurosci. 7, 1040–1047
98. Shen, D. et al. Automated morphometric study of
brain variation in XXY males. Neuroimage 23,
99. Giedd, J. N. et al. Puberty-related influences on brain
development. Mol. Cell. Endocrinol. 254–255,
100. Ernst, M. & Mueller, S. C. The adolescent brain:
insights from functional neuroimaging research. Dev.
Neurobiol. 68, 729–743 (2008).
101. Manganas, L. N. et al. Magnetic resonance
spectroscopy identifies neural progenitor cells in the
live human brain. Science 318, 980–985 (2007).
102. Steinberg, L. Cognitive and affective development in
adolescence. Trends Cogn. Sci. 9, 69–74 (2005).
103. Arguello, P. A. & Gogos, J. A. Modeling madness in
mice: one piece at a time. Neuron 52, 179–196
104. Hursh, J. Conduction velocity and diameter of nerve
fibers. Am. J. Physiol. 127, 131–139 (1939).
105. Rushton, W. A. A theory of the effects of fibre size in
medullated nerve. J. Physiol. 115, 101–122 (1951).
106. Schmidt-Nielson, K. Animal Physiology: Adaptation
and Environment 5th edn (Cambridge Univ. Press,
107. Eickhoff, S. B., Schleicher, A., Scheperjans, F.,
Palomero-Gallagher, N. & Zilles, K. Analysis of
neurotransmitter receptor distribution patterns in the
cerebral cortex. Neuroimage 34, 1317–1330 (2007).
108. Zilles, K., Palomero-Gallagher, N. & Schleicher, A.
Transmitter receptors and functional anatomy of the
cerebral cortex. J. Anat. 205, 417–432 (2004).
109. Chugani, H. T., Phelps, M. E. & Mazziotta, J. C. Positron-
emission tomography study of human brain functional
development. Ann. Neurol. 22, 487–497 (1987).
110. Huttenlocher, P. R. Synaptic density in human frontal
cortex - developmental changes and effects of aging.
Brain Res. 163, 195–205 (1979).
111. Rakic, P., Bourgeois, J. P. & Goldman-Rakic, P. S.
Synaptic development of the cerebral cortex:
implications for learning, memory, and mental illness.
Prog. Brain Res. 102, 227–243 (1994).
112. Kessler, R. C. & Wang, P. S. The descriptive
epidemiology of commonly occurring mental disorders
in the United States. Annu. Rev. Public Health 29,
The authors’ work is supported by the Canadian Institutes of
Health Research (T.P.), the Royal Society, UK (T.P.) and the US
National Institutes of Health (T.P., K.M. and J.N.G.).
DRD1 | DRD2
tomáš Paus’s homepage:
Matcheri Keshavan’s homepage:
Jay Giedd’s homepage:
All links Are Active in the online pdF
SCiEnCE AnD SoCiETY
science and ethics of ADHD
Abstract | What is attention-deficit hyperactivity disorder (ADHD)? Why are so
many children being diagnosed with ADHD and prescribed medication? Are
stimulant drugs an effective and safe treatment strategy? This article explores the
current state of scientific research into ADHD and the key social and ethical
concerns that are emerging from the sharp rise in the number of diagnoses and the
use of stimulant drug treatments in children. collaborations among scientists,
social scientists and ethicists are likely to be the most promising route to
understanding what ADHD is and what stimulant drugs do.
Attention-deficit hyperactivity disorder
(ADHD) is one of the most common child-
hood psychiatric disorders in the world1. Its
core symptoms are inattention, hyperactivity
and impulsiveness. Most children are first
diagnosed with ADHD when they reach
school age2 and approximately 75% of those
diagnosed are male3. The most common
forms of treatment for ADHD are the
stimulants methylphenidate and
Rising rates of ADHD diagnosis and
stimulant drug use in children have led
to a public debate over the validity of
the diagnosis, the root causes of ADHD
and the ethics of treating children with
psychotropic drugs. There are three par-
tially overlapping positions in the debate.
First, that ADHD is primarily caused by
a combination of biological factors. From
this perspective, diagnosis is valid and drug
treatment is justified because it corrects
an underlying neurochemical imbalance
that affects cognitive and motor functions.
Second, that ADHD is caused by a combi-
nation of biological and social factors; the
diagnosis does not yet adequately capture
the heterogeneity and complexity of the
disorder. This perspective accepts the utility
of stimulant drug medication, but some
nATURe ReVIeWS | neuroscience
VOLUMe 9 | DeceMBeR 2008 | 957
Nature Reviews | Neuroscience
N = 579
defiant disorder 40%
proponents are sceptical of the widespread
use of psychotropic drug treatments over
other interventions, such as behavioural
therapies5. Third, that ADHD is a valid
disorder but its primary causes are
environmental (for example, maternal
smoking, lead exposure, food additives
and so on)6–8. This perspective views early
recognition, prevention of exposure, and
raising awareness about predisposing
environmental factors as ways to reduce
dependence on stimulant medications9.
Any one of these positions involves a var-
iety of stakeholders: parents, teachers, clini-
cians, scientists, regulators, social scientists,
ethicists and children themselves. There
is a fourth position, which is sceptical that
ADHD is a real disorder. This position is
sometimes identified with scientologists,
but it is also represented by a separate, and
more thoughtful, sociological critique10,11.
In the past decade, scientific research has
focused on strengthening the first position,
with an emphasis on identifying primary
genetic causes of ADHD4. More-recent
evidence, however, suggests that complex
psychiatric disorders are mediated by a com-
bination of genetic and environmental fac-
tors4,12,13. Scientific research into the complex
and potentially multiple aetiologies of ADHD
is still in early stages14; however, it is attract-
ing a lot of attention as ADHD becomes a
global phenomenon: in the past decade rates
of diagnosis have increased sharply in most
countries around the world15. These increases
are linked to parallel growth in the
consumption of stimulant medications16. A
better scientific understanding of the aetiol-
ogy of ADHD might clarify whether the
growing number of school-age children that
are being diagnosed with ADHD and taking
stimulant drugs represents over-diagnosis and
overuse of stimulant treatments or an actual
increase in ADHD prevalence4,17.
Growing scientific evidence suggests that
ADHD cannot be explained by genetic or
environmental factors alone. Research that
integrates social and scientific perspectives
is likely to achieve a more complete explana-
tion. This article reviews the scientific and
social debates over ADHD and identifies key
areas in which social investigations should
be integrated with scientific research to gen-
erate richer models of the causes of ADHD
and better understanding of the validity of
the diagnosis. The ethics of ADHD diagno-
sis in children are also discussed, in order to
outline areas in which ethical analysis can
contribute to an understanding of the rela-
tive risks and benefits of ADHD diagnosis
and treatment approaches.
ADHD is characterized by a cluster of
behavioural symptoms that are considered
separate from, but highly correlated with,
other childhood psychiatric conditions, such
as conduct disorder and oppositional defiant
disorder18. The relationship between high
levels of co-morbidity (FIG. 1) and underlying
genetic factors is unclear12.
Two definitions are currently used in the
diagnosis of ADHD. American psychiatrists
follow the ADHD diagnosis described in the
Diagnostic and Statistical Manual of Mental
Disorders, 4th Edition (DSM-IV)19. DSM-IV
describes two primary categories of behav-
ioural symptoms: inattention and impul-
sivity–hyperactivity; and three subtypes of
ADHD: inattentive type, hyperactive–
impulsive type, and combined. The World
Health Organization’s manual, the
International Classification of Diseases,
10th edition (IcD-10) calls the condition
Hyperkinetic Disorder (HKD or HD)20.
ADHD and HD symptoms are very similar;
however, IcD-10 requires all three symptoms
— hyperactivity, inattention and impulsivity
— to be present for a diagnosis to be made.
A full diagnostic assessment for ADHD
should include an evaluation of the symptoms’
pervasiveness, duration, resultant impair-
ment and age of onset. Studies have found
that a diagnosis of ADHD is 3–4 times more
likely if DSM-IV criteria are used than if
IcD-10 criteria are used21,22. This is thought
to be due to the emphasis on impairment in
the IcD-10 diagnosis, the fact that IcD-10
requires more symptoms of the disorder
to be more pervasively present and the
fact that IcD-10 does not allow HKD to
be co-morbid with other child psychiatric
Although both the IcD-10 and the
DSM-IV diagnoses are reliable25,
neither DSM-IV nor IcD-10 captures the
phenotypic heterogeneity that is seen in
clinical contexts where ADHD is diagnosed.
This is because both manuals use a categori-
cal, rather than a dimensional, system of
classifying symptoms and making a
diagnosis12. categorical diagnosis requires
a hard distinction between normal and
pathological symptoms. This is in contrast
to classifying symptoms along a continuum,
or a dimensional spectrum, from normal to
dysfunctional. Both manuals are currently
under review and new editions will emerge
in the next few years. There is much
discussion over the possibility of moving
from categorical to dimensional diagnoses
in the next DSM26.
In addition to the complex descriptions
that are used to classify ADHD behaviours,
there are different methods for diagnosing
ADHD, especially in the United States27.
These range from child behaviour checklists
that elicit information from multiple sources
(such as the Connors Parent/Teacher Rating
Scales) to parent interviews28. In the United
States, the mental-health-related expertise of
the diagnosing clinician can vary consider-
ably (it is possible to obtain a diagnosis of
ADHD from primary-care physicians (gen-
eral practitioners), nurses, paediatricians,
psychiatrists and neurologists28), whereas
in most of europe, initial evaluations for
ADHD are usually performed in a specialist
Given the differences in diagnosing ADHD
described above, it is not surprising that
ADHD prevalence rates vary widely both
within and across countries. A recent meta-
analysis of ADHD prevalence rates by geo-
graphic region suggests that South American
countries have the highest prevalence (11.8%
of school-age children) and european coun-
tries have the lowest prevalence (4.6%)23.
Within-country estimates, based on indi-
vidual studies, show even greater variation:
Figure 1 | co-occurring disorders in the Multi-
modal treatment study of children with
Adhd. Participants in the National Institute of
Mental Health Multimodal Treatment study for
attention-deficit hyperactivity disorder (ADHD)
reflect the complex mental-health profiles of Us
children with ADHD. Only a third of the children
in the study had a diagnosis of ADHD alone. More
than half of the children had conduct or opposi-
tional defiant diagnoses in addition to having
ADHD, and a significant proportion of those with
conduct and oppositional diagnoses also had an
anxiety disorder. Figure modified, with permis-
sion, from REF. 18 (2001) Lippincott Williams &
958 | DeceMBeR 2008 | VOLUMe 9
Daily doses per 1000 inhabitants
US prevalence estimates vary from 2% to
18% of school-age children19; UK prevalence
estimates vary from 0.5% to 26% of school-
age children29–32. These variations could be
due to the use of different sources of evi-
dence — for example, diagnosis of a random
sample of school-age children or a survey of
paediatricians — which complicates a direct
comparison of the estimates.
More reliable information is available
on national and international increases in
ADHD diagnoses. These figures are extrapo-
lated from the growth in international
use of stimulant drugs — which are used
almost exclusively to treat ADHD (FIG. 2).
economists have found that in the past
decade, increases in the use of ADHD medi-
cations in non-US OecD (Organization for
economic cooperation and Development)
countries have surpassed rates of increase
in the United States15. The United States still
spends more money than all other countries
— 83% of the global market share — on
ADHD medications, but rates of increase
in US spending on ADHD medications can
be explained by the shift to more-expensive,
long-acting formulations such as concerta
(Alza corporation)15. In developing-world
nations, increases in annual use and spend-
ing on ADHD medications are greater
than 20%15. Thus, as some economists have
stated, “understanding determinants of use
of ADHD medications, and their costs, and
their potential risks and benefits, is now a
global issue” (REF. 15).
State of the science of ADHD
The social, clinical and behavioural com-
plexities of ADHD create enormous chal-
lenges for scientific research. Rather than
looking for discrete causal factors in ADHD,
investigations are increasingly focused
on identifying complex developmental
pathways that link genetic, biological and
environmental risk factors to phenotypic
expression in multiple different
Genetic factors in ADHD. Genome-wide
association studies have been largely
inconclusive, although one study has found
weak associations between variants of
the dopamine transporter (DAT) and the
dopamine receptor DRD4 and ADHD36.
Although these findings have been repli-
cated for several genes, overall results are
variable and reported effect sizes are small37.
Variations in the serotonin transporter gene
have also been implicated in susceptibility
to ADHD, although the role of serotonin in
ADHD is not well understood38.
The variability in findings and lack of
replication is presumed to be due at least
in part to diagnostic heterogeneity. To
address this problem, researchers have
begun to target measurable intermediary
neuro biological components (endopheno-
types), such as the dopamine system39. The
goal of identifying valid endophenotypes is
to increase the power of genetic research to
determine susceptibility genes for ADHD12.
When integrated into complex models of
neurodevelop mental pathways associated
with ADHD, genetic risks for ADHD could
theoretically inform ADHD diagnosis and
contribute to improved treatment
Neurobiology of ADHD. The well-established
dopamine theory of ADHD suggests that
dysfunctions in the dopamine neurotrans-
mitter system interfere with proper function-
ing in key neuropsychologic domains, such
as attention and motivation4,33. Thus, puta-
tive neuropsychological endophenotypes are
largely focused on executive-function defi-
cits that involve the dopamine system35. It is
unlikely, however, that executive-function
deficits are necessary or sufficient for
expression of the disorder14,40, and it is
unlikely that the dopamine system is
uniquely implicated in ADHD41. Studies in
animal models have shown that the neuro-
adrenergic and serotonergic neurotransmit-
ter systems are also affected by stimulant
drug treatments42. Animal models also con-
firm the hetero geneous origins of ADHD, as
animals with substantively different neural
defects model the behavioural symptoms
of ADHD42. eventually, neuro psychologic
heterogeneity is expected to identify distinct
subtypes of ADHD, which could shift
diagnostic attention from symptoms to
Neuroimaging findings in ADHD. A network
of distributed brain regions is thought to be
involved in attention, cognition and behav-
ioural self-regulation43. Indeed, structural
neuroimaging studies in ADHD research
suggest that patients have widespread ana-
tomical differences from controls; smaller
volumes in the dorsolateral prefrontal cortex,
the caudate nucleus, the corpus callosum
and the cerebellum have been reported44.
Functional neuroimaging studies predomi-
nantly using positron emission tomography
(PeT) and functional MRI (fMRI) support
the involvement of frontostriatal abnor-
malities (particularly in the dorsal anterior
cingulate cortex, the lateral prefrontal cortex
and the striatum) in ADHD45. The study of
neurobiological endophenotypes in ADHD
has led to a better understanding of the rela-
tionship between structural and functional
abnormalities in ADHD. Dopamine deficits
are thought to have a role in the anatomical
and functional differences observed in
dopamine-related brain areas, including
the caudate nucleus, the globus pallidus, the
corpus callosum and the cerebellum vermis46.
Volumetric and anatomical differences
in brain areas are integral to comprehensive
models of ADHD pathophysiology, and
they could theoretically be used to inform
Figure 2 | Worldwide consumption of methylphenidate. In 2003, Iceland and the United states
had the highest per capita consumption of methylphenidate in the world. Growth in consumption
between 1999 and 2003 was highest in european countries. The only country in which methylpheni-
date consumption decreased during this period was Israel. Figure reproduced, with permission, from
REF.115 (2005) International Narcotics Board.
nATURe ReVIeWS | neuroscience
VOLUMe 9 | DeceMBeR 2008 | 959
neuroimaging biomarkers of ADHD. Such
biomarkers could eventually become part
of a comprehensive clinical evaluation for
ADHD45. At present, however, both struc-
tural and functional neuroimaging data on
ADHD are inconclusive, owing in part to the
use of different imaging technologies across
studies and to a lack of adolescent and adult
data44. In addition, most imaging studies of
ADHD are underpowered, using samples
of fewer than 20 subjects per group44.
Treatment of ADHD
Despite the complexity of ADHD diagnosis,
there are effective treatments for children
that have been diagnosed with ADHD. In
the United States and increasingly in europe,
psychostimulants are first-line treatments for
the disorder. These drugs have been shown
to be more effective at treating ADHD
symptoms than behavioural therapy alone,
and also more effective than behavioural
therapy combined with drug treatment18.
Stimulants have been used to treat behaviour
problems in children since the 1950s. In
the 1970s, researchers showed that a posi-
tive response to stimulants is not limited
to children with ADHD: ‘normal’ children
show improvements in attention and focus
as well47. Therefore, to some degree, the
medications enhance performance rather
than treating the specific psychopathology.
How stimulants improve focus, atten-
tion and impulsive behaviour is still poorly
understood. They are generally thought to
affect brain sites associated with attention and
impulse control, including the prefrontal
cortex, the striatum and the cerebellar
vermis48–50. Psychostimulant action is closely
associated with the dopamine and noradren-
aline systems: they bind preferentially to
dopamine transporters to prevent dopamine
reuptake into presynaptic nerve endings51,52.
Both the dopamine and the noradrenaline
systems are implicated in cognitive deficits
that are related to ADHD, such as poor work-
ing memory and the inability to appropriately
inhibit responses33. In the future, pharmaco-
fMRI studies could be used to correlate neural
activity during cognitive tasks to medication
effects and, potentially, to tailor specific drug
treatments to the particular patient33.
Stimulants are administered in long- or
short-acting forms; most children now use
the long-acting forms, with effects that
last 8–10 hours. Although stimulant use is
associated with short-term improvements
on cognitive tasks, prolonged use has not
been found to be associated with long-term
improvements in academic achievement
when compared with baseline
Stimulant drug treatment for children
was long considered to be relatively safe55.
common side effects are usually mild, and
include appetite suppression and insomnia.
Recently, however, more-serious side
effects have led to new US Food and Drug
Administration (FDA) warnings. Since
February 2007 all FDA-approved drug treat-
ments for ADHD (methylphenidate, dexam-
phetamine and atomoxetine) have carried
a warning that their use can involve risk for
cardiovascular effects, growth suppression
and the development of psychosis or other
psychiatric conditions. Rare cases of sudden
death have been reported among children
using stimulant medications for ADHD. The
FDA warns that the use of these medications
by children with heart conditions should be
avoided or undertaken with great caution56.
The debate over ADHD and stimulant drugs
The global rise in ADHD diagnosis in
children and the increasing rates of stimu-
lant prescription have led to a vigorous,
often polemic, debate over the validity of
the ADHD diagnosis and the justification
for drug treatment. This divisive debate
no longer accurately reflects the state of
scientific understanding of ADHD, which
highlights the complexity and heterogeneity
of the disorder. The remainder of this article
focuses on long-standing social and ethical
concerns over ADHD and highlights areas of
potentially productive intersection between
these concerns and the goals of scientific
The validity of diagnosis
Diagnoses of psychiatric disorders are con-
troversial because they are based on clinical
assessment of behavioural symptoms:
there are no laboratory tests to determine
unequivocally whether a subject has the
disorder. In the case of ADHD, this problem
is exacerbated by the fact that ADHD symp-
toms are difficult to distinguish from normal
childhood behaviours41. As long as there is
no clear and indisputable scientific rationale
for the growing rates of ADHD diagnosis
and treatment in children4, the validity of
ADHD diagnosis will continue to come
under social and ethical scrutiny.
One school of thought argues that the
diagnosis is frequently used to serve social
or cultural purposes, such as bringing devi-
ant or socially undesirable behaviour under
medical surveillance and control57. Higher
than average ADHD prevalence rates in the
United States have been used to support
claims that ADHD is a product of Western
culture58. These arguments, which highlight
the ways in which ADHD diagnosis and
prevalence rates might reflect social and cul-
tural biases, are not necessarily in opposition
to the notion that ADHD is a real illness59.
The ‘science side’ of the debate over
ADHD diagnosis has tended to respond to
diagnostic-validity challenges by asserting
that ADHD is, in fact, a bona fide mental
disorder60 and by avoiding discussion of its
problematics, including the potential social
and cultural biases61 (see also BOX 1). This
is an ethical problem in so far as clarity
about the state of the science with regards
to the ADHD diagnosis is part of scientists’
responsibility to the public. It is also a posi-
tion that treats ADHD diagnosis as though
it were a concrete representation of disorder,
rather than an abstract approximation.
Thus, opportunities to combine scientific
and social expertise to work towards more-
accurate diagnoses and diagnostic methods
Social scientists and scientists can work
together in two areas that are currently prob-
lematic in ADHD diagnosis: standardization
and consistency. A number of authoritative
groups, including the American Association
of Pediatrics (AAP), the UK national
Institute of clinical excellence (nIce) and
the european network on Hyperkinetic
Disorders (eunethydis), are engaged
in efforts to standardize diagnoses62–64.
Implementing standardized diagnoses poses
challenges that are best addressed through a
combination of qualitative and quantitative
social analyses65. Implementation strategies
will need to be sensitive to social and indi-
A childhood behaviour disorder characterized by
persistent aggressive or anti-social behaviour that disrupts
the child’s environment and impairs his or her functioning.
Connors Parent/Teacher Rating Scales
Rating scales that are used to check for symptoms of
ADHD. Ideally they are filled out by both teachers
and parents to assist in measuring a child’s behaviour and
comparing it with that of other children of the same age.
Sets of rigid beliefs about social roles, behaviours, activities
and styles of self-presentation that are associated with
A pervasive, often unconscious, set of cultural beliefs and
prescriptions about what constitutes good mothering
and a good mother.
Oppositional defiant disorder
A childhood behaviour disorder characterized by a
persistent pattern of negative, hostile or defiant behaviour
that impairs the child’s social and academic functioning.
960 | DeceMBeR 2008 | VOLUMe 9
vidual variables that influence the uptake of
practice innovations and the translation
of evidence-based medicine into practice.
These variables can be either constraining
or adaptive66 and are dependent in part on
the nature, beliefs and practices of healthcare
organizations, the authority with which the
directive to innovate is communicated, the
behaviour and beliefs of individuals in the
organization, and the type of facilitation that
is required to enable the change process67,68.
Anticipation and analysis of potential
barriers to diagnostic standardization will be
likely to expedite implementation. However,
the research that is available is based largely
on Anglo-American data; little is known
about relevant institutional, social and indi-
vidual practices in other national contexts —
particularly in the developing world, where
rates of ADHD diagnoses are increasing.
exploratory qualitative studies could build
relevant social theory that would guide cul-
turally sensitive implementation strategies.
The effectiveness of these strategies and their
regional, national and international impact
would require assessment using standard-
ized outcome variables. Similarly, social-
science–science research collaborations
that focus on regional variations in ADHD
diagnoses have the potential to illuminate
the problem of inconsistency in ADHD
diagnoses within particular populations.
Regional and global variations in ADHD
diagnosis suggest that a distinction should
be made between the causes of ADHD and
the causes of over- and under-diagnosis of
ADHD. Although there is little systematic
understanding of this latter problem, it is
clear that there are important social influ-
ences. Some of these are well established,
including demographic factors, such as
ethnicity, education level and socioeconomic
status69–71; practitioner factors72; and geo-
graphic factors, including access to
psychiatric services70,73. The influence of
other social factors in ADHD diagnosis
— including community factors, such as
pressure within and pressure on schools3,74,
and family factors, such as parental expecta-
tions75 — is under-researched. cultural
trends, such as mothering ideology and
masculinity stereotypes, have also been pro-
posed to influence rates of ADHD diagno-
sis76–78. Data on these influences are derived
from studies using a variety of methodologi-
cal approaches, and thus the relative impact
of these factors is difficult to assess.
Macrosocial analyses, focusing on broad
national, state or regional factors, are also
being carried out to investigate the impact
of national policies and programmes on
ADHD diagnosis. In the United States, for
example, state and federal policies arguably
have a significant effect on the rates of
ADHD diagnosis. The US Individuals with
Disabilities Act (IDeA) provides a child
who has ADHD with additional educational
resources, which potentially benefits both
the child and their teacher79. The US man-
aged healthcare system can also be seen as
an important factor in psychiatric diagnoses.
Managed care encourages categorical diag-
noses and quick, cheap treatments — drugs
rather than behavioural therapy80. Finally,
the US pharmaceutical industry can also
influence ADHD diagnoses by marketing
drugs directly to the public through
direct-to-consumer (DTc) advertising81.
Further analysis of macro- and micro-
social factors (such as school, family and
community influences) in ADHD diagnosis
can contribute substantially to the scientific
problem of standardization and consistency
in ADHD diagnosis. Resolution of these
problems will have important clinical and
scientific implications. From a clinical per-
spective, children with significant needs will
be more likely to be identified and properly
treated. From a research perspective, mini-
mizing phenotypic variation across genetic
studies is likely to enable more successful
investigations into the genetic causes of
ADHD. Indeed, some researchers argue that
poor and inconsistent diagnoses of
psychiatric disorders might explain much of
the past failure of genetic-association studies82.
identifying risk factors in ADHD
As the importance of environmental factors
in determining ADHD outcomes becomes
clearer, scientific and social science expertise
can fruitfully intersect in planned prospec-
tive studies of ADHD. In order to access the
large samples that are required to detect
the complex influences of environmental
factors and gene–environment interactions
in ADHD, future research is likely to draw
on data from large national birth cohort
studies, such as the planned US national
children’s Study (ncS). By engaging a
multidisciplinary research team and by
developing innovative qualitative and
quantitative research methods to concep-
tualize environmental risk and protective
factors, test social and scientific hypotheses
and track ADHD phenotypes over time, it
should be possible to gain further
understanding of the risk factors for ADHD.
This type of approach should also allow the
design of interventions that are focused on
environmental risk and protective factors in
a specified sub-sample.
However, there are also ethical issues in
identifying individual and social risk factors
for ADHD. The identification of environ-
mental and genetic risks at the individual
and societal level and the implementation of
Box 1 | History of ADHD
To defend the validity of attention‑deficit
hyperactivity disorder (ADHD), scientists
occasionally draw on forms of evidence that
have popular appeal but that are unfortunately
palpably unscientific. For example, the National
Institute of Mental Health webpage on ADHD
opens with a historical narrative about the first
descriptions of ADHD, attributed to Dr Heinrich
Hoffman in 1845 and Sir George Still in 1902.
This story of the origin of ADHD diagnosis is
repeated in countless articles, books and
websites and is used as evidence that the
contemporary ADHD diagnosis is ‘real’ — in
effect proposing that if the diagnosis is old it must be real. This conclusion is neither logical nor
scientific. Moreover, Hoffman and Still were not actually describing ADHD as the diagnosis did not
exist at the time. Both physicians describe behaviours in children that overlap with the symptom
cluster that defines contemporary ADHD. Hoffman understood these behaviours to be sufficiently
common (that is, not abnormal) that he depicted them in a macabre illustrated children’s book that
has been a bestseller for generations (see figure)103. His popular character, Fidgety Phil (Zappel
Philipp), has warned generations of children about the consequences of fidgeting at the table. Still
attributed the behaviours he observed to “a lack of moral control” in children, an interpretation
that was aligned with contemporary eugenic theories about individuals who were ‘moral
defectives’ by virtue of heredity104–106. Neither Hoffman’s nor Still’s descriptions provide any
empirical evidence for the validity of ADHD; paradoxically, they do provide evidence that the
interpretation and classification of behaviour is culturally and historically embedded. Figure
reproduced, with permission, from REF.103 (2006) Belitha Press.
nATURe ReVIeWS | neuroscience
VOLUMe 9 | DeceMBeR 2008 | 961