Seminar1240 www.thelancet.com Vol 387 March 19, 2016.docx

Seminar
1240 www.thelancet.com Vol 387 March 19, 2016
Attention defi cit hyperactivity disorder
Anita Thapar, Miriam Cooper
Attention defi cit hyperactivity disorder (ADHD) is a
childhood-onset neurodevelopmental disorder with a prevalence
of 1·4–3·0%. It is more common in boys than girls. Comorbidity
with childhood-onset neurodevelopmental
disorders and psychiatric disorders is substantial. ADHD is
highly heritable and multifactorial; multiple genes and
non-inherited factors contribute to the disorder. Prenatal and
perinatal factors have been implicated as risks, but
defi nite causes remain unknown. Most guidelines recommend a
stepwise approach to treatment, beginning with
non-drug interventions and then moving to pharmacological
treatment in those most severely aff ected. Randomised
controlled trials show short-term benefi ts of stimulant
medication and atomoxetine. Meta-analyses of blinded trials
of non-drug treatments have not yet proven the effi cacy of
such interventions. Longitudinal studies of ADHD show
heightened risk of multiple mental health and social diffi
culties as well as premature mortality in adult life.
Introduction
Attention defi cit hyperactivity disorder (ADHD) is a
childhood-onset neurodevelopmental disorder char ac-
terised by developmentally inappropriate and impairing
inattention, motor hyperactivity, and impulsivity, with
diffi culties often continuing into adulthood. In this

Seminar, we aim to update and inform early career
clinicians on issues relevant to clinical practice and
discuss some controversies and misunderstandings.
Defi nitions of ADHD
ADHD is a diagnostic category in the American
Psychiatric Association’s Diagnostic and Statistical
Manual of Mental Disorders 4th edition (DSM-IV)1 and
the more recent DSM-5.2 The broadly equivalent
diagnosis used predominantly in Europe is hyperkinetic
disorder, which is defi ned in WHO’s International
Classifi cation of Diseases (10th edition; ICD-10).3 This
defi nition captures a more severely aff ected group of
individuals, since reported prevalence of hyperkinetic
disorder is lower than that of DSM-IV ADHD, even
within the same population.4 Key diagnostic criteria are
listed in the panel. DSM-5 has longer symptom
descriptors than those used in DSM-IV; these descriptors
also capture how symptoms can manifest in older
adolescents and adults. DSM-IV distinguished between
inattentive, hyperactive–impulsive, and combined sub-
types of ADHD; a diagnosis of the combined subtype
required the presence of symptoms across the domains
of inattention and hyperactivity–impulsivity. However,
ADHD subtypes are not stable across time,5 and DSM-5
has de-emphasised their distinctions. ICD-10 does not
distinguish subtypes; symptoms need to be present from
the three separate domains of inattention, hyperactivity,
and impulsivity for a diagnosis of hyperkinetic disorder.
The diagnosis of ADHD or hyperkinetic disorder also
requires the presence of symptoms across more than
one setting (eg, home and school) and requires that the
symptoms needed for diagnosis result in impairment,
for example in academic, social, or occupational

functioning. Onset must be early, although DSM-5 has
changed the age of onset from before age 7 years (ICD-10
and DSM-IV) to before age 12 years.
Like all complex medical and psychiatric disorders,
ADHD shows marked heterogeneity at clinical,
aetiological, and pathophysiological levels. Individuals
with a diagnosis of ADHD diff er from each other in
terms of their core symptom combinations, level of
impairment and comorbidities, as well as on other
background individual, family, and social factors.
For clinical purposes, defi ning ADHD categorically is
useful given that clinical decisions tend to be categorical
in nature—eg, whether to refer to specialist services or to
treat. However, like many medical disorders (such as
hypertension and diabetes), in terms of causes and
outcomes, ADHD can be viewed as a continuously
distributed risk dimension. In common with other
continuously distributed phenotypes (eg, blood pressure),
it could be argued that there is a lack of an objective
cut-point that defi nes the diagnostic threshold.
Indeed, individuals with subthreshold symptoms are at
heightened risk of adverse outcomes6 (as is seen in
hypertension). However, ultimately, categorical decisions
on resource allocation and treatment have to be made,
Lancet 2016; 387: 1240–50
Published Online
September 17, 2015
http://dx.doi.org/10.1016/
S0140-6736(15)00238-X
Child & Adolescent Psychiatry

Section, Institute of
Psychological Medicine and
Clinical Neurosciences, and
MRC Centre for
Neuropsychiatric Genetics and
Genomics, Cardiff University
School of Medicine, Cardiff , UK
(Prof A Thapar FRPsych,
M Cooper MRCPsych)
Correspondence to:
Prof Anita Thapar, Institute of
Psychological Medicine and
Clinical Neurosciences, Cardiff
University School of Medicine,
Hadyn Ellis Building, Maindy
Road, Cathays, Cardiff
CF24 4HQ, UK
[email protected] .ac.uk
Search strategy and selection criteria
To identify studies for this Seminar, we searched PubMed for
papers published between Jan 1, 2010, and March 31, 2015,
using the search terms “ADHD”, “aetiology”, “epidemiology”,
“prevalence”, “gender”, “time trends”, “prescribing”, “genetic”,
“prenatal”, “psychosocial”, “toxins”, “institutional rearing”,
“longitudinal”, “prognosis”, “animal model”, “biological

pathway”, “cognition”, “neuroimaging”, “comorbidity”,
“neuropsychological”, “medication”, “stimulants”,
“behavioural interventions”, “nonpharmacological
interventions”, “diet”, and “outcomes”. Only articles published
in English were included. Key recent reviews and book
chapters were also examined. To reduce the number of papers
cited, the most up-to-date review papers and meta-analyses
were used where possible. We selected papers according to our
judgment of the quality of the study or review paper, the
relevance to controversial or commonly misunderstood
issues, and whether fi ndings had clinical relevance.
We included older papers that we judged to be important.
http://crossmark.crossref.org/dialog/?doi=10.1016/S0140-
6736(15)00238-X&domain=pdf
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www.thelancet.com Vol 387 March 19, 2016 1241
and ICD-defi ned or DSM-defi ned diagnosis provides a
reliable way of balancing the risks and benefi ts of giving
an individual a diagnostic label and providing treatments
that are not free of adverse eff ects. A further challenge,
which occurs in all psychiatric disorders and some
neurological disorders (eg, migraine), comes from the
diagnosis being based on reported symptoms alone;
there are no biological tests. This diffi culty means that
even with clear-cut diagnostic criteria, there is potential
risk of overdiagnosis and underdiagnosis, which
underscores the importance of careful and rigorous
expert assessment.7 Concerns about underdiagnosis and
overdiagnosis are not restricted to ADHD or psychiatric
disorders.8

Epidemiology
In the general population, the estimated prevalence of
ADHD in children is 3·4% (95% CI 2·6–4·5) according
to the most recent meta-analysis,9 with lower rates of
around 1·4% reported for hyperkinetic disorder from
European studies.10 International comparisons show
that prevalence does not vary by geographical location
but is aff ected by heterogeneity in assessment methods
(eg, use of an additional informant to the parent or
carer) and diagnostic conventions (eg, ICD vs DSM).11
Notably, there is a marked under-representation of
studies on ADHD from low-income and middle-income
countries.
One common assumption is that ADHD must be a
modern occurrence. However, a case series of children
presenting with the characteristic clinical features was
published by the British paediatrician Sir George Still in
The Lancet in 1902,12 and there are descriptions that
pre-date this publication by several centuries. Time
trends studies of non-referred population cohorts in the
late 20th and early 21st centuries show no evidence of a
rise in rates of ADHD symptoms or diagnosis across
time.13,14 However, there has been a very marked rise in
the number of prescriptions issued for ADHD pharma-
cological treatment across high-income countries in the
past decade.15–17 Rises in clinic incidence and treatment
could simply indicate increased parent and teacher
awareness of ADHD or changes in the impact of
symptoms on children’s functioning, or both.18,19 Never-
theless, European studies have repeatedly reported that
despite the rise in ADHD treatment, the admin is trative
prevalence is lower than the population fi gure,
highlighting that in these countries there is still
underdiagnosis.17,20,21 However, in the USA, similar types
of studies show geographical variation in patterns

of underdiagnosis and overdiagnosis or in ADHD
medication prescribing.22,23 Such fi ndings highlight that
there is the potential for misdiagnosis and inappropriate
use of pharmacological interventions if safeguards are
not in place. These safeguards include ensuring full,
good-quality clinical assessments are undertaken, even
though these require time, and adherence to national
and international treatment guidelines. However, there
is no evidence of rising population rates of ADHD
explained by social change, contrary to the opinion of
some people.
An excess of aff ected male individuals is a strongly
consistent epidemiological fi nding, although the
male:female ratio of 3–4:1 recorded in epidemiological
samples is increased in clinic populations to around 7–8:1,
suggesting referral bias in relation to female patients with
ADHD.24 The same male preponderance is seen for other
neurodevelopmental disorders such as autism spectrum
disorder, intellectual disability (intelligence quotient [IQ ]
<70), and communication disorders.25
The natural history of ADHD is best examined in
prospective longitudinal studies. As is typical of
neurodevelopmental disorders, the core defi ning features
of ADHD tend to decline with age, although inattentive
features are more likely to persist. However, in line with its
heterogeneous clinical presentation, the develop mental
trajectories of ADHD are highly variable. Although
around 65% of patients continue to meet full criteria or
have achieved only partial remission by adulthood, some
patients do achieve full remission.26 Good-quality, large
epidemiological studies of the prevalence of ADHD in
adulthood are lacking, but one meta-analysis of adult
ADHD yielded a pooled prevalence of 2·5% (95% CI

2·1–3·1).27 However, there are still uncertainties as to what
constitutes the best way of defi ning ADHD (or indeed any
Panel: Key diagnostic symptoms of attention defi cit
hyperactivity disorder2
Inattentive symptoms
• Does not give close attention to details or makes careless
mistakes
• Has diffi culty sustaining attention on tasks or play activities
• Does not seem to listen when directly spoken to
• Does not follow through on instructions and does not
fi nish schoolwork, chores, or duties in the workplace
• Has trouble organising tasks or activities
• Avoids, dislikes, or is reluctant to do tasks that need
sustained mental eff ort
• Loses things needed for tasks or activities
• Easily distracted
• Forgetful in daily activities
Hyperactivity or impulsivity symptoms
• Fidgets with or taps hands or feet, or squirms in seat
• Leaves seat in situations when staying seated is expected
• Runs about or climbs when not appropriate (may present
as feelings of restlessness in adolescents or adults)
• Unable to play or undertake leisure activities quietly
• “On the go”, acting as if “driven by a motor”
• Talks excessively
• Blurts out answers before a question has been fi nished
• Has diffi culty waiting his or her turn
• Interrupts or intrudes on others

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neurodevelopmental disorder) in adulthood. DSM-5
explicitly allows for symptom decline and requires a
reduced number of symptoms for diagnosis of adult
ADHD.2 In clinical settings, diagnosis of ADHD in adults
who did not present in childhood requires some caution
in the absence of documented information because of the
diffi culty for young adults and those who know them to
date symptom onset retrospectively.28 Objective records
(eg, school reports) could help in this regard. Despite
these caveats, there is certainly suffi cient evidence to
conclude that ADHD is not simply a problem that most
children grow out of. However, transitioning from child to
adult mental health clinics is diffi cult because of a scarcity
of adult services.29
Early comorbidity
ADHD shows high concurrent comorbidity with other
neurodevelopmental disorders—namely, autism spec-
trum disorder, communication and specifi c learning or
motor disorders (eg, reading disability, developmental
coordination disorder), intellectual disability, and tic
disorders.30–32 Unsurprisingly, rates of comorbidity are
higher in individuals who are clinically referred than in
those who are not referred.33 ADHD also shows high
concurrent comorbidity with behavioural problems—
namely, oppositional defi ant and conduct disorders.31,34
Conduct disorder is a risk marker for greater
neurocognitive impairment and worse prognosis in
children with ADHD.35,36 This subgroup of children
with hyperkinetic conduct disorder is distinguished in

ICD-10 but not in DSM-5.
Risk factors
Overview
As for all complex disorders, no single risk factor is either
necessary or suffi cient to explain ADHD—many genetic
and non-genetic (or environmental) factors contribute to
risk, and the pattern of inheritance is multifactorial for
most aff ected individuals.
Genetics
ADHD is a familial disorder. Its relative risk is about
5–9 in fi rst-degree relatives of probands with ADHD.37
Many twin studies of ADHD from diff erent countries
have consistently yielded very high heritability estimates
of about 76%, a magnitude similar to that reported for
schizophrenia and autism.38
The genetic architecture of ADHD is similar to other
neuropsychiatric disorders such as schizophrenia. Several
diff erent classes of genomic variants have been identifi ed
to be associated with ADHD risk.39 These variants include
common (defi ned as >5% population frequency) DNA
sequence variants called single nucleotide polymorphisms
(SNPs), but associations have only been reported when
thousands of SNPs are combined into a composite
genetic risk score.40 Subtle chromosomal mutations,
such as rare (defi ned as <1% frequency) deletions and
duplications called copy number variants (CNVs), are also
associated with ADHD risk.41 These have larger eff ect
sizes but are uncommon.
Before whole-genome investigations, specifi c single
dopaminergic, serotonergic, and noradrenergic candidate
genes were signifi cantly associated with ADHD status

in meta-analyses.42,43 However, in the present era of
whole-genome investigation, psychiatric candidate gene
studies of DNA variants in single genes are viewed with
caution because of the potential for false positives.44
ADHD-associated genomic variants are non-specifi c;
composite genetic risk scores show signifi cant overlap
with those contributing to schizophrenia and mood
disorders.45,46 ADHD-associated CNVs also show overlap
with ones associated with schizophrenia, autism, and
intellectual disability.41,47 Although testing for rare CNVs
is now recommended for individuals with intellectual
disability, this is not the case for ADHD. Ascertaining
causality requires further and diff erent types of
investigation, as reviewed elsewhere.39
Although most cases of ADHD are multifactorial in
origin, there are several known, rare genetic syndromes
(such as fragile X syndrome, tuberous sclerosis, 22q11
microdeletion, and Williams syndrome) characterised by
high rates of ADHD and ADHD-like features. These
syndromes are also associated with high risk of other
disorders, such as autism (especially in fragile
X syndrome and tuberous sclerosis) and schizophrenia
(22q11 microdeletion syndrome). In typical clinic
populations with ADHD, there is no evidence that
routine screening for these genetic syndromes is
warranted in the absence of intellectual disability.48
Environment and gene–environment interplay
Environmental factors are also known to be important in
ADHD. Because evidence for modifi able causes can
aff ect clinical decision making, public health priorities,
and clinician and patient behaviour,49 we will discuss
whether fi ndings on individual environmental risks
meet accepted standards for inferring causation.50

Observational case-control and epidemiological studies
show that exposures to a range of prenatal and perinatal
factors, environmental toxins, dietary factors, and psycho-
social factors are all associated with ADHD.38 If these
associations are causal, it means manipulation of the risk
factor can alter the outcome. However, association does
not mean causation, because exposures to risks are not
randomly allocated and can be aff ected by unmeasured
confounders, selection factors, and reverse causation,
whereby the phenotype infl uences the environmental
exposure. Evidence for environmental causation must be
interpreted with these caveats in mind.
Prenatal and perinatal factors reported to be associated
with ADHD are low birthweight and prematurity,51 and
in-utero exposure to maternal stress, cigarette smoking,
alcohol, prescribed drugs (eg, paracetamol), and illicit
substances.38,52,53 In relation to prenatal smoking and
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stress, quasi-experimental designs suggest that most or
all of the association with off spring ADHD, unlike with
off spring birthweight, is explained by unmeasured
confounding factors.54–58
Environmental toxins, specifi cally in-utero or early
childhood exposure to lead, organophosphate pesticides,
and polychlorinated biphenyls, are risk factors for
ADHD, as reviewed elsewhere.38 Nutritional defi ciencies
(eg, zinc, magnesium, and polyunsaturated fatty acids),

nutritional surpluses (eg, sugar and artifi cial food
colourings), and low or high IgG food have not been
shown convincingly to precede ADHD and at present
should be regarded as correlates. Eff ective treatments for
any disorder, unlike prevention, do not necessarily have
to deal with its causes or origins.
Psychosocial risks, such as low income, family
adversity, and harsh or hostile parenting, although
robustly causal for some psychiatric disorders, are also
correlates rather than proven causes of ADHD.
Longitudinal studies,59 treatment trials,60 and a study of
children adopted away at birth61 suggest that observed
negative mother–child relationships (even in unrelated
mothers) arise as a consequence of early child ADHD
symptoms (reverse causation) and improve with
treatment. However, exposure to very severe, early
social deprivation seems to be diff erent and causal.
After being adopted away in the UK, Romanian orphans
raised in institutions and exposed to extreme early
privation in the fi rst year of life showed increased rates
of ADHD-like features, cognitive diffi culties, and
quasi-autistic features that persisted into adolescence.62,63
Psychosocial context may well shape ADHD presen ta-
tions and alter developmental trajectories, outcomes,
and impairments, but surprisingly this has not been
investigated widely (fi gure 1). Irrespective of the cause
of ADHD, treatment is based on clinical features and
not assumed aetiology.
As a fi nal word on risk factors, many individuals
mistakenly assume that the actions of genes (or biology)
and environment are distinct. Potentially important
environmental risks for ADHD and its outcomes may be
brought about as a consequence of genetic propensities
(gene–environmental correlation61). The eff ect of

environmental factors on clinical phenotype may also
depend on genetic liability. For example, animal studies
have robustly shown that environment can alter
behaviour in diff erent ways depending on the variant of
gene carried (gene–environment interaction39). Eff ects of
gene–environment interplay are subsumed in twin
heritability estimates. Finally, there is very good evidence
that environmental exposures result in biological
changes,49 including ones involving brain structure,
function, and altered DNA methylation (epigenetics).
These fi ndings highlight that genes, environment, and
biology work together. However, in man, these issues are
complex; they will not be discussed in detail here, but
have been reviewed elsewhere.38,39,49
Pathophysiology
Biology
The biological mechanisms through which genetic and
environmental factors act and interact to alter neuro-
development in ADHD are not yet understood and there
remains no diagnostic neurobiological marker. The
validity of animal models of ADHD are limited by our
incomplete understanding of its pathophysiology in
man and the extent to how well inattention, motor
overactivity, and impulsive responses on behavioural
tasks in non-human species represent ADHD.64
However, fi ndings in animal models have suggested
involvement of dopaminergic and noradrenergic
neurotransmission (in line with the neurochemical
eff ects of ADHD medications) as well as involvement of
serotonergic neurotransmission.65
Cognition
Although there is no cognitive profi le that defi nes
ADHD, defi cits in various neuropsychological domains
have been reliably identifi ed. In terms of executive

functioning, the most consistent and strong associations
are seen for response inhibition, vigilance, working
memory, and planning.66 In terms of non-executive
defi cits, associations are seen with timing,67 storage
aspects of memory,68 reaction time variability,69 and
decision making.70 However, there is substantial
heterogeneity in cognitive functioning even within
single samples,71 and there is not a straightforward
association between cognitive performance and the
trajectory of clinical symptoms.72,73 There is evidence,
though, that some cognitive defi cits are improved by
methylphenidate, with a meta-analysis showing
improvements in executive and non-executive memory,
reaction time, reaction time variability, and response
inhibition.74
Figure 1: Origins and trajectories of attention defi cit
hyperactivity disorder
(ADHD)
Multiple early risk factors contributing to the development of
ADHD
Genetics Early environment
(prenatal and postnatal)
ADHD Later risk and protective factors
modifying the course
Family and social environment
Genetics
Heterogeneous
outcomes

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Imaging
Functional MRI (fMRI) studies in patients with ADHD
have found abnormalities in the function of many neural
networks in response to cognitive tasks. A meta-analysis
of task-based fMRI studies identifi ed alterations in
several networks, including those related to attention
and executive function.75 In terms of brain structure, a
meta-analysis of structural MRI studies highlighted
alterations in the basal ganglia and limbic areas.76
In a meta-analysis of diff usion MRI studies investigating
white matter microstructure, alterations were reported
to be widespread, but most reliably seen in the right
anterior corona radiata, right forceps minor, bilateral
internal capsule, and left cerebellum.77 Reduced total
grey matter and altered basal ganglia volumes seem to
index familial risk for ADHD.78
The scientifi c literature is increasingly suggesting
that the pathophysiology of ADHD involves abnormal
interactions between large-scale brain networks; however,
current imaging studies do not yet have relevance to
clinical practice.79 Interpretation is complex because of
many factors, including the cross-sectional nature of
most studies. Longitudinal data regarding the trajectory
of cortical development suggest that the brain may show
maturational delay, with persistence of ADHD indexed
by progressive divergence from the normal trajectory,80
but it is not known whether this phenomenon can be
extrapolated to other metrics of structure, microstructure,

and function. The eff ect of pharmacological treatment is
also a consideration because there is some evidence to
suggest that it normalises macrostructure and function.81
Nonetheless, there is some evidence from longitudinal
studies of adults with childhood ADHD that grey and
white matter abnormalities persist well into adulthood.82,83
Clinical assessment
The assessment process for ADHD requires careful
clinical history taking that goes beyond asking yes or no
questions in relation to core ADHD symptoms. A missed
diagnosis has potential to jeopardise an individual’s
learning or occupational and social relationships, whereas
a misdiagnosis could lead to the use of pharmacological
treatment that is not needed. History taking should not
be reductionist—ie, exclusively focused on asking about
diagnostic items. A detailed developmental as well as
medical history and an assessment of family processes
and social circumstances (strengths as well as weaknesses)
are also required. Figure 2 summarises the key steps in
the assessment of children.
It is important to consider whether endorsed symptoms
are better explained by other diffi culties that are amenable
to intervention—eg, hearing diffi culties presenting as
inattention. However, diagnosis is based on clinical
phenotype and not generally excluded by presumed
cause. Information should be obtained from more than
one informant, including those who know the aff ected
individual best at home and at school (or college or work).
To decide which individuals need referral to a specialist
assessment service or to monitor treatment response, use
of standardised ADHD questionnaires (eg, Strength and
Diffi culties Questionnaire,84 Conners’ Parent and Teacher
Rating Scales85) are helpful, but these are not a substitute
for detailed history taking before diagnosis. Structured

interviews are more likely to be encountered in a research
setting, but might be valuable in a clinical context,
especially interviews that do not require extensive,
expensive training (eg, the Development and Wellbeing
Assessment).86 The use of structured interviews in a
clinical setting requires further investigation. ADHD
symptoms are commonly associated with a range of
neurobehavioural diffi culties, which could be comorbid
features of the disorder but should also be considered
as diff erential diagnoses because their treatments are
very diff erent.
Mental health symptoms, which should also be
screened for, include those of oppositional defi ant
disorder, conduct disorder, anxiety, and mood
disturbance. Developmental and learning problems
such as reading disorders, developmental coordination
disorder, and tic disorders are also common.87–89 Because
ADHD and autism spectrum disorder co-occur so
frequently,90 autistic symptomatology should be
considered. ADHD is also associated with lower IQ
or intellectual disability91 and emotion dysregulation
Figure 2: Summary of the clinical assessment process for
children
ADHD=attention defi cit hyperactivity disorder.
Obtain detailed clinical history from parents or carers and
young person
Carry out core ADHD symptom enquiry: are symptoms out of
keeping with
child's age and developmental stage?
Obtain information across settings; consider questionnaires as
an adjunct

Screen for associated difficulties (eg, mental health symptoms,
other
neurodevelopmental or learning problems)
• Developmental history (eg, motor delay)
• Medical history (eg, epilepsy)
• Family history (eg, mental health, educational history,
physical health
problems)
• Medical histories especially important in relation to cardiac or
other risk
factors if pharmacological treatment is being considered
Consider severity of symptoms, effects on functioning,
comorbid symptoms,
medical history, and the family and child's strengths, resources,
demands, and
psychosocial context when deciding on treatment options
Physical assessment:
• Signs of other disorders (eg, dysmorphic features, skin
lesions) and motor
coordination (eg, handwriting, balance); to be undertaken more
completely
if considering pharmacological treatment
• Baseline height, weight, blood pressure, pulse
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symptoms (eg, irritability),92 both of which can further
complicate the presentation and interpretation of
symptoms. In practice, it will be rare to fi nd an
individual who presents with so-called uncomplicated
ADHD, even if full diagnostic criteria for other
comorbid disorders are not met. This situation makes
formalising diff erential diagnoses conceptually diffi cult,
because in reality an individual with neurodevelopmental
problems is unlikely to have a pure presentation of any
one condition as a unifying explanation for their
diffi culties. A formulation should capture the full
range of developmental, behavioural, and psychiatric
diffi culties, even if some of these need to be described
in terms of subthreshold problems.
Neuropsychological testing does not have a role in
diagnosis of ADHD because cognitive processes are not a
defi ning characteristic.66 However, cognitive comorbidities
such as learning disability and dyslexia should be
considered, which may require specialist assessment
from education services.
Treatment
There are specifi c guidelines for the stepwise
management of ADHD, such as those developed by the
National Institute for Health and Care Excellence
(NICE)7 and the Scottish Intercollegiate Guidelines
Network (SIGN)93 in the UK, by the Eunethydis European
ADHD Guidelines Group (EAGG)94 in Europe, and by
the American Academy of Pediatrics (AAP)95 and the
American Academy of Child and Adolescent Psychiatry
(AACAP)96 in the USA. The main diff erence between
these guidelines is that US guidance does not preclude
the use of pharmacological treatment for preschool

children or for those with mild ADHD; practice that is
not recommended in Europe where a stepwise approach
is recommended. If pharmacological treatment is
prescribed, it should be in conjunction with behavioural
interventions—namely, optimised classroom manage-
ment strategies, parental psycho education, and behav-
ioural management tech niques. However, there is no
one-size-fi ts-all solution to management. Individual
circumstances such as current academic or employment
demands and medical history should be taken into
account, and appropriate evidence-based treatments for
comorbidities should also be initiated.
Non-pharmacological interventions have been
investigated extensively over the years. The only non-
pharma cological interventions that currently form a core
part of treatment guidelines are behavioural inter-
ventions. Initial results from the largest trial of ADHD
interventions so far, the multimodal treatment study of
children with ADHD (MTA),97 suggested that the
combination of intensive behavioural treatment plus
pharmacological treatment did not off er additional
benefi t over pharmacological treatment alone for core
ADHD symptoms, but that the combination might have
provided some benefi t in terms of associated symptoms
and levels of functioning as well as the need for a lower
drug dose. In a more recent series of meta-analyses
investigating randomised controlled trials of non-
pharmacological interventions, the investigators
concluded that, along with neurofeedback, cognitive
training, and restricted elimination diets, behavioural
interventions cannot be recommended as interventions
for core ADHD symptoms until better evidence of their
eff ectiveness is reported by blinded assessments.98
Elimination of artifi cial food colouring98 might be

benefi cial, but to what extent and for which population
of patients is unclear.99 A meta-analysis has shown that
children with ADHD have lower concen trations of
omega-3 fatty acids than controls and that supple-
mentation improves ADHD symptoms to a modest
degree (an eff ect size about a quarter as large of that
seen for pharmacological treatment); but whether
subnormal blood concentrations should be the
indication for treatment is not understood.100 However,
there is evidence from blinded randomised controlled
trials of a benefi cial eff ect of behavioural interventions
on parenting and child conduct problems,101 and there is
evidence that cognitive behaviour therapy may be useful
for adults with ADHD when used in conjunction with
pharmacological treatment.102
Stimulants such as methylphenidate and dexamfetamine
are the fi rst-line pharmacological treatments for ADHD,
and the noradrenaline reuptake inhibitor atomoxetine is
the second-line treatment. Each of these treatments
increases catecholamine availability. Meta-analyses have
provided evidence for the effi cacy of stimulants for ADHD
in children,103 in children with co-occurring autism
spectrum disorder,104 and in adults.105 Although it is
recommended that ADHD is treated in individuals with
autism spectrum disorder or intellectual disability, or
both, side-eff ects of pharmacological treatment in these
individuals are more common than in those with ADHD
alone.106,107 Meta-analyses have shown benefi cial eff ects of
atomoxetine in children108 and in adults.109 Extended-
release guanfacine and extended-release clonidine are
licensed for use in the USA. Atypical antipsychotics are
not indicated for treatment of core ADHD symptoms.
Pretreatment checks, including in relation to medical
and family medical history (in particular cardiac disorders),

are especially important if medication is to be initiated
(fi gure 2). Height, weight, blood pressure, and pulse
should be checked at baseline before starting treatment,
and compared with normative data. It is reasonable but
not mandatory to consider the routine performance of an
ECG before starting pharmacological treatment, and the
need to do so should be at the treating clinician’s discretion,
taking into account factors such as medical history, family
medical history, and physical examination fi ndings.7,110
It is best practice to start with a low dose, titrate up
according to response, and monitor side-eff ects carefully.7
The most common side-eff ects of medications for ADHD
are shown in the table. There is no evidence that
Seminar
pharmacological treatment for ADHD is associated with
changes in QT interval, sudden cardiac death, acute
myocardial infarction, or stroke.110 A comprehensive
review of best practice in managing adverse events
associated with pharmacological treatment for ADHD
has been published elsewhere.110 Once an optimum
response is achieved, height, weight, and growth will
need regular monitoring. NICE guidance recommends
that height is measured every 6 months in children and
young people; weight is measured 3 months and
6 months after initiation of treatment and every 6 months
thereafter in children, young people, and adults; and
height and weight in children and young people should
be plotted on a centile chart.7 Blood pressure and pulse
should also be plotted on a centile chart before and after

each change in dose and routinely every 3 months.7
Adverse side-eff ects of stimulant medication for ADHD
include appetite suppression and growth retardation,
which can be off set to a degree by so-called stimulant
holidays on days when symptom control is deemed less
crucial, such as weekends and holidays, and by adjusting
the timing of doses. Other side-eff ects of stimulants and
atomoxetine include gastrointestinal symptoms, cardiac
problems, insomnia, and tics (although tics are less
common with atomoxetine). Stimulants are controlled
drugs with potential for diversion for misuse, and if there
is a concern in this regard then an alternative drug may
be preferable.
Prognosis
Not only do core ADHD symptoms themselves persist,
but individuals with childhood ADHD are also at
substantial risk of adverse outcomes in adolescence
and adulthood. In this regard, ADHD behaves
dimensionally: there is no distinct threshold at which
adverse outcomes appear. A diagnosis of ADHD is
associated with low academic attainment and premature
cessation of education, and poor educational outcomes
also extend to individuals with subthreshold
symptoms.111 ADHD also predicts serious antisocial
behaviour, involvement with the police, and substance
misuse in adolescence.36
Until recently, few data for broad outcomes beyond
the third decade of life were available. However, one
long-term follow-up study has shown that childhood
ADHD (participants aged 6–12 years) is also associated
with adverse occupational, economic, and social
outcomes, antisocial personality disorder, and risk
of substance use disorders, psychiatric hospital

admissions, incarcerations, and mortality.112 A Danish
registry-based investigation showed substantially
increased mortality in adult life in individuals with
ADHD compared with individuals without the disorder.
This increase in mortality was mainly a result of
accidents, and was especially increased in those with
comorbid oppositional defi ant disorder, conduct
disorder, and substance misuse.113
A meta-analysis of ADHD in prison inmates showed
an estimated prevalence of 30·1% in youth prison
populations and 26·2% in adult populations, with the
risk for female prisoners being nearly as high as that for
male prisoners.114 Psychiatric comorbidity is high in
prisoners with ADHD, especially in adults.115 Although
randomised controlled trials of ADHD treatment have
reported immediate but not as yet longer term benefi ts,
there is epidemiological evidence that pharmacological
treatment might reduce criminal behaviour116 and
trauma-related visits to emergency departments.117
Most people with ADHD do not develop psychosis or a
mood disorder. The largest studies only fi nd a small
subgroup of individuals who additionally develop
schizophrenia or bipolar disorder.118,119 Evidence about
associations between ADHD and later unipolar
depression is inconsistent;112,120 this might be because
depression is more common in female patients who are
under-represented in ADHD samples.
Future research and clinical directions
The early age of onset, male preponderance, and
strong comorbidity with other childhood-onset neuro-
developmental disorders support the inclusion of
ADHD in the DSM-5 grouping of neurodevelopmental
disorders. The previous practice of not diagnosing

ADHD in the presence of autism spectrum disorder or
intellectual disability has been a crucial barrier to
research on aetiological and clinical overlaps and
distinctions as well as to clinical and educational
practice. Unfortunately, referral and treatment pathways
and service provision in health and education tend to be
diagnostically focused (ie, autism only or intellectual
disability only), although some clinics and services are
focusing more broadly on childhood neurodevelop-
mental disorders, a change which is welcomed and
supported by research.
Methylphenidate
(MPH)
Atomoxetine
(ATX)
Loss of appetite + +
Growth restriction ++ +
Other gastrointestinal symptoms: abdominal pain, nausea,
vomiting,
diarrhoea (MPH), constipation (ATX), dyspepsia, dry mouth
+ +
Increase in blood pressure and heart rate + +
Cough, nasopharyngitis + ··
Sleep disturbances ++ +
Tics + ··

Irritability, mood changes + +
Drowsiness + ++
Dizziness + +
Headache ++ +
+=common side-eff ect. ++=if the side-eff ect is common for
both drugs, the eff ect is more pronounced for this drug
compared with the other. ··=side-eff ect not common.
Table: Some of the more common side-eff ects associated with
pharmacological treatment
Seminar
We accept that for clinical practice, there is a need
for strict categories, otherwise diagnostic spread would
become at best unhelpful and at worst risky and
unethical (eg, use of pharmacological treatment where
not indicated) and application of evidence-based
treatments would become impossible (eg, interpreting
the severity of diffi culties of individuals included in a
trial). However, for aetiological and outcome research
purposes, there is strong evidence in favour of viewing
ADHD dimensionally. At present, we do not know what
sorts of dimensions best capture ADHD and at what
level they should be measured—eg, reported symptoms,
cognitive tests, brain imaging markers, or other
biological signatures.

Genetic research is progressing via large-scale
collaboration, but there is a need to understand the
clinical as well as biological meaning of fi ndings, if they
are to aff ect our understanding and treatment of ADHD.
Currently, there is no rationale for routine genetic
testing in ADHD because of limited predictive power.
However, because the disorder is heritable, rates of
ADHD in parents of those with ADHD are increased.
A pertinent future research question is how might
treatment of parent ADHD aff ect child ADHD features
and comorbidity? There is, for example, evidence that
treating parent depression seems to improve off spring
mental health.121,122 Another issue for future consideration
is that genetic and environmental risk factors that cause
ADHD are not necessarily the same as those that alter
the later course of the disorder or contribute to adverse
outcomes. What is greatly needed is research that tests
which environmental risks (eg, social and other
potentially modifi able risk factors) contribute to and
modify the longitudinal course of ADHD across time,
including better prognosis, with designs that can control
for unmeasured confounders and genetic contributions
from the aff ected person (eg, twin studies) and related
parents (eg, adoption studies). This could inform
interventions aimed at optimising outcomes.
So far, pharmacological and behavioural treatments for
ADHD have focused on symptomatic relief of the core
symptoms of inattention, overactivity, and impulsivity.
However, according to trial-based data, benefi ts seem to
be short-lived. Another issue is that treatment typically
begins after a child has already begun to fail across
multiple domains. ADHD in many respects behaves like
a chronic medical disorder. Many features remain
problematic long term, although the most prominent or
presenting features can change with age and development.

ADHD creates risks of its own and secondary mental
health problems commonly arise in mid-childhood and
after puberty. Almost certainly, for many individuals,
multimodal interventions that are carefully adjusted over
time to prevent complications will be needed, perhaps in
the way that is undertaken for optimising diabetes
control. How ADHD is best managed across the lifespan
and across key transition periods (eg, school entry,
comprehensive or high-school entry, transition to adult
services, and transition to parenthood) needs much more
investigation. Until now, guidelines have been based on
evidence, but unless research keeps pace, guidance will
have to be based on professional consensus, which is not
very satisfactory for a prevalent, impairing disorder.
Conclusions
ADHD is a very important condition because of its high
prevalence, persistence into adult life, and adverse
outcomes that extend beyond the aff ected individual.
Although ADHD is still viewed with scepticism by some
and often remains stigmatised by the media, the evidence
for it being a clinically and biologically meaningful entity
is robust and consistent across design type and sample.
There are established assessment methods and good
treatment evidence. However, as is true for any chronic
disorder, repeated assessment is likely to be needed and
treatment will typically need many adjustments over
time. Impairments beyond core diagnostic criteria,
developmental change, and an individual’s psychosocial
strengths, weaknesses, and resources are all important
aspects for consideration.
Contributors
AT drafted the initial outline and structure and wrote the fi rst
draft of
the summary and sections on introduction, defi nitions of

ADHD,
epidemiology, early comorbidity, genetics, environment and
gene–environment interplay, and future research and clinical
directions. MC wrote the fi rst draft of the sections on
pathophysiology,
clinical assessment, treatment, and prognosis, and prepared the
table,
panel, and fi gures. Both authors undertook scientifi c literature
searches
and edited the manuscript.
Declaration of interests
We declare no competing interests.
Acknowledgments
We have been funded by the MRC, ESRC, and the Wellcome
Trust.
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Reproduced with permission of the copyright owner. Further
reproduction prohibited without
permission.
Attention deficit hyperactivity disorderIntroductionDefinitions
of ADHDEpidemiologyEarly comorbidityRisk
factorsOverviewGeneticsEnvironment and gene–environment
interplayPathophysiologyBiologyCognitionImagingClinical

assessmentTreatmentPrognosisFuture research and clinical
directionsConclusionsAcknowledgmentsReferences
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Innovation
INNOVATION
SPOTLIGHT ON
1692 Dec09 Dyer Layout.indd 601692 Dec09 Dyer
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Five “discovery skills”
separate true innovators
from the rest of us.
| by Jeffrey H. Dyer, Hal B. Gregersen,
and Clayton M. Christensen

The Innovator’s
DNA
hbr.org | December 2009 | Harvard Business Review 61
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62 Harvard Business Review | December 2009 | hbr.org
The Innovator’s DNA
Innovation
INNOVATION
SPOTLIGHT ON
These are questions that stump senior executives,
who understand that the ability to innovate is the
“secret sauce” of business success. Unfortunately,
most of us know very little about what makes one
person more creative than another. Perhaps for this
reason, we stand in awe of visionary entrepreneurs
like Apple’s Steve Jobs, Amazon’s Jeff Bezos, eBay’s
Pierre Omidyar, and P&G’s A.G. Lafl ey. How do
these people come up with groundbreaking new
ideas? If it were possible to discover the inner work-
ings of the masters’ minds, what could the rest of us
learn about how innovation really happens?
In searching for answers, we undertook a six-
year study to uncover the origins
of creative – and oft en disrup-
tive – business strategies in par-

ticularly innovative companies.
Our goal was to put innovative
entrepreneurs under the micro-
scope, examining when and how
they came up with the ideas on
which their businesses were built.
We especially wanted to examine
how they diff er from other execu-
tives and entrepreneurs: Some-
one who buys a McDonald’s fran-
chise may be an entrepreneur,
but building an Amazon requires
different skills altogether. We
studied the habits of 25 innova-
tive entrepreneurs and surveyed
more than 3,000 executives and
500 individuals who had started
innovative companies or invented
new products.
We were intrigued to learn that
at most companies, top executives
do not feel personally responsible
for coming up with strategic inno-
vations. Rather, they feel responsi-
ble for facilitating the innovation
process. In stark contrast, senior
executives of the most innovative
companies – a mere 15% in our
study – don’t delegate creative
work. They do it themselves.
But how do they do it? Our research led us to
identify fi ve “discovery skills” that distinguish the
most creative executives: associating, questioning,
observing, experimenting, and networking. We

found that innovative entrepreneurs (who are also
CEOs) spend 50% more time on these discovery ac-
tivities than do CEOs with no track record for in-
novation. Together, these skills make up what we
call the innovator’s DNA. And the good news is, if
you’re not born with it, you can cultivate it.
What Makes Innovators Different?
Innovative entrepreneurs have something called
creative intelligence, which enables discovery yet
diff ers from other types of intelligence (as sug-
gested by Howard Gardner’s theory of multiple
intelligences). It is more than the cognitive skill of
being right-brained. Innovators engage both sides
of the brain as they leverage the fi ve discovery skills
to create new ideas.
In thinking about how these skills work together,
we’ve found it useful to apply the metaphor of DNA.
Associating is like the backbone structure of DNA’s
double helix; four patterns of action (questioning,
observing, experimenting, and networking) wind
around this backbone, helping to cultivate new in-
sights. And just as each person’s physical DNA is
unique, each individual we studied had a unique
innovator’s DNA for generating breakthrough busi-
ness ideas.
Imagine that you have an identical twin, en-
dowed with the same brains and natural talents
that you have. You’re both given one week to come
up with a creative new business-venture idea. Dur-
ing that week, you come up with ideas alone in
your room. In contrast, your twin (1) talks with 10
people – including an engineer, a musician, a stay-
at-home dad, and a designer – about the venture,

(2) visits three innovative start-ups to observe what
they do, (3) samples fi ve “new to the market” prod-
ucts, (4) shows a prototype he’s built to fi ve people,
and (5) asks the questions “What if I tried this?” and
“Why do you do that?” at least 10 times each day dur-
ing these networking, observing, and experiment-
ing activities. Who do you bet will come up with the
more innovative (and doable) idea?
“How do I fi nd INNOVATIVE PEOPLE
for my organization? And how can
I become more innovative myself ?”
The habits of Steve Jobs, Jeff
Bezos, and other innovative CEOs
reveal much about the underpin-
nings of their creative thinking.
Research shows that fi ve discov-
ery skills distinguish the most in-
novative entrepreneurs from other
executives.
DOING
Questioning » allows innovators
to break out of the status quo and
consider new possibilities.
Through » observing, innovators
detect small behavioral details –
in the activities of customers, sup-
pliers, and other companies – that
suggest new ways of doing things.
In » experimenting, they relent-

lessly try on new experiences and
explore the world.
And through » networking with
individuals from diverse back-
grounds, they gain radically
different perspectives.
THINKING
The four patterns of action »
together help innovators associate
to cultivate new insights.
IN BRIEF
IDEA
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Studies of identical twins separated at birth in-
dicate that our ability to think creatively comes
one-third from genetics; but two-thirds of the in-
novation skill set comes through learning – fi rst
understanding a given skill, then practicing it, ex-
perimenting, and ultimately gaining confi dence in
one’s capacity to create. Innovative entrepreneurs
in our study acquired and honed their innovation
skills precisely this way.
Let’s look at the skills in detail.

Discovery Skill 1: Associating
Associating, or the ability to successfully connect
seemingly unrelated questions, problems, or ideas
from diff erent fi elds, is central to the innovator’s
DNA. Entrepreneur Frans Johansson described this
phenomenon as the “Medici eff ect,” referring to the
creative explosion in Florence when the Medici fam-
ily brought together people from a wide range of
disciplines – sculptors, scientists, poets, philosophers,
painters, and architects. As these individuals con-
nected, new ideas blossomed at the intersections of
their respective fi elds, thereby spawning the Renais-
sance, one of the most inventive eras in history.
To grasp how associating works, it is important
to understand how the brain operates. The brain
doesn’t store information like a dictionary, where
you can fi nd the word “theater” under the letter
“T.” Instead, it associates the word “theater” with
any number of experiences from our lives. Some
of these are logical (“West End” or “intermission”),
while others may be less obvious (perhaps “anxiety,”
from a botched performance in high school). The
more diverse our experience and knowledge, the
more connections the brain can make. Fresh inputs
trigger new associations; for some, these lead to
novel ideas. As Steve Jobs has frequently observed,
“Creativity is connecting things.”
The world’s most innovative companies prosper
by capitalizing on the divergent associations of
their founders, executives, and employees. For ex-
ample, Pierre Omidyar launched eBay in 1996 aft er
linking three unconnected dots: (1) a fascination

with creating more-effi cient markets, aft er having
been shut out from a hot internet company’s IPO in
the mid-1990s; (2) his fi ancée’s desire to locate hard-
to-fi nd collectible Pez dispensers; and (3) the inef-
fectiveness of local classifi ed ads in locating such
items. Likewise, Steve Jobs is able to generate idea
aft er idea because he has spent a lifetime exploring
new and unrelated things – the art of calligraphy,
meditation practices in an Indian ashram, the fi ne
details of a Mercedes-Benz.
Associating is like a mental muscle that can grow
stronger by using the other discovery skills. As in-
novators engage in those behaviors, they build their
ability to generate ideas that can be recombined in
new ways. The more frequently people in our study
attempted to understand, categorize, and store new
knowledge, the more easily their brains could natu-
rally and consistently make, store, and recombine
associations.
Discovery Skill 2: Questioning
More than 50 years ago, Peter Drucker described
the power of provocative questions. “The important
and diffi cult job is never to fi nd the right answers, it
is to fi nd the right question,” he wrote. Innovators
constantly ask questions that challenge common
wisdom or, as Tata Group chairman Ratan Tata
puts it, “question the unquestionable.” Meg Whit-
man, former CEO of eBay, has worked directly with
a number of innovative entrepreneurs, including
the founders of eBay, PayPal, and Skype. “They get
a kick out of screwing up the status quo,” she told
us. “They can’t bear it. So they spend a tremendous
amount of time thinking about how to change the
world. And as they brainstorm, they like to ask: ‘If

we did this, what would happen?’”
Most of the innovative entrepreneurs we in-
terviewed could remember the specifi c questions
they were asking at the time they had the inspira-
tion for a new venture. Michael Dell, for instance,
told us that his idea for founding Dell Computer
sprang from his asking why a computer cost fi ve
times as much as the sum of its parts. “I would take
computers apart…and would observe that $600
worth of parts were sold for $3,000.” In chewing
over the question, he hit on his revolutionary busi-
ness model.
To question eff ectively, innovative entrepreneurs
do the following:
Ask “Why?” and “Why not?” and “What if?”
Most managers focus on understanding how to
make existing processes – the status quo – work a
little better (“How can we improve widget sales in
Taiwan?”). Innovative entrepreneurs, on the other
hand, are much more likely to challenge assump-
tions (“If we cut the size or weight of the widget
in half, how would that change the value proposi-
tion it off ers?”). Marc Benioff , the founder of the
online sales soft ware provider Salesforce.com, was
full of questions aft er witnessing the emergence of
Amazon and eBay, two companies built on services
delivered via the internet. “Why are we still loading
and upgrading soft ware the way we’ve been doing
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Innovation
INNOVATION
SPOTLIGHT ON
all this time when we can now do it over the inter-
net?” he wondered. This fundamental question was
the genesis of Salesforce.com.
Imagine opposites. In his book The Opposable
Mind, Roger Martin writes that innovative thinkers
have “the capacity to hold two diametrically op-
posing ideas in their heads.” He explains, “Without
panicking or simply settling for one alternative or
the other, they’re able to produce a synthesis that is
superior to either opposing idea.”
Innovative entrepreneurs like to play devil’s ad-
vocate. “My learning process has always been about
disagreeing with what I’m being told and taking
the opposite position, and pushing others to really
justify themselves,” Pierre Omidyar told us. “I re-
member it was very frustrating for the other kids
when I would do this.” Asking oneself, or others, to
imagine a completely diff erent alternative can lead
to truly original insights.
Embrace constraints. Most of us impose con-
straints on our thinking only when forced to deal
with real-world limitations, such as resource al-
locations or technology restrictions. Ironically,
great questions actively impose constraints on our

thinking and serve as a catalyst for out-of-the-box
insights. (In fact, one of Google’s nine innovation
principles is “Creativity loves constraint.”) To initi-
ate a creative discussion about growth opportuni-
ties, one innovative executive in our study asked
this question: “What if we were legally prohibited
from selling to our current customers? How would
we make money next year?” This led to an insight-
ful exploration of ways the company could fi nd
and serve new customers. Another innovative CEO
prods his managers to examine sunk-cost con-
straints by asking, “What if you had not already
hired this person, installed this equipment, imple-
mented this process, bought this business, or pur-
sued this strategy? Would you do the same thing
you are doing today?”
Discovery Skill 3: Observing
Discovery-driven executives produce uncommon
business ideas by scrutinizing common phenomena,
particularly the behavior of potential customers. In
observing others, they act like anthropologists and
social scientists.
Intuit founder Scott Cook hit on the idea for
Quicken fi nancial soft ware aft er two key observa-
tions. First he watched his wife’s frustration as she
struggled to keep track of their fi nances. “Oft en the
surprises that lead to new business ideas come from
watching other people work and live their normal
lives,” Cook explained. “You see something and ask,
‘Why do they do that? That doesn’t make sense.’”
Then a buddy got him a sneak peek at the Apple
Lisa before it launched. Immediately aft er leaving
Apple headquarters, Cook drove to the nearest res-

taurant to write down everything he had noticed
about the Lisa. His observations prompted insights
such as building the graphical user interface to look
just like its real-world counterpart (a checkbook,
for example), making it easy for people to use it.
So Cook set about solving his wife’s problem and
grabbed 50% of the market for fi nancial soft ware
in the fi rst year.
Innovators carefully, intentionally, and consis-
tently look out for small behavioral details – in the
activities of customers, suppliers, and other compa-
nies – in order to gain insights about new ways of
doing things. Ratan Tata got the inspiration that led
to the world’s cheapest car by observing the plight
of a family of four packed onto a single motorized
scooter. Aft er years of product development, Tata
Group launched in 2009 the $2,500 Nano using a
modular production method that may disrupt the
entire automobile distribution system in India. Ob-
servers try all sorts of techniques to see the world
in a diff erent light. Akio Toyoda regularly practices
Toyota’s philosophy of genchi genbutsu – “going to
the spot and seeing for yourself.” Frequent direct
observation is baked into the Toyota culture.
Discovery Skill 4: Experimenting
When we think of experiments, we think of scien-
tists in white coats or of great inventors like Thomas
Edison. Like scientists, innovative entrepreneurs ac-
tively try out new ideas by creating prototypes and
launching pilots. (As Edison said, “I haven’t failed.
I’ve simply found 10,000 ways that do not work.”)
The world is their laboratory. Unlike observers, who
intensely watch the world, experimenters construct
interactive experiences and try to provoke unortho-

dox responses to see what insights emerge.
The innovative entrepreneurs we interviewed all
engaged in some form of active experimentation,
whether it was intellectual exploration (Michael
Lazaridis mulling over the theory of relativity in
high school), physical tinkering (Jeff Bezos taking
apart his crib as a toddler or Steve Jobs disassem-
bling a Sony Walkman), or engagement in new
surroundings (Starbucks founder Howard Shultz
roaming Italy visiting coff ee bars). As executives
of innovative enterprises, they make experimenta-
tion central to everything they do. Bezos’s online
bookstore didn’t stay where it was aft er its initial
Sample of
Innovative
Entrepreneurs
from our Study
SAM ALLEN
ScanCafe.com
MARC BENIOFF
Salesforce.com
JEFF BEZOS
Amazon.com
MIKE COLLINS
Big Idea Group
SCOTT COOK
Intuit
MICHAEL DELL

Dell Computer
AARON GARRITY
XanGo
DIANE GREEN
VMWare
ELIOT JACOBSEN
RocketFuel
JOSH JAMES
Omniture
CHRIS JOHNSON
Terra Nova
JEFF JONES
NxLight; Campus
Pipeline
HERB KELLEHER
Southwest Airlines
MIKE LAZARIDIS
Research In Motion
SPENCER MOFFAT
Fast Arch of Utah
DAVID NEELEMAN
JetBlue; Morris Air
PIERRE OMIDYAR
eBay

JOHN PESTANA
Omniture
PETER THIEL
PayPal
MARK WATTLES
Hollywood Video
COREY WRIDE
Movie Mouth
NIKLAS
ZENNSTRÖM
Skype
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success; it morphed into an online discount retailer,
selling a full line of products from toys to TVs to
home appliances. The electronic reader Kindle is
an experiment that is now transforming Amazon
from an online retailer to an innovative electron-
ics manufacturer. Bezos sees experimentation as so
critical to innovation that he has institutionalized it
at Amazon. “I encourage our employees to go down
blind alleys and experiment,” Bezos says. “If we can
get processes decentralized so that we can do a lot
of experiments without it being very costly, we’ll get
a lot more innovation.”

Scott Cook, too, stresses the importance of cre-
ating a culture that fosters experimentation. “Our
culture opens us to allowing lots of failures while
harvesting the learning,” he told us. “It’s what sepa-
rates an innovation culture from a normal corpo-
rate culture.”
One of the most powerful experiments innova-
tors can engage in is living and working overseas.
Our research revealed that the more countries a
person has lived in, the more likely he or she is
to leverage that experience to deliver innovative
products, processes, or businesses. In fact, if man-
agers try out even one international assignment
before becoming CEO, their companies deliver
stronger fi nancial results than companies run by
CEOs without such experience – roughly 7% higher
market performance on average. P&G’s A.G. Lafl ey,
for example, spent time as a student studying his-
tory in France and running retail operations on U.S.
military bases in Japan. He returned to Japan later
to head all of P&G’s Asia operations before becom-
ing CEO. His diverse international experience has
served him well as the leader of one of the most
innovative companies in the world.
Discovery Skill 5: Networking
Devoting time and energy to fi nding and testing
ideas through a network of diverse individuals gives
innovators a radically diff erent perspective. Unlike
most executives – who network to access resources,
to sell themselves or their companies, or to boost
their careers – innovative entrepreneurs go out of
their way to meet people with diff erent kinds of
ideas and perspectives to extend their own knowl-

edge domains. To this end, they make a conscious
eff ort to visit other countries and meet people from
other walks of life.
They also attend idea conferences such as Tech-
nology, Entertainment, and Design (TED), Davos,
and the Aspen Ideas Festival. Such conferences
How Innovators Stack Up
This chart shows how four well-known innovative entrepreneurs
rank
on each of the discovery skills. All our high-profi le innovators
scored
above the 80th percentile on questioning, yet each combined the
dis-
covery skills uniquely to forge new insights.
Rankings are based on
a survey of more than
3,000 executives and
entrepreneurs.
100
80
60
40
PERCENTILE
Noninnovators

QUESTIONINGASSOCIATING OBSERVING
EXPERIMENTING NETWORKING
Michael Dell
Michael Lazaridis
Scott Cook
Pierre Omidyar
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Innovation
INNOVATION
SPOTLIGHT ON
draw together artists, entrepreneurs, academics,
politicians, adventurers, scientists, and thinkers
from all over the world, who come to present their
newest ideas, passions, and projects. Michael Laza-
ridis, the founder of Research In Motion, notes that
the inspiration for the original BlackBerry occurred
at a conference in 1987. A speaker was describing
a wireless data system that had been designed for
Coke; it allowed vending machines to send a signal
when they needed refi lling. “That’s when it hit me,”
Lazaridis recalls. “I remembered what my teacher
said in high school: ‘Don’t get too caught up with

computers because the person that puts wireless
technology and computers together is going to
make a big diff erence.’” David Neeleman came up
with key ideas for JetBlue – such as satellite TV at
every seat and at-home reservationists – through
networking at conferences and elsewhere.
Kent Bowen, the founding scientist of CPS tech-
nologies (maker of an innovative ceramic compos-
ite), hung the following credo in every offi ce of his
start-up: “The insights required to solve many of
our most challenging problems come from outside
our industry and scientifi c fi eld. We must aggres-
sively and proudly incorporate into our work fi nd-
ings and advances which were not invented here.”
Scientists from CPS have solved numerous complex
problems by talking with people in other fi elds. One
expert from Polaroid with in-depth knowledge of
fi lm technology knew how to make the ceramic
composite stronger. Experts in sperm-freezing tech-
nology knew how to prevent ice crystal growth on
cells during freezing, a technique that CPS applied
to its manufacturing process with stunning success.
Practice, Practice, Practice
As innovators actively engage in the discovery skills,
they become defi ned by them. They grow increas-
ingly confi dent of their creative abilities. For A.G.
Lafl ey, innovation is the central job of every leader,
regardless of the place he or she occupies on the
organizational chart. But what if you – like most ex-
ecutives – don’t see yourself or those on your team
as particularly innovative?
Though innovative thinking may be innate to

some, it can also be developed and strengthened
through practice. We cannot emphasize enough
the importance of rehearsing over and over the
behaviors described above, to the point that they
become automatic. This requires putting aside time
for you and your team to actively cultivate more
creative ideas.
The most important skill to practice is question-
ing. Asking “Why” and “Why not” can help turbo-
charge the other discovery skills. Ask questions
that both impose and eliminate constraints;
this will help you see a problem or opportunity
from a diff erent angle. Try spending 15 to 30
minutes each day writing down 10 new ques-
tions that challenge the status quo in your com-
pany or industry. “If I had a favorite question to
ask, everyone would anticipate it,” Michael Dell
told us. “Instead I like to ask things people don’t
think I’m going to ask. This is a little cruel, but
I kind of delight in coming up with questions
that nobody has the answer to quite yet.”
To sharpen your own observational skills,
watch how certain customers experience a
product or service in their natural environ-
ment. Spend an entire day carefully observing
the “jobs” that customers are trying to get done.
Try not to make judgments about what you see:
Simply pretend you’re a fl y on the wall, and
observe as neutrally as possible. Scott Cook ad-
vises Intuit’s observers to ask, “What’s diff erent
than you expected?” Follow Richard Branson’s
example and get in the habit of note taking
wherever you go. Or follow Jeff Bezos’s: “I take

pictures of really bad innovations,” he told us,
“of which there are a number.”
WHY DO INNOVATORS
question, observe, experiment,
and network more than typical
executives? As we examined what
motivates them, we discovered two
common themes: (1) They actively
desire to change the status quo, and
(2) they regularly take risks to make
that change happen. Throughout our
research, we were struck by the con-
sistency of language that innovators
use to describe their motives. Jeff
Bezos wants to “make history,” Steve
Jobs to “put a ding in the universe,”
Skype cofounder Niklas Zennström
to “be disruptive, but in the cause
of making the world a better place.”

These innovators steer entirely clear
of a common cognitive bias called
the status quo bias – the tendency to
prefer an existing state of affairs to
alternative ones.
Embracing a mission for change
makes it much easier to take risks
and make mistakes. For most of the
innovative entrepreneurs we studied,
mistakes are nothing to be ashamed
of; in fact, they are expected as a cost
of doing business. “If the people run-
ning Amazon.com don’t make some
signifi cant mistakes,” explained Be-
zos, “then we won’t be doing a good
job for our shareholders because we
won’t be swinging for the fences.”
In short, innovators rely on their

“courage to innovate” – an active
bias against the status quo and an
unfl inching willingness to take
risks – to transform ideas into power-
ful impact.
Put a Ding in the Universe
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To strengthen experimentation, at both the
individual and organizational levels, consciously
approach work and life with a hypothesis-testing
mind-set. Attend seminars or executive education
courses on topics outside your area of expertise;
take apart a product or process that interests you;
read books that purport to identify emerging trends.
When you travel, don’t squander the opportunity
to learn about diff erent lifestyles and local behav-
ior. Develop new hypotheses from the knowledge
you’ve acquired and test them in the search for new
products or processes. Find ways to institutional-
ize frequent, small experiments at all levels of the
organization. Openly acknowledging that learning
through failure is valuable goes a long way toward
building an innovative culture.

To improve your networking skills, contact the
fi ve most creative people you know and ask them
to share what they do to stimulate creative thinking.
You might also ask if they’d be willing to act as your
creative mentors. We suggest holding regular idea
lunches at which you meet a few new people from
diverse functions, companies, industries, or coun-
tries. Get them to tell you about their innovative
ideas and ask for feedback on yours.
• • •
Innovative entrepreneurship is not a genetic pre-
disposition, it is an active endeavor. Apple’s slogan
“Think Diff erent” is inspiring but incomplete. We
found that innovators must consistently act diff er-
ent to think diff erent. By understanding, reinforcing,
and modeling the innovator’s DNA, companies can
fi nd ways to more successfully develop the creative
spark in everyone.
Jeffrey H. Dyer ([email protected]) is a professor of
strategy at Brigham Young University in Provo, Utah,
and an adjunct professor at the University of Penn-
sylvania’s Wharton School. Hal B. Gregersen (hal.
[email protected]) is a professor of leadership
at Insead in Abu Dhabi, UAE, and Fontainebleau,
France. Clayton M. Christensen ([email protected]
hbs.edu) is a professor of business administration at
Harvard Business School in Boston.
Reprint R0912E To order, see page 131.

Try spending 15 to 30 minutes each day
writing down questions that challenge the
status quo in your company.
“The numbers aren’t working.”R
o
y
D
e
lg
ad
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