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ADHD and the symptomdimensions inattention,impulsivity, andhyperactivityJENS RICHARDT MØLLECAARD JEPSEN &MARIA MICHELPublished online: 24 Jan 2013.

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ARTICLE Nordic Psychology, 2006, 58 (2) 108-135

ADHD and the symptom

dimensions inattention,

impulsivity, and hyperactivity A review of aetiological twin studies

from 1996 to 2004

]ENS RICHARDT M0LLEGAARD JEPSEN MARIA MICHEL

Jepsen, J.R.M. & Michel, M. ADHD and the symptom dimensions inattention, impulsivity, and hyperactivity, Nordic Psychology, 58, 108-135

Attention-deficit hyperactivity disorder (ADHD) is a disabling condition with onset in early childhood. ADHD often co-occurs with educational failure and poor self-esteem. This litera­ture review includes twin studies published in English between 1996 and 2004. Our inclusion criterium was either a quantitative estimate of the heritability of ADHD, or of its inattentive and impulsive-hyperactive symptom-dimensions. This article also contains an introduction to the twin design as a method to estimate the influences from genetic and environmental sources on complex psychological traits. The methodological introduction contains a discussion of the validity of a basic assumption in the twin design referred to as "the equal environment assump­tion". All together, the studies reviewed include about 38.000 children. Based on parental information, the heritability estimates are generally very high and point to a dominant genetic influence on the symptom-dimensions associated with ADHD and on ADHD defined as a category. In contrast, the non-shared environmental factors are of less influence and the shared environmental factors are of no importance. The theoretical implications of these findings are briefly discussed and support the assumption of ADHD as a developmental disorder.

Correspondence: ]ens Richardt M0flegaard Jepsen, Engtoftevej 3, 3.tv., DK-1816 Frederiksberg C. E-mail: jensrichardt@get2net.dk.

Introduction In clinical child neuropsychological practice, many children and adolescents

with symptoms of inattention, behavioural impulsivity, or hyperactivity are

assessed. In Denmark, these symptoms can be diagnosed using the ICD-1 0

(WHO, 1992), most often as a "Disturbance of activity and attention" or as

"Attention deficit disorder without hyperactivity". The latter is included in the

rather unspecific diagnostic category "Other specified behavioural and emo­

tional disorders with onset usually occurring in childhood and adolescence".

Using DSM-IV (APA, 1994), these symptoms can be diagnosed as one of three

subtypes of Attention-Deficit/Hyperactivity Disorder (ADHD). The sample of

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children with ADHD created by the DSM-IV criteria significantly overlap the

sample of children with a "Disturbance of activity and attention" using the

ICD-1 0 criteria, although ICD-1 0 identifies a narrower group of children than

DSM-IV (Tripp et al., 1999). ADHD in childhood and adolescence is accompa­

nied by a broad range of behavioural, social, learning, and emotional problems,

e.g. low self-esteem. On top of these problems, ADHD is also associated with

an increased risk of other types of psychopathology and substance abuse. For

a substantial number of adolescents with the disorder, ADHD persists into

adulthood.

In the current scientific literature on ADHD, one can find aetiological hypoth­

eses that contradict the available evidence on this matter. Recently, limimi et al.

(2004) hypothesized that the behaviour labelled as ADHD in reality represents

aspects of interpersonal relations and is related to "the disappearance of the

childhood" in the modern western world. This idea contradicts the evidence of a

primary biological aetiology of ADHD, a view that is well validated and increas­

ingly accepted. The change of the aetiological model of ADHD from the former

psycho-social and interpersonal perspective to the current primarily biological

model of ADHD may be due to the results of twin- and adoption studies of psy­

chological traits and psychopathological disorders, including ADHD, that have

been done over the last 20 years. These findings have contributed to the increas­

ing acknowledgement of the genetic influence on human behaviour, personality

and mental disorders (Piomin et al., 2001 ).

The twin study is a quantitative genetic method used to estimate the relative

influences from both genetic and environmental factors on the differences in a

given trait among subjects. The twin study cannot detect which specific genes

or environmental factors are involved in a certain psychological trait or disorder

(Piomin et al., 2001 ).

Purpose The primary purpose of this article is to summarise the results of twin studies

of the genetic and environmental influences on both ADHD as a diagnostic

category, and on the ADHD-symptom dimensions inattention, impulsivity and

hyperactivity. We report the purposes, methods, and the major results from all

aetiological twin studies published in English from 1996 to 2004. The secondary

purpose is to present the twin study as a method, including its basic hypothesis.

The article also includes a short presentation of a well-established neuropsycho­

logical model of the inattention, impulsivity and hyperactivity symptoms.

The twin study is increasingly being used to investigate the aetiology of ADHD

and its co-morbid disorders (e.g. Burt et al., 2001 ). The twin studies on the co-

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110 fens Richardt M01/egaard Jepsen & Maria Michel NP, 2006 (2)

morbidity of ADHD and other behavioural and psychopathological disorders

are not included in this review even though we recognize that ADHD is often

associated with e.g. oppositional defiant disorder. This review only includes twin

studies on ADHD and the symptom dimensions inattention and impulsivity­

hyperactivity.

Presentation of a neuropsychological model of ADH 0 ADHD is a disorder that is empirically well researched. Most studies on ADHD

have primarily had a clinically descriptive character and have not been based

on a theoretical model of the disorder (Barkley, 1997 a). Thus, there was a need

for the development of a comprehensive neuropsychological theory on ADHD.

Russell A. Barkley developed a comprehensive neuropsychological theory on

ADHD based on a recent hypothesis on a reduced ability to inhibit behaviour

as the central psychological deficit. Barkley's model describes both the human

mental systems of self-control and the dysfunctions herein leading to symptoms

of inattention, impulsivity and hyperactivity. The theory also explains the emo­

tional, other behavioural and cognitive problems often seen in children and

adolescents with ADHD.

The model is inspired by an earlier neuropsychological theory on the human

ability to generate goal-directed and experience-based behaviour; i.e. behaviour

that is not determined by positive or negative reinforcements in the immediate

situation (pre-potent responses). The executive functions responsible for this type

of behaviour are primarily localised in the frontal lobes of the brain. These func­

tions are thought to have developed during human evolution, thereby creating

the possibility of both intentional behaviour and social interaction in groups

(Barkley, 2001 ).

In Barkley's model, the inability to inhibit behavioural impulses, is hypothesized

to be the core dysfunction in ADHD. The ability to perform behavioural inhibi­

tion encompasses several executive processes including the ability to inhibit and

postpone the execution of a pre-potent behavioural response. Intact behavioural

inhibition is seen as a prerequisite in order for a number of other secondary

executive functions to be able to influence the behaviour before it is executed.

These executive functions encompass verbal and nonverbal working memory,

self-regulation of affect/motivation and reorganization of behaviour. When these

executive functions are not given the possibility to influence the behaviour (due to

the basic deficient inhibitory ability), the resultant behaviour will be characterized

by irrelevant actions, insufficient inner control over behaviour, lack of flexibility,

etc. It is this kind of behaviour that has been labelled as inattentive, impulsive, and

hyperactive. The theory thus postulates that the essential dysfunction in ADHD

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is an executive dysfunction and not primarily an attentional dysfunction. This

theory on ADHD as a disturbance of executive functions has been summarized

as follows:

" .. ADHD is a developmental disorder of behavioural inhibition that impairs

the development of effective self-regulation (executive functioning) and is not, as

its name implies, chiefly a disorder of attention." (Barkley, 1997 b, 46).

Thus, based on this widely recognized neuropsychological model of ADHD,

inattention and impulsive-hyperactive symptoms can be viewed as behavioural

manifestations of executive dysfunctions.

Executive functions are traditionally measured by performance-based tasks

like e.g. the Wisconsin Card Sorting Test. This task demands attentional flexibil­

ity, working memory, and an ability to change behavioural sets in response to

feedback. Other assessment methods have been developed in order to quantify

executive functions, e.g. rating scales for parents and teachers. Only the study

by Kuntzi & Stevenson (2001) includes neuropsychological performance tasks in

the twin studies to be resumed here. Interviews and rating scales on inattention,

impulsivity, and hyperactivity were used in all the studies.

Introduction to the twin study design

Aetiological factors Twin- and adoption studies are able to segregate genetic factors from environ­

mental factors. Family studies cannot disentangle these factors because the

familiar transmission of a disorder or behavioural trait can happen via both

genetic and environmental factors (Thapar et al., 1995). Nevertheless, a newer

aetiological method within the family studies has been designed. The "blended

families design" is thought to be able to calculate the genetic influence on a

given behaviour and is used in mixed families, i.e. families with children from

different marriages, where the children are more or less genetically related

(Piomin, 2001; Rutter et al., 1999 b).

The twin study is based on the idea of relating the degree of behavioural similar­

ity between twins with the degree of genetic similarity between them. The twin

study is based on the fact that identical twins (monozygotic, MZ) are genetically

identical, whereas non-identical twins (dizygotic, DZ) twins on average share

only 50% of their genetic material. If genetic factors are important in a certain

type of behaviour or psychological trait, then the genetic identical twins are

expected to be more alike than the dizygotic twins (Piomin et al., 2001 ).

Because of this it is important to discriminate in the best possible way between

MZ and DZ twin pairs in order to have a reliable determination of the true twin

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112 /ens Richardt M01/egaard Jepsen & Maria Michel NP, 2006 (2)

status. This can be attained by means of biological laboratory tests, but such

methods are difficult to use in large epidemiological studies. Instead, rating scales

are often used to determine the twin status. Cohen et al. (1973) developed such

a parent rating scale including ten questions on the degree of physical similar­

ity between the twins. The physical traits to be rated on this three-points scale

included e.g. weight, height, facial features, colour of hair and eyes. In addition,

the rating scale included a global assessment of the degree of similarity between

the twins. It also included three questions about whether the twins had been

confused by the parents, by family members, or by others. In the scale validation

process, the results of the rating scale were compared to the results of a blood

sample analysis of 22 factors separately determined by one gene. If the twins

deviated from each other on one or more factors, the twins were categorized as

DZ and in the case of complete similarity they were categorized as MZ. Twin

status determined by this rating scale was 98% in accordance with the twin status

based on the biological analysis.

Adult twin status rating scales have been described as reliable even though

they may contain only a few questions. In contrast Hay et al. (2002) criticized the

use of twin status rating scales encompassing only a few questions to determine

zygosity in child populations.

The equal environments assumption in twin design The often larger similarity among MZ than among DZ twin pairs could hypothe­

tically be due to environmental factors and not only genetic influence (Piomin

et al., 2001 ). The basic assumption in the twin design is that MZ twins and

DZ twins are influenced to the same degree by the environment. This has also

been formulated as a hypothesis that the environmentally influenced similarity

is about the same in MZ twins as in DZ twins being raised in the same family

(Piomin et al., 2001 ). This basic assumption is termed the "equal environments

assumption". If this hypothesis is correct, then a larger degree of similarity in

a behavioural trait between MZ twin pairs than between DZ twin pairs must

be the result of genetic influence (Thapar et al., 1995). If this hypothesis is not

correct, then the greater behavioural similarity between MZ twins than between

DZ twins could partly be explained by environmental factors (Kendler et al.,

1993).

The validity of the "equal environments assumption" has been empirically

examined in different studies and a few of them will be summarised in the fol­

lowing.

Kendler et al. (1993) examined whether different expectations in the social

environment towards the MZ and DZ children could be a critique of the equal

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environments assumption; e.g. if parents had different expectations towards their

MZ twins than towards their DZ twins. Usually parents and other people expect

a higher degree of similarity in e.g. behaviour and abilities between MZ twins

than between DZ twins. In the study by Kendler and colleagues, the effect of these

expectations were elucidated by focusing on the twin pairs, whose twin status

was misclassified by both the twins themselves, their families, and their extended

social environment. Kendler et al. interviewed 1 033 adult twins about their psy­

chological symptoms e.g. depression, anxiety, and disturbed eating behaviour.

The twins were also interviewed about their subjective perception of their twin

status. About 10% of the MZ twin pairs erroneously thought they were DZ, while

only about 1% of the DZ twin pairs erroneously perceived themselves as MZ. The

biological twin status was assessed through evaluations of their degree of physical

similarity, and in case of doubt, a DNA-analysis was performed. The hypothesis

about the "equal environments assumption" could thus be tested comparing the

phenotypic similarity to both perceived twin status and biological twin status.

For all the examined disorders, no evidence for a significant effect of perceived

zygosity on resemblance was found. This result points to a weak influence on

these psychological symptoms from social and personal expectations based on

perceived twin status. This finding thus strengthens the validity of the "equal

environments assumption".

Older studies have shown that parents treat their MZ twin children more alike

than their DZ twin children. This environmental difference could, by a superfi­

cial glance, disqualify the hypothesis of the equal environment for MZ and DZ

twin children. Lytton (1977) proposed that parents might show a more similar

behaviour towards MZ twins because of the larger phenotypic similarity of these

twins and not just because of stereotyped expectations about larger similarity

among them. In order to examine this hypothesis, Lytton observed the social

interaction between 17 MZ and 29 DZ twin pairs (21f2 years of age) and their

parents. The behaviour of the parents towards the twins was classified as either

self-initiated or responding behaviour. Responding behaviour was defined as the

social response by the parent to a behaviour initiated by the child. The respond­

ing parent behaviours were excluded in the study, because only differences in

the parent initiated behaviour towards MZ twins compared to the parent initiated

behaviour towards DZ twins could be valid evidence of parental stereotyped

expectations based on twin status. This category of parent-initiated behaviour

was also less influenced by the immediate effects of the behaviour of the child

towards the parent. The parent-initiated behaviour was classified into one of

four categories: Command-prohibition, suggestion, positive action, and neutral

action. These four types of parental behaviour were compared between MZ and

DZ twin pairs. Among fathers, no differences in behaviour towards the two types

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114 }ens Richardt M01/egaard Jepsen & Maria Michel NP, 2006 (2)

of twins were found. Among mothers, only one statistically significant difference

was found in the behaviour category "suggestion". Lytton concluded that parents

in their spontaneous and self-initiated behaviour in general do not treat MZ twin

pairs as more similar than DZ twin pairs. Thus parents do not create differences

between MZ and DZ twin pairs based on stereotyped expectations, but they

respond to similarities and differences among the children. The results from this

study thus support the validity of the basal assumption in the twin design of an

equal environment for MZ and DZ twins.

Also, Morris-Yates et al. (1990) examined the validity of the hypothesis on

an equal environment for MZ and DZ twins. They administered retrospective

interviews to 343 adult same-sex MZ and DZ twin pairs about the degree of

similarity in their childhood- and adolescent social environment. The adult twins

also filled in the Eysenck questionnaires on personality and symptoms of anxi­

ety and depression. The study found that MZ twins report that they were treated

with excessive similarity by their parents, thus MZ twins report sharing a more

similar environment than DZ twins. This particular finding does not support the

hypothesis of equal environments; however, the degree of similarity in the paren­

tal treatment had no relation to the degree of similarity in personality, anxiety, or

depressive symptoms in the MZ and DZ twins. Based on this finding, Morris-Yates

et al. concluded that the hypothesis of the equal environment was valid:

"Closer analysis suggests that a large component of the greater similarity of

MZs environment during childhood and early adolescence is a consequence of

their genetic identity. Impositions of similarity by parents and others appear to

be of little significance. Therefore, for the purposes of most analyses, the equal

environments assumption is valid." (ibid, p. 325).

In the discussion of the equal environments assumption it has been argued that

MZ twins may have more similar experiences than DZ twins, because the MZ

twins are genetically more alike than DZ twins. It has been argued that genes

influence behaviour by which the individual forms and selects its environment.

In that way, genes also contribute to the differences in experiences between MZ

and DZ pairs. These differences in experiences are not thought of as in conflict

with the equal environments assumption, because the differences were not cre­

ated by the environment (Piomin et al., 2001 ). Rutter et al., (1999 a) criticised

the tendency in this argumentation to ignore the environmental influences, even

though they can be explained by the genetic differences among the individuals. In

contrast to Plomin, Rutter argued that there are no reasons to assume that e.g. the

scape-goating of a child have a reduced effect on the child, because the origins

of the scape-goating lay in genetically influenced aspects of either the parents or

the child's behaviour. Rutter consequently concluded:

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"The importance of the genetic origin of the environmental risk factor is undeni­

able but it is equally relevant that the proximal risk mechanism is environmentally

mediated ... " (ibid, p.6-7).

Plomin et al. (2001) discussed the validity of the "equal environments assump­

tion" from another angel. MZ twins may be exposed prenatally to larger envi­

ronmental differences than DZ twins. For example, the MZ twins have larger

differences in their birth weight than DZ twins, which may be explained by a

larger prenatal competition between the MZ twins that share the same chorion.

To the degree that MZ twins experience a less similar environment that DZ twins,

the genetic factor may be underestimated.

In conclusion, the validity of the "equal environments assumption" is empiri­

cally well examined using different methods. The hypothesis is considered valid

for most behavioural traits. This makes the twin study design a valid quantitative

genetic method in examining psychological dimensions (Piomin et al., 2001 ).

After a critical analysis of the methodological problems in the twin design, Rutter

et al. (1999 a) similarly concluded that the limitations in no way invalidate the

usefulness of this design, but only call for caution in the interpretation of find­

ings.

Models in twin design The twin design includes three basic models by which the influences from

genes, shared environment, and non-shared environment can be estimated. The

difference in the behavioural similarity between MZ and DZ twins creates the

basis for the calculation of the genetic influence on that behaviour. First, when

the behaviour is more alike between MZ twins than between DZ twins, this,

due to the "equal environments assumption", must be caused by genetic factors.

Secondly, any difference between the behaviour of MZ twin pairs must be due

to environmental factors, because these two children are genetically identical.

These environmental factors are named non-shared environmental factors and

they are indexed by the difference between the MZ twin pairs on a given mea­

sure. Non-shared environmental factors affect only one of the twins and may

encompass e.g. accidents, infection with a neuro-toxic virus, or attachment to

different social groups. The third model concerns the shared environmental

factors that affect both twins and may encompass e.g. social class and intactness

of the family. The family environment is thought of as the primary component

in the shared environmental factor (Burt et al., 2001 ). The influence from the

shared environmental factors is indexed by the part of the similarity between

DZ twins that is greater than expected from the genetic model (Faraone, 1996).

When the correlation between the behaviour of DZ twin pairs thus exceeds half

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the correlation between the MZ twins behaviour, this exceeding proportion is

interpreted as a result of influence from a shared environmental factor (Sherman

et al., 1997). As just explained, the twin design includes and calculates the

influence from two environmental factors and a genetic factor.

Heritability The term "heritability" is central in the aetiological twin studies on e.g. ADHD

and the symptom dimensions of inattention, impulsivity and hyperactivity. The

term heritability is associated with an aetiological multi-factorial model of a

behavioural trait or a clinical disorder, i.e. the genetic influence is thought of

as one causal factor among other factors (Rutter et al., 1990). Heritability is a

numeric value that expresses the size of the influence from genetic differen­

ces on the observed differences on a given behavioural trait (e.g. inattentive

behaviour) among a group of people. Thus, heritability is a statistical term

that describes the size of a genetic influence on the observed psychological

or behavioural differences among individuals. The concept of heritability does

not describe the size of the genetic influence on a single person's phenotype

(Piomin, 2001 ). The concept of heritability also appears as a "group heritability"

that is calculated based on the observed differences between two groups, e.g.

a group characterized by a high motor activity level, and a group with a low

motor activity level. Group-heritability expresses the genetic influence on the

membership of a group defined by extreme scores on a given measure, e.g. a

very high motor activity level (Kuntsi & Stevenson, 2000).

The calculation of heritability is based on observations in a certain population

at a certain time. Because of this, the heritability estimate may vary in different

populations and at different times (Piomin, 2001 ).

Faraone (1996) speculated whether the timing of a measurement of attentional

function during a child's developmental course would influence the estimation

of the relative aetiological influences from environment and genes. Faraone

explained the background for this consideration about fluctuating influences over

time from genes and environment as follows:

"Genes are switched on and off through the life cycle to meet the requirements

of the developing organism. Given that the brain is developing through childhood

and adolescence, it makes good sense to consider the possibility that the relative

contributions of genes and environment to attention problems might fluctuate

during development" (ibid, p. 597).

An example of the fluctuating genetic influence on a psychological trait can

be seen in a Dutch follow-up study on the genetic and environmental influences

on the development of general intelligence though the childhood years. Four IQ

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measurements in 209 twin pairs through their developmental course from 5 to

12 years of age revealed an increased genetic influence and a reduced influence

from the shared environment on their general intelligence through development

(Bartels et al., 2002).

Thus, the calculation of heritability is associated with some uncertainties,

and therefore Plomin et al. (1997) recommended that an estimate of heritability

based on a single study should be perceived as a crude estimate, unless the study

included many individuals.

Twin interaction- cooperation or competition The twin study design contains an uncertainty that stems from the interaction

between the twins. This twin interaction can be either competitive or coop­

erative (Rietveld et al., 2003). The effect of competition is also referred to as a

contrast effect and appears, when the behaviour of one twin causes the other

twin to behave differently. A cooperative effect appears, when the behaviour of

one twin causes the other twin to behave similarly (e.g. described Carey (1992)

a possible cooperative effect in criminal and antisocial behaviour).

An apparent cooperative or contrast effect can occur when parents fill in ques­

tionnaires about their twin children's behaviour. When parents in a twin study are

asked to assess and give information about the behaviour of their twins, they may

be inclined to compare the children with each other. In this way, the behaviour

of one twin can act as a standard for the assessment of the behaviour of the other

twin. The parents can either attach importance to the similarity or to the difference

between the behaviour of the twins. Data from twin studies can be analyzed for

the presence of contrast effect and/or rater bias (Rietveld et al., 2003).

Are twins representative of the general population? The difference in e.g. birth weight and time of birth between twins and single­

tons naturally raises the question as to what degree twin children can represent

the general population, primarily consisting of singletons. Differences between

twins and singletons can hypothetically reduce the validity of the generalization

of results from twin studies to singletons. Plomin et al. (1997) concluded that

twins do not differ considerably from singletons with respect to personality

and psychopathology. Because of this, the results from the twin design can

be generalized, and the method is suitable to study the genetic influence

on behavioural dimensions in the general population. Rutter et al. (1999 a)

discussed the importance of the greater risk of complications associated with

twin pregnancies than with pregnancies of singletons. They felt that neither the

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obstetric nor the perinatal complications had any influence on the validity of

twin studies of psychopathology, except in relation to mental retardation. Taken

together, the twin study design is evaluated to be a valid method to estimate

the genetic and environmental influences on the variation of a behavioural trait

in a population (ibid).

Diagnostic category or dimension It is a matter of debate whether a psychopathological condition is best descri­

bed as a dimension (a continuum) or if a categorical description in diagnostic

classes is more suitable.

In the case of conduct disorder and other types of more common types of

psychopathology, the range from more severe to less severe symptoms most

likely represents the same disturbance (Rutter, 1990). This makes a dimensional

description well suited and at the same time, a specific cut-off on this continuum

does not seem meaningful. In the case of other more severe and more seldom

psychopathological conditions like e.g. autism a categorical description seems

more suitable than a dimensional approach. Rutter also mentions anorexia ner­

vosa as an example of a disturbance where the less severe symptoms (dieting and

dissatisfaction with own body) may not represent the same disorder as represented

by the more severe symptoms.

In the DSM-IV, ADHD is defined as a category based on an observation of

the presence of a certain number of well-defined symptoms. Using a categorical

approach, the diagnostic criteria are either met or not. The disturbed functional

domains in ADHD (inattention, impulsivity and hyperactivity) can also be exam­

ined as dimensions. For this purpose e.g. rating scales are used to register the

symptoms. Some twin studies on the aetiology of ADHD have used a categorical

approach based on the diagnostic criteria from e.g. DSM-IV or DSM-111-R (APA,

1987). Other twin studies have examined the dysfunctional domains in ADHD

using a dimensional approach and utilized symptom-scales, neuropsychological

tests, or rating scales.

Psychopathological categories are diagnosed as either present or absent. That

is why the concept of concordance is used instead of correlation (Piomin et al.,

2001 ). Concordance is an index of risk. If the concordance in a twin study is

e.g. 1 0%, it means that if one twin has a certain disorder, then there is a 1 0%

likelihood that the other twin also has this disorder. Based on the twin concord­

ances, the heritability of a psychopathological disorder can be estimated. If MZ

twins have a concordance greater than the DZ twin concordance, it points to a

genetic influence on the disorder. If MZ and DZ twin concordances are the same,

heritability is zero (ibid).

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NP, 2006 (2)

Literature

ADHD and the symptom dimensions inattention, impulsivity, and hyperactivity

The literature used in this article has been found through a systematic search

in the databases PubMEd (MEDLIN E), EMBASE, and Psyclnfo through the years

1996 to 2004. In this paper we summarise all articles published from February

1st 1996 to April 1st 2004 that used the twin study design to investigate the

aetiology of ADHD. This review encompasses both twin studies using a cate­

gorical approach to ADHD (i.e. defined by authorized diagnostic criteria or

by criteria defined in the particular study) and studies using a dimensional

approach. The latter focuses on the degree of deviance in one or more of the

disturbed functional dimensions in ADHD (i.e. inattention, hyperactivity, and

impulsivity).

Summary of twin studies on AOH 0 and AOH 0-symptom dimensions

Gjone, Stevenson & Sundet (1996)

Purpose: Gjone, Stevenson & Sunde! (1996) assessed the genetic and environmental influences

on attention problems, using the Child Behavior Checklist (CBCL).

Method: The sample comprised same-sex twins between 5 to 15 years of age from the gen­

eral population in Norway. Parents of twin pairs from five national birth cohorts were contacted

by mail and asked to describe their children's behaviour by completing the CBCL rating scale.

Zygosity was determined based on parental information on a validated twin similarity question­

naire. The final sample included 526 MZ twin pairs and 389 DZ twin pairs. Data from the age

group 5 to 9 years and the age group 12 to 15 years were divided to detect possible age differences

in relative influence of genetic and environmental factors on attention problems.

Results: The heritability of attention problems showed no significant differences between

the two sexes or between the two age groups. The heritability estimates ranged from 66% to

78%. Estimates of influence from non-shared environmental factors ranged from 21% to 27%.

Contributions from shared environmental factors were little to none on attentional problems.

Heritability was also estimated regarding the severity of the attentional problems. The results

showed no significant changes in group heritability with increasing severity.

Sherman, McGue, & Iacono (1997a) Purpose: Sherman eta!. (1997a) examined concordance rates for ADHD, defined by DSM-111 and

DSM-111-R criteria, in MZ and DZ twins. Both teacher and parent information was used. In this

context the heritability of ADHD was calculated.

Method: Participants in the study were 194 MZ and 94 DZ male twin pairs, aged 11-12 years,

from an unselected population-based sample from Minnesota, USA. Exclusion criteria included

adoption and severe intellectual or physical disabilities. Zygosity was determined by a parental

questionnaire, an experimenter zygosity estimate, and an algorithm diagnosis including cephalic

index and fingerprint ridge count. In cases of disagreement between these estimates, serological

analysis was conducted.

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120 }ens Richardt M0flegaard Jepsen & Maria Michel NP, 2006 (2)

Teachers fulfilled a rating form including behaviour-items from existing teacher rating forms

and items covering the DSM-111 criteria for Attention disorder with hyperactivity and the DSM-111-R

criteria for ADHD. Mothers were given a diagnostic interview (Diagnostic Interview for Children

and Adolescent- Revised; DICA-R), with supplementary probes and questions to ensure complete

coverage of the disorders.

In this study, children who either met full criteria for, or fell one symptom short of, DSM criteria

were considered to have ADHD.

The subjects with ADHD were further subdivided; and given the diagnosis "pervasive ADHD"

when symptoms were reported in both the home and at school, and "situational ADHD" where

symptom criteria were reported by only mother or teacher respectively.

Results: For ADHD based solely on teacher ratings, a concordance for MZ twins of 0.53 and

for DZ twins of 0.37 were found. Heritability was 73% and contribution from non-shared envi­

ronmental factors was 27%. For ADHD based solely on mothers information, a concordance for MZ twins on 0.67 and

for DZ twins on 0.0 was found. Heritability was 89% and contribution from non-shared envi­

ronmental factors was 11%.

For ADHD, based on both teachers and mothers information, a concordance for MZ twins

on 0.58 and for DZ twins on 0.31 was found. Heritability was 79% and contribution from non­

shared environmental factors was 21%. Contributions from shared environmental factors was

non significant.

The high heritability indicates that the vast majority of the liability toADHD (defined by DSM-111

and DSM-111-R criteria) is associated with genetic factors.

Sherman, Iacono, & McGue (1997 b)

Purpose: Sherman et al. (1997) estimated genetic and environmental contributions to ADHD­

symptoms, using information from both teachers and mothers on the symptoms of the children.

Where the authors in their former study investigated heritability of ADHD as a category, in this

study they investigated the heritability of ADHD-symptom dimensions.

Method: Participants in the study was twin boys aged 11 to 12 years from the general popula­

tion in Minnesota, in total 194 MZ and 94 DZ twin pairs. Exclusion criteria included adoption

and severe physical or intellectual disabilities. Zygosity was determined by a parental question­

naire, an experimenter zygosity estimate, and an algorithm diagnosis including cephalic index

and fingerprint ridge count. In cases of disagreement between these estimates, serological analysis

was conducted.

Teachers completed a rating scale (MTFS Teacher Rating Form) covering the DSM-111 criteria

for attention disorder with hyperactivity and DSM-111-R criteria for ADHD, oppositional defiant

disorder and conduct disorder symptoms. Mothers were given a diagnostic interview (DICA-R),

covering disturbances including both external ising disorders (e.g. ADHD, oppositional and con­

duct disorders) and internalizing disorders (e.g. depression).

Results: Clear evidence for a genetic influence on the dimensions inattention and impulsivity­

hyperactivity was found. However, the correlations between the symptoms of the twins differed

according to the informant source, i.e. mother or teacher. Based on teacher ratings, a heritability

of inattention of 39% were found, with an influence from shared environmental factors of 39%

and from non-shared environmental factors of 22%. For the dimension impulsivity-hyperactivity

a heritability of 69% was found, and contribution from non-shared environmental factors of 31%. On this dimension no influence from shared environment was found.

Based on interviews with mothers, a heritability on inattention of 69% was found, influence

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NP, 2006 (2) ADHD and the symptom dimensions inattention,

impulsivity, and hyperactivity

from non-shared environmental factors comprising 31% and no influence from shared environ­

mental factors. For impulsivity-hyperactivity, a heritability of 91% was found, contribution from

non-shared environmental factors of 9% and no influence from shared environmental factors.

Levy, Hay, McStephen, Wood & Waldman (1997) Purpose: Levy et al. (1997) investigated the heritability of the symptom dimensions of ADHD and

of ADHD as a diagnostic category (using DSM-111-R criteria).

Method: The 14 symptoms from DSM-111-R were included in the questionnaire Australian Twin

Behaviour Rating Scale, which was mailed to families with 4- to 12-year old twins. Participants

were recruited from an Australian national twin register. The final sample included 1938 families

with 1919 male twins and 1957 female twins and their 1191 single-born siblings. The study

excluded families where a child had a major disability e.g. autism or Downs syndrome. Zygosity

was determined by a questionnaire with questions on similarity in physical features and frequency

of confusion by parents and others. In cases of doubt, an evaluation of physical resemblance was

made based on photos of the children.

Results: The correlation of ADHD-symptoms in MZ twins was higher than in DZ twins (r MZ

= .880 and r DZ = .488). The heritability of ADHD-symptoms was 75%. With a categorical

approach and a cut off of 8 symptoms a higher concordance in MZ twins than in DZ twins was

found (concordance MZ twins: 82.4% and concordance DZ twins: 37.9%). The heritability of

ADHD was found to be 91% and the effect of the shared environment 13%.

Nadder, Silberg, Eaves, Maes & Meyer (1998) Purpose: Nadder et al. (1998) examined the influence of genetic and environmental factors on

ADHD-symptoms.

Method: The final sample included 900 twins pairs aged 7-13 years from the general popu­

lation. The twins were part of a twin register in Virginia, USA. Zygosity was determined using

one question of physical similarity and one question of perceived zygosity. The study included

DZ twin pairs of different genders, which made it possible also to evaluate whether genes and

environmental factors affect the two genders in the same way. Parents participated in a telephone

survey to screen the children for 6 ADHD-symptoms. The validity of the telephone screening was

assessed in a comparison of the results with maternal ratings from the hyperactivity subscale of

the CBCL obtained in a previous study.

Results: Of the boys, 23.9% had 4 or more of the 6 ADHD-symptoms compared with only

13.2% of the girls. The heritability of ADHD-symptoms was 58% in girls and 61% in boys. Non­

shared environmental factors contributed with 42% in girls and 39% in boys. A contrast effect

was found in the study.

Steffenson, Larsson, Fried, El-Sayed, Rydelius, & Lichtenstein (1999) Purpose: The purpose of the study by Steffenson et al. (1999) was to evaluate whether the genetic

influence on ADHD-symptoms could be mediated by a genetic disposition for global maturity i.e.

a hypothesis, that maturational lag has an importance for ADHD. In this context, the influence

from genetic and environmental factors on ADHD-symptoms was calculated.

Method: The study included 8 to 9 year old twins from a population based Swedish Twin

Registry. Parents received a mailed questionnaire including the 14 ADHD items from DSM-111-R

and two questions concerning general maturity.

Zygosity was determined by one question regarding physical similarity in the children. The final

analysis included 731 same-sex MZ and DZ twin pairs and 317 DZ twin pairs of different sex.

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122 /ens Richardt Mrallegaard Jepsen & Maria Michel NP, 2006 (2)

Results: In this study, the results were calculated separately for boys and girls, and a different

heritability for ADHD was found for the two sexes. For girls, a heritability of 68%, an influence

from shared environmental factors of 12% and an influence from non-shared environmental fac­

tors of 19% was found. For boys, a heritability of 35%, an influence from shared environmental

factors of 40% and an influence from non-shared environmental factors of 25% was found.

Rhee, Waldman, Hay & Levy (1999) Purpose: Rhee et al. (1999) examined the heritability of ADHD-symptoms in the general popula­

tion and the influence from shared and non-shared environment including sex differences herein.

They also examined heritability in a group of children with many ADHD-symptoms.

Method: Participants were recruited from a national population-based and volunteer twin

registry in Australia and included twins between 3 and 15 years of age (1 034 MZ twin pairs and

1009 DZ twin pairs) and their 696 siblings between 3-18 years. Zygosity was determined based on

mothers information on physical similarity in an 11-item questionnaire. Mothers also completed

a questionnaire including 14 ADHD-symptoms (D5M-III-R). If a child had 8 or more symptoms

it was categorised as having ADHD. Heritability was calculated in four different subgroups of the

child population, e.g. a group comprising only twin pairs of the same sex. In addition, heritability

in individuals with 8 or more ADHD-symptoms in the same four subgroups was calculated.

Results: Heritability of ADHD-symptoms varied from 85% to 86% in the four subgroups, even

though two different models of genetic influence were used in the calculations.

Influence from shared environment on ADHD-symptoms was insignificant and influence from

non-shared environment was 14%-15%. The category of children with many ADHD-symptoms

(8 or more) was labelled "highly heritable", but heritability of ADHD-symptoms in the general

population was shown to be even higher.

Hudziak, Rudiger, Neale, Heath & Todd (2000) Purpose: Hudziak et al. (2000) calculated genetic and environmental influence on attentional

problems.

Method: Parents of same-sex twin pairs, aged 8 to 12 years, completed the questionnaire Child

Behavior Checklist (CBCL). CBCL contains 118 problem behaviours, some of which deal with

attentional problems. CBCL was primarily filled in by the mothers (92%). The twins were sampled

from the general population and took part in an ongoing Twin Study including all twins born

between 1975 and 1991 in Missouri, USA. The study on attentional problems encompassed 286

boy twin pairs (of these 129 MZ) and 206 girl twin pairs (91 MZ). Zygosity was determined by a

telephone interview through parental responses to questions about physical similarity, a method

that had formerly been validated.

Results: A stronger correlation of attentional problems in MZ than in DZ twin pairs was found

(r = .69 MZ boys; r = .26 for DZ boys; r = .66 for MZ girls; r = .20 for DZ girls). The heritability

of attentional problems was 60% for girls and 68% for boys. Shared environment were shown to

have no importance for attentional problems, and the influence from non-shared environmental

factors varied from 24% to 40%.

Thapar, Harrington, Ross, & McGuffin (2000)

Purpose: Thapar et al. (2000) investigated the aetiology behind ADHD where symptoms are seen

both at school and at home. The study therefore included both parent and teacher information

about the symptoms inattention, overactivity, and impulsivity in the children. In both D5M-IV and

ICD-10, the diagnostic systems require that symptoms of inattention and impulsive/hyperactive

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behaviour are manifest in more than one situation. In clinical practice this is often defined as the

presence of symptoms both at home and at school.

Method: After drop out and exclusion (e.g. in cases of mental retardation), the material

included 731 MZ twin pairs, 590 same-sex DZ twin pairs, and 599 opposite-sex twin pairs,

aged 5 to 17 years, from a population based twin register in Manchester, England. Mothers and

teachers were mailed a modified version of DuPaul ADHD Rating Scale, a questionnaire about

the symptoms of ADHD. If a child scored at least at the 8oth percentile, it was categorised as

having ADHD. Zygosity was determined by maternal response on the Cohen's questionnaire

about twin similarity.

Results: The heritability of ADHD, based on parental information alone, was 80%. The herit­

ability of ADHD was found to be 50% based on data solely from teachers. Finally, the heritability

of ADHD seen both at home and at school was 79% when calculations were based on both

parent and teacher information. The shared environment was shown to be without influence

on ADHD when calculations were based on data from mothers. Shared environment was also

without influence on ADHD based on information from both teachers and parents. In contrast

to this, the influence from shared environment was found to be 36% when based on teacher

information alone. Influence from non-shared environment was respectively 20% (based on

parent information), 14% (based on teacher information) and 21% (based on both parent and

teacher information).

Eaves, Rutter, Silberg, Shillady, Maes, & Pickles (2000)

Purpose: As part of an investigation of genetic and environmental components in ODD (oppo­

sitional-defiant disorder) and CD (conduct disorder) the authors examined the genetic and

environmental contributions to the three components in ADHD - inattention, impulsivity and

hyperactivity.

Method: The study was part of a longitudinal study of twins, aged 8 to 16 years, from the

general population in Virginia, USA. Parents and children were interviewed using the Child and

Adolescent Psychiatric Assessment (CAPA) that included two symptoms from each of the three

ADHD components. In this study a total of 1376 MZ and DZ twin pairs participated, where

zygosity was known with sufficient certainty and where at least one twin in the pair showed a

symptom of at least one of the aforementioned components.

Results: Based on parental information, a heritability ranging from 38% to 70% was found in

girls on the three components inattention, impulsivity, and hyperactivity- and for boys from 61%

to 74%. The lowest heritability was found for hyperactivity in girls (38%), whereas heritability

of impulsivity and inattention in girls showed more similarity to the heritability estimates found

in boys. In this study a great contrast effect was found. After correction for contrast effects, the

authors stated that there was little evidence that the genetic basis of ADHD is the same in boys

and girls.

Wilcutt, Pennington & DeFries (2000)

Purpose: Willcutt et al. (2000) examined the aetiology of the dimensions inattention and hyper­

activity/impulsivity and of ADHD.

Method: The study included 373 same-sex twin pairs, aged 8 to 18 years; where at least one

twin in the pair had exhibited learning difficulties in reading or mathematics. The twins were

recruited from Colorado Learning Disabilities Research Center. Zygosity was determined using

a modified version of a validated questionnaire, and in cases of doubt, a supplementary DNA

analysis was conducted.

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124 }ens Richardt M01fegaard Jepsen & Maria Michel NP, 2006 (2)

Mothers and a few fathers completed a diagnostic interview (Diagnostic Interview for Children

and Adolescents (DICA)), 50% as an interview and 50% as a questionnaire. Full scale IQ of

the children was assessed using WISC-R or WAIS, and the children also had a test of academic

achievement in reading and spelling.

DICA covered symptoms from the DSM-111 criteria for ADHD. 7 of these constituted an inat­

tention factor and 7 others a hyperactivity/impulsivity factor. An 8 symptoms cut-off was used as

criteria for ADHD. In addition, the cut-off criteria for extreme inattention were set at 6 symptoms

and for extreme hyperactivity/impulsivity at 3 symptoms.

Results: For ADHD (8 symptoms cut-off), a heritability on 98% was found. This result indicates

that ADHD (based on DICA) is almost entirely attributable to genetic factors. For other high cut-off

values (5, 6, 7, and 10 symptoms), a high heritability was also found, ranging from 92% to 98%.

The genetic influence thus contributed with almost the same strength regardless of whether the

diagnostic cut-off was set at 5 or 10 symptoms.

A heritability of 94% was found for high scores on the inattention dimension.

For high scores on the dimension hyperactivity/impulsivity, a heritability of 78% was found.

The heritability of extreme inattention was high whether or not the person also exhibited extreme

hyperactivity/impulsivity. In contrast, the heritability of extreme hyperactivity/impulsivity was only

high when the person also had many inattention symptoms, but low when the person did not

also exhibit symptoms of inattention.

Coolidge, Thede & Young (2000) Purpose: Coolidge et al. (2000) examined the relative contributions of genetic and environmental

factors to the co-morbidity of ADHD with conduct disorder (CD), oppositional defiant disorder

(ODD) or executive function deficits (EF) respectively. In this context the heritability of ADHD

also was calculated.

Method: The study included 224 twins (70 MZ pairs and 42 DZ pairs) from Colorado, USA,

with a mean age of 8 years. The participants were recruited through e.g. newspapers and adver­

tisements on the internet. Parents filled out a 200-item questionnaire (Coolidge Personality and

Neuropsychological Inventory), covering a range of diagnostic categories (DSM-IV) and neu­

ropsychological dysfunctions. Zygosity was determined using a questionnaire with items covering

physical similarities and mistaking the twins. Parents also filled out a demographic survey. They

were instructed to complete questionnaires for each child on separate days to reduce contrast

effect.

Results: The heritability of ADHD was 82%. Influence from non-shared environmental factors

was 18%, with no evidence of influence from shared environment. The study found that the co­

morbidity of ADHD with CD, ODD and EF was largely attributable to genetic influences. The

authors concluded that there is a common genetic vulnerability underlying a number of behav­

ioural and cognitive problems in children. The study found no evidence that shared environmental

factors contribute to the co-morbidity between these behavioural symptoms.

Kuntzi & Stevenson (2001) Purpose: Kuntzi and Stevenson (2001) combined two research approaches to hyperactivity in order

to make a behavioural genetic analysis of hyperactive behaviour and also of the psychological

mechanisms implicated in the disorder.

Method: The study included 268 same-sex twin pairs, age 7 to 11 years, sampled from the gen­

eral population. Parents and teachers filled out a questionnaire to assess hyperactivity (Conners'

Parent and Teacher Rating Scales). Some of the twin pairs were also assessed with a battery of

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psychological tests to estimate e.g. delay aversion and working memory. Three subgroups were

chosen for the analysis in this study:

a) One group for the study of genetic influence on hyperactivity as a dimension.

b) One group for the study of genetic influence on extreme hyperactivity, defined as a score 1.5

standard deviation above mean.

c) One group for the analysis of a possible common genetic influence on hyperactivity and the

psychological functions that are shown to be deviant in hyperactive children.

Zygosity was determined using a parent questionnaire. In cases of doubt three independent

raters evaluated photos of the children.

Results: a) In this study of hyperactivity as a dimension, heritability based on parent informa­

tion was found to be 71%. Non-shared environmental factors explained the remaining 29% of

the variance. Heritability based on teacher information was 57% and non-shared environmental

factors explained the remaining 43% of the variance.

b) In the study of extreme hyperactivity, a group heritability of 42% was found based on parent

information and of only 20% based on teacher information.

c) This study found that the variation in reaction times on a psychological test shares a genetic

basis with extreme hyperactivity. A group heritability of 64% was found. Furthermore, a common

genetic basis for extreme hyperactivity and a summed score of all the psychological test perform­

ances was found (with a group heritability of 80%).

Price, Simonoff, Waldman, Asherson & Plomin (2001)

Purpose: Price et al. (2001) investigated the heritability of hyperactive behaviour in preschool

children.

Method: Parents of all twins born in England and Wales in 1994 filled in a questionnaire when

the children were 2, 3 and 4 years old, with 4 questions from Revised Rutter Parent Scale for

Preschool children. Children with extreme pregnancy- or perinatal difficulties or chromosomal

anomalies were excluded from the study. The final sample included more than 2000 twin pairs.

Zygosity was determined based on a validated parent questionnaire.

Results: A high heritability of hyperactivity from 79% to 83% was found in the three age groups.

Influence from non-shared environmental factors was 17%-21%. No influence from shared

environmental factors was found.

Group heritability estimates for the most hyperactive 5%, 10%, and 20% of children at each

age group ranged from 83% to 93%. Influence from non-shared environmental factors was 7%

to 17%. No influence from shared environmental factors was found in these subgroups.

Genetic influence was thus found to be of equal importance across the continuum of hyper­

activity and inattention, including the most severely affected preschool children, suggesting that

ADHD may represent an extreme end of a behavioural dimension. This study found a substantial

genetic influence on hyperactivity and inattention for preschool ages, similar to what has been

found by other researchers for middle childhood and adolescence. This might express the continu­

ing influence of genetic factors on hyperactivity from infancy into adolescence.

Thapar, Harrington & McGuffin (2001)

Purpose: Thapar et al. (2001 l examined whether ADHD and conduct problems share common

risk factors. They also investigated whether the group of children with both ADHD and conduct

disorder make up a more heritable variant of ADHD. As part of the study, the heritability of

ADHD was calculated.

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126 }ens Richardt M01legaard Jepsen & Maria Michel NP, 2006 (2)

Method: The study included twins aged 5- 17 years from a population based twin register in

Manchester, UK. Questionnaires were mailed to parents and the final sample included informa­

tion from 2082 twin pairs. Zygosity was determined using a validated questionnaire about physical

similarity. Parents filled out a modified version of Dupaul ADHD Rating Scale, which, in addition

to the 14 ADHD-symptoms from DSM-111-R, also comprised four additional items to cover the

diagnostic criteria from ICD-1 0. Parents also completed the questionnaire Rutter's A Scale, which

includes conduct items. Occurrence of hyperactivity and conduct problems were defined by a

cut-off above 8oth centile on the two questionnaires respectively.

Results: In this study, a heritability of 80% was found for ADHD-related behaviour, influence

from non-shared environmental factors was 20%, and there was no influence from shared envi­

ronmental factors. It was concluded that when ADHD and conduct problems occur together, it

represents a genetic more severe variant of ADHD, even though heritability of conduct disorder

alone was not so high (47%). ADHD-related behaviour and conduct disorder share a common

genetic aetiology. The co-morbidity between ADHD and conduct disorder is mainly explained by

a common genetic risk factor, but a common non-shared environmental factor also contributes

hereto. The examination of data suggested that ADHD-related behaviour and conduct problems

are partly two distinct categories.

Martin, Scourfield & McGuffin (2002) Purpose: Martinet al. (2002) examined the degree of overlap between parent- and teacher reports

of ADHD-symptoms on the same questionnaires. Thus the aim was to use multiple informants to

assess the extent to which observer effects influence aetiological estimates. In the study heritability

was calculated based on parent- and teacher information respectively.

Method: From a population-based birth-register of all children born in Cardiff, South Wales,

twins between 5 and 16 years of age were found. The final sample included 278 MZ, 378 DZ and

14 pairs with unknown zygosity, in all 1340 children. Zygosity was determined using a validated

questionnaire with 6 items on physical similarity. Parents (usually mothers) and the children's

teachers reported symptoms of ADHD on the abbreviated Conners scale and the hyperactivity

subscale from Strengths and Difficulties Questionnaire (SDQ).

Results: Based on parent ratings, for the SDQ, the study found a heritability of 72%, influence

from non-shared environmental factors of 28% and no influence from shared environmental

factors. With regard to the Conners scale, a heritability of 74%, influence from non-shared envi­

ronmental factors of 26% and no influence from shared environmental factors was found.

Based on teacher ratings, for the SDQ, the study found a heritability of 81%, an influence

from non-shared environmental factors of 19%, and no influence from shared environmental

factors. Based on teacher information on Conners scale, a heritability of 80%, an influence from

non-shared environmental factors of 20%, and no influence from shared environmental factors

was found.

Kuntsi, Eley, Taylor, Hughes, Asherson, Caspi & MuffiH (2004) Purpose: Kuntsi et al. (2004) examined to what degree lower general intelligence (IQ), as can be

seen in persons with ADHD, are due to genetic or environmental factors. It has previously been

found that children with an ADHD-diagnosis, compared to control children, have a slightly lower

IQ (7-12 IQ-points lower). The background for the present study was that previous population

based research had found a negative correlation between ADHD-symptoms and general intel­

ligence, i.e. a tendency to lower IQ when more ADHD-symptoms are present (-.2 < r < -.4).

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NP, 2006 (2) ADHD and the symptom dimensions inattention,

impulsivity, and hyperactivity

Method: The study included 5-year old twins from two consecutive birth cohorts in England and

Wales. From this sample a high-risk group was chosen (with young age of the mother at first birth

(< 20 years) as a marker). 1116 families participated in the study and received home-visits.

Mothers were interviewed about the children's ADHD-symptoms (DSM-111 and the question­

naire Rutter Child Scale). Items from DSM-111 and Rutter Child Scale were also used for collecting

information from the teachers of the children about their current symptoms at school. In addition,

the children's general intelligence was assessed by two chosen subtests from an intelligence test

for preschool children (WPPSI-R). Zygosity was determined with a questionnaire and in cases of

doubt with DNA analyses.

IQ and ADHD could hypothetically be related to each other because of inattentive behaviour

and disinterest during test-taking. A videotaped and blinded observation of the behaviour of 400

children's test sessions had formerly ruled out this hypothesis, as less than 25% of the association

between IQ and ADHD (equal to two IQ-points) could be attributed to inattentive behaviour in

the test-situation.

Results: The study found a correlation between ADHD-symptoms and IQ of -D.28. The chil­

dren with an ADHD research diagnosis had a mean IQ of 89 compared to an IQ of 98 in the

control group.

Based on information from both parents and teachers, the genetic influence on ADHD­

symptoms was found to be 72%, and non-shared environmental factors contributed with the

remaining 28%.

The genetic influence on the ADHD diagnosis was 85% and contribution from non-shared

environmental factors was 15%.

86% of the correlation between lower IQ and ADHD-symptoms was accounted for by genetic

factors. Non-shared environmental factors accounted for the remaining 14%. One hundred

percent of the correlation between lower IQ and ADHD diagnosis (r = -D.34) was accounted for

by genetic influences.

Rietveld, Hudziak, Bartels, van Beijsterveld, & Boomsma (2004) Purpose: Rietveld et al. (2004) examined the size of genetic and environmental influences on

attention problems in boys and girls.

Method: The study included 2192 twins from a Dutch twin register, with complete data

regarding their attention functioning at the ages 3, 7, 10 and 12 years. At these age levels moth­

ers completed the ratings scale Child Behavior Checklist (CBCl), which has a special preschool

edition for the 3-year olds.

Results: The heritability of attentional problems and hyperactivity was almost 75% at all age

levels. Influence from non-shared environmental factors explained the remaining part of the

variation (about 25% including errors of measurement). No influence from shared environment

was found.

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128 }ens Richardt M0llegaard Jepsen & Maria Michel NP, 2006 (2)

Summary of aetiological twin studies of ADH 0 and of the symptom dimensions inattention and impulsivity­hyperactivity. Table 1 gives a summary of the essential characteristics and results in the twin

studies regarding genetic and environmental influences on ADHD and ADHD­

symptoms.

Table 1. Summary of heritability found in twin studies 1996 to 2004

Authors Year Final Age Clinical symptoms and Heritability Shared Non-number group categories/instrument (informant) environ- shared of parti- ment environ-

cipants ment

Gjone et 1996 1.830 5-15 lnattention/CBCL 66%-78% 0% 21%-

al. years (parents) 27%

Sherman 1997a 576 11-12 ADHD (OSM-111, DSM-111- 73% (teachers) 0% 27%

et al. years R)/ DICA-R 89% (mothers) 0% 11% 79% (teachers 0% 21% +mothers)

Sherman 1997b 576 11-12 lnattention(DSM-111, DSM- 39% (teachers) 39% 22%

et al. years 111-R)/DICA-R (mothers), 69% (mothers) 0% 31% MTFS-trf (teachers) Hyperactivity-impulsivity 69% (teachers) 0% 31% (DSM-111, DSM-111-R)/DICA- 91% (mothers) 0% 9% R (mothers), MTFS-trf (teachers)

Levy et al. 1997 5.067 4-12 ADHD-symptoms (DSM-111- 75% (parents) Not Not years R)/Australian Twin Behavior speci- speci-

Rating Scale lied lied ADHD (DSM-111-R)/ 91% (parents) 0% 13% Australian Twin Behavior Rating Scale

Nadder 1998 1.800 7-13 ADHD-symptoms (DSM- Girls: 58% 0% 42% et al. years 111-R, DSM-IV)/telephone (parents)

interview Boys: 61% 0% 39% (parents)

Steffenson 1999 2.096 8-9 ADHD-symptoms (OSM-111- Girls: 68% 12% 19% et al. years R)/rating scale (parents)

Boys: 35% 40% 25% (parents)

Rhee et al. 1999 4.086 3-15 ADHD-symptoms(DSM-111- 85%-86% 0% 14%-(twins) years R)/rating scale (parents) 15% 696(sib-lings) 3-18 ~ 8 ADHD-symptoms highly herit-

years (DSM-111-R)/ rating scale able

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NP, 2006 (2)

Authors Year Final Age number group of parti-dpants

Hudziak 2000 984 8-12 et al. years

Thapar 2000 3.840 5-17 et al. years

Eaves et 2000 2.752 8-16 al. years

Willcut 2000 746 8-18 et al. years

Coolidge 2000 224 8 years et al. (mean)

Kuntzi & 2001 536 7-11 Stevenson years

Price et al. 2001 > 4.000 2, 3 and 4 years

Thapar 2001 4.164 5-17 et al. years

Martin 2002 1.340 5-16 et al. years

ADHD and the symptom dimensions inattention, impulsivity, and hyperactivity

Clinical symptoms and Heritability Shared Non-categories/instrument (informant) environ- shared

ment environ-ment

Inattention (CBCU Girls: 60% 0% 32%-Boys: 68% 40% (mothers)

ADHD/DuPaul 80% (parents) 0% 20% ADHD Rating Scale 50% (teachers) 36% 14% (ADHD defined as 80% 79% (parents 0% 21% percentile) +teachers)

Inattention, impulsivity and Girls: 38%- Not Not hyperactivity/CAP A 70% (parents) speci- speci-

fied fied

Boys: 61%- Not Not 74% (parents) speci- speci-

fied fied

ADHD (DSM-111)/DICA (8 98% (mothers) Not Not symptoms in DICA) speci- speci-

fied fied Inattention 94% (mothers) Not Not

speci- speci-fied fied

Hyperactivity/impulsivity 78% (mothers) Not Not speci- speci-fied fied

ADHD (DSM-IV)ICPNI 82% (parents) 0% 18%

Hyperactivity/Canners 71% (parents) 0% 29% Parent and Teacher Rating 57% (teachers) 0% 43% Scales

Hyperactivity/Revised 79%-83% 0% 17%-Rutter Parent Scale for (parents) 21% Preschool Children

ADHD-related behaviour 80% (parents) 0% 20% (DSM-111, ICD-1 0)/DuPaul ADHD Rating scale, Rutters A scale

ADHD-symptoms/SDQ 72% (parents) 0% 28% 81% (teachers) 0% 19%

ADHD-symptoms!Conners 74% (parents) 0% 26% Scale 80% (teachers) 0% 20%

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130 }ens Richardt MflJIIegaard Jepsen & Maria Michel

Authors Year Final Age Clinical symptoms and Heritability number group categories/instrument (informant) ofparti-cipants

Kuntzi 2004 2.232 5 years ADHD-symptoms (DSM- 72% (parents et al. 111)/Rutter Child Scale +teachers)

ADHD (DSM-111)/Rutter 85% (parents Child Scale +teachers)

Rietveld 2004 2.192 3, 7, Hyperactivity and inatten- 75% (mothers) et al. 10 and tion/CBCL

12 yrs

DICA-R: Diagnostic Interview for Children and Adolescents- Revised, MTFS-trf: Minnesota Twin Family Study- teacher rating form, CBCL: Child Behavior Checklist, CAPA: Child and Adolescent Psychiatric Assessment, DICA: Diagnostic Interview for Children and Adolescents, CPNI: Coolidge Personality and Neuropsychological Inventory, SDQ: Strengths and Difficulties Questionnaire

NP, 2006 (2)

Shared Non-environ- shared ment environ-

ment

0% 28%

0% 15%

0% 25%

Where the authors have reported the influence from shared environment e.g. as insignificant, we report the influence as 0%.

Conclusion The twin design can differentiate between and quantify influences from genes,

shared environment, and non-shared environment on a psychological trait or on

a psychopathological category. During the last 15 years, a substantial number of

aetiological twin studies of ADHD and of the symptom dimensions inattention

and impulsivity-hyperactivity have been conducted. All the 18 twin studies from

1996 to 2004 that have been summarised in this article have based their esti­

mates of genetic and environmental influences on data from either interviews

or rating-scales. Together the studies include a huge number of children and

adolescents (over 38000 individuals). There is substantial agreement between

the results of the twin studies even though different rating scales and interviews

have been administered in order to describe the behaviour of the children- and

even at different age levels. In addition different methods have been used to eva­

luate the twin status of the subjects. Based on parental information, all results

point to a dominant genetic explanation of ADHD and of ADHD symptoms.

Somewhat inconsistent with all other studies, the study of Steffenson et al.

(1999), which was also based on parent data, found an unusually low heritabi­

lity of ADHD-symptoms in boys, while the heritability of ADHD-symptoms in

girls to a larger degree was in accordance with other findings. In this particular

study (Steffenson et al., 1999) the twin status of the participants was assessed

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NP, 2006 (2) ADHD and the symptom dimensions inattention,

impulsivity, and hyperactivity

with only one single item. In testing for zygosity, studies of adults have shown

that a few items are sufficient; in childhood this is not the case (Hay et al.,

2002). Thus the use of only a single item on zygosity in the study of Steffenson

et al. (1999) may have contributed to a less valid classification of the children

in MZ or DZ and therefore to a less valid estimation of heritability.

Several of the research groups have proposed that twin studies optimally ought

to encompass descriptions of the children's behaviour in several different situa­

tions in order to control for a possible situational variation in attention behaviour

e. g. in school and at home (e. g. Gjone et al., 1996 & Hudziak et al., 2000).

This could be accomplished by collecting data from both parents and teachers.

Information about the behaviour of the children at home is often given by the

mothers. It might further strengthen the credibility of the twin study results if

information about behaviour in the home environment was collected from both

parents (Cooligde et al., 2000).

In studies where information about the children are given by two different

informants e.g. mothers and teachers, differences in the aetiological pattern can

be seen depending on whether information are given by teachers or by parents.

An influence from shared environment and a lower heritability is found when

information about the children is based solely on teacher ratings. This difference

is difficult to explain but may be the result of situational differences in the behav­

iour of the children. In addition teachers may to a larger degree than parents mix

up what behaviour belongs to which twin when behaviour in different situations

are to be remembered and reported in rating scales. Teachers may possibly also

over-report ADHD-symptoms due to a confusion of ADHD-symptoms with other

behavioural symptoms, and mothers may under-report ADHD-symptoms due to

a lack of access to a large reference group (Sherman et al., 1997 a).

Based on parent information, the influences from genes appear to be the

dominant cause of ADHD and ADHD symptoms. Thus in most of the studies

summarised here, a high heritability, between 70% and 90%, has been found.

The documentation of the dominant genetic aetiological factor in ADHD (defined

by different criteria) and ADHD-symptoms is in agreement with the results from

adoption studies (e.g. Sprich et al., 2000). Barkley et al., (2002) described the

strong genetic influence on ADHD as follows:

"The genetic contribution to these traits is routinely found to be among the

highest for any psychiatric disorder (70-95% of trait variation in the population),

nearly approaching the genetic contribution to human height."

The non-shared environment is the second-largest aetiological factor in ADHD

and in ADHD symptoms. In most of the summarised studies, the influence from

non-shared environmental factors varies from 10% to 30%. Finally, the shared

environmental factor has none or only inferior aetiological influence on ADHD

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132 /ens Richardt M(!JI/egaard Jepsen & Maria Michel NP, 2006 (2)

and ADHD symptoms. Thus most of the studies summarised in this article find

no influence from shared environment.

All the twin studies found between 1996 and 2004 are epidemiological inve­

stigations. Therefore they describe the existence of a strong genetic influence on

the normal variation in inattention and impulsivity-hyperactivity in the general

population. However, some of these twin studies have also examined genetic and

environmental influences in groups of children and adolescents with an exces­

sive number of ADHD-symptoms. In these groups of children and adolescents

with exceptionally many symptoms of inattention and impulsivity-hyperactivity,

a very high genetic influence has been found (e.g. Levy et al., 1997). These

findings are of particular relevance for the clinical practice with these children

considering that to our knowledge, no studies have been conducted in the period

from 1996 to 2004, which include twin pairs with at least one child of the pair

having a clinical diagnosis of ADHD (Thapar, 2000). Furthermore, attentional

problems measured with a rating scale are not a direct measure of ADHD. They

have nevertheless been shown to be a marker for a diagnosis of ADHD (Rietveld

et al., 2004).

The non-shared environmental factors contribute to make children in the same

family different. As mentioned above, the influence from the environment on inat­

tention and impulsivity-hyperactivity is predominantly of this non-shared type.

In contrast, the shared environment for children in the same family contributes

very little to ADHD or to ADHD symptoms. Thus the environment not shared

by siblings in a family has far more effect on ADHD and ADHD-symptoms than

the environment shared by the children. Shared environmental factors such as

e.g. parents socio-economic status, their style of upbringing, and the emotional

climate in the home have an inferior or no aetiological influence on ADHD and

ADHD-symptoms. Aetiological theories hypothesising the shared family environ­

mental factors as the primary causes of psychopathology have no validity regard­

ing the aetiology of ADHD and ADHD-symptom dimensions. If one for purely

hypothetical reasons would disregard the biological non-shared environmental

factors as e.g. pregnancy and delivery complications and at the same time ignore

psycho-social non-shared environmental factors outside the family, then all this

non-shared environmental influence may predominantly consist of the unique

relation between the parent and the child. This specific psychosocial factor, i.e.

the relation or the attachment between parent and child, would, even under these

unrealistic magnifying conditions, at most explain about 30% of the variance in

ADHD-symptoms in the population. Thus aetiological theories focusing on the

individual attachments between parents and their children must be considered

highly insufficient as explanatory models.

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NP, 2006 (2) ADHD and the symptom dimensions inattention,

impulsivity, and hyperactivity

Most twin studies described the ADHD-symptoms in a dimensional mode using

e.g. rating scales. As an exception, Levy et al. (1997) used both a dimensional

and a categorical approach in their twin study. The categories of ADHD were

defined by the presence of at least 5 or 8 symptoms. This study made it possible

to compare the heritability based on a dimensional approach with the heritability

in the two defined ADHD-categories. The heritability based on the two ADHD­

categories was not significantly larger than the heritability based on the dimen­

sional or "trait" approach. Based on this finding the authors argued that ADHD

(here defined as more than five, respectively eight, ADHD-symptoms) represents

the extreme end of a continuum in the population rather than a distinct category

with an especially high heritability. The authors therefore proposed perceiving

ADHD as a deviance from a norm rather than a distinct category, as is also done

concerning e.g. mental retardation.

The dominant influence of genes on both ADHD and ADHD symptoms strong­

ly supports Barkley's (1997) suggestion to categorise ADHD as a developmental

disorder in line with e.g. dyslexia and autism spectrum disorders.

To the extent that inattention, impulsivity, and hyperactivity actually reflect

executive dysfunction, the twin study results may suggest that executive dysfunc­

tions also are under primary genetic aetiological influence. This hypothesis is

only partly supported by a twin study of genetic and environmental influences on

executive function measured by the Wisconsin Card Sorting Test (WCST) (Anokhin

et al., 2003). In this study a moderate genetic influence on outcome measures

from WCST were found (heritability from 37% to 46%).

Until now, the behavioural genetic twin studies have primarily focused on

aetiological factors in a single psychopathological disorder like e.g. ADHD. In

the literature there now seems to be a tendency to shift away from this focus

on a single psychopathological disorder or behavioural dimension to a focus

on the aetiology of co-morbid psychopathological disorders. This new focus on

aetiological factors in co-existent problems is very relevant for clinical practice

because different mental and behavioural problems so often are seen together

in the same child. In clinical practice, one can often encounter e.g. co-morbid

aggressive behaviour and ADHD, anxiety and ADHD, or inattention and execu­

tive dysfunctions. As an example, Schmitz & Mrazek (2001) found the relation­

ship between attention problems and co-morbid criminal behaviour to be under

substantial genetic influence (79%).

LITERATURE American Psychiatric Association (1987) Diagnostic and statistical manual of mental disorders;

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