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The Intergenerational Transmission of Anxiety: A Children-of-Twins Study


Abstract and Figures

The transmission of anxiety within families is well recognized, but the underlying processes are poorly understood. Twin studies of adolescent anxiety demonstrate both genetic and environmental influence, and multiple aspects of parenting are associated with offspring anxiety. To date, the children-of-twins design has not been used to evaluate the relative contributions of genetic transmission compared with direct transmission of anxiety from parents to their offspring. Anxiety and neuroticism measures were completed by 385 monozygotic and 486 dizygotic same-sex twin families (37% male twin pair families) from the Twin and Offspring Study in Sweden. Structural equation models tested for the presence of both genetic and environmental transmission from one generation to the next. For both anxiety and neuroticism, the models provide support for significant direct environmental transmission from parents to their adolescent offspring. In contrast, there was no evidence of significant genetic transmission. The association between parental and offspring anxiety largely arises because of a direct association between parents and their children independent of genetic confounds. The lack of genetic transmission may reflect there being different genetic effects on these traits in adolescence and adulthood. Direct environmental transmission is in line with developmental theories of anxiety suggesting that children and adolescents learn anxious behaviors from their parents through a number of pathways such as modeling. Future analyses should combine children-of-twins data with child twin data in order to examine whether this direct effect solely represents parental influences on the offspring or whether it also includes child/adolescent anxiety evoking parental anxiety.
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The Intergenerational Transmission of Anxiety:
A Children-of-Twins Study
Thalia C. Eley, Ph.D., Tom A. McAdams, Ph.D., Fruhling V. Rijsdijk, Ph.D., Paul Lichtenstein, Ph.D., Jurgita Narusyte, Ph.D.,
David Reiss, M.D., Erica L. Spotts, Ph.D., Jody M. Ganiban, Ph.D., Jenae M. Neiderhiser, Ph.D.
Objective: The transmission of anxiety within families is well
recognized, but the underlying processes are poorly un-
derstood. Twin studies of adolescent anxiety demonstrate
both genetic and environmental inuence, and multiple
aspects of parenting are associated with offspring anxiety. To
date, the children-of-twins design has not been used to
evaluate the relative contributions of genetic transmission
compared with direct transmission of anxiety from parents to
their offspring.
Method: Anxiety and neuroticism measures were completed
by 385 monozygotic and 486 dizygotic same-sex twin fam-
ilies (37% male twin pair families) from the Twin and Offspring
Study in Sweden. Structural equation models tested for the
presence of both genetic and environmental transmission
from one generation to the next.
Results: For both anxiety and neuroticism, the models pro-
vide support for signicant direct environmental transmission
from parents to their adolescent offspring. In contrast, there
was no evidence of signicant genetic transmission.
Conclusions: The association between parental and off-
spring anxiety largely arises because of a direct association
between parents and their children independent of genetic
confounds. The lack of genetic transmission may reect there
being different genetic effects on these traits in adolescence
and adulthood. Direct environmental transmission is in line
with developmental theories of anxiety suggesting that chil-
dren and adolescents learn anxious behaviors from their
parents through a number of pathways such as modeling.
Future analyses should combine children-of-twins data with
child twin data in order to examine whether this direct effect
solely represents parental inuences on the offspring or
whether it also includes child/adolescent anxiety evoking
parental anxiety.
AJP in Advance (doi: 10.1176/appi.ajp.2015.14070818)
Anxiety disorders are the most common group of disorders,
with a lifetime prevalence of about 30% (1). They are asso-
ciated with a wide array of personal, nancial, and societal
costs (2), making research into their etiology a priority. A
notable feature of anxiety disorders is that they start early in
life, with a mean age at onset of 11 years (1). It is therefore
crucial to understand the development of anxiety symptoms
in young people.
One of the most robust features of anxiety disorders is that
they run in families (3). This association has been widely
explored, and there is evidence for a number of contributing
mechanisms. First, children and adolescents can develop
symptoms of anxiety by vicarious learning, whereby off-
spring watching anxious behaviors in their parents then
model these behaviors themselves (4). Second, anxious mothers
may have a more anxious parenting style, including holding
more negative expectations and showing greater intrusive-
ness, overprotection, and expressed anxiety (5, 6), although it
should be noted that most studies that have found this as-
sociation focused on families in which the child also had an
anxiety disorder or heightened anxiety symptoms. Third, as
well as parents inuencing their offspring, there is evidence
for the reverse effect. Specically, studies have found that
parents of offspring with anxiety disorders show higher levels
of parental overprotection and rejection and lower levels of
emotional warmth (7, 8). However, these studies do not take
into account another possibility, whereby genes that affect
parent anxiety and child/adolescent anxiety also inuence
parenting, thus leading to a confounding of genetic and en-
vironmental inuences.
Twin studies consistently reveal mild to moderate genetic
inuences on a wide range of child and adolescent anxiety
measures, including trait anxiety (9), disorder-related symp-
toms assessed by self-report (10) and parent-report (11), and
anxiety disorders (12, 13). Similarly, studies of adults reveal
mild to moderate genetic inuences on trait anxiety (14),
anxiety symptoms (15), and anxiety disorders (16). This sug-
gests that thetransmission of anxietyphenotypes from parents
to their children could be explained, at least partially, by ge-
netic inuences. It is noteworthy that there is considerable
ajp in Advance 1
genetic overlap across symptoms reecting different anxiety
diagnoses (such as separation anxiety, social anxiety, and
general anxiety) in child (17, 18), adolescent (10), and adult (10,
19) samples. Furthermore, epidemiological studies have found
evidence for substantial heterotypic continuity within the
anxiety disorders (i.e., continuity of anxiety over time does
not sit within diagnostic boundaries [20]). Thus, a child who
presents with separation anxiety may develop generalized
anxiety in adolescence and panic disorder in adulthood. This
heterotypic continuity, combined with the genetic overlap
found between different types of anxiety measures, suggests
that for examination of transmission of anxiety one should
use a broad measure of anxiety symptomatology reecting
general vulnerability to anxiety disorders.
In addition to providing evidence for genetic inuences,
twin studies also provide support for a signicant role of the
shared environment (21), nongenetic inuences that con-
tribute to family members resembling one another, and the
nonshared environment, that which leads to differences
among family members. The contribution of shared environ-
ment to variation in anxiety is consistent with the evidence
described above for the importance of family environment in the
development of anxiety in children. For example, siblings may
show similar levels of anxiety because they were both exposed to
the same level of parental-expressed anxiety. In summary, there
is evidence to support a role for both genetic and environmental
inuences on anxiety in adults and in children and adolescents;
however, to our knowledge no study to date has explicitly tested
the relative contribution of genetic and en vironmental inuences
to the transmission of anxiety within families. This is important
because we might target interventions for pediatric anxiety
differently if intergenerational transmission is largely a result of
genes versus resulting from the family-wide environment.
Although pediatric twin studies are able to ascertain the
proportion of variance in child/adolescent phenotypes due to
genetic and environmental inuences, they cannot specify
the extent to which genes and the environment contribute to
transmission from parents to their children. For this, other
genetically sensitive designs are needed. The children-of-
twins model is one such design and involves adult twin pairs
and their offspring (22). By comparing correlations between
children and their parent and contrasting this with corre-
lations between children and their parents identical cotwin,
we can learn about the inuence of living with ones parent
over and above simply receiving 50% of their genes. Fur-
thermore, by comparing the extent to which correlations
between children and their twin uncle/aunt (avuncular
correlations) differ for monozygotic and dizygotic twin
families, we can infer the extent to which genetic and en-
vironmental factors inuence transmission from one gen-
eration to another. Children share a greater level of genetic
inuence with their uncle/aunt when in monozygotic fam-
ilies than when in dizygotic families (see Figure 1). Thus, if
children resemble their uncle/aunt to a greater extent in
monozygotic families than in dizygotic families, this implies
a genetic inuence on transmission of the trait of interest. In
contrast, if these two sets of correlations are similar, and are
signicantly lower than the parent-child correlations, this is
indicative of an environmental mode of transmission. While
transmission of both depression and internalizing symptoms
within families has been found to be a result of environmental
transmission independent of genetic effects (2325), the
transmission of anxiety-related traits within families has yet
to be explored using the children-of-twins design.
In the present study,we used the Children of Twins design to
examine the relative contribution of genetic and environmental
inuences to transmission of broadly assessed anxiety from
one generation to another.For this analysis, we used a measure
of anxious personality in parents and a measure of anxiety
symptoms in the offspring. For simplicity, from herein we use
the word anxietyalone when referring to the transmission of
parental anxious personality to offspring anxiety symptoms
while specifying all other types of anxiety as applicable. As
a comparison, we also repeated analyses for neuroticism, given
FIGURE 1. Genetic Correlations Between Family Members in the
Children-of-Twins Study Design for Both Monozygotic (MZ) and
Dizygotic (DZ) Families
Twin 1
Section A
Twin 2
Ospring Ospring
Twin 1
Section B
Twin 2
Ospring Ospring
Section A represents MZ correlations, and Section B represents DZ
correlations. ajp in Advance
that this personality trait shows strong phenotypic and genetic
correlations with anxiety (26).
Data were drawn from the Twin and Offspring Study of
Sweden and comprised information on 387 monozygotic twin
families and 489 dizygotic twin families. A twin family com-
prised a twin pair, each twins spouse, and one of each of their
adolescent children. Only same-sex twin pairs were used, and
twin offspring were selected so that cousins were the same
sex as one another and did not differ in age by more than
4 years. Thirty-seven percent of twin pairs were male, and
52% of offspring were male. At the time of data collection,
the mean age of offspring in the Twin and Offspring Study
of Sweden sample was 15.7 years (SD=2.4; range 1122). The
mean age of twins in the sample was 44.8 years (SD=4.9; range
3260), and for spouses the mean age was 45.5 years (SD=5.4;
range=2565). After complete description of the study was
given, written informed consent was obtained. Further in-
formation on the Twin and Offspring Study of Sweden sample
is provided elsewhere (27).
Parental anxious personality was self-reported by twins using
20 items from the Karolinska Scales of Personality (28, 29).
Items were oriented toward either social (I often feel un-
certainwhen I meet peopleI dont know verywell) or physical
(sometimes my heart beats hard or irregularly for no par-
ticular reason) aspectsof anxiety, in addition to general worry
(I often worry about little things which others see as un-
important). Respondents used a Likert scale ranging from
0 (not at all) to 3 (very) true. Item scoreswere summed to give
an overall anxiety rating. Cronbachs alpha was 0.90.
Offspring anxiety symptoms were measured using items
from the Child Behavior Checklist (30). Twins, their spouses,
and offspring all reported on offspring behavior over the
previous 6 months. A previous study aimed at developing
DSM-oriented scales from Child Behavior Checklist items
(31) was used to guide the selection of items included in our
anxiety scale, and as with the parental anxiety symptoms,
the focus was on items that reect social (clings to adults
or too dependent)andphysical(Imnervous,highstrung,
or tense) aspects of anxiety, as well as general worry (I
worry quite a lot). Items were scored on a scale ranging
from 0 (not) to 2 (very/often) true. Items from all three re-
porters (which correlated from 0.25 to 0.45) were summed
to create an overall anxiety score to provide the broadest
and most objective measure possible. Cronbachsalphawas
Neuroticism was self-reported for both twins and off-
spring using the neuroticism scale of the Eysenck Personality
Questionnaire (32). The scale comprised nine yes/no items
(such as are you often worried without knowing why?)
scored 1/0 for yes/no. Item scores were summed to give an
overall neuroticism rating. Cronbachs alpha was 0.72 for
parents and 0.67 for offspring.
Analyses on anxiety included 385 monozygotic twin families
and 486 dizygotic twin families. However, the neuroticism
measure was only included in the second cohort of the study,
resulting in a reduced sample comprising 222 monozy-
gotic families and 293 dizygotic families for the neuroticism
Genetic analyses were conducted in the structural equation
modeling program OpenMx (33). Prior to analyses, residuals
were taken to control for twin sex and age as is standard practice
in twin analyses (34). All variables were log-transformed to
correct for skew. We tted structural equation models to the
data using maximum likelihood estimation. Models allowed us
to quantify the effects of additive genetic (A), common envi-
ronmental (C; nongenetic effects that make members of a nu-
clear family similar to one another) and nonshared environmental
(E; environmental effects that make members of a family
different from one another) effects on parental anxiety. By
comparing the magnitude of monozygotic twin correlations
(attributable to the combined effects of A+C) to dizygotic twins
(attributable to 0.5*A+C), genetic and environmental inu-
ences can be estimated. Comparing monozygotic and dizygotic
avuncular correlations and parent-child correlations allows
for the estimation of genetic and nongenetic intergenerational
pathways. Comparing correlations between cousins from
monozygotic families with those of dizygotic families allows
for the estimation of the role of familial and nonshared en-
vironmental effects on offspring anxiety.
The model used is shown in Figures 2 and 3. It is note-
worthy that the path from parent phenotype to offspring
phenotype reects the direct inuence of a parents behavior
on his or her offspring. Because this is manifested through the
environment, we describe it as environmentaltransmission,
but it should be noted that this pathway also reects gene-
environment correlation if there is genetic inuence on the
parent phenotype. Second, as in all children-of-twins models,
there was no shared environment factorfor the offspring part
of the model, since this would result in there being too many
paths for the data available. The signicance of the environ-
mental (fromparent to offspring phenotype) andgenetic (from
A1:to offspring phenotype) intergenerational pathways was
tested by creating submodels in which they were xed to zero.
Both chi-square difference tests and Akaikes information
criterion were used to assess whether submodels were a sig-
nicantly worse t to the data than the full model. All analyses
were repeated controlling for assortative mating, but results
were substantively similar (see the online data supplement).
The correlation between the anxiety measures and neurot-
icism was 0.70 for parents and 0.42 for offspring. Correlations
between twin parents and their offspring for both anxiety
ajp in Advance 3
measures and neuroticism are summarized in Table 1. Several
ndings from this table are worth noting. First, there is ev-
idence for genetic effects on both anxious personality and
neuroticism in the parents, as indicated by the larger mono-
zygotic correlations compared with dizygotic correlations
(e.g., 0.55 compared with 0.20, respectively, for anxiety).
Second, there is evidence for genetic inuence on offspring
anxiety symptoms and neuroticism given the larger corre-
lations for cousins from monozygotic families compared
with dizygotic families (e.g., 0.08 compared with 20.03, re-
spectively, for anxiety). Third, there is marginal evidence for
genetic effects on transmission of anxiety given the larger
avuncular correlations (offspring 1parent 2 and vice versa)
for monozygotic families compared with dizygotic families
(0.11 compared with 0.02, respectively). However, these
values are both small, and for neuroticism, this pattern is not
seen (0.03 compared with 0.07 for monozygotic and dizygotic
families, respectively). Overall, these data do not suggest
substantial genetic transmission of broadly assessed anxiety
or neuroticism. Finally, there is modest evidence for envi-
ronmental transmission of both anxiety and neuroticism,
given the larger parent-offspring than avuncular correlations
in both monozygotic and dizygotic families. For example, in
monozygotic families, while the avuncular correlation for
anxiety was 0.11, the parent-offspring correlation was 0.20.
FIGURE 2. Results From the Full Unconstrained Model for Anxiety
(0.43, 0.59)
(0.00, 0.08)
(0.00, 0.43)
(0.00, 0.11)
(0.57, 1.00)
(0.40, 0.54)
(0.12, 0.34)
A1 = Additive genetic eects on parental anxiety
C1 = Shared-environmental eects on parental anxiety
E1 = Nonshared environmental eects on parental anxiety
A1’ = Genetic eects common to parental and ospring anxiety
A2 = Familial eects specific to ospring anxiety
E2 = Nonshared environmental eects on ospring anxiety
The pathway between A1 and A1is xed to 0.50 because parents and
offspring share 50% of their genome.
FIGURE 3. Results From the Full Unconstrained Model
for Neuroticism
(0.00, 0.46)
(0.00, 0.36)
(0.00, 0.78)
(0.00, 0.92)
(0.08, 0.99)
(0.54, 0.75)
(0.13, 0.39)
A1 = Additive genetic eects on parental neuroticism
C1 = Shared-environmental eects on parental neuroticism
E1 = Nonshared environmental eects on parental neuroticism
A1’ = Genetic eects common to parental and ospring neuroticism
A2 = Familial eects specific to ospring neuroticism
E2 = Nonshared environmental eects on ospring neuroticism
The pathway between A1 and A1is xed to 0.50 because parents and
offspring share 50% of their genome. ajp in Advance
The t indices from the model-tting analyses for twin
parents and their offspring for both anxiety and neuroticism
are presented in Table 2. It is noteworthy that the power to
detect genetic effects in the child part of the model was low,
given that the genetic resemblance between cousins from
monozygotic families compared with dizygotic families was
0.25 compared with 0.125. In both cases, the model restricted
to environmental transmission only, from which the genetic
transmission path was removed (model 3), provides a good
t to the data indicating that genetic transmission is not
a signicant contributor to overall model t. In contrast, for
both anxiety and neuroticism, the genetic transmission-only
model, in which the environmental transmission path was
dropped, provides a signicantly poorer t to the data pro-
viding support for the environmental transmission pathway.
However, given the complexity of thesemodels, we provide the
results for the full model rather than the best-tting model
(Figures 2 and 3). Examination of the condence intervals for
the environmental transmission and genetic transmission paths
for both anxiety and neuroticism revealed that the condence
interval for the environmental transmission pathway, going
from parent to offspring, did not include zero. In contrast, in
both cases, the genetic transmission path (from A1to off-
spring phenotype) did include zero.
This is the rst study, to our knowledge, to examine the
transmission of anxiety using a children-of-twin design. These
analyses provide support for the direct, environmentally
mediated transmission of anxiety from parents to their ado-
lescent offspring over and above any genetic confounding of
this association. It is noteworthy that the analyses do not
provide support for genetic transmission being a signicant
inuence, given the assumptions of our model that the same
genetic factors inuence both adolescent and adult anxiety.
These two ndings will be discussed in turn.
There are three potential interpretations of the environ-
mental inuence on the association between parent and
offspring anxiety. The rst is that parental anxiety itself
results in a rearing environment that is conducive to the
development of anxiety in young people. This could operate
through a number of mechanisms. One is vicarious learning
(4), whereby the young person learns to be fearful of certain
environmental stimuli by observing the presence of that fear
in his or her parent(s). For example, if an adolescent wit-
nesses repeated examples of parental anxiety in response to
ambiguous or only mildly threatening behavior, he or she will
learn that the world is an unsafe place. Such learning can also
take place through hearing explanations or interpretations of
ambiguous or mildly negative experiences that emphasize the
threat content of that experience, reecting anxiety-related
information processing on the part of the parent (35, 36). In
both these instances, while there may be a genetic inuence
on the parents expressed anxiety (as seen in the models
here), the way in which the anxiety is transmitted is through
a direct environmental pathway between the parents be-
havior and the offspring. The second interpretation of this
environmental pathway is that it reects anxious parents
engaging in negative parenting behaviors that promote
anxiety in their offspring. However,although anxious parents
have been shown to be more likely to display overcontrolling
behavior (5, 37), and to be more negative and critical of their
offspring (5), this is most commonly found in the context of
the child/adolescent displaying high anxiety.This leads to the
third interpretation, which is that anxiety in the offspring
inuences the parenting he or she receives. This is compatible
with ndings that parents of anxious children/adolescents
TABLE 1. Correlations Between Twin Parents and Their Offspring for Anxiety and Neuroticism
Monozygotic Twin Families Dizygotic Twin Families
Twin Parent 1 Twin Parent 2 Offspring 1 Twin Parent 1 Twin Parent 2 Offspring 1
Twin parent 2 0.55 0.48
to 0.61
0.20 0.11
to 0.28
Offspring 1 0.20 0.16
to 0.25
0.11 0.04
to 0.18
0.20 0.16
to 0.25
0.02 0.05
to 0.08
Offspring 2 0.11 0.04
to 0.18
0.20 0.16
to 0.25
0.08 0.03
to 0.19
0.02 0.05
to 0.08
0.20 0.16
to 0.25
0.03 0.12
to 0.05
Twin parent 2 0.36 0.25
to 0.46
0.26 0.15
to 0.36
Offspring 1 0.21 0.15
to 0.27
0.03 0.06
to 0.12
0.21 0.15
to 0.27
0.07 0.02
to 0.15
Offspring 2 0.03 0.06
to 0.12
0.21 0.15
to 0.27
0.16 0.01
to 0.29
0.07 0.02
to 0.15
0.21 0.15
to 0.27
0.03 0.09
to 0.15
Parent-child correlations constrained to be equal across zygosity types.
ajp in Advance 5
display parenting behaviors thatexacerbatetheanxietysymp-
toms (8, 37). One study of anxious children found that associ-
ations between negative parenting behaviors and child-expressed
anxiety during a task were far stronger for mothers who were
also anxious compared with mothers who were not anxious
(5). This suggests that there are likely to be effects in both di-
rections. Whatever the mechanism, the present study is the rst
to demonstrate that the association between parent and child
anxiety persists after accounting for genetic confounding.
The lack of evidence for genetic transmission of anxiety
within families may at rst appear surprising, given the her-
itability estimates found for both anxiety and neuroticism.
However, it is consistent with other ndings on internalizing
problems, which have similarly shown evidence only for
environmental transmission (2325, 38). There are at least
three possible explanations for this apparent lack of genetic
transmission for anxiety-related phenotypes within families.
The rst relates to the assumptions of our model, that the
same genes inuence both adult and adolescent anxiety. At
present, the twin literature is inconclusive on this issue. Two
studies, one of mixed anxiety/depression (39) and the other of
anxious cognitions (40), both across adolescence and into
young adulthood, identied considerable continuity of ge-
netic factors. In contrast, two studies of mixed anxiety/
depression (41) and fears (42) from adolescence into young
adulthood found only modest stability with considerable
genetic innovation. Thus, it remains unclear the extent to
anxiety-related phenotypes. Given this, it is plausible that
while parental anxiety is genetically inuenced, these genes
are different from those relevant to the development of
adolescent anxiety. Testing this hypothesis would require
children-of-twins data on which we had measures from
adolescence on the adult parent twins. Currently, no such
data set exists, although the number of longitudinal child twin
studies in which the children are entering young adulthood is
encouraging from this perspective (43, 44). Second, it is also
possible that the heritability
estimate for anxiety pheno-
types obtained from child/
adolescent twin studies in-
cludes interactions between
genetic factors and the shared
environment. Such interac-
sign would be included in the
heritability estimate (45), but
in the children-of-twins de-
sign we use this would not be
the case because the effects of
the shared environment can-
not be estimated in the off-
spring generation. Given that
shared environment is found
to be signicant more often in
child anxiety phenotypes than
in other types of psychopathology, this is another plausible
explanation. Third, it is possible that measurement error re-
duced the paths between the generations thus reducing our
ability to detect genetic transmission. However, the study used
relatively standard questionnaire measures for which there is at
least adequate reliability.
This study has a number of notable strengths. It is the rst
children-of-twins analysis of transmission of anxiety from
parents to their adolescent offspring. It uses a relatively large
data set that provides good statistical power. Finally, we
provide an internal replication by considering neuroticism in
addition to anxiety. However, there are a number of limi-
tations. First, while the study was fairly large, one always
achieves greater power with larger samples. As shown in
Table 1, there was a modest difference between the avuncular
correlations for anxiety from monozygotic families compared
with dizygotic families (0.11 and 0.02, respectively), which
suggests modest genetic inuence, that may have proved
signicant with a larger sample. For neuroticism, there was
no indication of genetic transmission, even in the correla-
tional data. Second, although these ndings provide support
for direct transmission, the use of cross-sectional data means
that they do not indicate the direction of effect. Finally, it is
possible that parents with higher levels of anxiety over-reported
anxiety in their offspring, resulting in a bias in parent-offspring
correlations at the upper end of the distribution. However, mean
levels of anxiety do not differ across our monozygotic families
compared with our dizygotic families, and thus any bias asso-
ciated with higher anxiety should not affect our estimates of
genetic and environmental inuences or the direct transmission
In summary, the association between parentaland offspring
anxiety remains after accounting for genetic transmission.
These results are consistent with a direct, environmen-
tally mediated effect of parent anxiety on offspring anx-
iety or could reect anxious adolescents eliciting anxiety
in their parent. Longitudinal analyses using an extended
TABLE 2. Fit Indices From Model-Fitting for Twin Parents and Their Offspring on Anxiety
and Neuroticism
Model Fit Measure
2LL Akaike Information Criterion
df x
df p
Saturated 9582.91 2704.91 3439
Full model 9610.65 2694.65 3458 27.74 19 0.09
Direct transmission only
9611.16 2693.16 3459 0.51 1 0.47
Genetic transmission only 9625.15 2707.15 3459 14.5 1 ,0.001
Saturated 5717.71 1649.71 2034
Full model 5741.33 1635.33 2053 23.62 19 0.21
Direct transmission only
5742.06 1634.06 2054 0.73 1 0.39
Genetic transmission only 5756.44 1648.44 2054 15.12 1 ,0.001
The overall model t is assessed by 2LL, which is minus twice the log likelihood.
The chi-square for model 2 each time is the difference in minus twice the log likelihood (2LL) between the full genetic
and the phenotypic saturated model; in contrast, the chi-square for models 3 and 4 is the difference in 2LL between
each model and the full genetic model (model 2).
The best-tting model. ajp in Advance
children-of-twins design will be useful in exploring these
questions further.
From Kings College London, MRC Social, Genetic and Developmental
Psychiatry Research Centre, the Institute of Psychiatry, Psychology and
Neuroscience, London; the Department of Medical Epidemiology and
Biostatistics, Karolinska Institutet, Stockholm, Sweden; the Department of
Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Yale
Child Study Center, New Haven, Conn.; the Ofce of Behavioral and Social
Sciences Research, NIH, Bethesda, Md.; the Department of Psychology,
George Washington University, Washington, DC; and the Department of
Psychology, The Pennsylvania State University, University Park, Pa.
Address correspondence to Dr. Eley ( or Dr. McAdams
Drs. Eley and McAdams contributed equally to the work.
Supported by the Leverhulme Trust (RPG-210, principal investigator,
Thalia Eley, Ph.D.). The Twin and Offspring Study in Sweden was supported
by grant R01MH54610 from NIMH.
This study presents independent research part-funded by the National
Institute for Health Research (NIHR) Biomedical Research Centre at South
London and Maudsley NHS Foundation Trust and Kings College London.
The views expressed are those of the author(s) and not necessarily thoseof
the NHS, the NIHR, or the Department of Health.
The authors report no nancial relationships with commercial interests.
Received July 2, 2014; revisions received Oct. 23, Nov. 25, and Dec. 18,
2014; accepted Jan. 13, 2015.
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... Moreover, it is clear that this intergenerational transmission of anxiety is not solely (or even largely) attributable to genetic processes; environmental factors have also been shown to contribute substantially to the transmission of anxiety within families [3]. The focus of the research that has sought to understand these environmental processes has been largely on parenting, and it seems likely that a number of parental processes are at play. ...
p>Background: Anxiety is the most common childhood mental health condition and is associated with impaired child outcomes, including increased risk of mental health difficulties in adulthood. Anxiety runs in families: when a parent has anxiety, their child has a 50% higher chance of developing it themselves. Environmental factors are predominant in the intergenerational transmission of anxiety and, of these, parenting processes play a major role. Interventions that target parents to support them to limit the impact of any anxiogenic parenting behaviors are associated with reduced anxiety in their children. A brief UK-based group intervention delivered to parents within the UK National Health Service led to a 16% reduction in children meeting the criteria for an anxiety disorder. However, this intervention is not widely accessible. To widen access, a 9-module web-based version of this intervention has been developed. This course comprises psychoeducation and home practice delivered through text, video, animations, and practice tasks. Objective: This study seeks to evaluate the feasibility of delivering this web-based intervention and assess its effectiveness in reducing child anxiety symptoms. Methods: This is the protocol for a randomized controlled trial (RCT) of a community sample of 1754 parents with self-identified high levels of anxiety with a child aged 2-11 years. Parents in the intervention arm will receive access to the web-based course, which they undertake at a self-determined rate. The control arm receives no intervention. Follow-up data collection is at months 6 and months 9-21. Intention-to-treat analysis will be conducted on outcomes including child anxiety, child mental health symptoms, and well-being; parental anxiety and well-being; and parenting behaviors. Results: Funding was received in April 2020, and recruitment started in February 2021 and is projected to end in October 2022. A total of 1350 participants have been recruited as of May 2022. Conclusions: The results of this RCT will provide evidence on the utility of a web-based course in preventing intergenerational transmission of anxiety and increase the understanding of familial anxiety.</p
... Previous integrative models on the transmission of anxiety and depressive symptoms from mother to child have proposed several biological and environmental mechanisms (Stein et al., 2014;Goodman & Gottlib 1999;Beijers et al., 2014). First, shared genetic factors play an important role in this transmission (Eley et al., 2015;Goodman, 2020). For example, heritability estimates of anxiety and depression are ranging from 30% to 50% (Fernandez-Pujals et al., 2015;Hettema et al., 2001). ...
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Maternal prenatal distress (i.e., anxiety and depressive symptoms) increases the risk for childhood behavioral and emotional problems. So far, the potential role of maternal bonding in this association still needs further study. Maternal prenatal distress can affect the development of maternal bonding from pregnancy onwards. Maternal prenatal and postnatal bonding in turn have been shown to predict child behavioral functioning. We aimed to investigate whether maternal prenatal and postnatal bonding mediate the association between maternal prenatal distress and toddlers’ internalizing and externalizing problems. Data from a Dutch prospective longitudinal sample ( N = 666) were used to conduct single and multiple mediation models. Mothers reported prenatal anxiety (State Anxiety Inventory) and prenatal depressive symptoms (Edinburgh Postnatal Depression Scale) at 24 weeks’ gestation and maternal prenatal bonding (Maternal Antenatal Attachment Scale) at 32 weeks’ gestation. At 6 weeks and 6 months postpartum mothers completed questionnaires to assess maternal postnatal bonding (Maternal Postnatal Attachment Scale). Mothers reported child internalizing and externalizing problems (Child Behavior Checklist) at 28 months postpartum. Maternal prenatal and postnatal bonding mediated the link between maternal prenatal anxiety and child externalizing problems but not internalizing problems. Only maternal bonding 6 months postpartum mediated the link between maternal prenatal depressive symptoms and child internalizing problems but not externalizing problems. Our study showed that maternal postnatal bonding more consistently mediated links between measures of maternal prenatal distress and child behavioral and emotional problems than maternal prenatal bonding. Interventions reducing maternal prenatal distress and promoting maternal bonding should be developed.
... This is consistent with evidence of causal effects of maltreatment on psychopathology from Mendelian randomization 42 , co-twin control 43 and other quasi-experimental studies 44 . We also found that parental mental illness was associated with internalizing and externalizing problems independent of genetic confounding, which supports evidence from children-of-twins and adoption studies [45][46][47] . In contrast, we found that parental substance abuse, parental criminality and parental separation were predominantly associated with internalizing and externalizing problems via genetic confounding. ...
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Children who experience adversities have an elevated risk of mental health problems. However, the extent to which adverse childhood experiences (ACEs) cause mental health problems remains unclear, as previous associations may partly reflect genetic confounding. In this Registered Report, we used DNA from 11,407 children from the United Kingdom and the United States to investigate gene–environment correlations and genetic confounding of the associations between ACEs and mental health. Regarding gene–environment correlations, children with higher polygenic scores for mental health problems had a small increase in odds of ACEs. Regarding genetic confounding, elevated risk of mental health problems in children exposed to ACEs was at least partially due to pre-existing genetic risk. However, some ACEs (such as childhood maltreatment and parental mental illness) remained associated with mental health problems independent of genetic confounding. These findings suggest that interventions addressing heritable psychiatric vulnerabilities in children exposed to ACEs may help reduce their risk of mental health problems. In 11,407 children, Baldwin et al. report gene–environment correlations between polygenic scores for psychiatric disorders and adverse childhood experiences, as well as partial genetic confounding of associations between adverse childhood experiences and mental health.
... Anxiety typically runs in families, with a 2-7 times increased risk for offspring of parents with anxiety disorders (8). A recent twin study found support for a direct environmental transmission of anxiety between parents and children (9). A main mechanism may be the parenting style of anxious parents often characterized by overprotection and modeling anxiety (10). ...
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Offspring of parents with anxiety disorders have an increased risk of developing anxiety themselves. Very few studies have evaluated interventions aiming to prevent anxiety in offspring of anxious parents. This study was a small (N=40) randomized pilot study with three arms evaluating the feasibility of a novel parent support group for anxious parents, the Supporting Anxious Parents Program (SAPP). The primary objective was to evaluate the acceptability of the SAPP. In addition, we also evaluated preliminary effects on child anxiety, parent risk factors, and quality of life, and feasibility of the study design. Excessive parental worry and anxiety and having a child not meeting criteria for an anxiety disorder (6-12 years old), served as inclusion criteria. Thirteen parents were randomly allocated to a group-based intervention, 14 to an individual Internet-based version of the intervention, and 13 to a waitlist control condition. The intervention was developed to target three risk factors involved in the parent-child transmission of anxiety; criticism/low warmth, overprotective behaviors, and modeling of anxiety. The results showed that parents were generally very satisfied with the intervention. We did not find any significant decreases in child anxiety in the intervention conditions. However, for the parents, we found preliminary support for reduced overprotective behaviors, reduced worry, and increased quality of life. The study design was found to be feasible. According to the results, a revision of the intervention is recommended before a full randomized controlled trial could be conducted.
... Infants born to depressed or anxious parents inherit genes predisposing them to depression and anxiety. They grow up in a depressed and anxious home environment where PNE triggers insecure emotional and behavioral responses in young children [56][57][58]. When parents have high negative emotions, young children perceive PNE and develop insecurity. ...
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This study aimed to investigate the relationship between parents’ perceived social support (PSS) and young children’s approaches to learning (ATLs) in rural China, as well as the mediating effect of the home learning environment (HLE) and the moderating effect of parental negative emotions (PNE). Using the cluster random sampling method, 2714 kindergarteners (Mage = 52.99 months, SD = 10.28; 52.00% boys; 27.43% only child) were recruited from rural areas of eight provinces in China. With questionnaires, parents reported their PSS and PNE, HLE, and the children’s ATLs. The results indicated that: (1) parents’ PSS positively predicted children’s ATLs; (2) the HLE partially mediated the relationship between parents’ PSS and children’s ATLs; and (3) PNE moderated the relationship between parents’ PSS and children’s ATLs. Thus, the results supported a moderated mediation model on the relationship between parents’ PSS and young children’s ATLs, with the HLE as a mediator and the parents’ PSS as a moderator. These findings offer new avenues for intervening and supporting the development of young children’s ATLs.
Trauma-related disorders are debilitating psychiatric conditions that affect people who have directly or indirectly witnessed adversities. Experiencing multiple types of traumas appears to be common during childhood, and even more so during adolescence. Dramatic brain/body transformations occurring during adolescence may provide a highly responsive substrate to external stimuli and lead to trauma-related vulnerability conditions, such as internalizing (anxiety, depression, anhedonia, withdrawal) and externalizing (aggression, delinquency, conduct disorders) problems. Analyzing relations among neuronal, endocrine, immune, and biochemical signatures of trauma and internalizing and externalizing behaviors, including the role of personality traits in shaping these conducts, this review highlights that the marked effects of traumatic experience on the brain/body involve changes at nearly every level of analysis, from brain structure, function and connectivity to endocrine and immune systems, from gene expression (including in the gut) to the development of personality.
Distinguishing between the effects of nature and nurture constitutes a major research goal for those interested in understanding human development. It is known, for example, that many parent traits predict mental health outcomes in children, but the causal processes underlying such associations are often unclear. Family‐based quasi‐experimental designs such as sibling comparison, adoption and extended family studies have been used for decades to distinguish the genetic transmission of risk from the environmental effects family members potentially have on one another. Recently, these designs have been combined with genomic data, and this combination is fuelling a range of exciting methodological advances. In this review we explore these advances – highlighting the ways in which they have been applied to date and considering what they are likely to teach us in the coming years about the aetiology and intergenerational transmission of psychopathology.
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Objectives To gain insight into the nature of maternal anxiety among mothers from diverse cultures through exploring the components of maternal anxiety and ways mothers cope with it in order to assist helping professionals in providing psychoeducation and counseling to mothers who experience intense anxiety regarding their children. Methods In this qualitative study, 17 mothers participated in cognitive interviews conducted as a part of the maternal anxiety scale development. Data from semi-structured interviews was explored using thematic analysis. Results Four themes related to mothers’ experiences of anxiety emerged from the data: (1) maternal insecurities and social comparison, (2) coping with anxiety, (3) dependence versus autonomy, (4) cultural considerations. Conclusions for Practice The results of this study can be used by helping professionals working with mothers by implementing emotion regulation skills for maternal anxiety that are described in the implications section of the paper.
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Parental depressive symptoms are associated with emotional and behavioural problems in offspring. However, genetically informative studies are needed to distinguish potential causal effects from genetic confounds, and longitudinal studies are required to distinguish parent-to-child effects from child-to-parent effects. We conducted cross-sectional analyses on a sample of Swedish twins and their adolescent offspring (n = 876 twin families), and longitudinal analyses on a US sample of children adopted at birth, their adoptive parents, and their birth mothers (n = 361 adoptive families). Depressive symptoms were measured in parents, and externalizing and internalizing problems measured in offspring. Structural equation models were fitted to the data. Results of model fitting suggest that associations between parental depressive symptoms and offspring internalizing and externalizing problems remain after accounting for genes shared between parent and child. Genetic transmission was not evident in the twin study but was evident in the adoption study. In the longitudinal adoption study child-to-parent effects were evident. We interpret the results as demonstrating that associations between parental depressive symptoms and offspring emotional and behavioural problems are not solely attributable to shared genes, and that bidirectional effects may be present in intergenerational associations.
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Parental psychopathology, parenting style, and the quality of intrafamilial relationships are all associated with child mental health outcomes. However, most research can say little about the causal pathways underlying these associations. This is because most studies are not genetically informative and are therefore not able to account for the possibility that associations are confounded by gene-environment correlation. That is, biological parents not only provide a rearing environment for their child, but also contribute 50% of their genes. Any associations between parental phenotype and child phenotype are therefore potentially confounded. One technique for disentangling genetic from environmental effects is the children-of-twins (COT) method. This involves using data sets comprising twin parents and their children to distinguish genetic from environmental associations between parent and child phenotypes. The COT technique has grown in popularity in the last decade, and we predict that this surge in popularity will continue. In the present article we explain the COT method for those unfamiliar with its use. We present the logic underlying this approach, discuss strengths and weaknesses, and highlight important methodological considerations for researchers interested in the COT method. We also cover variations on basic COT approaches, including the extended-COT method, capable of distinguishing forms of gene-environment correlation. We then present a systematic review of all the behavioral COT studies published to date. These studies cover such diverse phenotypes as psychosis, substance abuse, internalizing, externalizing, parenting, and marital difficulties. In reviewing this literature, we highlight past applications, identify emergent patterns, and suggest avenues for future research. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
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The present longitudinal study responds to a need for new perspectives and research tools for studying school transition stress by identifying changes in student role strains and assessing sex differences in strain changes during the transition from elementary school to a sixth-through eighth-grade middle school Findings, consistent with predictions, include (a) students did not experience more strain in the team-taught middle school program than in elementary school, (b) boys experienced more strains in elementary school than did girls but were not more bothered by the strains, and (c) boys exhibited relatively greater declines in the number and magnitude of strains during the transition to middle school than did girls. The role strain approach promises to be a useful tool for identifying strains that may affect early adolescents' adjustments to school transitions. This type of research also may help practitioners construct school environments that maximize opportunities for human development.
Objective: The anxiety and depressive disorders exhibit high levels of lifetime comorbidity with one another. The authors examined how genetic and environmental factors shared by the personality trait neuroticism and seven internalizing disorders may help explain this comorbidity. Method: Lifetime major depression, generalized anxiety disorder, panic disorder, agoraphobia, social phobia, animal phobia, situational phobia, and neuroticism were assessed in over 9,000 twins from male-male, female-female, and opposite-sex pairs through structured diagnostic interviews. Multivariate structural equation models were used to decompose the correlations between these phenotypes into genetic and environmental components, allowing for sex-specific factors. Results: Genetic factors shared with neuroticism accounted for between one-third and one-half of the genetic risk across the internalizing disorders. When nonsignificant gender differences were removed from the models, the genetic correlations between neuroticism and each disorder were high, while individual-specific environmental correlations were substantially lower. In addition, the authors could identify a neuroticism-independent genetic factor that significantly increased risk for major depression, generalized anxiety disorder, and panic disorder. Conclusions: There is substantial, but not complete, overlap between the genetic factors that influence individual variation in neuroticism and those that increase liability across the internalizing disorders, helping to explain the high rates of comorbidity among the latter. This may have important implications for identifying the susceptibility genes for these conditions.
Although the last edition of this book was published only a decade ago, there would be little point basing this narrative on the genetics chapter presented in the last edition – because the field has changed enormously. In particular, there has been a shift away from simply enquiring about the extent to which child and adolescent anxiety is due to genes and the environment, to focusing upon more detailed questions about how these estimates vary with regard to factors such as age and sex, as well as investigating other ways in which genetic and environmental influences upon anxiety are mediated and moderated. Addressing a wider range of issues has led to a body of literature that is too large to exhaustively review in this chapter. Hence, this chapter will focus on a selection of some of the most important research studies in the field. The chapter begins with a discussion of long-standing research methods and key early findings from which the field has developed. Novel findings and methods of investigation are then highlighted to provide the reader with knowledge about the types of issues that are likely to be addressed in chapters written on child and adolescent anxiety another 10 years from now. How do we know about the genetic basis of anxiety? By observing the world around us, it is clear that anxiety runs in families (i.e., is familial). Anxious children are met at the school gates by anxious parents, whereas carefree parents seem to produce children temperamentally similar to themselves. Supporting these observations are data from family studies, which show clearly that anxiety runs in families (see Creswell, Murray, Stacey, & Cooper, Chapter 14, this volume). For example, one study found that children of anxious parents are more likely to be diagnosed with an anxiety disorder as compared to children of parents with dysthymia or who have never been mentally ill (Turner, Beidel, & Costello, 1987).
Importance: The DSM-5 classifies mood and anxiety disorders as separate conditions. However, some studies in adults find a unidimensional internalizing factor that underpins anxiety and depression, while others support a bidimensional model where symptoms segregate into distress (depression and generalized anxiety) and fear factors (phobia subscales). However, little is known about the phenotypic and genetic structure of internalizing psychopathology in children and adolescents. Objective: To investigate the phenotypic associations between depression and anxiety disorder symptom subscales and to test the genetic structures underlying these symptoms (DSM-5-related, unidimensional and bidimensional) across 3 developmental stages: childhood, adolescence, and early adulthood. Design, setting, and participants: Two population-based prospective longitudinal twin/sibling studies conducted in the United Kingdom. The child sample included 578 twins (mean age, approximately 8 and 10 years at waves 1 and 2, respectively). The adolescent and early adulthood sample included 2619 twins/siblings at 3 waves (mean age, 15, 17, and 20 years at each wave). Main outcomes and measures: Self-report symptoms of depression and anxiety disorders. Results: Phenotypically, when controlling for other anxiety subscales, depression symptoms were only associated with generalized anxiety disorder symptoms in childhood (r = 0.20-0.21); this association broadened to panic and social phobia symptoms in adolescence (r = 0.17-0.24 and r = 0.14-0.16, respectively) and all anxiety subscales in young adulthood (r = 0.06-0.19). The genetic associations were in line with phenotypic results. In childhood, anxiety subscales were influenced by a single genetic factor that did not contribute to genetic variance in depression symptoms, suggesting largely independent genetic influences on anxiety and depression. In adolescence, genetic influences were significantly shared between depression and all anxiety subscales in agreement with DSM-5 conceptualization. In young adulthood, a genetic internalizing factor influencing depression and all anxiety subscales emerged, alongside a small significant genetic fear factor. Conclusions and relevance: These results provide preliminary evidence for different phenotypic and genetic structures of internalizing disorder symptoms in childhood, adolescence, and young adulthood, with depression and anxiety becoming more associated from adolescence. The results inform molecular genetics research and transdiagnostic treatment approaches. The findings affirm the need to continue examining the classification of mood and anxiety disorders in diagnostic systems.