The relation between frontal EEG asymmetry and the
D.J.A. Smit ,, D. Posthuma ,, D.I. Boomsma E.J.C. De Geus ,
a Department of Biological Psychology, Vrije Universiteit of Amsterdam, van der Boechorststraat 1, 1081 BT Amsterdam, The Netherlands
b Centre of Neurogenomics and Cognition Research (CNCR), Vrije Universiteit of Amsterdam, Amsterdam, The Netherlands
Received 9 December 2005; accepted 16 June 2006
Frontal asymmetry of EEG alpha power (FA) may index the risk for anxiety and depression. Evidence linking FA to the underlying biological
mechanisms is scarce. This is unfortunate because FA has potential as a biological marker to support gene finding in anxiety and depression. Weexamined the heritability of FA in 732 twins and their singleton siblings, and established the genetic and environmental contribution to the relationbetween FA and the risk for anxiety and depression. Multivariate models showed that FA is heritable only in young adults (males 32% and females37%) but not in middle-aged adults. A significant relation between FA and the risk for anxiety and depression was only found in young adultfemales. This relation was explained by shared genes influencing both EEG and disease risk. Future studies on asymmetry of left and right frontalbrain activation should carefully consider the effects of sex and age.
# 2006 Elsevier B.V. All rights reserved.
Keywords: Twins; Sex differences; Age cohorts; Endophenotype
Because affective style is related to the liability to develop
psychopathology such as depression and anxiety disorders a
Frontal asymmetry of EEG alpha power (FA) has been
relation between FA and depression and anxiety can be
studied extensively as a correlate of individual differences in
emotional responding. These studies assume that alpha power
many studies provided findings consistent with this view (for an
acts as an inverse index of activity: a synchronous state of
overview, see Coan and Allen). For example, FA has been found
oscillations reflects inactivity of the underlying neural substrate
to differ between clinically depressed patients and non-
(). This assumption has been supported by fMRI
and PET studies that showed a decrease in cortical blood flow
responders and non-responders to fluoxetine
Greater left hemispheric activity has been associated
with approach related behavioral tendencies, and greater right
hemispheric activity with withdrawal related tendencies. In the
negative affectivity also holds in infants of depressed mothers
extant literature, therefore, it is hypothesized that FA acts as an
index of the basic emotional dimension of approach versus
patients () or unipolar depression patients
this basis individual differences in asymmetric frontal activity
). The latter indicates that FA is a marker for the
are hypothesized to indicate individual differences in affective
liability for depression rather than the depressive state itself.
Taken together, these studies have established a secure footholdfor FA as a biological marker for depression.
FA has focused on its relation to psychopathology and otherbehavioral phenotypes, but evidence linking FA to the underlying
* Corresponding author. Tel.: +31 20 598 8787; fax: +31 20 598 8832.
biological mechanisms is scarce. This is unfortunate because FA
0301-0511/$ – see front matter # 2006 Elsevier B.V. All rights reserved.
D.J.A. Smit et al. / Biological Psychology 74 (2007) 26–33
has potential significance as a so-called endophenotype to
depression data were available for 9088 twins and non-twin siblings. These
support gene finding in depression. Endophenotypes are
were divided into two age cohorts based on the twins age on 1 January 1999: ayoung adult cohort (under 35) with 3879 males and 5364 females, and a middle-
psychophysical or psychophysiological phenotypes that are
aged cohort (over 35) with 647 males and 1232 females. On average 2.20
constituents of the causal pathway from gene to phenotype. They
represent the expression of a subset of genes from the whole set of
A subset of twins and siblings were invited for detailed psychophysiological
genes causing the genetic part of phenotypic variation. As such,
study in the laboratory. For the present study, twins were invited who had
they can be useful when the great number of genes involved in the
previously participated in EEG or cardiovascular research. In addition, weinvited their non-twin siblings. A total of 760 subjects from 309 twin families
phenotype of interest reduces the statistical power in linkage and
accepted the invitation to participate. As with the survey sample, the EEG
association studies. Ideally, endophenotypes possess several
sample consisted of two age cohorts based on the age of the twins: a younger
features (): (i) they are stable, (ii) heritable, (iii)
cohort (M = 26.2 years, S.D. = 4.1) and a middle-aged cohort (M = 49.4 years,
and correlated with the phenotype of interest, and (iv) the
S.D. = 7.2). Participating families consisted of one to seven siblings (including
relations in (ii) and (iii) share a common genetic source.
twins). On average, 2.50 participants per family participated. Informed consentwas obtained in writing for the EEG study. Both the EEG and the questionnaire
Although studies show that the requirements (i) stability and
studies received approval from the appropriate ethical committees.
(iii) correlation to the risk for depression have been met withsuccess (
The experimental protocol and background EEG registration has been
to FA and to the association between FA and depression is still
scarce. Several conference abstracts reported on the genetic basis
a brief description will be repeated here. The experimental protocol consisted of
two parts. During one part, psychometric intelligence, inspection time, andreaction times were assessed. During the other, EEG was measured at rest and
offspring correlation of r = 0.46 in a family study of alcoholic
during various reaction time tasks. The order of the two parts of the protocol was
and depressed patients and controls, providing evidence for
randomized across family members. Consequently, half of EEG registration
familial influences in FA. used a twin study to
sessions were during morning hours, and half were in the afternoon.
further show that these familial influences reflected genetic
Subjects were seated in a comfortable reclining chair in a dimly lit, sound
influences. In 60 pairs of 17-year-old female twins, they found
attenuated, and electromagnetically shielded room. They were instructed torelax and minimize eye and body movement. Resting background EEG was
33% of FA variability to be under genetic control. In a thesis,
registered for 3 min under both eyes open and eyes closed instructions with 19
reported that genetic influences explained a modest
Ag/AgCl electrodes mounted in an electrocap. Signal registration was con-
22% of the variation in mid-frontal FA in 66 female twin pairs,
ducted using an AD amplifier developed by Twente Medical Systems (TMS;
and no significant heritability in males from a normal population.
Enschede, The Netherlands) for 657 subjects (381 young, 380 middle-aged) and
Recently, reported a modest mid-frontal FA
NeuroScan SynAmps 5083 amplifier for 103 subjects (24 young, 80 middle-aged). Signals were continuously represented online on a Nec multisync 17 in.
heritability of 31% within a young adult female sample.
computer screen using Poly 5.0 software or Neuroscan Acquire 4.2. Standard
Here we aim to extend the knowledge base on the genetics of
10–20 positions were F7, F3, F1, Fz, F2, F4, F8, T7, C3, Cz, C4, T8, P7, P3, Pz,
FA by examining FA from resting EEG in large set of twin pairs
and their singleton siblings. Additionally we aim to establish the
NeuroScan subjects Fp1, Fp2, and Oz were also recorded, but not included in
genetic and environmental contribution to the relation between
the analysis. The vertical electro-oculogram (EOG) was recorded bipolarlybetween two Ag/AgCl electrodes, affixed 1 cm below the right eye and 1 cm
FA and the risk for anxiety and depression. Anxiety disorders
above the eyebrow of the right eye. The horizontal EOG was recorded bipolarly
have not been studied extensively in relation to FA, and the
between two Ag/AgCl electrodes affixed 1 cm left from the left eye and 1 cm
results are less conclusive than for depression
right from the right eye. An Ag/AgCl electrode placed on the forehead was used
as a ground electrode. Impedances of all EEG electrodes were kept below 3 kV,
and impedances of the EOG electrodes were kept below 10 kV. The EEG wasamplified, digitized at 250 Hz and stored for offline processing. Amplifier filter
are highly comorbid with depression. Moreover, the genetic
settings for TMS were a single order FIR bandpass filter with cutoff frequencies
variance of these phenotypes reflects for the most part a common
of 0.05 and 30.0 Hz. NeuroScan filter settings were a lowpass filter at 50.0 Hz.
genetic source (;). We hypothesize that the common
genetic factor underlying the risk for anxiety and depression isreflected in individual differences in FA. Since sex differences in
Computation of FA used the EEG recorded during the eyes closed condition.
the heritability of FA as well as in the relation between FA and
Signals at leads F3 and F4 were analyzed using NeuroScan software version 4.2.
depression have been reported, we stratified our sample
The signals were recalculated with averaged earlobes (A1 and A2) as reference.
The 3 min recording was cut into 43 epochs of 1024 data points (4.096 s). Any
linear trend was removed from EEG by fitting and subtracting the regressionline for each epoch separately. Next, epochs were excluded per lead when EOG
channels showed more than 400 mV and EEG more than 175 mV deviation fromground in either direction. EEG traces were then visually inspected per subject
for remaining artifact due to muscle activity, swallowing, eye movement, badrecordings, and externally induced artifacts (e.g., experimenter initiated reset
The sample of this study was derived from an ongoing twin family study on
pulses, electrical hum). Only epochs with extreme magnitudes of muscle
mental and physical health in participants of the Netherlands Twin Registry
artifacts and eye movements were excluded. Subjects with less than 22 valid
(NTR). Families with adult twins have been receiving surveys on lifestyle and
epochs after visual inspection were considered unreliable and set to missing (22
health every 2/3 years since 1991 Anxiety and
epochs ensure at least 1 min and 30 s of data per subject.). The number of
D.J.A. Smit et al. / Biological Psychology 74 (2007) 26–33
subjects with valid data on both F3 and F4 was 732. shows the exact
after normalization of the Anx, Neu, SoA, and Dep scores. This factor score
composition of the final sample per age cohort and zygosity of the twins.
summarizes the genetic risk for anxiety and depression and has been found to
For all remaining, artifact-free epochs, power spectra were calculated with a
have a heritability of about 60% (Forty-six subjects
Hamming window for 5% of the epoch duration at the beginning and end of the
(seven young adult females) of the subjects with EEG data did not have survey
epochs. Power spectra were averaged, resulting in a single spectrum with a
data available on any of these time points.
resolution of about 0.25 Hz (1000/4096 Hz). Alpha power was defined as thesum of all data points in the range from 8.0 Hz up to but not including 13.0 Hz.
Prior to genetic model fitting we tested: (1) whether the twin data could be
generalized to a singleton population by comparing the means and (co-)var-
where higher scores reflect lower left alpha power, and consequently higher left
iances of twins and singleton siblings, and (2) the equivalence of means and
cortical activation, relative to the right cortex.
variances across MZ and DZ twins. Significance of these differences were tested
Up to 20% of the population may exhibit low or very low alpha synchro-
by four group omnibus tests, that is, for all four sex by cohort groups
nization () yielding denominator values that
are close to zero. This can result in an unstable and noisy FA measure. In
Genetic statistical analysis of the power spectra of the sample was repeated
accordance with Anohkin et al., we repeated our analyses after excluding
in young males, young females, middle-aged males, and middle-aged females.
subjects with the lowest average frontal EEG power. This subject selection
A linear regression model was employed to include effects of the covariate of
aimed to reduce the adverse effects of noise amplification due to the nature of
age on the observed scores within each group, formally represented as:
mi = b0 + b1 agei, where mi is the expected value of individual i, agei theindividual’s age in years at time of measurement, b0 the intercept, and b1 is
Structural Equation Modeling implemented in the program Mx version 1.57
estimated the contribution of additive genetic variation (s2 ),
Questionnaires were sent in 1991, 1993, 1995, 1997, 2000, and 2002 to twin
shared environmental variation (s2 ), or non-shared environmental variation
families and their siblings who had indicated that they were willing to
(s2 ) to the observed interindividual variation in power spectra using the full
participate in the survey study. A detailed description of the survey content
information Maximum Likelihood Estimation (MLE) procedure
and response rates at each wave can be found in Data on
Sources of shared environmental variation by definition include
trait anxiety (Anx), neuroticism (Neu), somatic anxiety (SoA), and anxious
all environmental influences that twins and siblings from the same family share,
depression (Dep) from three waves were analyzed (1997, 2000, and 2002). Trait
while sources of non-shared environmental variation refer to the environmental
anxiety and anxious depression were collected using the Dutch versions of the
variation that is unique for an individual and that is not shared with other family
Spielberger Anxiety Inventory (STAI; and the Young
members. For two members of a DZ twin pair (and sibling pairs) who are raised
Adult Self Report scale (YASR; Neuroticism and somatic
in the same home and share on average 50% of their segregating genes, the
anxiety were assessed with the Amsterdamse Biografische Vragenlijst (ABV;
correlation between shared environmental influences (C) was fixed at 1, the
). The item content of the ABV neuroticism scale is very similar to
correlation between additive genetic influences (A) at 1/2, and the correlation
that of the Eysenck Personality Questionnaire. From these traits a factor score
between dominant genetic influences (D) at 1/4. For two members of an MZ
was calculated after weighing each trait to maximize heritability of the factor
twin pair correlations between shared environmental, additive genetic, and
score. As depression has repeatedly been shown to differ in genetic makeup
dominant genetic influences were all fixed at 1. Correlation between non-shared
environmental influences (E), by definition, is set to zero for both MZ and DZ
the subscale weights were calculated separately for males and females:
twins. Thus, the expectation for the total variance is s2 þ s2 þ s2 þ s2 , the
expectation for the covariance between MZ twins is s2
expectation for DZ twins/sibling pairs is ð1=2Þs2 þ ð1=4Þs2 þ s2 . Heritability
¼ 0:144 Â Anx þ 0:117 Â Neu þ 0:039 Â SoA þ 0:064 Â Dep;
is calculated as the proportional contribution of genetic variation to the totalobserved variation (ðs2 þ s2 Þ=ðs2 þ s2 þ s2 þ s2 Þ).
The twin design with additional siblings does not allow the simultaneous
estimation of dominant genetic and common environmental effects
If the DZ correlation is larger than half the MZ correlation, this
¼ 0:133 Â Anx þ 0:117 Â Neu þ 0:066 Â SoA þ 0:053 Â Dep;
will be taken as evidence of common environmental effect and s2 will be set to
zero. If the DZ correlation is less than half the MZ correlation, this will be taken
as evidence of dominant genetic effects and s2 will be set to zero. In addition, to
Table 1Number and composition of families per age cohort and zygosity of the twins
Families with both twins + 2 or more siblings
Families with 1 twin + 2 or more siblings
Note: We based family composition on the participating offspring only. For example, a family with ‘both twins only’ could potentially consist of more than twochildren, but these did not participate in the EEG experiment. MZM: MZ male twins; MZF: MZ female twins; DZM: DZ male twins; DZF: DZ female twins; OS:opposite sex twins.
D.J.A. Smit et al. / Biological Psychology 74 (2007) 26–33
estimate dominant genetic effects sample sizes must be very large
We will therefore attempt to estimate this effect in the
Phenotypic correlations between FA and the risk for anxiety and depression
FA in middle-aged subjects (M = 0.35, S.D. = 0.098) was
higher than in young adult subjects (M = 0.54, S.D. = 0.111).
The ANOVA showed the effect of cohort to be significant (F(1,
728) = 6.84, MSE = 0.011, p < 0.01). Neither the main effect
of sex or the sex by cohort interaction were significant.
3.2. FA split-half reliability and temporal stability
3.4. Association between FA and the risk for anxiety anddepression
The split-half reliability, as an indication of measurement
error, can be considered a ceiling for the MZ twin correlation.
depicts the correlations between frontal asymmetry
We selected 10% of the subjects at random to compute FA at
and the risk for anxiety and depression for each sex by age
odd and even epochs separately. The resulting split-half
cohort group. In addition, it shows the intrapair correlations
correlation was 0.87 suggesting that MZ correlations are bound
after removing the subjects with the 10, 20, and 30% lowest
average frontal power scores (). It is clear
To compute temporal stability, 32 subjects were invited back
that the association was significant only in young females.
after a period varying from 354 to 1322 days. Of those, 27 had
Hence (bivariate), genetic modeling proceeded in the separate
valid data available on F3 and F4 on both occasions. Temporal
stability calculated as the correlation coefficient between bothmeasurement occasions was 0.44. Jointly these analyses
3.5. Twin correlations and heritabilities for the risk for
indicate that individual differences in FA are reliable and
For all four groups variances and means did not differ
significantly between MZ twins, DZ twins, and singletonsiblings. Likewise, DZ twin, twin–sibling, and sibling–sibling
Generally, studies into hemispheric asymmetry limit their
correlations were not found to differ. Further analyses therefore
samples to right-handed individuals as handedness may be
assumed these parameters to be equal, which increases the
confounded with the lateralization of brain function. We tested
this assumption by comparing FA scores of left against right-
shows the resulting intrapair correlations obtained for
handed subjects and with a one-way univariate ANOVA with
the different sex by zygosity groups. Correlations differed
age and sex as covariates. Nine individuals indicated to be
between the cohorts, although the effect was rather small given
ambidextrous or did not provide an answer. Although the
the large sample size (x2(5) = 15.00, p = 0.010). Correlations did
proportion of left-handers was slightly higher in the young
not differ between the sexes. The intrapair correlations suggested
adult cohort (N = 384, P = 13.3%) than in the middle-aged
dominant genetic effects as the DZ/sibling correlations were
cohort (N = 339, P = 11.8%), this difference was not sig-
below half the MZ correlations. These effects were significant for
nificant (x2 < 1). Although left-handed subjects (M = 0.032)
young adult males and middle-aged females. Heritabilities were
based on the summed additive and dominant genetic effects for
(M = 0.046), the effect did not reach significance (MSE =
these groups. For young adult females and middle-aged males
0.011, F (1) = 1.41, ns). Additionally, we tested whether twin
only additive genetic effects contributed to heritability.
pairs discordant for handedness differed from twins con-cordant for handedness. If left-handedness causes a mirroring
3.6. Twin correlations and heritabilities for FA
of brain function lateralization, twin pairs discordant forhandedness should show a negative, or at least a reduced,
As with the risk for anxiety and depression, no differences
intrapair correlation compared to concordant twin pairs.
were found in the means and variances between the zygosity
Maximum likelihood estimation of the correlations did not
groups (MZ, DZ) and in the means, variances and correlations
show evidence for an effect of concordance for either MZ or
DZ twin pairs (both x2(1) < 1). From these results, we
shows the sibling correlations for male MZ twins,
concluded that handedness is not a confound of FA, and
female MZ twins, male DZ twins plus all other non-identical
subsequent analyses used all pairs, including left-handed
male–male sibling relations, female DZ twins plus all other
subjects and pairs discordant for handedness.
non-identical female–female sibling relations, and opposite sex
D.J.A. Smit et al. / Biological Psychology 74 (2007) 26–33
Table 3Twin correlations and heritabilities of FA and the risk for anxiety and depression
Note: MZM: MZ male twins; DZM: DZ male twins and same-sex siblings; MZF: MZ female twins; DZF: DZ female twins and same-sex siblings; OS: opposite sextwins and siblings. DZ and opposite sex correlations entail all fraternal sibling relations and are corrected for intrapair age and sex differences. ns: p > 0.05.
a N represents the total sum of all possible sibling pairs, e.g., a family with one sister and two MZ brothers has two opposite sex sibling pairs, and one male MZ twin
pair. Note that during statistical analyses these sibling relations within a single family were not treated as independent.
b Heritability (h2) was modeled including dominant genetic effects (ADE). In all other cases, only additive genetic effects and unique environmental effects were
twin and sibling relations. These intrapair correlations are given
anxiety and depression is due to genes or environmental
for the full EEG sample including those subjects without
factors shared between the two variables. That is, insofar FA
questionnaire data available on any occasion. In the young
and anxiety and depression correlate, how much of that shared
cohort, DZ/sibling correlations were less than half the MZ
variance can be attributed to genetic sources, and how much
correlations. This pattern of twin correlations suggests the
to environmental sources. Since a significant correlation
presence of genetic dominance, but in view of the sample size
between FA and the risk for anxiety and depression was only
for FA genetic dominance was not explicitly modeled
found in young females, we limited the bivariate genetic
analysis to this group. As the best fitting models in young
Common environmental variation did not contribute
females estimated additive genetic and unique environmental
significantly to the observed variation in FA and we proceeded
effects (AE) on both the risk factor score and FA in the
by fitting a model with additive genetic and unique environ-
univariate cases, the bivariate models, too, estimated AE
mental influences only (AE). Under this model, FA heritability
was significant only in the younger cohort (32% males, 37%
The results showed that environmental correlations were
females). These models were refitted after excluding the 10%,
close to and not significantly different from zero at all
20% and 30% of subjects that scored lowest on the average of
selection criteria (all x2 < 1, ns). The genetic correlations
F3 and F4 power. Heritability estimates in the middle-aged
were not significant in the full sample (x2(1) = 2.18,
cohort remained non-significant. In the young males, evidence
p = 0.14), borderline significant after 10% of the subjects
for a genetic contribution disappeared.
with the lowest frontal alpha were excluded (x2(1) =3.54, p = 0.06), and significant after 20 and 30% of the
3.7. Genetic and environmental contribution to the
subjects with the lowest frontal alpha were excluded
association between FA and the risk for anxiety and
(x2(1) > 5.17, p < 0.05). These results suggest that the
observed correlation between FA and the risk for anxiety anddepression in young females can be explained by shared
Bivariate genetic analyses were used to determine whether
genetic sources and not by an overlap in environmental
the observed correlation between FA and the factor score for
D.J.A. Smit et al. / Biological Psychology 74 (2007) 26–33
The finding that the relation between FA and anxiety and
depression is restricted to females is in keeping with much of
FA has been put forward as a biological marker for the risk
the previous literature. Studies that related FA to psychopathol-
for anxiety and depression (for reviews:
ogy were often limited to female subjects, or included a
majority of females in their samples. This can be observed in
disorders and have found to be influenced by overlapping
the exhaustive summary of studies relating FA to psycho-
). FA has therefore great potential to be used as a
has been explicitly noted by others ). Of
so-called endophenotype in studies searching for genes that
those that included an adult sample, five report exclusively on
influence the shared neurobiological pathways that are affected
in these disorders. Two requirements, however, are that FA is
heritable and that the genes influencing FA also influence the
risk for anxiety and depression. Here we explored this question
in male and female twins and their siblings in two different age
Our results show that frontal asymmetry was only heritable
in young adulthood and was higher in young females (37%)
than in young males (32%). FA heritability in young females
contrast, only two studies report on a majority of males
rose slightly after selecting subjects with sufficient frontal
A stronger case for sex differences comes from studies that
heritability disappeared. It may therefore be concluded that
directly compared results from males and females (
heritability is more robust in young adult females. These
results are consistent with the previous twin studies on FA in
young female adults that reported heritabilities of 33%
activity only in depressed females not responsive to fluoxetine
treatment and no effects in males or responsive females.
found an effect in males opposite of that of
heritability of 22% in females and no significant heritability
females, that is, higher left frontal activity for males with family
in males. With regard to cohort differences, none of these
previous studies had included subject groups with mean ages
interaction effects between depression liability and sex in an
older than 21, so we cannot compare our results in adults to
ANOVA predicting FA depending on the reference montage:
with vertex (Cz) as reference, FA was related to increased
The heritability of young adult FA seems rather low, but it
liability of depression in females, and not in males. In the field
must be appreciated that resting FA consists of a mixture of trait
activity in anxious 8- and 10-year-old girls and greater left
Equation Modeling on data recorded during four recording
frontal activity in 11-year-old boys. Similar sex differences
have been reported in studies investigating defensiveness as
40% of total FA variance to be state and 60% trait variance.
Heritability of FA, therefore, was bound by a maximum of 60%.
These results, plus the results presented here, provide evidence
The contribution of state and trait variance may be unequally
for sex differences in the relation between FA and anxiety or
distributed across gender. Females may be more reactive to the
experimental procedures involved in the EEG recordings
perhaps in interaction with traits that are known to modulate
clearly reveals that while infants, adolescents, and especially
young adults have been studied extensively, older adults are
recording environment is more anxiogenic in women than in
men, and this reactivity is genetically determined, then trait
on subjects of 37 years on average, found evidence of group
variance in women will show larger heritability estimates.
differences between depressed and non-depressed subjects
To index the risk for anxiety and depression we used a factor
score obtained from multiple scales at multiple measurement
similar results with a measure related to FA in a sample of 43–
occasions. As reported previously, this factor score is about
57 years. found that self-reported well-being
60% heritable in both males and females (
was related to greater left fronto-central activity in subjects 57–
The relation between the factor score and FA was not
significant in older subjects or in young adult males. As with
between a young adult and an elderly age group in the relation
heritability, young females were the positive exception. Only in
between FA and defensiveness. Other studies included both
this group, the relation between FA and the risk for anxiety and
younger and older subjects, but did not report their data
depression became significant after excluding subjects with the
lowest average frontal EEG power as suggested by
). In contrast to these previous results, the
D.J.A. Smit et al. / Biological Psychology 74 (2007) 26–33
current results showed no evidence of a relation between FA
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be surprising. In the middle-aged cohort variance in FA only
Boomsma, D.I., Vink, J.M., van Beijsterveldt, T.C., De Geus, E.J., Beem,
reflected the accumulated effects of environmental factors and
A.L., Mulder, E.J., Derks, E.M., Riese, H., Willemsen, G.A., Bartels, M.,
life events unique to family members. Because the young
van den Berg, M., Kupper, N.H., Polderman, T.J., Posthuma, D., Rietveld,
cohort showed that FA and the factor score were correlated
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entirely by underlying genetic factors, the lack of a correlation
between FA and the risk for anxiety and depression simply may
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Frontiers of Science Program RG0154/1998-B and the
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In the absence of the drug in the urine, the colored antibody-colloid gold AMP AMPHETAMINE conjugate moves with the sample fluid by capillary action along the membrane until it reaches the immobilized drug conjugate in the test band MonlabTest® region. At this point, the antibody-colloid gold conjugate reacts with the pre-coated drug conjugate to produce a visible pink colored line as
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