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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 Boomsma, D.I., Beem, A.L., van den Berg, M., Dolan, C.V., Koopmans, and the risk for anxiety and depression in a large middle-aged J.R., Vink, J.M., De Geus, E.J., Slagboom, P.E., 2000. Netherlands twinfamily study of anxious depression (NETSAD). Twin Research 3 (4), Dutch sample. In view of the genetic analyses, this should not 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 M.J., Stubbe, J.H., Knol, L.I., Stroet, T., van Baal, G.C., 2002. Nether-lands Twin Register: a focus on longitudinal research. Twin Research 5 entirely by underlying genetic factors, the lack of a correlation between FA and the risk for anxiety and depression simply may Bruder, G.E., Stewart, J.W., Tenke, C.E., McGrath, P.J., Leite, P., Bhattacharya, simply reflect the absence of heritable influences on FA in this N., Quitkin, F.M., 2001. Electroencephalographic and perceptual asymme- try differences between responders and nonresponders to an SSRI anti- In short, the relation between FA and the risk for anxiety and depressant. Biological Psychiatry 49 (5), 416–425.
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