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The Genetic Epidemiology of Irrational Fears and Phobias in Men
Kenneth S. Kendler, MD;
John Myers, MS;
Carol A. Prescott, PhD;
Michael C. Neale, PhD
Arch Gen Psychiatry. 2001;58:257-265.
ABSTRACT
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Background Much of our knowledge of the role of genetic factors in the etiology
of phobias comes from one population-based sample of female twins. We examined
the sources of individual differences in the risks for phobias and their associated
irrational fears in male twins.
Methods In personal interviews with both members of 1198 male-male twin pairs
(707 monozygotic [MZ] and 491 dizygotic [DZ]) ascertained from a population-based
registry, we assessed the lifetime history of agoraphobia and social, animal,
situational, and blood/injury phobias as well as their associated irrational
fears. Twin resemblance was assessed by means of probandwise concordance,
odds ratios, tetrachoric correlations, and univariate and multivariate biometrical
model fitting.
Results The suggestive results obtained by analysis of phobias only were supported
by analyzing both fears and phobias. All 5 phobia subtypes aggregate within
twinpairs. This aggregation is due largely or solely to genetic factors with
heritability of liabilities ranging from 25% to 37%. Multivariate analysis
revealed a common genetic factor, genetic factors specific to each subtype,
and a common familial-environmental factor.
Conclusions In male subjects, genetic risk factors, which are partially common across
all subtypes and partially subtype specific, play a moderate role in the etiology
of phobias and their associated irrational fears. Family environment probably
has an impact on risk for agoraphobia and social phobia. The genetic liability
to blood/injury phobias is not distinct from those of the more typical phobias.
INTRODUCTION
FAMILY STUDIES suggest that phobias are familial,1, 2, 3, 4, 5, 6
but cannot clarify the origin of this family resemblance. Twin studies of
self-reported fears consistently have suggested a significant role for genetic
factors.7, 8, 9, 10, 11
By contrast, twin studies of clinically defined phobias have, with one exception,
suffered from very small samples sizes with resultant low power to discriminate
alternative models of familial transmission.12, 13, 14
This exception is our previous study of phobias in female-female twins from
the Virginia Twin Registry.15, 16, 17
These reports examined 5 types of phobias—agoraphobia (AgP), social
phobia (SoP), animal phobia (AnP), situational phobia (SiP), and blood/injury
phobia (BiP)—and reached the following conclusions. First, all phobia
subtypes are moderately familial. Second, familial aggregation of AgP, SoP,
and AnP is due to genetic factors. For SiP and BiP, results based on our first
assessment15, 16 suggested that
twin resemblance might result from familial-environmental factors. However,
when our analyses included a second assessment interview,17
the added power obtained through control of measurement error suggested that
the results for these phobia subtypes were similar to those for the others
(ie, the familial transmission due solely to genetic factors). Third, high
levels of comorbidity were seen between the phobia subtypes.15
Contrary to results from family studies,4 the
best-fitting multivariate model suggested common genetic and individual-specific
environmental factors that influenced risk for all phobia subtypes, as well
as genetic and environmental factors unique to each subtype. However, these
analyses did not include BiP, which was assessed at a later wave. Blood/injury
phobia differs from typical phobias,18 where
exposure to phobic stimuli (eg, snakes, heights, and public speaking) usually
produces increased sympathetic activity (eg, tachycardia, increased blood
pressure, sweating, and flushing). By contrast, in individuals with BiP, exposure
to phobic stimuli (eg, needles and blood) usually increases parasympathetic
activity (eg, bradycardia, hypotension, pallor, and fainting). Given these
differences, would the genetic and environmental risk factors for BiP be distinct
from those for the other phobia subtypes?
In this report, using our recently studied sample of male-male twin
pairs ascertained from the same registry, we address the following questions:
1. What are the sources of individual differences in risk for the 5
phobia subtypes in male twins?
2. Do irrational fears without impairment reflect a milder form of the
same liability dimensions as classic phobias? If so, will including such fears
in the modeling improve power and the ability to discriminate competing models?
3. What is the level of comorbidity among individual phobia subtypes
in this population sample? To what degree do genetic and environmental common
factors contribute to the observed patterns of comorbidity, and will these
common factors have less impact on the liability to BiP than on the liability
to the more typical phobia subtypes?
SUBJECTS AND METHODS
SAMPLE AND ASSESSMENT PROCEDURES
This report is based on data from the second wave of interviews in our
study of adult twins from the Virginia Twin Registry (now part of the Mid-Atlantic
Twin Registry), details of which have been outlined previously.19
Briefly, twins were eligible for participation if one or both members were
successfully matched and if they were white, a member of a multiple birth
that included at least 1 male, and born between 1940 and 1974. Of 9417 eligible
individuals for the first wave, 6814 (72.4%) completed initial interviews.
For those who completed the initial interview, we recontacted them to schedule
a second interview at least 1 year later. Where possible, this interview was
completed face-to-face (79.4% of sample). Of the eligible individuals, 5629
(82.6%) were successfully interviewed. To assess test-retest reliability,
150 members of male-male twins were reinterviewed a mean (± SD) of
4.4 ± 1.1 weeks after their initial interview.
The current report is based on 1198 male-male pairs (707 monozygotic
[MZ] and 491 dizygotic [DZ]) with complete data on irrational fears and phobias
from the second-wave interview and 544 interviewed individual twins (254 from
MZ and 290 from DZ pairs) with complete data whose co-twins did not complete
a second-wave interview.
At the second-wave interview (1994 through 1998), subjects were aged
20 to 58 years (mean ± SD, 36.8 ± 9.1 years). Interviewers had
a master's degree in a mental health–related field or a bachelor's degree
in this area plus 2 years of clinical experience. Members of a twin pair were
interviewed by different interviewers unaware of clinical information about
the co-twin. Zygosity diagnosis was performed using a discriminant function
analysis based on 6 standard zygosity questions. The algorithm was developed
on 227 twin pairs who underwent genotyping using 8 or more highly polymorphic
DNA markers.19
We assessed a lifetime history of phobias with an adaptation of the
phobic disorders section of the Diagnostic Interview Schedule (DIS) Version
III-A.15, 20 The 22 specific individual
fears that were assessed are outlined in Table 1. We also asked respondents "Is there anything else you've
been unreasonably terrified to do or be near?" If any phobia described in
response to this question best belonged with 1 of the 5 specific subtypes,
it was so treated. Other phobias mentioned in response to this question (eg,
fear of darkness) were included in our analysis of any phobia, but were not
counted as belonging to a specific subtype.
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Table 1. Specific Irrational Fears and Phobias in 2940 Male Twins*
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In the DIS, to be considered a phobia, the fear must result in seeing
a physician, taking medications, or reporting that the fear or its avoidance
"interfered with life or activities a lot." Given the low and variable rates
of treatment seeking for phobias,21 we defined
phobias solely through a modification of the third criterion, objective impact
of the fear on respondent behavior. In contrast to the DIS, where the respondent
makes the judgment about fear-associated interference, in our interview, the
interviewer made this assessment.
STATISTICAL ANALYSIS
The univariate and multivariate twin models used in this report are
described elsewhere.15, 22 We assume
that variation in liability to phobias results from the following 3 sets of
factors: (1) additive genetic (A), which contribute twice as much to the correlation
in MZ twins as DZ twins; (2) family or common environment (those familial
factors such as parental attitudes that are shared by members of a twin pair)
(C), which contribute equally to the correlation in MZ and DZ twins; and (3)
individual specific environment (E), which reflect environmental experiences
not shared by members of a twin pair and therefore contribute to differences
between them in their phobia histories.
Our multivariate twin analyses decompose into genetic and environmental
sources the variance in phobia liability and the covariance in liability among
different phobia subtypes. We attempt, in these analyses, to explain the correlations
between the phobia subtypes as resulting from a small number of latent factors.
Multivariate genetic analysis goes beyond traditional factor analysis in providing
insight into the causes of resemblance among variables.
Two alternative multivariate models that describe how genetic and environmental
factors influence covariation are tested. Genetic and environmental factors
could influence covariation through a single common pathway.23
By contrast, in the independent pathway model, genes and the environment contribute
to covariation through separate genetic and environmental latent factors.
Having 5 phobia subtypes, two factors were potentially identifiable.
However, we focused on single common factor models, because this was the approach
used previously.15 The relationship between
the common genetic factor and BiP was evaluated by setting the connecting
path to 0 and examining the change in fit.
To use complete twin pairs and twins whose co-twin was not interviewed,
we used an Mx option24 to fit models by maximum
likelihood. During optimization, trial values of the parameters are used to
generate a predicted covariance matrix and a matrix of thresholds. For any
particular observation, the overall matrix is filtered to create a submatrix
matching those observations that are present. Likewise, the corresponding
subset of the matrix of thresholds is created. These matrices are then used
to compute the log-likelihood of the observation in question. The log-likelihoods
of all cases are summed to obtain the log-likelihood of the sample, which
is maximized using numerical optimization software. An advantage of this method
is that it reduces the possible impact of cooperation bias by using information
on potential differences in the prevalence of phobias in those twins with
vs those without a co-twin participating to obtain a better estimate of true
prevalences.
Because maximum likelihood analysis of raw ordinal data does not provide
an overall test of goodness of fit, we compare relative fits against the full
model. Twice the difference in log-likelihood between the full model and submodel
tested yields a statistic that is asymptotically  2, with degrees
of freedom equal to the difference in the number of parameters in both models.
Alternative models are evaluated for the optimal balance between explanatory
power and parsimony, which is operationalized by Akaike's Information Criterion
(AIC).25, 26
Because unreasonable fears are more common than phobias, analysis including
fears would have increased power.27 Such analysis
would be appropriate if fears and phobias resulted from a single continuum
of liability, a hypothesis testable by the multiple-threshold model.28 For our analyses, P indicates phobias only, and FP,
fears and phobias.
We tested the equal environment assumption that exposure of MZ and DZ
twin pairs to environmental risk factors for fears and phobias was equally
correlated by predicting twin concordance for phobias, controlling for zygosity
by means of the similarity of environmental experiences of the twins in childhood29 and adulthood.
RESULTS
TEST FOR BIASES AND RELIABILITY
We performed 12 analyses predicting twin concordance for each phobia
subtype and any phobias from the similarity of their childhood environment
and the frequency of adult contact. Three were significant at the 5% level;
2, in the direction opposite that predicted. Controlling for zygosity, twin
pairs with more similar childhood environments were significantly less likely
to be concordant for AnP (21 = 5.55; P = .02) and SiP (21 = 4.10; P = .04). Those in frequent adult contact were significantly more likely
to be concordant for SiP (21 = 5.27; P = .02).
Short-term test-retest reliability for irrational fears and phobias,
as assessed by the coefficient and the tetrachoric correlation, were modest
to moderate (Table 2). With the
exception of social fears/SoP, irrational fears were more reliably reported
than phobias. The reliability of the assignment of a phobia given an irrational
fear was particularly modest. Consistent with our previous results,17 individuals may be more reliable at recalling irrational
fears than they are at reporting their behavioral consequences.
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Table 2. Test-Retest Reliability of Irrational Fears, Phobias, and
Phobias for 150 Subjects Who Admit to Fears*
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DESCRIPTION BY INDIVIDUAL FEAR
Many more individuals endorsed an irrational fear than met criteria
for an associated phobia (Table 1).
However, this ratio differed widely. For example, although 46% of individuals
who feared being in crowds met criteria for AgP, the parallel figures for
fears of needles, giving a speech, and snakes were 18%, 15%, and 14%, respectively. Table 1 also presents, within each of the
phobia subtypes, the proportion of individuals who met criteria for phobia
based on each specific fear. The most common impairing fears for each subtype
were being in crowds for AgP, giving a speech for SoP, snakes for AnP, other
high places for SiP, and dentists or hospitals for BiP.
The most common phobia subtype was SiP, followed by SoP, BiP, AnP, and
AgP. No significant differences were seen in the prevalence of the phobia
subtypes or any phobia in MZ vs DZ twins (results not shown).
TWIN RESEMBLANCE
Twin resemblance was seen for all 5 of the phobia subtypes in MZ twins,
with the odds ratios (ORs) ranging from 2.30 for SoP to 4.64 for AnP (Table 3). In DZ twins, twin resemblance
was seen for AgP, SoP, and AnP, but not for SiP or BiP. For all phobia subtypes
as well as for any phobia, the OR and tetrachoric correlations in MZ twins
exceeded those seen in DZ twins, suggesting the importance of genetic risk
factors.
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Table 3. Prevalence and Measures of Similarity for Phobias in MZ and
DZ Male-Male Twin Pairs*
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UNIVARIATE MODEL FITTING TO PHOBIAS ONLY
Table 4 shows the results
of model fitting for each of the phobia subtypes and for any phobia. For AgP
and SoP, the full ACE model suggested that twin resemblance resulted from
both genetic and familial-environmental factors. When we tested the simpler
AE and CE models in these 2 phobias, they produced nearly identical fits. Table 4 presents results for the AE model.
The CE model produced the following estimates for c2 and e2: -0.29 and 0.71,
respectively, for AgP, and 0.17 and 0.83, respectively, for SoP. The E-only
model, by contrast, fit more poorly for both phobias. Although AgP and SoP
aggregated within twin pairs, we had no power to distinguish the degree to
which this was due to genetic and/or environmental mechanisms.
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Table 4. Model-Fitting Results for Phobias in Male-Male Twin Pairs*
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For AnP, SiP, BiP, and any phobia, c2 was estimated at 0 in the full model, indicating that twin resemblance
was ascribed entirely to genetic factors. In each case, the AE model fit somewhat
better than the CE model, with estimates of heritability ranging from 0.22
(for any phobia) to 0.35 (for AnP). The very wide confidence intervals (CIs)
on these heritability estimates are noteworthy. Furthermore, using the more
rigorous 2 difference test, we could not reject the CE against
the ACE model at any level approaching statistical significance. Indeed, even
the test for familial aggregation of phobias (the ACE vs E-only model) was
significant only for AgP (22 = 6.05; P = .05), AnP (22 = 6.65; P = .04), SiP (22 = 7.02; P = .03), and any phobia (22 = 10.83; P = .004).
UNIVARIATE MODEL FITTING TO FEARS AND PHOBIAS
We began by testing with the multiple threshold model28
the assumption that irrational fears and phobias represented differing points
on a single continuum of liability. Although none of the results for the 5
phobia subtypes, examined separately in MZ and DZ twins, were statistically
significant, the results for any phobia were significant in both twin groups
(MZ, 25 = 80.0; P<.001;
DZ, 25 = 67.7; P<.001).
Therefore, we proceeded with model fitting using the trivariate classification
of unaffected, fear only, and phobia for the 5 specific subtypes of fears
and phobias only. The test-retest reliability for this trichotomy is shown
in Table 2.
The magnitude of the polychoric correlations for fears/phobias in MZ
and DZ twins (Table 3) are generally
similar to those seen with phobias only (although there are some exceptions,
eg, AgP). However, as expected, the SEs of these correlations are substantially
smaller than those seen with phobias alone.
The pattern of modeling results for fears and phobias (Table 5) differed from that found with phobias alone in 3 important
ways. First, the full or ACE model suggested for all 5 phobia subtypes that
the familial aggregation of phobia susceptibility was due solely to genetic
factors. For each phobia/fear, AE was the best-fit model, with estimates of
the heritability of liability ranging from 0.24 for SoFP to 0.43 for AgFP.
Second, the statistical power with which we could reject alternative models
was substantially greater. Using the 2 difference test, we
could reject the CE model against the ACE model at or near the 5% level for
the following 4 of the 5 fear/phobia subtypes: AgFP (21 = 3.64; P = .06), AnFP (21 = 11.87; P<.001), SiFP (21 = 8.09; P = .004), and BiFP (21 = 3.21; P = .07). For all fears/phobias,
we could reject the E only (or no familial transmission model) with confidence,
ie, AgFP (22 = 21.49; P<.001),
SoFP (22 = 22.97; P<.001),
AnFP (22 = 42.17; P<.001),
SiFP (22 = 34.32; P<.001),
and BiFP (22 = 25.30; P<.001).
Third, the CIs around the parameter estimates were considerably narrower when
we considered both fears and phobias in the model fitting compared with phobias
alone.
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Table 5. Model-Fitting Results for Fears and Phobias in Male-Male Twin
Pairs*
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COMORBIDITY AMONG PHOBIA SUBTYPES AND MULTIVARIATE MODEL FITTING
Substantial comorbidity exists among all combinations of the phobia
subtypes (Table 6). As measured
by OR or tetrachoric correlations, the highest comorbidity is seen between
AgP and SoP, followed by SoP and BiP. The pattern of comorbidity of BiP is
similar to that seen with more "typical" phobias.
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Table 6. Tetrachoric Correlation and Odds Ratios Between Phobias*
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Because of greater statistical power and stability of estimates, we
performed multivariate model fitting with fears and phobias, the results of
which are outlined in Table 7.
Model 1 was the full independent pathway model with the A, C, and E common
factors as well as the A, C, and E factors specific to each phobia subtype.
When we tried to simplify this to a common pathway model, the fit deteriorated
substantially, and the AIC increased. Therefore, in subsequent models, we
set to 0, in turn, the C common factor (model 3), the A common factor (model
4), the E common factor (model 5), the phobia-specific C paths (model 6),
and the phobia-specific A paths (model 7). The AIC improved only for model
6. Indeed, the fit of the model was unchanged when constraining to zero C
paths unique to each phobia.
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Table 7. Multivariate Model-Fitting Results for Specific Fears/Phobias*
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We then tested the relationship between the genetic risk factors for
BiFP and the more typical phobias. Starting with model 6, we constrained to
0 the path from the common genetic factor to BiFP, thereby forcing all genetic
risk for BiFP to be independent of the other phobia subtypes. This model fit
substantially more poorly than model 6, with a deterioration of 6.5 2 units (P = .01).
Parameter estimates for the best-fit model 6 are seen in Figure 1 and Table 8.
Five results are noteworthy. First, contrary to the hypothesis that the genetic
risk factors for BiFP are distinct from those for the more typical phobias,
BiFP actually had the highest loading on the common genetic factor. Second,
the best-fit model also contained genetic risk factors specific to each phobia
subtype. These genetic-specific factors were most important for SoFP, AnFP,
and SiFP. Third, unlike the univariate analysis for fears/phobias (but more
like the univariate analyses for phobias alone), we found evidence of the
impact of shared environment, but only in the form of a common factor. This
common factor significantly affected only AgFP and SoFP. Fourth, the best-fit
model contained one common E factor. That is, some environmental experiences
that were unique to individual twins influence the general risk for fears/phobias.
This factor had highest loadings on AgFP and SoFP. Finally, substantial specific
E loadings were seen for all subtypes, which would represent an admixture
of measurement error and environmental experiences that predisposed uniquely
to individual phobia subtypes.
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Results from the best-fitting multivariate genetic model for the
subtypes of phobias (model 6). A indicates additive genetic; C, common or
shared family environment; E, individual specific environmental effects; subscript
C, phobia common factors; and subscript S, additive genetic and individual-specific
environmental effects specific to each phobic subtype. Thus, AC
refers to the additive genetic common factor (additive genes that influence
liability to all phobia subtypes); CC, the shared environmental
common factor; and ES, individual-specific environmental experiences
that uniquely influence liability only to 1 phobia subtype. The magnitude
of each path, as estimated using model 6, is shown. Squaring these path or
standardized partial regression coefficients gives the proportion of variance
in the observed variable accounted for by the latent factor.
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Table 8. Sources of Variance in Liability to Individual Phobia Subtypes
From Best-Fit Fear/Phobia Multivariate Model
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COMMENT
We addressed 3 questions about the genetic epidemiology of irrational
fears and phobias in male-male twin pairs from a population-based registry.
We examine these questions in turn.
Individual phobia subtypes and any phobia aggregated within twin pairs.
For AnP, SiP, BiP, and any phobia, the best-fit model suggested that familial
aggregation was due solely to genetic factors with modest heritabilities.
For AgP and SoP, model fitting could not distinguish between genetic and familial-environmental
sources of twin resemblance. For all the phobia subtypes, power was limited,
and CIs for the parameter estimates were broad.
Many twins in our sample reported irrational fears without objective
impact on their lives. Given our need for greater statistical power to resolve
sources of individual differences and the low reliability with which individuals
recalled whether the fears were impairing, we applied the multiple-threshold
model28 to a trichotomous classification of
all individuals into unaffected, fear only, and phobia. Results from these
analyses indicated that for all the phobia subtypes, the pattern of results
within MZ and DZ twins pairs were consistent with the hypothesis that fears
were a milder manifestation of the same liability dimension that produced
clinical phobias. We found similar results in our female twins.17
We repeated our analysis using this trichotomous classification, with
results that were substantially clearer than those obtained for phobias alone.
With the increased statistical power, evidence of familial-environmental effects
on AgP and SoP disappeared. The best-fit model for all the phobia subtypes
suggested that familial resemblance was due solely to genetic factors, again
with modest heritability estimates, but now with considerably smaller CIs.
We recently fitted multiple threshold models to data on fears and phobias
from the previously studied female-female pairs17
to which our current results can be compared usefully. We used a measurement
model based on 2 waves of interviews from which we can derive expected heritability
from a single interview: for AgFP, 0.47; for SoFP, 0.31; for AnFP, 0.27; for
SiFP, 0.26; and for BiFP, 0.32. These results, well within the 95% CIs obtained
in the male sample, suggest that the role of genetic factors in liability
to irrational fears and phobias are probably similar in men and women.
Similar to other community samples,15, 30
substantial comorbidity was seen between phobia subtypes. Multivariate twin
modeling is a powerful method to examine the contributions of genetic and
environmental factors to observed patterns of comorbidity. Given the higher
test-retest reliability and greater power and stability of parameter estimates
associated with adding of information on irrational fears, we included these
along with phobias in our multivariate analyses. The best-fit model contained
3 common factors (reflecting genetic and shared and unique environments) that
influenced liability to all forms of phobia. In addition, each phobic subtype
had evidence of genetic and unique environmental factors specific to that
phobia.
The pattern of results we obtained was similar to that in our previous
multivariate analysis in women (which contained only 4 phobia subtypes)15 in 2 important ways. In both sexes, certain genetic
factors influenced risk for all phobia subtypes, whereas others specifically
influenced risk for individual phobic subtypes. In both sexes, the loadings
of AnP on this common genetic factor were higher than those for the other
typical phobias of AgP, SoP, and SiP. We also saw evidence that in men and
women, certain individual environmental experiences increased risk nonspecifically
for all phobic subtypes, whereas others were phobia-subtype specific in their
impact. However, 2 differences are noteworthy. First, we found evidence in
our multivariate analysis in men but not in women of shared environmental
effects that had a significant impact on AgP and SoP. These results suggest
that twin siblings shared some environmental experiences in their family or
community that influence risk specifically for AgP and SoP. Second, the pattern
of loadings for phobia-specific genetic factors differed between the sexes.
For example, we found in women much larger contributions of phobia-specific
genetic influences for AgP than AnP, whereas in men the findings were reversed.
Further research will be required to determine if these and other differences
seen in both sexes are substantive in nature or due to stochastic fluctuations
in patterns of phobia resemblances in twin pairs.
Our multivariate analyses also permitted us to evaluate the hypothesis
that the genetic risk factors for BiP are distinct from those for the more
typical phobia subtypes. Our results were inconsistent with this hypothesis.
Indeed, BiP had the highest loading on the common genetic factor, and we could
not set that path to 0 without a substantial deterioration in fit. The more
typical phobias and BiP probably share common early fear pathways that then
diverge in their outflow to the hypothalamus and autonomic pathways.31 These findings suggest that genetic risk factors
for phobias in men act largely on the individual differences in the sensitivity
of those early fear pathways shared by BiP and the more typical phobias.
These analyses should be considered in the context of 2 potential methodological
limitations. First, our criteria for phobias differ from those proposed in
recent DSM editions.32, 33
For example, our interviewer-based assessment of impairment, although more
objective, may produce a lower threshold for interference than the self-report
measure used in the DIS. Our definition may also be broader than that proposed
in DSM-III-R criteria32
in that we require objective impact on respondent behavior rather than the
significant interference with normal routine in DSM-III-R. However, DSM-III-R would include an unreasonable
fear that produced marked distress, whereas we did not. The Epidemiological
Catchment Area screened for a more limited number of phobic stimuli (14 specific
fears) and produced a lifetime prevalence for any phobia in men of 10.4%,30 about half of what we found in this study. By contrast,
compared with our results, the National Comorbidity Study found much higher
rates of SoP in men (11.1%)34 and slightly
lower rates of AgP (3.5%).
Second, a lifetime history of irrational fears and phobias was assessed
in this study at a single point in time. If uncorrelated in twin pairs, unreliability
of measurement is indistinguishable from the effects of true individual specific
environment in our twin models. Our short-term retest reliability found most
tetrachoric correlations for fears and phobias ranging from 0.60 to 0.85.
These results suggest that a substantial proportion of what we call E in our
models in fact represents unreliability of measurement. If our twin models
were corrected for this effect, as shown in the female sample,17
the estimates of the heritability of liability to phobias (ie, the genetic
proportion of reliable variance) would be considerably higher than those reported
herein.
AUTHOR INFORMATION
Accepted for publication October 10, 2000.
This work was supported by grants MH/AA-49492 and MH-54150 and Research
Scientist awards MH-01277 (Dr Kendler) and MH-01458 (Dr Neale) from the National
Institutes of Health, Bethesda, Md. We acknowledge the contribution of the
Virginia Twin Registry, now part of the Mid-Atlantic Twin Registry, to ascertainment
of subjects for this study. The Mid-Atlantic Twin Registry, directed by Linda
Corey, PhD, and Lenn Murrelle, PhD, has received support from the National
Institutes of Health, the Carman Trust (Richmond, Va), and the WM Keck (Los
Angeles, Calif), John Templeton (Radnor, Pa), and Robert Wood Johnson (Princeton,
NJ) Foundations.
These data were collected under the direction of Patsy Waring, Sarah
Woltz, MA, and Frank Butera, MS.
From the Virginia Institute for Psychiatric and Behavioral Genetics
(Drs Kendler, Prescott, and Neale and Mr Myers) and the Departments of Psychiatry
(Drs Kendler, Prescott, and Neale and Mr Myers) and Human Genetics (Drs Kendler
and Neale), Medical College of Virginia of Virginia Commonwealth University,
Richmond.
Corresponding author and reprints: Kenneth S. Kendler, MD, Department
of Psychiatry, Medical College of Virginia of Virginia Commonwealth University,
800 E Leigh St, PO Box 980126, Richmond, VA 23298-0126.
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