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Depression in offspring following severe prenatal stress
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Depression in offspring following severe prenatal stress
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DEPRESSION IN OFFSPRING FOLLOWING SEVERE PRENATAL STRESS
Copyright 1998
by
Jennifer Bunn Watson
A Thesis Presented to the
FACULTY OF THE GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
MASTER OF ARTS
(Clinical Psychology)
December 1998
Jennifer Bunn Watson
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UMI Number: 1394795
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U N IV ERSITY O F S O U T H E R N C A L IFO R N IA
T H E G R A D U A T E S C H O O L
U N IV E R S I T Y P A R K
L O S A N G E L E S . C A L IF O R N IA 9 0 0 0 7
This thesis, •written by
Jennifer Bunn Watson
under the direction o f he.r.— Thesis Committee,
and approved by all its members, has been pre
sented to and accepted by the Dean of The
Graduate School, in partial fulfillment of the
requirements for the degree of
Master of Arts in Clinical Psychology
ISv COMMITTEE
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List of Tables
Table 1. Hamilton Depression mean scores (with standard
deviations) for exposed and control subjects by trimester.
Table 2. Hamilton Depression trimmed mean scores (with standard
deviations) for exposed and control subjects by trimester
with 20% trimming.
Table 3. Self-Rating Depression Scale mean scores (with standard
deviations) for exposed and control subjects by trimester.
Table 4. Self-Rating Depression Scale trimmed mean scores (with
standard deviations) for exposed and control subjects by
trimester with 20% trimming.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.
Abstract
In 1976 a severe earthquake (7.8) struck Tangshan, China. The earthquake
provides the opportunity to examine the impact of maternal stress on fetal
neurodevelopment. It was hypothesized that exposure to this severe earthquake is related
to increased depressive symptomotology in the offspring.
Depressive symptomotology was examined in 1215 18-year old students using the
Hamilton Depression Scale (HAMD) and the Self Rating Depression Scale. Half were
exposed to the Tangshan earthquake in utero, and the other half were not exposed
(controls). The exposed subjects are equally distributed across all nine months of
gestation for earthquake exposure; control subjects were born a year later and matched for
birth date.
Exposure to maternal stress in utero was associated with more depressive
symptoms in exposed subjects as compared to control subjects on the HAMD,
Yuen's(688.9)=7.8,p<001 and the SDS, Yuen’s(72S.l)=2.5,p=01.
Earthquake exposure while in utero may have negative effects on mood later in
life.
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Background
Animal Studies of Teratogens
Animal research has demonstrated that maternal stress during a critical period of
gestation may adversely affect the fetus. In 1964 Thompson and Quinby reported that
dams who were severely stressed during pregnancy produce pups that evidence reduced
locomotion in the open-field test. A review by Archer and Blackman (1971) of the early
research on the influence of prenatal stress on the offspring revealed that stress during
gestation may have an influence on offspring behavior; however the nature and direction
of these potential behavioral changes were inconsistent. Weinstock, Fride, and Hertzberg
(1988) noted that the following experimental design factors could have shaped the findings
in the Archer and Blackman review: “type of behavioral test on the offspring, the
maternal environment at the time of stress, the intensity of stress, its timing and frequency
throughout gestation in relation to critical stages of fetal development, the reaction of the
hippocampo-hypothalamo-hypophyseal-adrenal (HP A) systems of the mother and fetus to
the stressor.” To address the question what role do timing and frequency of stress have
on the developing fetus, Fride and Weinstock (1984) administered daily noise stress to
pregnant rats on a regular basis. A measure of the plasma corticosterone levels of stressed
and control (not exposed to noise stress) dams revealed that by the third exposure to the
loud noise the plasma levels of the stressed dams had adapted to the level of the control.
Fride and Weinstock (1984) then employed a noise schedule where the stressor was
administered on an unpredictable basis and the maternal plasma levels alternated between
being abnormally high and low during the last week of pregnancy. From these findings
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Weinstock et al. concluded that the timing of the stress and the administration of the stress
(randomly versus regular intervals) affected the maternal corticosterone response (1988).
An investigation by Alonso, Arevalo, Agonso, and Rodriguez (1991) examined the
effects of maternal stress (during the second half of gestation) on the behavior of the
offspring. The main finding o f this study by Alonso et al. was that female rats at age 80
days and at 200 days who were exposed to stress as fetuses exhibited an increase in
immobility on the Porsolt test as compared to female controls (1991). According to
Porsolt (1977) immobility on the Porsolt test represents behavioral despair which has been
adopted by many animal researchers as a model of depression in rats. In a follow up study
Alonso, Navarro, and Rodriguez (1994) found that the female rats who were exposed to
stress as fetuses exhibited more immobility (depression) on the Porsolt test as adults; in
addition, these stressed rats showed a reduction of dopamine turnover in the nucleus
accumbens and the effect on the right nucleus accumbens was higher than on the left
accumbens.
A study comparing rats that were submitted to stress prenatally to those exposed
postnatally found that adult prenatally stressed rats demonstrated high anxiety-like
behavior when exposed to novelty and increased secretion of corticosterone in response to
stress as compared to adult rats who were stressed postnatally (Vallee, Mayo, Dellu,
Moal, Simon, & Maccari, 1997). Adult rats who were exposed to stress prenatally
(random noise and light stress) were less active in an open field and had significantly
elevated plasma corticosterone after each open field exposure when compared to controls
(Fride, Dan, Feldon, Halevy & Weinstock, 1986). An investigation of the long term
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changes in the HPA axis after prenatal stress (Maccari, Piazza, Kabbaj, Barbazanges,
Simon, & Le Moal, 1995) found that prenatal stress protracts the stress-induced
corticosterone response in adult rats and the researchers attributed the prolonged stress-
induced corticosterone response in prenatally stressed adult rats to the reduction in
corticosteroid receptors in the brain. From this finding Maccari et al. concluded that
“changes in the activity of the HPA axis may be one of the biological substrates of the
long-term effects of certain perinatal events” (1995).
Human studies of teratogens
Early studies exposing pregnant women to teratogens documented the adverse
effects that such teratogens have on the human fetus. Radiation treatment to the mother
was reported to have ill effects on the offspring, including physical malformities (Goldstein
& Murphy, 1929). The administration of thalidomide to pregnant women during a week
of the first trimester was also noted to result in congenital deformities in the newborns
(McBride, 1961).
Influenza in the mother during the second trimester has been demonstrated to have
a potentially teratogenic effect on the fetus. An increase in adult schizophrenia diagnoses
was reported in populations who suffered an influenza infection during their second
trimester of gestation (Mednick, Machon, Huttunen, & Bonnet, 1988). This finding by
Mednick et al. (1988) has been replicated in a number of studies, supporting the
hypothesis that at least one form of schizophrenia has a neurodevelopmental origin
(O’Callaghan, Sham, Takei, Glover, & Murray, 1991; Kendell & Kemp, 1989; Barr,
Mednick, & Munk-Jorgensen, 1990; Kunugi, Nankos, & Takei, 1992; Waddington, 1992;
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4
Welham, McGrath, & Pemberton, 1993; Machon, & Mednick, 1994; Fahy, Jones, Sham,
Takei & Murray, 1993). This neurodevelopmental hypothesis of schizophrenia proposes
that the second trimester is a critical period of development of the fetal brain, and
disruption of the brain’s neurodevelopmental process may result in one form of
schizophrenia.
Effects of Prenatal Stress on Offspring
Studies examining the negative effects of maternal stress on the fetus have found
that maternal stress increases circulating cortisol (Demyttenaere, Nijs, Evers-Kiebooms, &
Konincky, 1989) in the mother which is then distributed to the fetus (Zarrow, Philpott, &
Denenberg, 1970). In addition, human fetuses whose mothers experienced a severe stress
during gestation, evidenced increased pre-term deliveries (Crow & Done, 1992) and lower
birth weights (Kunugi et al., 1992; Lou, Hansen, Nordentoft, Pryds, Jensen, Nim &
Hemmingsen, 1994; Waddington, 1992). A notable study by Selten, van Duursen, van der
Graaf, Gispen, & Kahn (1997) found that exposure to a maternal stress (1953 Dutch
flood) was associated with an increased risk for psychotic illness in the offspring. Selten
et al. (1997) concluded that the association between increased risk for psychotic illness
and maternal stress may be due to “maternal glucocorticoids crossing the placenta and
disturbing the child’s brain development.”
A study of birth records by Jones and Tauscher reported a higher incidence of birth
defects in census tracts lying within the 90 dbA loudness contours of the Los Angeles
International Airport as compared to census tracts in the rest of LA County which
suggests that loud noise may be contributing to negative outcomes in the offspring (1978).
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5
An additional study involving pregnant mothers who were exposed to airport noise found
that the female offspring who had the highest noise exposure as measured by
questionnaires administered to the mothers were significantly smaller in gestational length
as compared to controls (Schell, 1981). Investigations that have examined functioning in
prenatally stressed offspring have found that mothers’ psychosocial stress significantly
diminishes the neurological optimality o f her newborn (Lou et al., 1994).
Mechanism by which maternal stress may negatively affect the fetus
The negative effect of maternal stress on a fetus may be due in part to the release
of stress hormones. When the mother experiences a severe stress, stress hormones
(corticosteroids) are released from her adrenal cortex. (Corticosteroids are comprised of
aldostrin, androgens, and cortisol, with the cortisol, or glucocorticoids being the largest
component.) This hypersecretion of glucocorticoids in the mother continues until the
termination of the stress or until the glucocorticoids inhibit the secretion through a
negative feedback loop. The stress hormones are fat-soluble; thus, the glucocorticoids are
transported via the placenta, directly to the developing fetus.
The Neurodevelopmental Hypothesis
By the fifth month of gestation the human fetus possesses the majority of neurons
that will comprise the neocortex. During the second trimester, rapid proliferation,
migration, and differentiation occurs in the central nervous system (CNS) (Nowakowski,
1991). Thus, the CNS is undergoing expeditious development of many critical areas
during the second trimester of gestation. Disruption occurring during active development
o f brain areas may inhibit the development, migration, positioning, and/or connections of
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6
the neurons. Disruption o f the migratory process has been associated with a variety of
diseases including mental retardation, dyslexia, and schizophrenia. Kovelman and Scheibel
reported the existence of ectopic neurons in area CA1 of the hippocampus in brains of
patients with severe schizophrenia which may be do to abnormal neuronal migration
(1984). In addition to migration, differentiation is a crucial component to successful CNS
development. Differentiation is a very complex course, entailing processes such as
programmed pruning, retraction of exuberant collaterals, and the elimination of synapses
during CNS development. A number of processes are involved in controlling
differentiation of the nervous system including steroidal hormones (Arnold & Breedlove,
1985; Arnold & Gorski, 1984; Nordeen, Nordeen, Sengelaub & Arnold, 1985).
Affective Disorders and Teratogens
It is possible that some affective disorders, like some forms of schizophrenia, have
a neurodevelopmental source. Recent MRI studies revealed a reduction of total cerebral
volume and hypoplasia in the medial temporal lobe of depressed patients. These
neurostructural findings have been interpreted as being supportive of a
neurodevelopmental etiology of bipolar affective disorder (Nasrallah, 1991; Olsen, 1991).
Two previous studies have investigated the possibility that a teratogen such as an influenza
virus in the pregnant mother could be related to the development of an affective disorder
in the adult offspring. Machon, Mednick, and Huttunen found that among people
exposed to the Helsinki influenza in the second trimester there was a significant increase in
the proportion of individuals diagnosed with affective disorders (1997). Furthermore, the
Machon et al. study reports that the effect was stronger in males than females, as well as
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7
stronger in unipolar forms versus bipolar forms (1997). A retrospective study of 120
mothers of bipolar patients reported an increase in first trimester maternal respiratory
infection (i.e., influenza and febrile cold) as compared to matched controls (Stoeber,
Kocher, Franzek, & Beckmann, 1997). Crow and Done examined subjects who were
exposed to the 1957 influenza virus and reported a small (but insignificant) increase in
affectively ill patients based on mother reports that were collected at the time of delivery
(1992).
Depression and Glucocorticoids
The biological markers that have been most consistently demonstrated in
depressive illness are abnormalities in the hypothalamic-pituitary-adrenal axis (HPA)
(Dinan, 1994). Researchers have postulated that there may be a high level of
glucocorticoid receptors in depressed patients (Dinan, 1994), and more specifically, the
lymphocyte glucocorticoid type II receptor may be altered (Sallee, Nesbitt, Dougherty, &
Hilal, 1995). Further research has proposed that the elevated cortisol levels associated
with depression may feedback onto the brain and exacerbate depressive symptoms
(Murphy & Wolkowitz, 1993). In addition, treatment of some chronically depressed
patients has involved the administration of glucocorticoid antagonists (Murphy, Filipini, &
Ghadirian, 1993). These studies suggest that glucocorticoids may play a major role in
some forms of depression.
Interaction of Gender and Prenatal Stress
There is some discrepancy in the literature regarding which gender may be the
most affected by a prenatal stressor. The studies by Alonso et al. (1991; 1994) indicate
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that the female rats who are exposed to maternal stress during gestation were more
negatively affected than male rats who were also exposed. However, the Fride and
Weinstock investigation involving the administration of a noise stress to pregnant rats
noted negative outcomes in the offspring regardless of the offsprings’ gender (1984).
Research with humans has found that male subjects who were exposed to a teratogen as a
fetus exhibited an increased rate of affective disorders as compared to females (Machon et
al., 1997).
Purpose of this Study
In 1976 a severe earthquake (7.8, Richter Scale) struck Tangshan, China resulting
in 240,000 deaths, thousands of injuries, and widespread destruction o f houses and basic
services. However, this catastrophic event (which was unpredictable and uncontrollable)
may serve as a natural experiment. We examined offspring of women who were exposed
to the earthquake during pregnancy to determine if the stress of the quake had long-term
negative affects on the fetuses who are adults. It is probable that the stress of the
earthquake resulted in the elevation of glucocorticoids (stress hormones) in the pregnant
mothers living in Tangshan. Considering the results of animal studies, it was hypothesized
that this elevation of glucocorticoids in the pregnant women may have produced a chronic
elevation in the fetuses’ level of glucocorticoids. In turn this elevation of glucocorticoids
may have resulted in a decrease in central corticosteroid receptors, and/or elevated
glucocorticoid levels may have adversely affected the fetuses’ developing HPA axis. Thus,
individuals who endured the prenatal stress of the earthquake may be at risk for later adult
depression. Studies involving the teratogenic effects of an influenza virus on the fetus
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9
during the second trimester of gestation indicate that the timing of exposure to the
earthquake may play a critical role in the later development of adult depression.
Therefore, we hypothesized:
1.) Subjects who were exposed to the earthquake while in utero will report more
depression as adults than the control subjects who were not exposed to the
earthquake.
2.) A comparison of exposed subjects to their season-of-birth matched controls by
trimester will show that the second trimester exposed subjects endorse more
depressive items on the depression measures as compared to the matched second
trimester control subjects. However the first and third exposed will not
demonstrate as much of a difference when compared to their season-of-birth
matched controls.
3.) Among those exposed, trimester-two exposed subjects will also exhibit
significantly higher depression scores as compared to subjects exposed to the
quake during the first or third trimesters of gestation.
4.) Although the animal and human research differs on which gender demonstrates a
greater effect for depression after exposure to maternal stress, the human data
presents a stronger effect for males. Thus, of the male and female subjects in this
study who were exposed to the earthquake in utero, the male subjects will exhibit
an increased level of depressive symptoms as compared to the female exposed
subjects.
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10
5.) The offspring of mothers who report being stressed by the earthquake will have
more depression than subjects whose mothers report not being stressed by the
quake.
Methods
The stress associated with the severe earthquake in Tangshan, China in July of
1976 serves as a natural experiment for examining the critical prenatal period in which a
severe stress to the mother would have a deleterious effect on the fetus. Data were
collected from 1215 18-year old students. Approximately half of the students (N=611)
were exposed to the severe earthquake while in utero, and 604 additional students who
were not exposed to the earthquake served as controls.
Subjects
The exposed group consists of 611 high school seniors attending one of the
eleven, major Tangshan schools who were fetuses at the time of the earthquake. The
mothers of the subjects resided within the city of Tangshan, China on July 28, 1976. The
subjects were randomly drawn from the approximately 8,000 seniors who are currently
attending the eleven high schools.
1. First trimester exposed. Subjects bom January 29, 1977 to April 28, 1977
comprise the subjects who were exposed to the earthquake during their first
trimester of gestation.
2. Second trimester exposed. Subjects born October 29, 1976 to January 28, 1977
comprise the subjects who were exposed to the earthquake during their second
trimester of gestation.
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11
3. Third trimester exposed. Subjects bom July 29, 1976 to October 28, 1976
comprise the subjects exposed to the earthquake during their third trimester of
gestation.
The control group was assessed exactly one year after the exposed group and
consists of 604 high school seniors, attending one of the eleven major schools in
Tangshan, China who were bom exactly one year after the exposed group. Thus, the
control subjects were not exposed to the earthquake as fetuses.
1. First trimester control. Subjects born January 29, 1978 to April 28, 1978
comprise the first trimester control subjects.
2. Second trimester control. Subjects born October 29, 1977 to January 28, 1978
comprise the second trimester control subjects.
3. Third trimester control. Subjects born July 29, 1977 to October 28, 1977
comprise the third trimester control subjects.
Selection criteria for exposed and control groups. The 1215 exposed and
control subjects were matched for birth date so there are an approximately equal number
o f subjects representing months one through nine of gestation. Assessment of the control
subjects one year after the exposed group, resulted in an exposed and control group that
were both 18 years of age at the time of testing. In addition, selecting subjects who have
the same months of birth, controls for the possible effect of season of birth. (To control
for the possibility that exposed subjects may be more likely to drop out of school,
Tangshan school officials were interviewed. These officials reported that “almost all”
children remained in school until age 19.)
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12
Measurements and Procedure
Data were gathered from two sources:
1. The 1215 students who are categorized as control and exposed completed a battery of
questionnaires at school in a large auditorium. All questionnaires were in Chinese.
2. The mother of each student involved in the study was given a questionnaire regarding
her whereabouts at the time of the earthquake, experiences during the earthquake and her
emotional reaction to the quake.
Depression Scales. The Hamilton Depression Scale (HAMD) was given to all
subjects to assess levels of depression (Hamilton, 1964). The HAMD is utilized
internationally and is commonly used in China. An additional depression measure, the Self-
Rating Depression Scale (SDS), was given to the students to provide additional data on
potential depressive symptomatology (Zung, 1983). The SDS is also in common use in
China. The scales were administered as part of a battery of tests given to all subjects in a
classroom setting.
M other questionnaires. A questionnaire designed to assess the mother’s
physical and emotional state directly after the earthquake was sent home with each
student to be filled out by their biological mother (see Appendix A). The mother
questionnaire also provides a general assessment of each mother’s experiences during the
earthquake and emotional state directly after the earthquake; thus, we have a measure of
the physical impact, emotional impact, and stress caused by this natural disaster. (Data
were not collected for subjects who did not reside with their biological mothers.)
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13
Analyses
Depression Scales: In the test battery administered to the subjects, two of the
scales (HAMD and SDS) assess depressive symptomatology. Since the HAMD is
widely used in clinical and research settings in China, results from the HAMD were
utilized to test the five hypotheses regarding depression. We conducted a 2x3x2
Analysis of Variance (ANOVA) comparing the exposed group to the control group, the
three trimesters o f exposure, and males versus females with the HAMD as the dependent
variable was conducted. Individual Yuen’s tests with 20% trimming were then
performed to test hypotheses one through five (Yuen, 1974). The Yuen’s compares
trimmed means and provides good control for skewed distributions, outliers, and heavy
tailed distributions (Wilcox, 1996). Hypotheses two and three involve multiple
comparisons; thus a Bonferroni correction was utilized to control for Type I error. A
bivariate correlation was also utilized for hypothesis five to examine the association
between duration of stress experienced by the mother and the depression scores of the
offspring. Additional analyses of an exploratory nature were conducted with the SDS to
determine if this additional depression measure supports the findings from the HAMD.
The analyses performed with the SDS followed the same format as those conducted with
the HAMD.
Mother Questionnaire: For the exposed group, 411 of the mothers completed the
Mother Questionnaire. The 411 mothers who completed the Mother Questionnaire had an
approximately equal distribution across months of exposure. Intensity (item eight) and
duration (item nine) of stress were assessed by the Mother Questionnaire (see Appendix
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14
A). A mother was categorized as having experienced emotional distress if she endorsed
any of the symptoms on item eight; thus a stressed group (N=296) and a non-stressed
group (N=l 15) of mothers was created. A Yuen’s test was utilized to compare the
offsprings’ HAMD scores for the stressed and non-stressed group of mothers. In addition
to assess for a possible association with the mother’s rating of the duration o f her
symptoms (item nine on Mother Questionnaire) and the offsprings responses on the
HAMD, a Pearson correlation was conducted for those subjects whose mothers reported
being stressed.
Results
HAMD Results
The result of an omnibus F-test comparing the exposed subjects to the control,
the three trimesters of exposure, and males to females with HAMD as the dependent
variable indicated a significant effect, F(2,1202)=3.15, p=.04. The overall mean scores
on the HAMD for the exposed and control subjects are presented by trimester and by
gender in Table 1. As can be seen in Table I the exposed group reports more depressive
symptoms than the control, and on the average the mean scores for the males on the
HAMD are higher than the scores of the females.
Table 1. Hamilton Depression mean scores (with standard deviations) for exposed and
control subjects by trimester.
HAMD
Exposed Control
Males Females
(N=295) (N=316)
Males Females
(N=250) (N=353)
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15
Trimester 1 7.2(5.7) 6.1(4.7) 4.0(4.1) 3.4(3.6)
Trimester 2 7.5(5.4) 5.9(5.0) 5.1(4.4) 5.3(5.2)
Trimester 3 6.8(5.4) 7.0(4.7) 6.2(5.6) 4.6(5.0)
Total 7.2(5.5) 6.3 (4.8) 5.3(5.0) 4.3 (4.6)
Overall Exposed Overall Non-Exposed
6.8(5.2) 4.7(4.8)
The first hypothesis, that the exposed subjects (N=611) would have elevated
scores on the HAMD as compared to the non-exposed subjects (N=604) was confirmed
with a Yuen’s test, (688.9)=7.8, p< .001. There was a marked difference between the
exposed and the controls with the exposed subjects having significantly higher HAMD
scores than the controls. Table 2 presents the trimmed mean HAMD scores and
standard deviations for the exposed and control subjects by trimester and by gender
using 20% trimming.
Table 2. Hamilton Depression trimmed mean scores (with standard deviations) for
exposed and control subjects by trimester with 20% trimming.
HAMD
Exposed Control Significance Level
(N=611) (N=604) Yuen’s Test
Trimester 1 5.78(.39) 2.73(.26) p<001
Trimester 2 6.06(.46) 4.25(.32) p=001
Trimester 3 6.29(.42) 4.34(.38) p<001
Total________ 6.02Q42) 3.66Q19) pC.OOl
The second hypothesis (subjects exposed during the second trimester would
report higher levels of depression than their season-of-birth matched controls) was
examined with a Yuen’s test for two independent groups. In addition Yuen’s tests were
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16
performed comparing the first and third trimester exposed subjects with their season-of-
birth matched controls on the HAMD. To control for Type I error a Bonferroni
correction was utilized. Since three comparisons were conducted a significance level of
.017 was utilized. The second trimester exposed subjects exhibited significantly higher
scores on the HAMD when compared to the second trimester controls, Yuen’s(218.8) =
3.23 p=.001. A comparison of the first trimester exposed to the first trimester control
subjects resulted in the exposed subjects having significantly higher HAMD scores than
the controls, Yuen’s(221.9) = 6.58 p<001. The third trimester exposed subjects
endorsed more depressive symptoms on the HAMD as compared to the third trimester
controls, Yuen’s(226.6) = 3.46 p<001. All three trimesters of exposed subjects had
significantly higher depression scores on the HAMD than their season of birth matched
controls.
Hypothesis three (subjects exposed to the earthquake during their second
trimester of gestation would experience elevated levels of depression as compared to
subjects exposed to the quake during trimesters one or three), was examined with the
following three Yuen’s tests: 1.) second trimester with first trimester, 2.) second
trimester with third trimester, and 3.) first trimester with third trimester. To control for
Type I error a Bonferroni correction with a significance level of .017 was utilized. The
first comparison of HAMD scores for trimesters one and two was not significant,
Yuen’s(241.3) = .46, p=.65. Subjects exposed to the quake during trimester two did not
differ significantly from subjects exposed during trimester three on the HAMD,
Yuen’s(237.0) = 38, p=.71. A final comparison of HAMD scores for subjects exposed
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17
during trimester one to the HAMD scores for subjects exposed during the third trimester
of gestation revealed no significant difference between the two groups on HAMD scores,
Yuen’s(240.2) = .89 p=. 37.
We examined the hypothesis that males (N=295) exposed to maternal stress in
utero would exhibit more depression than exposed females (N=316) with a Yuen’s test.
There was a trend toward a significant difference between the male and female exposed
subjects with the males (trimmed mean = 6.49) having higher HAMD scores than the
females (trimmed mean = 5.66), Yuen’s(322.9) = 1.63, p=. 10.
Finally, the HAMD scores of exposed subjects whose mothers reported being
stressed (N=296) (endorsing any of the items on question 8 of the Mother
Questionnaire) were compared with a Yuen’s test to the scores of exposed subjects
whose mothers reported that they did not experience stress (N=115) after the
earthquake. A non-significant trend was found between the offspring o f stressed
mothers as compared to offspring of non-stressed with the offspring of stressed mothers
having higher scores on the HAMD, Yuen’s(34l.0)=1.64, p=. 10. For the offspring of
mothers who reported experiencing stress from the quake, a significant positive
correlation between duration of stress (as measured by item 9 on the Mother
Questionnaire) and HAMD scores resulted, (293) r =.1289, p=.03.
SDS Results
The analyses conducted with the HAMD scores were repeated with the subjects’
responses to the SDS to determine if the results of the SDS would corroborate the
findings from the HAMD. An omnibus F-test comparing the exposed subjects to the
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18
control, the three trimesters of exposure, and males to females with SDS as the
dependent variable indicated a significant effect, F(2,1202)=3.28, p=.04. The overall
mean scores on the SDS for the exposed and control subjects are presented by trimester
and by gender in Table 3.
Table 3. Self-Rating Depression Scale mean scores (with standard deviations) for exposed
and control subjects by trimester.
SDS
Exposed Control
Males Females Males Females
(N=295) (N=316) (N=250) (N=353)
Trimester 1 39.4(7.9) 40.0(9.1) 40.6(7.9) 36.6(7.7)
Trimester 2 39.2(7.8) 40.0(8.7) 37.0(6.5) 39.1(9.0)
Trimester 3 38.9(7.9) 40.1(8.9) 40.8(9.2) 38.8(8.9)
Total 39.2(7.9) 40.0(8.9) 39.5(8.2) 38.0(8.5)
Overall Exposed Overall Non-Exposed
39.6(8.4) 38.6(8.4)
The first hypothesis, that the exposed subjects (N=611) would have elevated
scores on the SDS as compared to the non-exposed subjects (N=604) was confirmed
with a Yuen’s test, (728.1)=2.5, p=.01. This finding that the exposed subjects have
significantly higher SDS scores than the controls supports the previous finding with the
HAMD that the exposed have higher levels of depression as compared to the controls.
Table 4 presents the trimmed mean SDS scores and standard deviations for the exposed
and control subjects by trimester and by gender using 20% trimming.
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19
Table 4. Self-Rating Depression Scale trimmed mean scores (with standard deviations)
for exposed and control subjects by trimester with 20% trimming.
SDS
Exposed Control Significance Level
(N=611) (N=604) Yuen’s Test
Trimester 1 39.05(.90) 39.77(1.18) NS
Trimester 2 38.27(.78) 36.75(.84) NS
Trimester 3 38.98(.99) 37.6(1.07) NS
Total________38.75Q35) 37.50(.36) p=.01
The second hypothesis that subjects exposed during the second trimester would
report higher levels of depression than their season-of-birth matched controls (i.e.,
second trimester controls) was examined with a Yuen’s test with SDS scores as the
dependent variable.. To determine if the first and third trimester exposed subjects would
demonstrate a similar effect when compared to their season-of-birth matched controls on
the SDS Yuen’s tests were also performed. To control for Type I, error a Bonferroni
correction was utilized. Since three comparisons were conducted, a significance level of
.017 was utilized. There were no significant differences between the second trimester
exposed and the second trimester non-exposed subjects on the SDS. In addition, no
significant differences resulted from individual Yuen’s tests comparing the first trimester
exposed to the first trimester non-exposed and comparing the third trimester exposed to
the third trimester non-exposed on the SDS.
The third hypothesis (subjects exposed to the earthquake during their second
trimester o f gestation would experience elevated levels of depression as compared to
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20
subjects exposed to the quake during trimesters one or three), was examined with the
following three Yuen’s tests using SDS as the dependent variable: 1.) second trimester
with first trimester, 2.) second trimester with third trimester, and 3.) first trimester with
third trimester. To control for Type I error a Bonferroni correction with a significance
level of .017 was utilized. Subjects exposed to the quake during trimester two did not
differ significantly from subjects exposed during trimesters one or three on the SDS.
A Yuen’s test comparing the exposed males to the exposed females conducted
with the SDS scores as the dependent variable was not significant. In addition there was
no significant difference on a Yuen’s test between the SDS scores for the subjects’
whose mothers reported experiencing stress after the earthquake when compared to the
subjects whose mothers did not report being stressed. No significant correlation resulted
between SDS scores and the duration of stress experienced by the mother.
Discussion
The main purpose of this study was to determine if exposure to a severe maternal
stress (major earthquake) in utero increases risk for adult depression. Our main
hypothesis was confirmed by the data; the subjects in this study who were exposed to the
earthquake as fetuses demonstrated a marked increase in the number of depressive
symptoms they endorsed on two different measures of adult depression (HAMD and SDS)
when compared to age and season-of-birth matched controls.
We interpret the above finding as follows. The stress of the earthquake most likely
resulted in the release of stress hormones (an elevation of glucocorticoids) in the pregnant
women. This physiological reaction in the mother may have had an adverse effect on the
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21
fetuses’ developing HPA axis and/or glucocorticoid receptors. Animal researchers
studying the long-term effects of prenatal stress have concluded that alterations in the
activity of the HPA axis may be associated with perinatal events (Maccari et ah, 1995). In
our study, the exposed group’s endorsement of a higher number of depressive symptoms
appears to be associated with exposure to a prenatal stress. An alteration in the HPA axis
during the perinatal period may be influencing the exposed subjects’ expression of
depressive symptoms.
It should be noted that the level of depressive symptoms endorsed by the exposed
sample on the HAMD and SDS does not signify clinical depression. It may be that the
elevated scores on the depression measures are indicative of a temperament that is
associated with fetal exposure to a maternal stress. It is also possible that the increased
number of depressive symptoms in the exposed group may be a risk factor for the
development of depression.
Based on the findings from the animal literature (Alonso et al., 1990; Alonso et
al., 1993) and the human literature (Machon et al., 1997), we predicted that the
difference between the second-trimester exposed and the second-trimester control
subjects would be greater than the difference between the first and third trimester
exposed subjects and their season-of-birth matched controls. However, we found that all
exposed subjects had increased levels of depression on the HAMD regardless of the
timing of their exposure to maternal stress. We also hypothesized that within the
exposed sample, second-trimester exposed subjects would report elevated levels of
depression as compared to subjects exposed during the first or third trimester of
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22
gestation. This hypothesis was not supported by the data. We found no significant
difference between the first, second, and third trimester exposed subjects on the HAMD
or the SDS. In our study, the stressful event experienced by the mother was a major
earthquake (7.8 Richter); thus the women may have continued to feel stressed due to
experiences such as the destruction of homes, deaths of family and friends, and shortage
of food. We may not have found a specific trimester effect because of this long-term
stress endured by the mother.
A non-significant trend emerged in the analyses that compared the number of
depressive symptoms reported by the male and female exposed subjects. The male
exposed subjects on the average reported that they experienced more depressive
symptoms than the females. Although this difference in the male and female subjects was
not significant, the slight difference warrants further investigation. It may be that a
comparison of the distributions of the male and female scores would result in a
significant difference between the groups.
Within the exposed group, the offspring of mothers who reported being stressed
by the earthquake had slightly higher scores on the HAMD as compared to offspring of
non-stressed mothers. Although the difference was not significant, it does suggest that
the mothers’ stress may be associated with the offsprings’ experience of a higher number
of depressive symptoms during adulthood. Of the mothers who did report being stressed
during the earthquake, the mothers who experienced a longer duration of stress had
offspring who tended to endorse more depressive symptoms on the HAMD. The
questionnaire completed by the mothers was administered retrospectively. The mother
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23
may be inclined to over or under estimate the stress and emotional distress she
experienced during the earthquake. Thus, results from the analyses involving the mother
questionnaires should be interpreted cautiously.
This study does have limitations. The gestational age of the subjects at the time
of exposure was estimated from their date of birth. Thus, we are not accounting for the
incidences of pre- and post-term births. We do not have medical records for the
mothers; therefore, we cannot control for the physical injuries she endured. We are also
lacking medical records for the offspring which would allow us to control for the
potential mediating effects of factors like obstetrical complications on our findings.
Future research in this area should involve a direct measure of glucocorticoid
levels in prenatally stressed offspring to determine if there is a physiological change
associated with maternal stress. In addition assessing the stress-induced corticosterone
response in offspring exposed to prenatal stress would allow researchers to determine if
these individuals are at increased risk for having a negative response (such as depression
or anxiety) when they encounter a stressful situation.
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24
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Appendix A. The Mother Questionnaire.
Parents of :
Greeting! Some days before, we examined your child’s physicaL and mental health. We
checked the brain CT, electroencephalogram, IQ test, psychology test, etc. We want to
notify you that the results for these examines were in the normal range.
We have the following items that are related to the earthquake, please have the student’s
mother fill them out. Thank you for your co-operation.
Name: Gender: Educational Level: Occupation:
Name of the place you work (phone # )___________________________
Address in detail
1. During the earthquake, where did you live?
2. During the earthquake, where were you? (1) sleeping (2) working (3) entertaining
3. During the earthquake, were you buried in the ruins? Yes No
4. How did you get out from the ruins? (1) get out of it naturally (2) self help
(3)rescued by someone else
5. How long were you buried in the ruins?
(1) few minutes (2) more than 10 minutes (3) one hour (4) couple of hours
(5) more than one day
6. What was your physical injured condition, including faint? How long did you faint?
Where your head smashed, skull cracked, arms and legs broken, muscles twisted, etc.?
Please describe:
7. What was your treatment situation after you were injured?
(1) go to other place for treatment (2) stayed in the same place for treatment
(3) didn’t get any treatment (4) operation (5) treated by medication
(6) physical therapy
8. After the earthquake, what was your mental condition? Did any of the follow occur?
(1) fretful
(4) sad
(7) over sensitive
(10) no emotional reaction
(13) whole body feel uncomfortable
(2) nervous and unease
(5) depressed
(8) regretful
(11) didn’t speak
(14) perplexed
(3) frighten
(6) apathetic
(9) excited
(12) sleep problems
(15) rapid heart beat
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29
(16) despair (17) can’t recognise relatives (18) want to die
(19) others (please specify)
9. The above situation continued for how long?
(1) couple of hours (2) couple of days (3) couple of month (4) over a year
(5) over three years (6) over five years (7) over ten years
(8) until now
10. After the earthquake, what was your health condition? Did you have any body illness?
(including high blood pressure, heart disease, ulcer, skin infection, etc.)
11. During the earthquake, your family relatives’ injured and death condition, including:
grandfather, grandmother, mother-in-law, father-in-law, brother-in-law, sister-in-law,
uncle, aunt, mother, father, brother, sister, son, and daughter.
12. Was your child bom after 10 months of pregnancy and bom naturally? Does any of
these apply:
(1) difficult delivery; (2) premature birth; (3) Caesarean section;
(4) suffocate; (5) use clamps and walk, talk time.
After filling out this form, please mail it to:
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Asset Metadata
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Watson, Jennifer Bunn
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Depression in offspring following severe prenatal stress
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Master of Arts
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Clinical Psychology
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