Journal of Obstetrics and Gynaecology (2 0 0 2 ) V ol. 2 2 , No.
3 , 2 6 0 – 2 6 6
OBSTETRICS
Prenatal anger effects on the fetus and neonate
TIFFANY FIELD, 1 M. DIEGO, 1 MARIA HERNANDEZ-REIF, 1 F. SALMAN, 1
S. SCHANBERG, 2 CY NTHIA KUHN, 2 REGINA YANDO, 3 and DEBRA BENDELL4
1
Touch Research Institutes, University of Miami School of Medicine, 2 Duke University
School of Medicine, 3 Harvard Medical School, and 4 UCLA School of Medicine, USA
Summary
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14
One hundred and sixty-six women were classified as
experiencing high or low anger during the second trimester of
pregnancy. The high-anger women also had high scores on
depression and anxiety scales. In a follow-up across
pregnancy, the fetuses of the high-anger women were noted
to be more active and to experience growth delays. The high-
anger mothers’ high prenatal cortisol and adrenaline and low
dopamine and serotonin levels were mimicked by their
neonates’ high cortisol and low dopamine levels. The high-
anger mothers and infants were also similar on their relative
right frontal EEG activation and their low vagal tone. Finally,
the newborns of high-anger mothers had disorganised sleep
patterns (greater indeterminate sleep and more state changes)
For personal use only.
and less optimal performance on the Brazelton Neonatal
Behavior Assessment Scale (orientation, motor maturity and
depression). These data highlight the need for prenatal
intervention for elevated angry mood during pregnancy.
Introduction
Several recent studies have documented the negative
effects of prenatal depression and anxiety on the fetus
(Glover et al., 1999; Dieter et al., 2000; Field et al.,
2000) and the neonate (Abrams et al., 1995; Jones et al.,
1998; Lundy et al., 1999). These have included
increased fetal activity and delayed fetal growth, and at
the neonatal stage non-optimal performance on the
Brazelton scale, increased indeterminate sleep, reduced
vagal tone, relative right-frontal EEG activation and
neurotransmitter/neurohormone profiles matching the
depressed mothers’ prenatal profiles, including
increased cortisol and noradrenaline (Lundy et al.,
1999) and decreased dopamine and serotonin (Field et
al., 2000). Although less is known about the effects of
elevated prenatal anxiety on the fetus and neonate,
Glover et al. (1999) have suggested that anxiety effects
would be mediated by elevated noradrenaline levels and
the resulting increase in uterine artery resistance,
decrease in blood flow and increased intrauterine
growth retardation. Inasmuch as depression and anxiety
are often comorbid (Field et al., 2000), their independent
effects may be difficult to untangle.
Anger is still a third negative emotion that can occur
during pregnancy. Although pregnancy anger has not
been the subject of any published papers, a recent study
on pregnancy depression yielded more frequent
Correspondence to: Tiffany Field PhD, Touch Research Institutes, University of Miami School of Medicine, Department of
Pediatrics (D-820), PO Box 016820, Miami, FL 33101 USA. Email: tfield@med.miami.ed u
ISSN 0144– 3615 print/ISSN 1364– 6893 online/02/030260– 07
DOI: 10.1080/01443610220130526
significant correlations between pregnancy anger and
neonatal outcome measures than correlations between
pregnancy depression or anxiety and neonatal outcome
measures (Field et al., 2000). These data highlight the
need to further explore the effects of anger as a primary
and/or comorbid pregnancy variable.
The somewhat limited literature on anger would pre-
dict that unexpressed or unacceptable (to the subject)
anger would be accompanied by depression and physi-
ological arousal. In one study, individuals who
considered anger an unacceptable emotion were more
likely to have a depressed mood and greater activation
of the sympathetic nervous system (Mancuso, 2000). In
another study, high anger-out individuals showed the
greatest increases in adrenocorticotrophic hormone
concentrations during acute psychological stress (e.g.
public speaking) (al’Absi et al., 2000). In contrast, in a
study on controlled expression of anger, both depres-
sion and physiological arousal were reduced (Dahlen
and Deffenbacher, 2000). Similarly, constructive angry
behaviour has been noted to be a significant predictor of
lower physiological arousal (lower blood pressure)
even when controlling for anxiety and depression
(Davidson et al., 2000a). Further, matching angry facial
expressions in a backward masking paradigm has been
associated with distinct facial muscle reactions that
correspond with even a very short exposure (30 ms)
(Dimberg et al., 2000), and with increased regional
cerebral blood flow in the left and right amygdala as
assessed by functional magnetic resonance imaging
(Hariri et al., 2000). In the same study, labelling the
angry expression was associated with an increase in
regional cerebral blood flow in the right prefrontal
cortex.
Further evidence for these associations comes from
cognitive therapy (Dahlen and Deffenbacher, 2000) and
exercise (at least 2–3 times/week) interventions show-
ing that anger, depression, anxiety and physiological
arousal could be decreased even though, by at least one
account, anger (anger-in and anger-out), aggression,
depression and anxiety have been notably stable across
at least an 8-year period (rs = 0·47–0·75) (Magai, 1999).
Intervention models that have been effective with
anxiety disorders have also been effectively used with
anger-related difficulties (Brondolo et al., 1997).
Taylor & Francis Limited, 2002

Further, data from other literature suggest that these
three emotions are comorbid with depression, anger and
anxiety sharing many clinical features. For example,
depression and anger comorbidity were noted in a study
showing greater serotonergic dysfunction in depressed
individuals having anger attacks (Fava et al., 2000).
The purpose of the present study was to determine
the effects of high anger as self-reported on the profile
of mood states scale (POMS) during pregnancy on fetal
development and neonatal outcomes. In addition, an
attempt was made to establish the relative amounts of
the outcome variance that could be explained by prena-
tal anger and the comorbid emotions, depression and
anxiety.
Methods
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14
Participants
The women were recruited during the second trimester
(mean = 20·1 weeks; range = 18–22 weeks) from
obstetrician–gynaecologists’ offices. The women’s
medical charts were reviewed to screen out any women
who showed recreational drug use during pregnancy
based on routine drug screens. The final sample
included 166 pregnant women of lower–middle socio-
economic status (mean = 2·9 on the Hollingshead index,
1975). The women averaged 27·7 years of age, 37%
were single, and their ethnicity was distributed: 35%
African-American, 28% Hispanic, 28% white Non-
Hispanic and 9% other. Eighty-four per cent of the
For personal use only.
infants were full term (mean = 37 weeks) and healthy
and 55% were female. Based on the profile of moods
anger scale scores the mothers were divided by a
median split into high-and low-anger groups. The two
groups differed on several demographic variables (see
Table I) including that the higher anger group was
comprised of (1) younger mothers, P<0·05; (2) a greater
percentage of black mothers, P<0·05; (3) a greater per-
centage who were single; and (4) a greater percentage
of males born to high-anger mothers.
Procedure
At their prescribed ultrasound session (mean gesta-
tional age = 20·1 weeks) the mothers were given the
profile of mood states (POMS) (McNair et al., 1971),
Table I. Means for demographic variables
Groups
Variables Low anger
Mother age 2 8·47
Mother SES 2·81
Mother ethnicity(%)
Anglo 3 3·1
Hispanic 27·1
Black 2 8·8
Other 1 1·0
Marital status (%)
Single 18·9
Married 8 1·1
Divorced
Infant sex (%)
Male 3 5·2
Female 64 ·8
Prenatal anger effects 261
the Center for Epidemiological Studies depression scale
(CES-D) (Radloff, 1977), the Spielberger trait anxiety
inventory (Spielberger et al., 1970), and the behavioral
inhibition system/behavioral approach system Scale
(BIS/BAS) (Carver and White, 1994). The ultrasound
sessions were coded for fetal activity, and the ultra-
sonographers’ estimates of weight and growth were
recorded. First-morning urine samples were obtained
from the mothers during the prenatal visit and from
them and their newborns within 24 hours of delivery.
The CES-D and POMS were given again shortly after
the delivery, and the medical records were used to score
the obstetric complications scale (OCS) and the
postnatal complications scale (PNS) (Littman and
Parmelee, 1978). The Brazelton Neonatal Behavior
Assessment Scale (Brazelton, 1984) was also measured
within the first 2 days after birth. In addition, at that
time the mothers’ and newborns’ EKGs and EEGs were
recorded and the neonate’s sleep states and activity
were coded.
Measures
Profile of mood states (POMS). (McNair et al.,
1971). The POMS consists of 15 items on rating
depressed mood, nine items on anxiety and 12 items on
anger. They are rated on five-point scales ranging from
(0) ‘not at all’ to (4) ‘extremely’ using words such as
‘blue’ and ‘sad’. The scale has adequate concurrent
validity, good internal consistency (r= 0·95; McNair and
Lorr, 1964) and it is an adequate measure of intervention
effectiveness (Pugatch et al., 1969).
Center for epidemiological studies depression
scale (CES-D; Radloff, 1977). TheCES-Disa20-
item self-report scale designed to measure depressive
symptoms including depressed mood, feelings of guilt,
worthlessness, helplessness and hopelessness, loss of
energy and sleep and appetite disturbances (Radloff and
Teri, 1986). The 20 symptoms are rated for frequency
(over the past week) from ‘rarely or none of the time’ to
‘most or all of the time’. A summary score ranges from
0 to 60 by summing all items. Reliability and validity
have been acceptable across a variety of demographic
characteristics including age, education, geographic
High anger F P
2 6·92 3·8 4 0·05
3·0 4 2·2 8 ns
c2 P
2 2·6 9·7 4 0·05
2 7·8
4 1·7
7·9
c2 P
4 4·1 6·7 9 0·03
5 2·9
2·9
c2 P
5 8·1 5·0 9 0·02
4 1·9
 26 2 T. Field et al.
area and racial, ethnic and language groups (Radloff
and Teri, 1986). The CES-D was given to the mother at
the time of prenatal recruitment and again within 24
hours following delivery.
The state trait anxiety inventory. (Spielberger et
al., 1970). This was used to assess levels of anxiety.
This 20-question four-point Likert scale forms a
summed score from 20 to 80 for the trait subscale.
Higher scores indicate greater anxiety. The state
anxiety scale is comprised of 20 items and assesses how
the subject feels at that moment in terms of severity
(‘not at all’ to ‘very much so’). The trait anxiety scale is
comprised how the subject ‘typically feels’. Character-
istic items include: ‘I feel nervous’ and ‘I feel calm’.
The scores increase in response to stress and decrease
under relaxing conditions (Spielberger et al., 1970).
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14
Research has demonstrated that the state-trait anxiety
inventory has adequate concurrent validity and internal
consistency (r = 0·83).
The behavioral inhibition system/behavioral
approach system scale (BIS/BAS) (Carver and
White, 1994). The BIS/BAS is a 24-item questionnaire
consisting of personal statements followed by four
severity options ranging from very true to very false.
The BIS/BAS is designed to assess the tendency to
behave in response to reward or in response to punish-
ment. The behavioral inhibition system (BIS) scale
For personal use only.
examines behaviour in response to punishment and the
behavioral approach system (BAS) scale of the
questionnaire examines behaviour in response to
rewards and is comprised of three subscales: BAS fun,
BAS reward and BAS drive. BIS/BAS difference
scores are obtained by subtracting Z-transformed BIS
scores from BAS scores. Positive scores denote
greater BAS activity, while negative scores denote
greater BIS activity. The BIS/BAS and EEG activity
are significantly related in non-depressed (Sutton and
Davidson, 1997) and depressed (Diego et al., 2002)
samples.
Fetal activity. This assessment was made at 18–22
weeks (mean = 20·1 weeks). For this assessment the
technician positioned the scanner to obtain a lateral
view of the fetus. The observer, who was blind to the
mother’s group assignment, then watched the fetus for
5 consecutive minutes. Every 3 seconds (a total of 100
samples), a tape-recorded cue (heard through an
earphone) prompted the observer to record the fetal
activity categories including: (a) single limb move-
ments, (b) multiple limb movements and (c) gross body
movements. Inter-rater reliability, calculated on one-
third of the sample for two observers, yielded the
following Kappa values: single limb movements = 0·82;
multiple limb movements = 0·86; gross body move-
ments = 1·00. For the data analyses, the percentage of
time the fetus engaged in total movement, as well as
each movement category, was calculated. No effort was
made to discern fetal behaviour states because they
cannot be identified reliably before 36 weeks’ gestation
and most particularly during a 5-minute clinical fetal
ultrasound examination without confirmation through
fetal heart rate monitoring.
First-morning urine samples. First-morning urine
samples were collected from the women at their ultra-
sound visit and from both the women and their
newborns within 24 hours following delivery. Newborn
first-morning urine samples were collected in the
nursery. The samples were frozen and sent to Duke
University to be analysed by technicians who were
‘blind’ to group assignment. The urines were assayed
for nor-adrenaline, adrenaline, dopamine, serotonin and
cortisol levels after correcting for creatinine levels.
Nor-adrenaline, adrenaline and cortisol levels were
assessed because of their previously reported positive
association with prenatal anger (al’Absi et al., 2000;
Field et al., 2000), dopamine because of a recent animal
model implicating a negative association between
dopamine levels and depression (Weiss et al., 1996)
and serotonin because of its association with anger
(Fava et al., 2000).
Obstetric complications. Obstetric complications
were assessed on the obstetric complications scale
(OCS) (Littman and Parmelee, 1978), which is
comprised of 41 items taken from the medical charts
and rated as optimal or nonoptimal.
Postnatal complications. Postnatal complications
were quantified using the postnatal complications scale
(PNS) (Littman and Parmelee, 1978), which consists of
10 items rated as optimal or non-optimal.
Brazelton neonatal behavior assessment scale
(Brazelton, 1984). This measured was on the first
afternoon after birth. The Brazelton assessments were
performed by researchers who were trained to 0·90
reliability and were blind to the group classification of
the mothers and infants. This neurobehavioural exami-
nation consists of 28 items, each scored on a nine-point
scale, and 20 elicited reflexes, each scored on a three-
point scale. The infant’s performance was summarised
according to the traditional Lester et al. (1982) clusters,
and Lester and Tronick’s (1992), unpublished scale)
depression, excitability and withdrawal factors.
Sleep/wake behaviour. Sleep/wake behaviour
was deotaped continuously in compressed time
(3 hours’ sleep coded in 1 hour using time lapse video)
for an inter-feeding interval (2–3 hours) before the
Brazelton Scale was measured on the first afternoon
after birth. Thoman’s studies of term infants’ sleep
patterns suggest that an interfeeding interval time frame
can provide a representative sample (Thoman, 1975),
and Sostek and Anders (1975) have used ‘nap’ record-
ings of this duration. The videotapes were coded for all
movements that occurred during that period onto a
laptop computer according to the procedures we have
used in our other sleep studies (Scafidi et al., 1986).
Before sleep state coding the examiner was trained to
0·90 reliability. An adaptation of Thoman’s sleep state
criteria was used to define sleep/wake behaviour cate-
gories (Thoman, 1975). Sleep was assessed because
less quiet and more indeterminate (uncodable) sleep
was associated with right frontal EEG activation in
infants of depressed mothers in our previous study
(Jones et al., 1998).

EEG for a baseline measure of relative right or
left frontal EEG activation. At the neonatal stage
the EEG was recorded while the infant was in a quiet
alert state in a bassinet. The researcher was blind to the
mother’s depression status. EEG and behaviour were
recorded for 3 minutes while the infant was awake and
alert. We have reported significant 1–3-month stability
of EEG asymmetry (r= 0·45) (Jones et al., 1996) as well
as significant 3-month to 3-year stability (Jones et al.,
1997). At a separate time during the session the
mother’s EEG was recorded while she sat quietly with
her eyes open for 3 minutes.
EEG recording. The EEG for both the mother and
infant were recorded using Lycra stretchable caps
(manufactured by Electro-Cap, Inc.) that were posi-
tioned on the subject’s head using anatomical
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14
landmarks (Blom and Anneveldt, 1982). Electrode gel
was injected into the electrodes at the following sites:
F3, F4, P3, P4, T3, T4, O1, O2 and Cz (used as the
reference during recording for the majority of subjects),
and impedances were brought below 5000 ohms. Addi-
tional electrodes were positioned on the external
canthus and above the supra-orbit of the right eye to
record the subject’s EOG, which was used to determine
horizontal and vertical eye movement artefacts.
The EEG signals were obtained using a Grass Model
12 Neurodata Acquisition System with filters set at 1
Hz high-pass and 100 Hz low-pass and a gain of 20 000.
Before data collection, the signal for each channel was
For personal use only.
calibrated. The output was directed to a Dell 325 D PC
fitted with Analog Devices RTI-815 A/D board. The
sampling rate was 512 samples per second and the data
were streamed across the computer screen and then
saved to a hard disk using data acquisition software
(Snapstream, v. 3·21, HEM Data Corp. 1991).
EEG analyses. The EEG data were analysed using
an EEG analysis software package (EEG Analysis
System v. 5·3, James M. Long, 1987–1990). The first
step of this process involves computing EEG offline to
derive a computer-averaged reference, followed by the
manual elimination of sections of data that are unusable
due to artefact (eye movements, muscle activity or
technical difficulties). The remaining artefact-free data
were analysed spectrally using discrete Fourier trans-
forms to yield power data for the 1–30 Hz frequency
bands in 1 Hz bins. The infant EEG data were plotted
spectrally revealing that the majority of activity fell
within the 3–13 Hz frequency bins. The 3–13 Hz has
also been used in previous newborn EEG research
(Jones et al., 1999). Data analyses were conducted on
Table II. Self-report measures prenatally and postnatally (SDs in parentheses)
Groups
Variables Low anger
POMS– anger 2·7 2(2·17 )
Prenatal CES-D 10·7 7(7·49 )
Postnatal CES-D 7·3 0(6·68 )
STAI– prenatal 31·3 8(8·77 )
STA I– postnatal 31·1 5(8·51 )
BAS-BIS difference 0·0 5(0·75 )
Prenatal anger effects 263
the natural log power data for both hemispheres in the
frontal and parietal regions. Frontal alpha laterality
ratios (FLR) were computed by obtaining the difference
of the mean log power density scores of a right hemi-
sphere site and its homologous left hemisphere site
(LnRight–LnLeft). A score of zero represents hemi-
spheric symmetry, a negative score represents relative
right frontal activation and a positive score represents
relative left frontal activation.
Vagal tone. For this measure heart rate was
recorded for a 15-minute period while the infant was in
an infant seat and the mother seated on a chair. Vagal
tone was assessed by placing 3 EKG electrodes on the
infant’s chest and back regions. The electrodes were
connected to a Grass Model 12 Neurodata Acquisition
system preamplifier with bandpass frequencies set at
1.0 and 100 Hz and a gain of 2000. The output was
directed to a Dell 325 D PC fitted with Analog Devices
RTI-815 A/D board. The data were streamed across the
computer screen at a sampling rate of 512 samples per
second and then saved to a hard disk using data
acquisition software (Snapstream, v. 3·21, HEM Data
Corp. 1991). After scoring for artefact, EKG data were
converted to inter-beat intervals (IBI) using an EKG
analysis program (James Long Company, Caroga Lake,
NY, USA) and then to vagal tone using Delta-Biomet-
rics, Inc., Mxedit software, which utilizes an algorithm
developed by Porges (1991).
Results
As can be seen in Table II, the high-anger group women
also had high depression and high anxiety scores both
prenatally and postnatally. In addition, the high-anger
group women had elevated cortisol and adrenaline levels
and lower dopamine and serotonin levels prenatally (see
Table III). At the postnatal period the high-anger moth-
ers’ cortisol and nor adrenaline levels were elevated
similar to their own prenatal levels and their infants’
postnatal cortisol levels were elevated, and their
dopamine levels were lower.
As can be seen in Table IV, the high anger mothers
and their infants were showing right-frontal EEG acti-
vation, and the vagal tone of the mothers and their
infants was lower. As noted in Table V, the infants of
high-anger mothers showed a greater number of state
changes (see Table V).
Table VI shows the Brazelton Neonatal Behavior
Assessment Scale scores. The infants of the high
prenatal anger mothers had less optimal orientation,
motor organisation and depression scores.
High anger F P
17 ·8 8(7·7 0) 8 6·25 0·00 1
19 ·8 2(8·9 6) 2 8·09 0·00 1
14 ·4 8(11 ·48) 1 4·31 0·00 1
44 ·35 (10·16) 43·51 0 ·001
41 ·5 5(9·5 2) 3 0·72 0·00 1
0 ·0 2(0·9 1) 0·2 1 ns
 26 4 T. Field et al.

Table III. Means for prenatal and postnatal neurotransmitters and neurohormones (ng/mg) (SDs in
parentheses)

Groups
Variable Low anger High anger F P
Biochemical
Prenatal (mother)
Cortisol 2 53·4 4(16 4·05 ) 32 4·48 (178 ·13) 2·95 0·05
Noradrenaline 53·8 0(26 ·1 1) 54 ·16(24 ·38) 0·07 ns
Adrenaline 5·0 4(3·30 ) 6 ·55(4·7 4) 2·76 0·05
Dopamine 3 35·7 7(10 7·83 ) 26 1·32 (123 ·21) 3·02 0·00 5
Serotonin 49 56·2 4(25 45·3 8) 3 984 ·92(21 00 ·7 5) 2·71 0·05
Postnatal (mother)
Cortisol 1 94·1 6(92 ·2 4) 27 0·79 (211 ·32) 2·58 0·05
Noradrenaline 31·0 5(15 ·8 3) 45·92(24 ·23) 3·83 0·01
Adrenaline 4·2 7(2·90 ) 5 ·19(1·9 9) 1·37 ns
Dopamine 2 59·7 7(11 4·98 ) 25 3·47 (94·9 3) 0·23 ns
Serotonin 45 60·2 8(33 04·0 2) 4 495 ·60(21 91 ·8 6) 0·08 ns
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14

Infant
Cortisol 4 41·0 5(17 7·54 ) 52 6·50 (199 ·92) 2·60 0·05
Noradrenaline 56·5 5(38 ·5 8) 63 ·47(33 ·95) 0·67 ns
Adrenaline 5·8 3(3·31 ) 4 ·91(3·0 8) 1·01 ns
Dopamine 5 00·9 0(24 2·72 ) 35 5·62 (253 ·64) 3·07 0·05
Serotonin 94 06·2 7(75 02·2 8) 6 635 ·74(53 56 ·2 6) 1·21 ns

Table IV. Means for prenatal complications and physiological variables (SDs in parentheses) (high values are
optimal except for fetal activity)

Groups
Variables Low anger High anger F P
For personal use only.

Fetal activity 2 2·82(17·23) 37 ·0 2(30 ·09) 3 ·3 2 0·0 5

Obstetric complications 97 ·8 8(26 ·0 6) 94 ·4 1(24·8 3) 0·22 ns
Postnatal complications 14 8·28 (27·7 1) 1 27 ·7 7(36 ·79) 4 ·7 3 0·0 5
Frontal asymmetry– mother 0·01 (0·15 ) -0·13(0·19) 7 ·6 0 0·0 1
Frontal asymmetry– infant 0·03 (0·11 ) -0·05 (0·12 ) 4·9 3 0·0 5
Vagal tone– mother 4 ·1 1(0·4 6) 3 ·8 4(0·2 1) 6 ·6 6 0·0 1
Vagal tone– infant 4·7(1·2 8) 4 ·2 2(0·3 5) 2 ·8 2 0·0 5

Table V. Means for newborn sleep variables (SDs in parentheses)

Groups
Variables Low anger High anger F P
Sleep scale
Deep sleep 25 ·74 (23 ·75) 3 6·91 (2 5·65 ) 2·11 ns
Active sleep 1 2·68 (13·60 ) 13 ·61 (1 1·63 ) 0·06 ns
REM sleep 14 ·37 (20·00) 1 2·78 (1 3·05 ) 0·10 ns
Drowsy 9 ·16 (11 ·63) 3·48 (8 ·60) 1·48 ns
Alert inactive 5 ·21 (8·44) 2·65 (5 ·01) 3·30 ns
Awake active 4·26 (7·26) 3·48 (8 ·06) 0·11 ns
Fussing/crying 4 ·00 (7·4 1) 3·13 (5 ·35) 0·19 ns
Indeterminate sleep 39 ·84 (27 ·23) 4 8·91 (1 9·58 ) 1·57 ns
Number of state changes 34 ·21 (20 ·43) 5 1·85 (2 8·73 ) 5·05 0·0 5
Postnatal total movement 0 ·61 (0·1 0) 0·65 (0 ·17) 0·93 ns

Discussion The mimicking of the mothers’ prenatal neurotrans-

That the high-anger group experienced high depres-
sion and anxiety scores was not surprising, given the
comorbidity of these emotional states in other studies
(Field et al., 2000; Glover et al. 1999). Elevated pre-
natal cortisol and noradrenaline and low levels of
dopamine and serotonin typically accompany preg-
nancy depression (Field et al., 2000), although their
association with anger has not been reported before.
mitter/neurohormone profile by neonates has also been
previously reported for prenatal depression (Lundy et
al., 1999; Field et al., 2000), but this is the first time a
matching of prenatal maternal and neonatal biochemi-
cal profiles has been reported for high-anger women.
Similar remarks could be made for the parallel relative
right-frontal EEG activation noted at the neonatal
period in the high-anger mothers and their infants.
 Prenatal anger effects 265

Table VI. Means for Brazelton neonatal behavior assessment scale scores (SDs in parentheses)

Groups
Variable Low High F P
Brazelton
Habituation 5·67 (1·72 ) 5·10 (2 ·18) 1 ·80 ns
Orientation 4·73(1·58 ) 3·82 (1 ·79) 6 ·19 0 ·0 5
Motor organisation 4·53 (0·95 ) 3·94 (1 ·42) 5 ·16 0 ·0 5
Range of state 3·82 (1·17 ) 3·50 (1 ·14) 1 ·64 ns
State regulation 4·18 (1·41 ) 4·06 (1 ·69) 0 ·13 ns
A utonomic stability 6 ·27(1 ·5 7) 5·7 7(2·0 7) 1·5 8 ns
Reflexes 2 ·90(2 ·4 8) 2·5 3(1·7 1) 0 ·6 8 ns
Withdrawal symptoms 2·74 (1·98 ) 3·30 (2 ·11) 1 ·59 ns
Excitability 2·15(1 ·7 0) 2·40 (1 ·56) 0 ·49 ns
Depression 2·03 (1·56 ) 4·20 (3 ·01 17·6 7 0·001

Although this has been reported repeatedly for NIMH merit award (MH no. 46586) to Tiffany Field and
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14

depressed mothers and infants (Dawson et al., 1992;
Jones et al., 1996; Field et al., 2000), this again is the
first observation of this matching of EEG patterns in
angry mothers and their infants. The relative right-
frontal EEG activation noted in our high-anger moth-
ers and infants is consistent with greater blood flow
reported for the functional MRIs in the right prefrontal
cortex (Hariri et al., 2000).
The frequent report of low vagal tone in depressed
mothers and infants was also replicated here on the
high-anger mothers and infants. Elevated stress bio-
chemistry and lower vagal activity (sympathetic
For personal use only.
funding by Johnson and Johnson.
References
Abrams S.M., Field T., Scafidi F. and Prodromidis M. (1995)
Maternal ‘depression’ effects on infants’ Brazelton Scale
performance. Infant Mental Health Journal, 16, 231–235.
al’Absi M., Bongard S. and Lovallo W.R. (2000) Adrenocor-
ticotropin responses to interpersonal stress: effects of overt
anger expression style and defensiveness. International
Journal of Psychophysiology, 37, 257–265.
Blom J.L. and Anneveldt (1982) An electrode cap tested.
Electroencephalography and Clinical Neurophysiology,

activation) would have been predicted by studies on 54, 591–594.

anger reviewed in the introduction (al’Absi et al., 2000;
Davidson et al., 2000; Mancuso, 2000). The greater
number of state changes during sleep and the less opti-
mal orientation, motor organisation, range of state and
depression scores on the Brazelton are consistent with
reports on prenatal depression stress effects on neonatal
sleep and behaviour (Abrams et al., 1995; Jones et al.,
1996; Lundy et al., 1999; Field et al., 2000).
These non-optimal neonatal outcomes highlight the
need for prenatal intervention. Anger and its associated
depression and anxiety emotions and physiological
arousal have been notably reduced by cognitive therapy
(Dahlen and Deffenbacher, 2000) and by exercise
(Hassmen et al., 2000). In addition, we have shown that
pregnancy massage therapy can reduce at least depres-
sion and its associated stress hormones/
neurotransmitters, resulting in more optimal neonatal
outcomes (Field et al., 2000). In addition to finding
cost-effective prenatal interventions, research is needed
on separating the effects of prenatal anger and comor-
bid emotional states such as depression and anxiety. If,
like depression, anger also contributed to prematurity
and low birth weight it would also be important to find
a prenatal marker variable that could predict premature
delivery, as Wadhwa et al. (1998) have found that 28-
week gestation cortisol assays predict at 0·98 reliability
the likelihood of preterm delivery. Interventions could
then be mounted to prevent this outcome for women
with high anger during pregnancy.
Acknowledgements
We would like to thank the mothers and infants who partici-
pated in this study. This research was supported by an NIMH
Senior Research Scientist Award (MH no. 00331) and an
Brazelton T.B. (1984) Neonatal Behavior Assessment Scale.
Philadelphia, Lippincott.
Brondolo E., DiGiuseppe R. and Tafrate, R.-C. (1997)
Exposure-based treatment for anger problems: focus on the
feeling. Cognitive and Behavioral Practice, 4, 75–98.
Carver C.S. and White T.L. (1994) Behavioral inhibition,
behavioral activation, and affective responses to impending
reward and punishment: The BIS/BAS scales. Journal of
Personality and Social Psychology, 67, 319–333.
Dahlen E.R. and Deffenbacher J.L. (2000) A partial compo-
nent analysis on Beck’s cognitive therapy for the treatment
of general anger. Journal of Cognitive Psychotherapy, 14,
77–95.
Davidson K., MacGregor M.W., Stuhr J., Dixon K. and
MacLean D. (2000a) Constructive anger verbal behavior
predicts blood pressure in a population-based sample.
Health Psychology, 19, 55–64.
Davidson R.J., Putnam K.M. and Larson C.L. (2000b) Dys-
function in the neural circuitry of emotion regulation—a
possible prelude to violence. Science, 289, 591–594.
Dawson G., Klinger L.G., Panagitotides H., Hill D. and
Spieker S. (1992) Frontal lobe activity and affective behav-
ior of infants of mothers with depressive symptoms. Child
Development, 63, 725–737.
Diego M.A., Field T. and Hernandez-Reif M. (2002) Frontal
EEG asymmetry and BIS/BAS in intrusive and withdrawn
mothers. Infant Mental Health Journal, in press.
Dieter J., Field T., Jones N.A., Lecanuet J.P., Hernandez-Reif
M. and Salman F.A. (2000) Maternal depression and
increased fetal activity. Manuscript submitted for
publication.
Dimberg U., Thunberg M. and Elmehed K. (2000) Uncon-
scious facial reactions to emotional facial expressions.
Psychological Science, 11, 86–89.
Fava M., Vuolo R.D., Wright E.C., Nierenberg A.A., Alpert
J.E. and Rosenbaum J.F. (2000) Fenfluramine challenge in
unipolar depression with and without anger attacks.
Psychiatry Research, 94, 9–18.
 26 6 T. Field et al.
Field T., Diego M., Dieter J., Hernandez-Reif M., Schanberg
S., Kuhn C., Yando R. and Bendell D. (2000) Prenatal
depression effects on the fetus and the newborn. In review.
Glover V., Teixeira J., Gitau R. and Fisk N.M. (1999)
Mechanisms by which maternal mood in pregnancy may
affect the fetus. Contemporary Reviews in Obstetrics and
Gynecology, 1–6.
Hariri A.R., Bookheimer S.Y. and Mazziotta J.C. (2000)
Modulating emotional responses: effects of a neocortical
network on the limbic system. Neuroreport , 11, 43–48.
Hassmen P., Koivula N. and Uutela A. (2000) Physical
exercise and psychological well-being: a population study
in Finland. Preventive Medicine, 30, 17–25.
Hollingshead A. (1975) Four-factor Index of Social Status.
New Haven, CT, Yale University.
Jones N.A., Field T., Fox N.A., Davalos M., Lundy B. and
Hart S. (1998) Newborns of mothers with depressive symp-
toms are physiologically less developed. Infant Behavior
and Development, 21, 537–541.
Lester B., Als H. and Brazelton T.B. (1982) Regional obstet-
J Obstet Gynaecol Downloaded from informahealthcare.com by The University of Manchester on 12/20/14
ric anesthesia and newborn behavior: a reanalysis toward
synergistic effects. Child Development, 53, 687–692.
Littman D. and Parmelee A. (1978) Medical correlates of
infant development. Pediatrics, 61, 470–474.
Lundy B.L., Jones N.A., Field T., Nearing G., Davalos M.,
Pietro P., Schanberg S. and Kuhn C. (1999). Prenatal
depression effects on neonates. Infant Behavior and
Development , 22, 121–137.
Magai C. (1999) Personality change in adulthood: loci of
change and the role of interpersonal processes.
International Journal of Aging and Human Development,
49, 339–352.
Mancuso R.A. (2000) Anger ideals and their impact on
For personal use only.
emotional and physiological reactivity (socialization, emo-
tional, reactivity). Dissertation Abstracts International,
Section B, Sciences and Engineering, 60, 3620.
McNair D.M. and Lorr M. (1964) An analysis of mood in
neurotics. Journal of Abnormal Social Psychology, 69,
620–627.
McNair D.M., Lorr M. and Droppleman L.F. (1971) POMS
profile—Profile of Mood States. San Diego, CA,
Educational and Industrial Testing Services.
Porges S.W. (1991) Vagal tone: a mediator of affect. In: The
Development of Emotion Regulation and Dysregulation.
Edited by Garber J. and Dodgel K.A. Cambridge,
Cambridge University Press.
Pugatch D., Haskell D. and McNair D.M. (1969) Predictors
and patterns of change associated with the course of time
limited psychotherapy. Mimeo Report.
Radloff L.S. (1977) The CES-D Scale: a self-report depres-
sion scale for research in the general population. Journal of
Applied Psychological Measures, 1, 385–401.
Radloff L.S. and Teri L. (1986) Use of the Center for Epide-
miological Studies Depression Scale with older infants.
Clinical Gerontologist, 5, 119–135.
Scafidi F., Field T., Schanberg S., Bauer C., Vega-Lahr N.,
Garcia R., Poirier J., Nystrom G. and Kuhn C.M. (1986)
Effects of tactile/kinesthetic stimulation on the clinical
course and sleep/wake behavior of preterm neonates. Infant
Behavior and Development, 9, 91–105.
Sostek A.M. and Anders T.F. (1975) Effects of varying
laboratory conditions on behavioral-state organization of 2
and 8-week-old infants. Child Development, 46, 871–878.
Spielberger C., Gorsuch R.L. and Lushene R.E. (1970) The
State Trait Anxiety Inventory. Palo Alto, CA, Consulting
Psychologists Press.
Sutton S.K. and Davidson R.J. (1997) Prefrontal brain
asymmetry: a biological substrate of the Behavioral
Approach and Inhibition Systems. Psychological Science,
8, 204–210.
Thoman E.B. (1975) Early development of sleeping behav-
iors in infants. In: Behavior and Development in Infancy:
Human and Animal Studies, edited by Ellis N.T. New
York, John Wiley & Sons.
Wadhwa P.D., Porto M., Garite T.J., Chicz-DeMet A. and
Sandman C.A. (1998) Maternal corticotropin-releasin g
hormone levels in the early third trimester predict length of
gestation in human pregnancy. American Journal of
Obstetrics and Gynecology, 179, 1079–1085.
Weiss J.M., Demetrikopoulos M.K., West C.H.K. and
Bonsall R.W. (1996) Hypothesis linking the noradrenergic
and dopaminergic systems in depression. Depression, 3,
225–245.