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This is to certify that the
dissertation entitled

MATERNAL CORTISOL AS A MEDIATOR OF
PRENATAL STRESS AND INFANT REGULATION

Doctoral

DEVELOPMENT

presented by

Shallimar M. Jones

has been accepted towards fulfillment
of the requirements for the

 

degree in Psychology

AW

' Majdr Professor's Signature
’0 ”8’0 9’

Date

MSU is an afiinnative—acfion, equal-opportunity employer

PLACE IN RETURN BOX to remove this checkout from your record.
To AVOID FINES return on or before date due.
MAY BE RECALLED with earlier due date if requested.

 

DATE DUE

DATE DUE

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6/07 p:/CIRCIDateDue.indd-p.1

 

MATERNAL CORTISOL AS A MEDIATOR OF PRENATAL STRESS AND
INFANT REGULATION DEVELOPMENT

by

Shallimar M. Jones

A DISSERTATION

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY
Department of Psychology

2007

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ABSTRACT

MATERNAL CORTISOL AS A MEDIATOR OF PRENATAL STRESS AND
INFANT REGULATION DEVELOPMENT

By

Shallimar M. Jones
Maternal experience of stress during pregnancy can have a lasting impact on infant
regulation development. Research suggests that the Hypothalamic Adrenal (HPA) axis
transmits maternal stress to the fetus and that these effects can be observed in infant
regulatory behaviors such as temperament and sleep patterns. However, examining
prenatal maternal cortisol as a mediator of prenatal maternal stress and infant regulation
has not been observed in human populations. Therefore, the present study investigated
this relationship using a prospective design with a community sample of 92 participants
in the 3rd trimester of their pregnancies. Participants were interviewed a second time
when the infants were 3 months old. A.M. and PM. salivary maternal cortisol and self
report measures for prenatal stress (depression, anxiety, life stress, daily hassles, and
perceived stress) and pregnancy related conditions were examined at Time 1. At Time 2,
self report measures of postnatal stress (depression, anxiety, life stress, daily hassles, and
perceived stress), general health, infant sleep and temperament with the Infant Behavior
Scale were completed. Hierarchical Linear Regression controlling for postnatal stress,
showed that cortisol was not a significant mediator. However, prenatal stress did predict
aspects of infant regulation. Specifically, mental stress predicted infant activity (beta = -
.24, p<.05) and sleep (beta = .40, p<. 05) and life stress predicted attention (beta = -.24,
p<.05). Postnatal analyses (controlling for prenatal stress) showed that, perceived stress

experienced by the mother directly (beta = .21 , p <05) and indirectly through parenting

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effects (beta = -.24, p<.05) attention. Implications from this study not only highlight the
need for further research on the role of cortisol as a mediator of prenatal stress and infant
regulation, but also the need to incorporate these findings into clinical and physical

assessments for earlier identification of pregnant women whose children may be at risk

for possible negative developmental consequences.

C0pyfight By
SHALLIMAR M. JONES

2007

First and forest

at with encou'agcrtte:
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ACKNOWLEDGEMENTS
First and foremost I would like to thank God for giving me strength to complete
this journey. Secondly I would like to thank all of my family and friends for providing
me with encouragement and support when I needed it. I would also like to give a special
thanks to my advisor Dr. Bogat, for your guidance through this process. In addition, I
would like to give a special thank you to my classmates; your encouragement was greatly

appreciated.

NRODL'CTION .....

Stress During P’
HPA Axis ...... i
HPA and Offsp'
Postnatal Strexx
Prenatai Stress .-.
Stress in Humn I

Pit'lis'.

Prcm'...

Stress and the li
PS silt
PIL’T..:’. ;
P\\gkt
Postnatal Strm 1
Parent:
PIL’l‘uial
Rdlit.l;"..1
Hm Itht

METHODS ........
Participants...
Measures

-...

 

TABLE OF CONTENTS

INTRODUCTION ............................................................................. 1
Stress During Pregnancy in Animals ................................................ 4
HPA Axis ............................................................................... 8
HPA and Offspring Development ..................................................... 12
Postnatal Stress and Parenting Offspring ........................................... 14
Prenatal Stress and Parenting Offspring .............................................. 18
Stress in Humans ....................................................................... 19

Prenatal Stress and Fetal Outcomes ....................................... 22

Prenatal Stress and Birth Outcomes ....................................... 24

Prenatal Stress and Infant Outcomes ...................................... 28
Prenatal Stress and Childhood and Adolescent Outcomes ............ 29
Prenatal Stress and Adult Outcomes ..................................... 30

Stress and the HPA Axis in Humans ................................................ 31
PS stress hormones and Fetal Development ............................. 34

Prenatal Stress Hormones and Infant Development ................... 36
Psychological stress, hormones, and infant outcomes ................ 37
Postnatal Stress in Humans ............................................................. 38
Parenting and Postnatal Stress ............................................. 39

Prenatal Stress, Hormones and Later Outcomes. . . . . . . . . . . . . . . ..40
Rationale ..................................................................... 43
Hypotheses .................................................................. 44
METHODS ...................................................................................... 48
Participants .......................................................................... 48
Measures ............................................................................. 49
Demographics .............................................................. 49

Maternal Health ............................................................ 49

Physical Health Symptomatology ....................................... 49

Center for Epidemiological Studies Depression Scale. . . . . . ....50

State Trait Anxiety Inventory ............................................ 50

Perceived Stress Scale ...................................................... 50

Life Experiences Survey ................................................. 51

Daily Hassles Questionnaire ............................................. 51

Birth, pregnancy, and delivery questionnaire .......................... 52

Infant Care Scale ........................................................... 52

Infant Behavior Questionnaire ............................................ 52

Cortisol ...................................................................... 53

Infant Sleep ................................................................. 53
Procedure ........................................................................... 54
Recruitment .................................................................. 54

Data Collection and Data Entry .......................................... 56
RESULTS .......................................................................................... 56
Initial Data Construction ......................................................... 56

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DISCL'SSIOX ......

REFERENCES .....

Irnputation ................................................................... 56

Variable Construction ..................................................... 57
Preliminary Data Analysis ................................................ 58
Frequency Analysis ....................................................... 63
Correlations of All Variables ............................................. 63
Hypothesis A: PS will have a direct effect on infant regulation. . . . . . . ..63
Mental Stress and Infant Regulation ................................... 63

Life Stress and Infant Regulation ....................................... 63

Perceived Stress and Infant Regulation ................................ 63
Hypothesis B: PS will have a direct effect on cortisol ........................... 64
Stress and A.M. Cortisol ................................................. 64

Stress and P.M. Cortisol .................................................. 64
Hypothesis C: Cortisol Predicting Infant Regulation ............................ 64
A.M. Cortisol Predicting Infant Regulation ........................... 64

P.M. Cortisol Predicting Infant Regulation ............................ 64
Hypothesis D: Cortisol Mediating Prenatal Stress and Infant Regulation... . .64
Hypothesis E: Prenatal Stress Predicting Postnatal Stress ....................... 64
Hypothesis F: Postnatal Stress Predicting Infant Regulation .................... 65
Mental Stress Predicting Infant Regulation ........................... 65

Life Stress Predicting Infant Regulation .............................. 65

Perceived Stress Predicting Infant Regulation ........................ 65

Hypothesis G: Postnatal Stress Predicting Parenting Competency. . . . ..65
Hypothesis H: Parenting Competency Predicting Infant Regulation... . . . . ....65
Hypothesis 1: Parenting Competency Mediating Postnatal Stress and Infant

Regulation ............................................................. 66
DISCUSSION .............................................................................. 66
REFERENCES ............................................................................. 76

vii

Appcrtdtt
Append:
Appendt

Appendix

APPENDICES

Appendix A: Demographics .......................................................... 98
Appendix B: Maternal Health ...................................................... 101
Appendix C: Physical Health Symptoms .......................................... 104

Appendix D: Center for Epidemiological Studies Depression Scale... . 1 06

Appendix E: State-Trait Anxiety Inventory ....................................... 108
Appendix F: Perceived Stress Scale ............................................... 111
Appendix G: Life Experiences Survey ............................................ 113
Appendix H: Daily Hassles Questionnaire ......................................... 117
Appendix 1: Birth, pregnancy, and Delivery Questionnaire .................... 1 19
Appendix J: Infant Care Scale ...................................................... 124
Appendix K: Infant Behavior Questionnaire ...................................... 126
Appendix L: Cortisol .................................................................. 130
Appendix M: Infant Sleep ............................................................ 132
Appendix N: Flyers ................................................................... 134
Appendix 0: Screen .................................................................. 136
Appendix P: Consent Forms ........................................................ 138
Appendix Q: Recontact Information ............................................... 139

viii

 

figure 1: Medution _\

LIST OF FIGURES

Figure 1: Mediation Model Hypothesized Relationships ................................. 62

ix

 

iii: 1: Demographic I).
Table}. Demographic \

left-123: Table of Means

   
 
 

Tale 4: Table of Comet:

his 5: Correiations of A.

lit-3e 7: Hypothesis A; .\1
his 8: Hypothesis A: V
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LIST OF AND TABLES

Table 1: Demographic Description of Sample .................................................. 145
Table 2: Demographic Variables for T2 ........................................................ 146
Table 3: Table of Means for Imputed vs. Non-Imputed Data ............................... 147

Table 4: Table of Combined Imputed and Non-imputed Data for Study Variables. . . .. 148

Table 5: Correlations of All Variables .......................................................... 149
Table 6: Hypothesis A: Mental Stress Predicting Infant Activity .......................... 150'
Table 7: Hypothesis A: Mental Stress Predicting Distress To Limitations ............... 151
Table 8: Hypothesis A: Mental Stress Predicting Smiling.....................................152
Table 9: Hypothesis A: Mental Stress Predicting Duration of Orienting ................. 153
Table 10: Hypothesis A: Mental Stress Predicting Sleep ..................................... 154
Table 11: Hypothesis A: T1 Life Stress Predicting Activity .................................. 155
Table 12: Hypothesis A: Life Stress Predicting Distress to Limitations .................... 156
Table 13: Hypothesis A: Life Stress Predicting Smiling ..................................... 157
Table 14: Hypothesis A: T1 Life Stress Predicting Duration of Orienting ................. 158
Table 15: Hypothesis A: Tl Life Stress Predicting Sleep ................................... 159
Table 16: Hypothesis A: T1 Perceived Stress Predicting Activity .......................... 160
Table 17: Hypothesis A: T1 Perceived Stress Predicting Distress to Limitations ....... 161
Table 18: Hypothesis A: T1 Perceived Stress Predicting Smiling ........................... 162
Table 19: Hypothesis A: T1 Perceived Stress Predicting Duration of Orienting ......... 163
Table 20: Hypothesis A: Tl Perceived Stress Predicting Sleep ............................. 164
Table 21: Hypothesis B: T1 Mental Stress Predicting A.M. Cortisol ...................... 165
Table 22 Hypothesis B: T1 Life Stress Predicting A.M. Cortisol ......................... 166

12:-Eli: Hypothesis B
Table 3-1: Hypothesis 8;
1:51:35: Hypothesis B
lib-1:36: Hypothesis 3 I
It's}: 37. Hypothesis C

Table 38: Hypothesis C 'T

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Table 23: Hypothesis B: Tl Perceived Stress Predicting A.M. Cortisol . .........167

Table 24: Hypothesis B: T] Mental Stress Predicting P.M. Cortisol ...................... 168
Table 25: Hypothesis B: T] Life Stress Predicting P.M. Cortisol ........................... 169
Table 26: Hypothesis B: T1 Perceived Stress Predicting P.M. Cortisol ................... 170
Table 27: Hypothesis C: T1 A.M. Cortisol Predicting Activity ............................ 171
Table 28: Hypothesis C T1 A.M. Cortisol Predicting Distress to Limitations . . ..172
Table 29: Hypothesis C: T1 A.M. Cortisol Predicting Distress to Smiling . . 1 73
Table 30: Hypothesis C: T] A.M. Cortisol Predicting Duration of Orienting 1 74
Table 31: Hypothesis C: T] A.M. Cortisol Predicting Sleep ............................... 174
Table 32: Hypothesis C: T1 P.M. Cortisol Predicting Activity ............................. 175
Table 33: Hypothesis C: Tl P.M. Cortisol Predicting Distress to Limitations . .....l77
Table 34: Hypothesis C: T1 P.M. Cortisol Predicting Distress to Smiling ............... 178
Table 35: Hypothesis C: T1 P.M. Cortisol Predicting Duration of Orienting ............179
Table 36: Hypothesis C: T1 P.M. Cortisol Predicting Sleep ............................... 180

Table 37: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and
Activity ....................................... 181

Table 38: Hypothesis D: Tl A.M. Cortisol As A Mediator of T1 Life Stress and
Activity ........................................ 182

Table 39: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and
Activit y ........................................ 183

Table 40: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and
Distress to Limitations ...................... 184

Table 41: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Life Stress and Distress
to Limitations ............................... 185

Table 42: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and
Distress to Limitations ...................... 186

xi

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Table 57:

Table 58:

Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and
Smiling ......................................... 187

Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Life Stress and
Smiling ........................................ 188

Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and
Smiling .......................................... 189

Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and
Duration of Orienting .......................... 190

Hypothesis D: T] A.M. Cortisol As A Mediator of T1 Life Stress and Duration
of Orienting ................................... 191

Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and
Duration of Orienting ........................ 192

Hypothesis D T1 A.M. Cortisol As A Mediator of T1 Mental Stress and
Sleep ........................................... 193

Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Life Stress and
Sleep ........................................... 194

Hypothesis D: Tl A.M. Cortisol As A Mediator of T1 Perceived Stress and
Sleep ............................................ 195

Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress and
Activity ......................................... 196

Hypothesis D: T] P.M. Cortisol As A Mediator of T1 Life Stress and
Activity ........................................ 197

Hypothesis D: Tl P.M. Cortisol As A Mediator of T1 Perceived Stress and
Activity ......................................... 198

Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress and
Distress to Limitations ....................... 199

Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Life Stress and Distress
to Limitations ............................... 200

Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and
Distress to Limitations ...................... 201

Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Mental Stress and
Smiling ......................................... 202

xii

 

Title 59: Hypothesis D

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Table 59: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Life Stress and

Smiling ........................................ 203
Table 60: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and
Smiling ........................................ 204
Table 61: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Mental Stress and
Duration of Orienting ..................... 205
Table 62: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Life Stress and Duration
of Orienting ................................. 206
Table 63: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and
Duration of Orienting ...................... 207
Table 64: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress and
Sleep .......................................... 208
Table 65: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Life Stress and
Sleep .......................................... 209
Table 66: Hypothesis D T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and
Sleep ........................................... 210
Table 67: Hypothesis E: T1 Mental Stress Predicting T2 Mental Stress ................... 211
Table 68: Hypothesis E: T1 Life Stress Predicts T2 Life Stress ............................ 212
Table 69: Hypothesis E: T1 Perceived Stress Predicts T2 Perceived Stress . . . . . . .213
Table 70: Hypothesis F: T2 Mental Stress Predicting Activity .............................. 214
Table 71: Hypothesis F: T2 Mental Stress Predicting Distress to Limitations... . . . . . . ....215
Table 72: Hypothesis F: T2 Mental Stress Predicting Smiling ............................... 216
Table 73: Hypothesis F: T2 Mental Stress Predicting Duration of Orienting .............. 217
Table 74: Hypothesis F: T2 Mental Stress Predicting Sleep ................................. 218
Table 75: Hypothesis F: T2 Life Stress Predicting Activity .................................. 219
Table 76: Hypothesis F: T2 Life Stress Predicting Distress to Limitations ................ 220

Table 77: Hypothesis F: T2 Life Stress Predicting Smiling .................................. 221

xiii

Table 78: Hypothesis F: T2 Life Stress Predicting Duration of Orienting ................. 222

Table 79: Hypothesis F: T2 Life Stress Predicting Sleep ..................................... 223
Table 80: Hypothesis F: T2 Perceived Stress Predicting Activity ........................... 224
Table 8]: Hypothesis F: T2 Perceived Stress Predicting Distress to Limitations. . . . ..225
Table 82: Hypothesis F: T2 Perceived Stress Predicting Smiling ........................... 226
Table 83: Hypothesis F: T2 Perceived Stress Predicting Duration of Orienting. . . . ....227
Table 84: Hypothesis F: T2 Perceived Stress Predicting Sleep .............................. 228
Table 85: Hypothesis G: T2 Mental Stress Predicting Parenting Competency ............ 229
Table 86: Hypothesis G: T2 Life Stress Predicting Parenting Competency ................ 230

Table 87: Hypothesis G: T2 Perceived Stress Predicting Parenting Competency ........ 231

Table 88: Hypothesis H: T2 Parenting Competency Predicting Activity ................... 232
Table 89: Hypothesis H: T2 Parenting Competency Predicting Distress to

Limitations ........................... 233
Table 90: Hypothesis H: T2 Parenting Competency Predicting Smiling ................... 234

Table 91: Hypothesis H: T2 Parenting Competency Predicting Duration of Orienting..235
Table 92: Hypothesis H: T2 Parenting Competency Predicting Sleep ...................... 236

Table 93: Hypothesis I: Parenting Competency Mediating T2 Mental Stress and
Activity ............................... 237

Table 94: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Distress
to Limitations ....................... 238

Table 95: Hypothesis I: Parenting Competency Mediating T2 Mental Stress and
Smiling .............................. 239

Table 96: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Duration
Of Orienting ........................ 240

Table 97: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and
Sleep .................................. 241

xiv

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Table 98: Hypothesis 1: Parenting Competency Mediating T2 Life Stress and
Activity ............................... 242

Table 99: Hypothesis 1: Parenting Competency Mediating T2 Life Stress and Distress to
Limitations ........................... 243

Table 100: Hypothesis I: Parenting Competency Mediating T2 Life Stress and
Smiling ............................... 244

Table 101: Hypothesis 1: Parenting Competency Mediating T2 Life Stress and Duration
of Orienting .......................... 245

Table 102: Hypothesis I: Parenting Competency Mediating T2 Life Stress and Sleep...246

Table 103: Hypothesis 1: Parenting Competency Mediating T2 Perceived Stress and
Activity ............................... 247

Table 104: Hypothesis I: Parenting Competency Mediating T2 Perceived Stress and
Distress to Limitations ............. 248

Table 105: Hypothesis 1: Parenting Competency Mediating T2 Perceived Stress and
Smiling ............................... 249

Table 106: Hypothesis I: Parenting Competency Mediating T2 Perceived Stress and
Duration of Orienting .............. 250

Table 107: Hypothesis 1: Parenting Competency Mediating T2 Perceived Stress and
Sleep .................................. 251

XV

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INTRODUCTION

The purpose of this study is to examine the relationship between psychosocial and
physiological measures of stress during pregnancy and early infant regulation behavior
(i.e. infant temperament and sleeping pattern) in humans. The idea that maternal
emotions can influence infant regulation development has long been accepted (F eirreira,
1965). The most extensive examination of this issue has been conducted in animals.
Research in animals has demonstrated that offspring exposed to prenatal stress in the
form of unpredictable noise, (Schneider, 1992), motor restriction (Deminiere et a1.,
1992), or crowding (Dahlof, Hard, & Larsson, 1978) of the mother went on to exhibit
fearful behaviors, decreased exploration of novel environments, learning difficulties, and
problems with physical and motor development during infancy and into adulthood
(Meek, Burda, & Paster, 2000; Schneider et a1., 1992, Grimm & Frieder, 1987;
Weinstock, Matlinda, Maor, Rosen, & McEwen, 1992). Many researchers believe that
the effects of prenatal stress on infant regulation are mediated by the physiological stress
response of the maternal hypothalamic-pituitary—adrenal (HPA) axis (Barbazanges,
Piazza, 1e Moal, & Macccari, 1996; Weinstock, 1997).

One of the hormones involved in the stress response is cortisol. Research in
animals has demonstrated a relationship between maternal stress and increased
circulating corticosterone (cortisol in humans) within the mother (Arishima, Nakama,
Morikawa, Hashimoto, & Eguchi, 1977; Zarrow, Philpott, & Denenberg, 1970) and
within the fetus (Gitau, Cameron, Fisk, & Glover, 1998; Stewart, Rogerson, & Manson,
1995). Research has shown that rats exposed to prenatal stress display greater and

prolonged elevation of adrenal hormones as adults (Clarke, Wittwer, Abbott, &

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Schneider, 1994; Fride, Dan, Feldon, Halevy, & Weinstock, 1986). This is problematic
because many researchers believe that prenatal exposure to stress may permanently alter
the neural circuitry of a developing organism (Benes, 2000; Meaney et a1., 1996), leaving
it more vulnerable for future emotional dysregulation, psychopathology, and a host of
other difficulties during later development (Meyer et a1., 2001). In fact, research has
demonstrated that chronic exposure to stress and the circulating hormone cortisol, has
been associated with a variety of physical problems including cardiovascular diseases,
irnmuno-suppression, insulin resistance, and neuro-degenerative diseases (Mchwen &
Sapolsky, 1995; Meaney 1996) as well as psychological problems such as excessive fear,
anxiety, and depression in both humans and animals (Meyer, Chrousos, & Gold, 2001).

The postnatal environment also affects the development of an organism.
Specifically, the effect of prenatal stress on subsequent infant physiology and behavioral
development has also been shown to be impacted by postnatal maternal care. Work with
rodents has demonstrated that high levels of maternal care may mediate the expression of
fearfulness and circulating corticosterone in their offspring (Caldji, Tannenbaum,
Sharma, Francis, Plotsky, & Meany, 1998; Lui et a1. 1997; Sapolsky, 1997).
Unfortunately, most of these studies did not consider the influence of the prenatal
environment. Using a cross fostering design to examine prenatal stress, Maccari, Piazza,
Kabbaj, Barbazanges, Simon and Le Moal (1995) found that the effects of prenatal stress
environment could be influenced by postnatal parenting.

There is some evidence that a parallel relationship between prenatal stress and
infant development may be true in the human population as well. Unlike animals where

the idea of stress is easily operationalized, this is not so easily accomplished in the human

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population. Stress during pregnancy has been conceptualized as the experience of life
events or daily hassles (DaCosta, Brender, & Larouche, 1998; Zuckerman, Amaro,
Bauchner, & Cabral, 1989), psychological distress such as anxiety (Hobel, Dunkel-
Schetter, Roeshc, Castro, & Arora, 1999), perceived stress (Sable & Wilkinson, 2000), or
as a combination of all of these (Lobel, Dunkel-Schetter, & Scrimshaw, 1992). In
addition, most studies on humans either examine stress during pregnancy and its
relationship to early infant birth outcomes or they examine stress during the postnatal
period. Studies conducted on the impact of prenatal stress on birth outcomes have
documented that prenatal stressors are related to birth outcomes such as preterm delivery,
decreased head circumference, pregnancy complications, or lower birth weight (Lou et
a1., 1994; Dunkel-Schetter, 1998; Paarlberg, Bingerhoets, Passchieir, Dekker, & van
Geijn, 1999). Research in the postnatal period has also demonstrated an effect of
postnatal stressors of the mother on infant motor and emotional development (Meijier,
1985; Warren, Gunnar, Kagan, Anders, Simmons, Rones, Wease, et a1., 2003).

Currently, there is only a small body of literature that prospectively examines the
connection between prenatal stress and infant development. One of the few prospective
studies in this area, conducted by Huizink, de Medina, Mulder, Visser, and Buitelaar
(2002), found that prenatal stress in the form of perceived stress and pregnancy anxiety
was related to difficult infant behavior and attention regulation at 3 and 8 months. In
addition, work by de Weerth, van Hees, and Buitelaar (2003) has demonstrated that
mothers with high levels of cortisol during pregnancy not only delivered sooner than low
cortisol mothers, but their infants also displayed more crying, fussing, and negative facial

expressions. Unfortunately, these studies did not consider the influence of postnatal

 

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stress. Therefore it is difficult to determine if the effects of prenatal stress significantly
contribute to later infant development over and above postnatal stress. One study that did
control for postnatal anxiety, found that maternal anxiety during pregnancy predicted
later behavioral and emotional problems in children 4 years of age (O’Connor, Heron,
Golding, Beveridge, & Glover, year). However this study did not account for postnatal
parenting behavior which, in addition to stress, has also been shown to be an important
predictor of infant development in both humans and infants (Teicher, Andersen, Polcari,
Anderson, Navalta, & Kim, 2003).

Given the delicate nature of a developing fetus, prenatal exposure to stress
through circulating hormones can be detrimental to subsequent development. Therefore,
the purpose of this study is to examine the relationship between prenatal stress and infant
regulation development. In order to account for postnatal variables, postnatal stress and
parenting will also be accounted for.

Stress During Pregnancy in Animals

The idea that stress during pregnancy can impact fetal development, has long
been established (Ferreira, 1965). Most of the early studies examining stress began in the
19703. The term “stress” has been defined in a number of ways. The two oldest
definitions of stress are rooted in the biological model and the engineering model. In the
biological model, the main idea was to identify biologically-based reactions that could be
generalized from individually taxing situations (Selye, 1956). In the engineering model,
however, stress refers to an applied external force that when present, exceeds the carrying

capacity of the material (Smith, 1987). Stress research in animals uses a combination of

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these definitions by examining the effects of externally induced stressors and their effects
on the biological and social development of an organism.

To induce stress in animals, pregnant mothers (mostly rodent or nonhuman
primates) have been subjected to a variety of stressors that have ranged from painful to
less painful. For example, with rodents some researchers have used crowding (Dahlof et
a1., 1978), repetitive tail shocks (Takahashi, Haglin, & Kalin, 1992), saline injections
(Peters, 1990), or restraint (Herrenkohl & Whitney, 1976; Herrenhol, 1976; Derniniere et
a1., 1992) as stressors. While other researchers examining nonhuman primates have used
noise (Schneider, 1992) or social stress such as removing a pregnant animal from its
home cage and placing it in a new unfamiliar environment (Schneider & Coe, 1993).

Research in this area has demonstrated that the type of stressor can have
differential outcomes on later development. Velazquez-Moctezuma et a1. (1993) used
four different prenatal stress (PS) conditions in rodents and found that restraint and sleep
deprivation were correlated with later sexual behavior in males, while immersion in cold
water was not. Other researchers have also found differential patterns in the type of PS
and later offspring outcomes. For example, Takahashi et a1. (1990) found that random
electric shock was associated with fewer vocalizations, while Williams et a1. (1998)
found that restraint was associated with more vocalizations in rodents.

The timing of the stressor may also be a factor in many PS conditions. In a study
of PS examining rodents during the beginning, middle, and end of pregnancy, it was
found that later adult exploration was highly associated with PS in the early part of

pregnancy (Suchecki & Neto, 1991). Other studies with nonhuman primates have shown

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that PS administered across gestation rather than mid-gestational stress was related to
later neuromotor development (Schneider & Coe, 1993).

Although stressors differ in severity and timing, overall PS has been associated
with negative birth outcomes and early developmental delays as well as later adult
developmental delays in motor, learning, emotional, and neurological development in
animals. Currently most studies examining PS typically focus on later adult animal
outcomes rather than early developmental effects of PS. Research on early development
has shown that rhesus monkeys exposed to early PS had lower birth weight than non PS
monkeys (Schneider et a1., 1999). In rodents, Meek et a1. (2000) found that when
pregnant mice were randomly exposed to handling, noise, increased temperatures, or light
for 45 minutes during the last week of pregnancy, a variety of early developmental
indices were disturbed in the offspring. Specifically, they found that stressed pups were
initially smaller than non stressed pups, had fewer teeth at birth, and were less likely to
rotate at 3 days than non-stressed pups.

PS has also been associated with delayed motor development in animals. For
example, Drago, Di Leo, and Giardina, (1999) found that rats exposed to PS exhibited
delayed neonatal sensorimotor reflexes. Meek et a1. (2000) reported that PS rats were
less likely to climb, respond to tail pulling, or demonstrate clinging in the first week of
life. Other studies have found that infant PS squirrel monkeys demonstrated poorer
muscle tone, coordination, self-feeding, and response speeds than non PS monkeys.
These results are consistent with other research on adult rodents that demonstrate
continued motor delays (Grimm & Frieder, 1987; Lambert, Kinsley, Jones, Klien, Peretti,

& Stewart, 1995). This pattern has also been observed in nonhuman primates as well.

 

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Specifically, Schneider (1992b) reported that at 6 months, squirrel monkeys demonstrated
lower levels of gross motor behavior than non PS monkeys.

In addition to delayed motor development, cognition is also affected by PS.
Research shows that adult rats exposed to PS have difficulty learning new tasks such as
water mazes or reversal of previously learned discrimination tasks (Amsten, 2000; de
Quervain, Roozendaal, & McGaugh, 1998; Grim & Frieder, 1987; Meek et a1., 2000;
Thompson et a1., 1962). In one of the earliest studies on this topic, Thompson et al.
(1962) reported that PS rodents demonstrated a higher number of errors and needed more
time to complete mazes than non PS rats. Grim and Frieder (1987) reported that PS rats
learned mazes at a slower rate than non PS rats. In nonhuman primates, Schneider
(1992c) observed that PS monkeys took longer to locate partially obstructed objects than
non PS monkeys.

Other studies have documented disturbed emotional responses (or anxiety-like
symptoms) in animals exposed to PS as well. According to Weinstock (2001),
observation of rats exposed to an unfamiliar peer revealed that 30% of PS rats initiated
contact compared to 90% of controls. Other studies have demonstrated increased startle
responses, increased defecation, freezing, decreased ultra-sonic vocalizations, and altered
sleep patterns in rats (Fride et a1., 1986; Fride & Weinstock, 1984; Takahashi, Haglin, &
Kalin, 1992). In nonhuman primates exposed to PS, abnormal social behavior has also
been observed. Specifically, at 2 years of age, PS rhesus monkeys displayed fewer
incidents of exploration in novel environments, reduced play, and increased clinging

behaviors when placed in unfamiliar environments as compared to controls (Coe,

 

 

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Kramer, Czeh, Gould, Reeves, Kirschbaum, & Fuchs, 2003; Schneider, 1992a;
Schneider, 1992b).

Animals exposed to PS also exhibit a variety of neurological deficits. Coe et al.
(2003) examined PS in a sample of rhesus monkeys. The researchers exposed pregnant
monkeys to daily stress for 25% of their 24 week gestation period. PS during early and
late gestation resulted in inhibited cell grth of the dentate gyrus and decreased
hippocampal volume in both PS conditions. This is important for several reasons. First,
the dentate gyrus is responsible for the generation of new cells (Gould & Tanapat, 1999;
Altman & Bayer, 1990; Bayer, 1980). It is formed during gestation and continues to
develop postnatally (Gould & Tanapat, 1999; Altman & Bayer, 1990; Bayer, 1980), so a
reduction of this structure early on could effect subsequent cell growth. Second, the
hippocampus is involved in episodic and declarative memory, spatial learning, and is also
involved in the stress response (McEwen, Margarinos, & Reagan, 2002). Therefore a
reduction of this structure could explain some of the cognitive deficits exhibited by these
animals. Further, because many believe that the stress response system mediates the
relationship between PS and later development (Dodic et al., 2002; Maccari, Darnaudery,
Morley-Fletcher, Zuena, Cinque, & Van Reeth, 2003; Owen, Andrews, & Matthews,
2005; Nyirenda & Seckl, 1998; van den Bergh, Mulder, Mennes, & Glover, 2005 ;
Wadhwa et a1., 2001), disruption of this structure may affect the effectiveness of the
stress response.
HPA Axis

When an organism encounters stressful stimuli, the Hypothalamic Adrenal

Pituitary (HPA) axis responds. The first system that responds is the sympathetic nervous

 

 

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system (Kalat, 1998; Korte, 2001). Here the “fight or flight” system is activated and the
body immediately responds with an increase of catecholamines such as cortisol, which
are hormones that elevate blood sugar and metabolism to aid in an increased fuel supply
needed to respond to the situation (Kalat, 1998; Korte, 2001). As a part of this system,
the HPA axis is also activated. This system is slower than the sympathetic system and
involves the release of glucocorticoids (GC) which serve as the end product of the
negative feedback loop which inhibits the stress response (Francis & Meaney, 1999;
Meaney et a1 1996; Vazquez, 1998; Weinstock, 2001).

In the HPA pathway, the paraventricular nucleus of the hypothalamus responds to
external stressors by releasing corticotropin releasing hormones (CRH) and arginine
vasopressin (AVP) to signal the anterior pituitary gland to secrete adrenocorticotropic
hormone (ACTH) (Francis et al., 1996; Francis & Meaney, 1999; Meaney et al., 1996;
Vazquez, 1998; Weinstock, 2001). In the bloodstream, this hormone ultimately
stimulates the adrenal cortex to release the steroid hormones GC. GCs are most
commonly in the form of corticosterone in rodents (or cortisol in humans and nonhuman
primates). They serve to mobilize energy via increasing circulating glucose levels and
also act on areas of the brain such as the hippocampus and amygdala to affect learning
and memory (Francis et al., 1996; Francis & Meaney, 1999; Meaney et al., 1996; Owen
et al., 2005; Vazquez, 1998; Weinstock, 2001). Although the mobilization of energy
constitutes an important coping mechanism, prolonged exposure to high levels of
corticosterone hormones leads to cardiovascular diseases, neuronal death, decreased
immune response, as well as inhibited growth and reproduction in the long term because

energy is being directed to other parts of the body (Mchwen & Sapolsky, 1995; Tsigos

 

 

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& Chrousos, 2002; Vazquez, 1998; Weinstock, 2001). Accordingly, in order to be
effective, the stress response system must be kept under strong regulation by rapidly
responding to stimuli and quickly returning to baseline (Huznik, 2004; Vazquez, 1998;
Weinstock, 2001).

The response of the stress system is regulated by a negative feedback system
(Francis et al., 1996; Francis & Meaney, 1999; Huznik, 2004; Meaney et al., 1996;
Vazquez, 1998; Weinstock, 2001) involving circulating levels of GCs (Korte, 2002;
Huznik et al., 2004; Ratka, Sutano, Bloemers, & De Kloet, 1989; Rue] & De Kloet, 1985;
Vazquez, 1998). GCs bind to two types of receptors: mineralcorticoid (MR) receptors or
glucocorticoid receptors (GR). They are each located in the hippocampus, septum, and
amygdala (Korte, 2002; Maccari et al., 2003; Mastorakos & Ilias, 2003; Ratka et al.,
1989; Ruel & De Kloet, 1985; Vazquez, 1998; Weinstock, 2001). However, GRs are
also located in other parts of the brain, with the highest concentration in the
hypothalamus, hippocampus, and pituitary (Korte, 2002; Maccari et al., 2003;
Mastorakos & Ilias, 2003; Ratka et al., 1989; Ruel & De Kloet, 1985; Vazquez, 1998).
GCs bind mostly to MRS in basal conditions, whereas during times of stress and circadian
peak, GCs mostly bind to GRs (Korte, 2002; Maccari et a1., 2003; Mastorakos & Ilias,
2003; Ratka et al., 1989; Rue] & De Kloet, 1985; Vazquez, 1998). Regardless, both MR3
and GRs respond to levels of circulating GCs by inhibiting the release of CRH in the
HPA axis at its source, namely, the hypothalamus. Given this position, GCs and GRs are
“part of a complex signaling system between the external environment, the brain, and the
periphery” (Huznik et al., 2004, p. 121) which help to regulate the stress system.

Although the stress response system follows the same general pattern during

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pregnancy, there are some major distinctions fi'om the non-pregnancy state. The major
difference is that during pregnancy the circulating levels of CRH are estimated to be at
least 2-10 times higher than non-pregnancy levels (Huznik et al., 2004). One of the
reasons for this increased level is that unlike non-pregnancy states, during pregnancy the
placenta, deciduas, and fetal membranes also produce CRH (Huznik et a1., 2004; Grino et
al., 1987; Mastorakos & Ilias, 2003; Owen et al., 2005; Petraglia et al., 1996; Smith,
1999; van den Bergh et al., 2005). Although CRH produced by the placenta is
chemically synonymous to hypothalamic CRH, it is not regulated by the negative
feedback loop as in the normal HPA axis (Majzoub & Karalis, 1999; Challis, Matthews,
van Meir, & Rameriez, 1995). Instead, the production and regulation of CRH during
pregnancy operates in more of a positive feedback system (Majzoub & Karalis, 1999;
Challis et a], 1995).

There are several aspects to the positive feedback system; namely, the mother,
fetus, and the placenta each interact with one another to produce stress hormones.
Specifically, although the placenta individually produces CRH, maternal CRH production
also serves to potentiate placental production of CRH (Huizink, 2004; Kofrnan, 2002;
Linton et al., 1993; Mastorakos & Ilias, 2003). This in turn, increases both maternal and
fetal levels of corticosterone (cortisol in humans and primates). Fetal CRH is also
influenced by the production of placental CRH. Placental CRH, stimulates the fetal HPA
axis and thereby potentiates its production of cortisol. This serves to increase placental
CRH as well. Since placental CRH crosses both the maternal and fetal stress systems, it
serves to potentiate circulating levels of CRH and cortisol on both sides. This results in a

state of hypercortisolism that persists from around the 8th week of pregnancy and

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eventually peaks during the third trimester in preparation for birth in humans (Huizink et
al., 2004; Korte, 2002; Mastorakos & Ilias, 2003; Owen et al., 2005; Smith, 1999; van
den Bergh, 2005).

Fortunately, all the circulating cortisol from the mother does not reach the fetus
due to the presence of 11 B-hydroxy-steriod-dehydrogenase type 2 (1 lBHDS2) (Schoof,
Frobenius, Kirshbaum, Repp, Kneer et al., 2001; Seckl, 1997). Located in the placenta,
IIBHDSZ metabolizes some maternal cortisol. However, llBHDSZ can have large
variations between placentas (Welber, Seckl, & Holmes, 2001), so fetal exposure to
maternal cortisol can also vary. Nonetheless, even with llBHDSZ, maternal cortisol has
been shown to account for 33 — 40% of the variation in fetal cortisol (Gitau et al., 1998;
2001; 2003).

HPA and Offspring Development

Researchers examining this relationship have found that maternal stress hormones
mediate offspring stress responses. For example, Barbazanges et al. (1996) performed an
adrenalectomy and blocked corticosterone secretion in rodents. They then compared the
offspring of mothers exposed to PS with an intact stress system to mothers with blocked
corticosterone secretion. Results showed that when the pups were exposed to restraint
stress, pups of mothers with an intact system demonstrated an overall 30 to 70%
reduction of MR3 and GRs (respectively) at 21 and 90 days of age. They also exhibited
higher basal levels of circulating corticosterone and a longer activation of corticosterone
secretion than the blocked condition. Oddly, the pups in the blocked condition did not
display a reaction to stress. However, when pregnant mothers with the blocked

corticosterone system were injected with corticosterone, results were comparable to those

12

 

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with the intact system. This suggests that the presence of maternal corticosterone is
essential for the development of the offspring stress response. However, overexposure to
corticosterone can actually be detrimental to fetal and later adult development (Korte,
2002).

Weinstock et al. (1992) found that when pregnant rodent moms were exposed to
P8, their offspring had fewer GRs than non-PS rodents. In fact, in PS rats, the basal level
of corticosterone was 3x higher than in non-PS rats. This could be due in part to the
decreased GRs. In addition, they also engaged in more defecation and wall seeking when
placed in an open field test. Fride et al. (1986) found that the effects of PS persist over
time. When adult rats were repeatedly exposed to stress, corticosterone in non PS rats
ceased to rise after the 4th exposure, but corticosterone continued to rise until the 8th
exposure in PS rats. They also found that PS rats displayed initially higher releases of
corticosterone than non PS rats. Research has also shown that rats exposed to PS also
have higher morning basal levels of corticosterone than non PS rats (W einstock, 1997).

Similar results have also been found in humans and non-human primates.
However unlike rodents, human and non-human primate fetuses are afforded some
protection from maternal stress hormones. Specifically, the enzyme 11 B-hydroxysteroid
dehydrogenase (located in the placenta), binds to maternal cortisol and renders it inactive
(Huizink, 2004; Linton et al., 1993; Kofrnan, 2002; Mastorakos & Ilias, 2003; Suda et al.,
1988). In spite of this protection, there is still a strong linear relationship between
maternal and fetal cortisol (Gitau, Cameron, Fisk, & Glover, 1998), suggesting that a
significant amount of unaltered maternal cortisol continues to cross the placental barrier.

Considering that brain development in humans and non-human primates occurs

13

 

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mostly in-utero (Matthews, 2000), PS can have lasting effects on fetal development.
Work with rhesus monkeys has demonstrated that monkeys exposed to PS had higher
basal levels of cortisol than non PS monkeys (Clarke & Schneider, 1993). Other research
reported that at 4-years-of-age rhesus monkeys exposed to PS displayed enhanced ACTH
activity, but not cortisol activity in baseline or activation levels (Clarke, Wittwer, Abbott,
& Schneider, 1997). The physiological effects of stress have also been examined in
monkeys by externally administering ACTH during mid-gestation for a period of 14 days
(Schneider, Coes, & Lubach, 1992). This resulted in delayed motor development,
increased irritability, and shorter attention spans of 2-week-old infants. Other studies
found that baseline cortisol and ACTH were normal at 8 months but were elevated at 18
months in PS monkeys (Clarke et al., 1994; Schneider et al., 1998). Overall, the
literature suggests that PS has a significant impact on later development in both rodents
and non-human primates. Unfortunately most of these studies do not address the
postnatal environment; namely, they fail to address the impact of parenting behaviors on
infant development.
Postn_atal Stress and Parenting Offspring

Research has shown that stimulation during infancy has an enduring impact on
long term development in both humans and animals (Pfeifer, Rotundo, Myers, &
Denenberg, 1976). In his early studies of this effect in rats, Seymour Levine (1957)
found that when pups were removed from their nest and mildly shocked they exhibited,
as adults, lower levels ACTH. These animals also showed a greater ability to rapidly
habituate to novel situations (Levine 1960; Levine & Broadhurst, 1963; Levine,

Hallmeyer, Kara, & Denenberg 1966; Williams & Wells 1970;), were less susceptible to

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autoimmune diseases, and lived longer than non-manipulated rats (Levine, 1962). Even
as infants, the stimulated pups opened their eyes earlier, achieved motor coordination
sooner, and weighed more than the control group (Levine, 1960). Interestingly, these
effects were similar to those reported earlier by Wieninger (1954), who, instead of using
physical stress, “gentled” the pups by stroking them with the hand every day. The effects
that Levine observed were paradoxical because stimulation that was intended to be
painful and stressful, and which was hypothesized to produce negative long term effects,
instead, produced positive effects (see Pfeifer et al., 1976).

One of the first explanations of how early stimulation may affect subsequent
development was proposed by Levine (1962) and is now known as the “direct action
hypothesis.” He reported that, in one of his control groups, removing a pup from the nest
without further treatment showed the same beneficial effects on adult stress regulation as
that seen in the removal-plus-shocking group, and that, by comparison, it was the
undisturbed group which showed deficits. From these findings, he proposed that early
exposure to “noxious chronic stimulation” (including the stress of maternal separation),
modified the development of physiological systems that affect stress regulation in
adulthood (Bell et al., 1970). Although a direct effect of stimulation on the pups certainly
occurs, this hypothesis did not explain how aversive stimulation and non-aversive
stimulation could produce the same beneficial outcomes (Bell et al., 1970).

While conducting similar experiments, later research found that handling not only
disrupted the pups, but the mother as well (Bruno, Blass, Amin, 1982; Levine, 1967;
Levine & Mullins, 1966; Bell et al, 1970; Smotherman & Bell, 1980; Smotherman,

Brown, & Levine, 1977; Pfeifer et a1 1976). On this basis, it was proposed that the

15

 

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disruption caused by “the experimental stimulation of pups directly affects maternal
behavior and indirectly produces long-lasting effects on the behavior and physiology of
pups” (Smotherman, 1980, p. 169). This statement situates maternal behavior as the
primary mediating factor of handling effects, not the direct experience of handling on the
pups themselves.

The maternal mediation hypothesis emphasizes the fact that stressed pups bring a
different set of stimulation cues to the nurturing context that affects maternal behavior.
Specifically, it was found that upon return to the nest, pups emit increased ultrasonic
vocalizations (Bell et a1, 1970; Bruno et al., 1982; Hofer, 1987; Smotherman et al., 1970;
Smotherman & Bell, 1980) to which the mother responds by increasing pup-directed
behaviors such as nursing, nest building, licking, and grooming (Bell et al., 1970; Levine,
1960). It was further demonstrated that brief handling (removal of pups from nest) also
had a constant effect on mother-pup interactions that lasted throughout the neonatal
period (Bruno et al., 1970; Francis & Meaney, 1999; Levine, 1960; Levine & Mullins,
1966). As measured by increased CORT levels, studies have shown that handling stresses
not only the pups, but the dams a well. This increased stress is also reflected in maternal
grooming behavior. Specifically, mothers of handled and non-handled pups spend
relatively the same amount of time on the nest (Francis & Meaney, 1999; Smotherman &
Bell, 1980), however, only the dams in the handled groups spent the most time licking
and grooming their pups (Francis & Meaney, 1999; Smotherman, 1982). On the other
hand, extended periods of handing have been related to depression like symptoms in
dams where they engage in less pup grooming, more anxious behavior in novel

environments, less aggression in intruder tests, and fewer escape behavior (Boccia &

16

 

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Pederson, 2001; Boccia, Razzoli, Vadlamundi, Prasad, Caleffie, & Pederson, 2007).

Changes in maternal behavior have also been related to direct (non pup elicited)
stimuli. For example, when CORT was added to the drinking water of lactating dams, it
was positively related to maternal licking and grooming behavior (Rees, Pansear, Steiner,
& Fleming, 2004, 2006). Other work has directly exposed lactating dams to intruder odor
which not only increases maternal CORT but grooming behavior as well (Moles,Rizzi, &
D'Amato, 1994). Although studies of these offspring are not presently available in the
literatures, one can assume (based on what is known about maternal behavior and
offspring development) that these offspring experience the same benefits as other
offspring in the handled condition. In sum, this shows that stress can impact offspring by
direct exposure and indirectly via the dam.

While the maternal mediation hypothesis solved many questions, other questions
remained concerning the physiological mediation of the same effects. On this issue,
Meaney et al. (1992) determined that the receipt of increased maternal care causes an
increase in the GR receptor mRN A in the hippocampus via the release of serotonin
induced in this area by maternal handling and licking. This physiological change was
deemed crucially important because, as previously mentioned, GRs are directly involved
in the negative feedback loop that regulates the activity of the HPA axis.

Overall, these results show that parenting can mediate the relationship between
external stress and infant development. Unfortunately, most of the studies in this area are
restricted to rodents. This is problematic because unlike humans and non-human
primates, the rodent brain is only about 12% of its adult weight at birth (Clancy et al.,

2001 ). Therefore most of these effects cannot be generalized to other animal populations

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where the majority of brain development occurs in utero. In fact, since postnatal days 12-
14 are most comparable to near-term fetal development in humans (Clancey et a1., 2001),
it may be that the maternal mediation hypothesis model is a better predictor of PS rather
than postnatal stress in human and non-human primate populations. In addition, most of
these studies do not take the prenatal environment into account when examining postnatal
stress. Therefore, without considering both environments, the picture of stress and infant
development is not complete.
Prenatal Stress and ParentingOffspring

There is some research to suggest that the postnatal environment can moderate
abnormal emotional reactivity seen in PS animals (Meaney et al., 1989; Wakshlak &
Weinstock, 1990). Most of the work in this area has been conducted on rodents.
Maccari, Piazza, Kabbaj, Barbazanges, Simon and Le Moal (1995) examined the effects
of prenatal stress and parenting behavior in a cross fostering design. The researchers
placed PS rat pups with adopted mothers shortly after birth and compared them to pups
raised by the biological mother. They found that the adopted mothers displayed more
maternal behavior in the form of licking and grooming than biological mothers.
Consistent with the previous reports of maternal behavior, the adopted pups also showed
a decreased response of HPA activity than non—adopted pups. Other research has shown
similar results. Lordi, Patin, Protais, Meillier, and Caston (2000) found that rats exposed
to PS and then raised in an enriched environment had less anxiety in stressful and basal
conditions than PS rats in non-enriched environments. One reason for the difference
between adopted and non-adopted environments may be the effect that PS has on

postnatal maternal behavior. Specifically, Damaudery, Buee, Biltart, and Maccari (2004)

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found that mothers exposed to chronic stress during pregnancy displayed more freezing
and anxiety-like behaviors than non-stressed mothers. Unfortunately, maternal behavior
was not observed in this study. Therefore it may be that stress during pregnancy not only
alters fetal development, but it may have a lasting impact on postnatal maternal behavior.
Given this, it may be that postnatal parenting behaviors can serve to either attenuate or
potentiate the effects of PS.

Stress in Humans

Unfortunately stress in the human population cannot be as easily defined as it is in
the animal population. Defining stress based on the biological (Selye, 1956) or the
engineering model (Smith, 1987) fails to consider the multidimensionality of stressors in
humans (Lazarus, 1991; Wheaton, 1999). Researchers have defined stress in humans
according to external events, internal events, or as a combination of both (Aldwin, 1994;
Lazarus & Folkman, 1984; Pearlin & Schooler, 1978).

When stress is considered as an external event it typically refers to the occurrence
of a particular stressor (Aldwin, 1994; Lazarus & Folkman, 1984; Pearlin & Schooler,
1978). A stressful life event (or stressor) is defined as “a condition of threat, or structural
constraint that, by its very occurrence or existence, calls into question the operating
integrity of the organism” (Wheaton, 1999, p. 281). Stressors can be events such as the
death of a loved one, daily hassles, or domestic violence (Pearlin et al. 1981; Taylor,
Repetti, & Seernan, 1997; Wheaton, 1999). Depending upon the severity and/or the
occurrence of the stressor, it is classified as either a discrete, chronic, or traumatic life
event (Pearlin et al., 1981; Wheaton, 1999).

A discrete stressor is described as an event that has a clear termination but may or

19

may not possess a definite beginning (Wheaton, 1999). An example of a discrete stressor
would be the final day of work at a job an individual did not like. There may or may not
have been a set point at which the person began to despise the job, but the last day
signifies a clear termination of the stressor.

A chronic stressor on the other hand is defined by three criteria. Similar to a
discrete stressor, the first condition of a chronic stressor is that it does not necessarily
have a set beginning (Wheaton, 1999). Rather a chronic stressor leaves “the individual
feeling as if there is a problem but little understanding as to how it developed” (p. 283).
The second condition is that the stressor(s) be continuous in the sense that it occurs
within the “daily roles or activities” (p. 283) experienced in the normal life of an
individual. Finally, unlike discrete stressors which have a set ending, chronic stressors
can continue indefinitely. An example of a chronic stressor would be poverty (Ennis et
al., 2000; Pearlin et al. 1981). A person living in poverty may or may not know how they
came to be poor, but due to their condition they are faced with various stressors that
impact their daily life. Some of the stressors they face are associated with dwelling in
high crime neighborhoods, poor health care, fewer access to resources, lack of
employment opportunities, and other daily strains associated with this position (Ennis et
al., 2000; McLoyd, 1998).

The final category of stressors is referred to as traumatic events. Although events
in this category can occur as either discrete or continuous events, this category is separate
because of the severity of the event. Due to the magnitude of the stressor, traumatic
events are “thought to have greater potential for long-term impacts than most other

stressors” (Wheaton, 1999, p. 285). An example of a traumatic event would be physical

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abuse. If a woman experiences physical abuse once, this would be considered a discrete
traumatic stressor. However if she experiences physical abuse repeatedly over time, this
would be considered a continuous traumatic stressor. According to Wheaton, continuous
traumatic stressors are thought to be the “single most virulent form of stressful
experience” (p. 286).

Internal events or the strain placed upon an individual are also considered to be
stressors (Aldwin, 1994; Lazarus, 1983; Lazarus & Folkman, 1985; Pearlin & Schooler,
1978). The internal state of the organism can refer to the perception of stressfulness of an
event or the emotional state of the organism. For example, although the occurrence of an
event can be stressful, it also depends on how stressful an individual perceives the event.
Consider the death of a close relative. Generally many would think that this would be
stressful for a person to endure. However, what if the person never knew the relative or
what if they did not like them at all? In this case, the death of their relative may not be a
negative stressor at all, instead they may even be happy that the person died.

Another type of internal stressor is emotional distress. According to Lazarus
(1983), the state of depression or anxiety leads to certain cognitive appraisals of events.
For example, the state of depression or anxiety sets a person on cue to selectively take in
and perceive stimuli in a negative or threatening way (Beck, 1998). This constant intake
of negative or threatening information eventually strains the organism and becomes
harmful over time (Selye, 1974).

The transaction between internal and external events is also considered to be an
essential aspect of stress. According to Lazarus and Folkrnan (1984) stress is the “person

environment-transaction.” Specifically in the transactional model it is theorized that

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stress is the balance between the occurrence of the event, how the event is appraised, and
how one emotionally responds to or views the event.

Each of these types of stress are plausible indicators of stress for humans.
However, none of these definitions considers stress within the context of the HPA axis.
As previously mentioned, the HPA axis is aroused when an organism perceives a
stimulus to be threatening (Kalat, 1998; Korte, 2001). Given this, it seems that it is not
necessarily the occurrence of an event that matters; rather it is also how the person
responds to the event that leads to activity of the HPA axis. Therefore, it may be that the
best definition of stress considers all of these events as in the Lazarus and F olkman
(1984) model, but instead focuses on the perception of stressfirlness of discrete, chronic,
or traumatic events rather than simply relying on their occurrence. Further, given that the
perception of the event is influenced by mental stress such as anxiety and depression, it
would also seem that this construct is important to include in a physiological definition of
stress as well. Unfortunately though, this definition of stress which focuses on the
general stress perception, stress appraisal of life events or daily hassles and mental stress
has not been widely explored in research within this population. Instead, the more
traditional definitions of stress (individually examining depression, anxiety, life events or
daily hassles) have been used to examine the impact of PS on fetal, birth, early infant,
and adult outcomes using both retrospective and prospective designs.

Prenatal Stress and Fetal Outcomes. A variety of stressors during pregnancy have
been found to correlate with a variety of fetal responses. For example, Van den Bergh
(1990) examined anxiety during the 37th and 40th weeks of pregnancy. She also measured

fetal motor responses via ultrasound. Results showed a significant association between

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high levels of anxiety and fetal movement. Unfortunately, this study had a small sample
size (N=30) and used a self reporting format without controlling for pregnancy
complications, therefore these results have several confounders and may not generalize to
the larger population. Groome, Swiber, Bentz, Holland, and Atterbury (1995) also
examined anxiety in a sample of pregnant women and fetal behavior through an
ultrasound. Unlike Van den Bergh (1990), they found that mothers who were high in
anxiety had fetuses who exhibited fewer body movements and more sleep than other
fetuses.

Other research has examined PS and fetal heart rate. Monk, F ifer, Myers, Sloan,
Trien, and Hurtado (2000) examined anxiety during the 3rd trimester and fetal responses
in 20 women. Using the Stroop color-word task to induce stress, the investigators
examined the effect of PS on maternal and fetal heart rate. When examined as a whole
there was no connection between maternal anxiety and fetal heart rate. However, when
the sample was split into high and low anxiety, the fetuses of mothers in the high anxiety
group exhibited significantly higher heart rates when presented with the Stroop test.
Though with the low sample size this study may not have been able to replicated.
DiPeietro, Costigan, and Gurewitsch (2003) found similar results when they examined
women at 24 and 36 weeks at gestation. Results showed that induced maternal stress
from the Stroop color-word task was associated with increased variability in fetal heart
rate and suppression of motor activity. Although it did not control for other confounders
such as income or other health related outcomes, this study performed baseline and

manipulation measures of fetal movement on 137 women. Overall, these studies exhibit a

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connection between the maternal experience of stress during pregnancy and its impact on
fetal behaviors.

Prenatal Stress and Birth Outcomes. PS has been most widely studied in regards
to birth outcomes. In this literature, stress is conceptualized as the occurrence of a
stressor (DaCosta, Brender, & Larouche, 1998; Hedgaard, Henriksen, Scher, Hatch, &
Sabroe, 1996; Hobel, Dunkel-Schetter, Roesch, Castro, & Arora, 1999; Wadhwa,
Sandman, Porto, Dunkel-Schetter, & Garite, 1993), the perception of a stressor (Sable &
Wilkinson, 2000), how one emotionally responds to stress (Hobel et al., 1999;
Killingsworth, Rini, Dunkel-Schetter, Sandman, & Wadhwa, 1999; Wadhwa et al., 1993),
or a multidimensional concept that includes all of the above (Lobel, Dunkel-Schetter, &
Scrimshaw, 1992; Huznik et al., 2003).

The examination of life events during pregnancy and its association with birth
outcomes is one of the most common approaches used in this area. Most approaches rely
on the total number of life events experienced during a set time (Lobel, 1993). There are
some reports that demonstrate a relationship between these stressors and birth outcomes
(Brandt & Neilson, 1992; Gunter, 1963; Newton, Webster, Binu, Maskrey, & Phillips,
1979; Suarez, Cardarelli, & Hendricks, 2003) while other reports do not support this
finding (Aurelius et al., 1984; Ching & Newton, 1983; Hedegaard et al., 1996; Mutale,
Creed, Maresh, & Hunt, 1991; Obel, Hedegaard, Henriksen, Secher, & Olsen, 2003). For
example, Paarlberg et al. (1999) found that daily hassles experienced during the 1St
trimester were associated with low birth weight. Newton and Hunt (1984) examined total
life events during the third trimester and found that they were related to preterm delivery

as well. In another study, Brandt and Nielson (1992) examined the impact of chronic

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work stress during pregnancy and birth outcomes. They found that these women were at
risk for lower birth weight, spontaneous abortion, as well as stillbirth.

Traumatic stress also has an impact on birth outcomes. Glynn, Wadhwa, Dunkel-
Schetter, Chicz-DeMet, and Sandman (2000) found that the traumatic stress of
experiencing an earthquake during pregnancy was associated with shorter gestational
length. Specifically, women who experienced the earthquake early in pregnancy were
more likely to deliver premature than late gestation exposure. Other research by Hansen,
Lou, and Olsen (2000) found that women who experienced the death of an older child
during the 1St trimester of pregnancy, were more likely to have children with cranial
malformations.

Some studies, though, have found contradictory results. Hedegaard et a1. (1996)
used a prospective design with a Danish sample to examine stressful life events during
the 16‘h and 30th week of pregnancy and preterm delivery. They found that the
experience of life events was not associated with preterm delivery. Obel et al. (2003)
also examined a Danish population of 4638 pregnant women. They found that life
events were not associated with decreased head circumference at birth. Given the
location of this population it is possible that these studies may not generalize to other
countries. Overall, the literature is very much divided on the impact of life event stress
and birth outcomes. One possibility for this may be flaws in the studies that impact their
ability to detect significant associations. These studies each examine different types of
stressors and birth outcomes, so the results do not generalize to all life events or
outcomes. It is possible that certain life events (i.e., discrete, chronic, or traumatic

stressors) are each individually associated with specific types of birth outcomes.

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How a stressor is perceived also has an impact on birth outcomes. For example,
although Hedegaard et al. (1996) did not find an association between the occurrence of
life events and birth outcomes, they did find that individual appraisal of the event was
associated with risk for preterm delivery. However, since this was a self-report design
rather than a combined standardized interview and self-report methodology, it is difficult
to determine if the same results would have been produced. Sable and Wilkinson (2000)
used a retrospective design to examine perceived stress during pregnancy. They found
that women who perceived that stress occurred during most of their pregnancy were 1.5
times more likely to deliver very low birth weight babies than other mothers who did not.

There is also a body of literature that examines the relationship between
emotional state of the mother and birth outcomes. In general, depression is the most
frequently reported mental health problem for women (Weisman, Bruce, Leaf, F lorio, &
Holzer, 1991; Kessler, McGonagle, Zhao, Nelson, Hughes, Eshleman, et al., 1994). The
estimated lifetime prevalence for depression in women is between 10.2% (Weisman et
al., 1991) and 21.3% (Kessler et al., 1994). During pregnancy though, roughly 25 - 30%
of women display elevated symptoms of depression (Klein & Essex, 1994/1995).
Hoffman and Hatch (2000) assessed depression in each trimester of pregnancy for a
sample of women. They found that in poor women, depression during the 28th week of
pregnancy was associated with decreased birth weight and may be related to restricted
fetal growth. Within 24 hours of birth, studies have shown that babies born to depressed
mothers show less activity, less endurance, longer time to habituate to visual stimuli, and
more irritability than babies of non-depressed mothers (Abrams, Field, Scafidi, &

Prodromidis, 1995; Field, 1995; Hernandez-Reif, Field, Diego, & Largie, 2002).

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Anxiety however, is the most widely examined emotional state during pregnancy.
Rini, Dunkel-Schetter, Wadhwa, and Sandman (1999) examined the combined
contribution of pregnancy-related anxiety and state-trait anxiety during the 22nd to 28th
week of pregnancy on 230 Hispanic and White women. They found that women who
experienced higher anxiety during pregnancy were more likely to experience preterm
delivery than women with lower anxiety. Wadhwa et al. (1993) sampled women who
were between the 22"d and 28th week of pregnancy. They found that anxiety was
associated with gestational age and preterm delivery. Unlike most studies both of these
used an ethically diverse primarily low income population. Although both examined
birth records and used self-report, neither study controlled for income differences within
their population. This is important because low income women may not have access to
services like other women, this in turn could impact their delivery complications. Other
studies that examined anxiety during pregnancy also found a relationship with birth
outcomes. For example Dayan et al. (2002) examined anxiety during the 20-28‘h weeks
of pregnancy. They found that anxiety was related to preterm labor. Page] et al. (1990)
found that anxiety during pregnancy was related to 5 minute APGAR scores but not to 1
minute scores or birth weight.

Based on the Lazarus and Folkman (1984) theory, some researchers have used a
multidimensional conceptualization of stress to examine its relationship to birth
outcomes. Lobel et a1. (1992) used the combined standardized score of number of life
events, total life event distress, anxiety, and general perceived stress during pregnancy to
represent the latent stress variable. They found that although the number of life events

was not related to birth outcomes, life event distress, anxiety, and general perceived stress

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was significantly related to low birth weight and preterm delivery. Wadhwa et al. (1993)
used a similar technique and combined daily hassles, chronic stress, and perceived stress
into one score. The results revealed that the combined life events score was related to
low birth weight. However, these results were correlational and therefore, did not take
other confounding variables into consideration. Recent work by Dole, Savitz, Picciotto,
Siega-Riz, McMahon and Buekens (2003) also examined anxiety, life events, and general
perceived stress during the 24th and 29‘h week of pregnancy. They found that women
who experienced anxiety were more likely to deliver prematurely. In addition women
who experienced anxiety and high perceived stress were also at risk for preterm delivery.
Overall these studies show that PS is related to delivery complications.

Pren_atal Stress and Infant Outcomes. PS is also associated with infant and child
development. For instance, Allen, Lewinson, and Seeley (1998) examined the infants of
mothers who experienced emotional difficulties during pregnancy. These infants were
almost 2.5 times more likely to exhibit disruptive disorders than other infants. Currently
there are a few studies that have examined PS and infant outcomes using a prospective
design. Van den Bergh (1990) examined anxiety during late pregnancy and later infant
temperament. Results demonstrated that anxiety during pregnancy was significantly
correlated with difficult temperament at 10 weeks and again at 7 months. Anxiety during
the last trimester of pregnancy and infant behavior at 1 year and again at 2 years, revealed
similar results (Brouwers, van Baar, & Pop, 2001). After accounting for income,
smoking and alcohol use, and depression during pregnancy, prenatal anxiety was related
to poor attention and reactivity at 1 year of age. PS accounted for 22% of the variance in

decreased mental development at 2 years of age. Huizink et al. (2002) examined a

28

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combined measure of PS as a predictor of infant temperament at 3 and 8 months. After
accounting for pre and postnatal depression, they found that prenatal anxiety accounted
for 3.8% of the variance in attention regulation in 3 month old infants. Perceived stress
accounted for 8% of the variance in difficult behavior at 3 months. The prenatal anxiety
and perceived stress together accounted for 5% of the variance in attention at 8 months.
O’Connor, Heron, Golding, and Glover (2002) also examined anxiety during the last
trimester of pregnancy in almost 8,000 women. Controlling for pregnancy and delivery
complications and alcohol and smoking, they found that children of mother’s in the top
15% of anxiety at 18 or 32 weeks were at least 2 to 3 more likely to emotional or
behavioral problems that were more that 2 standard deviations above the mean. The data
here shows that the effects of PS also extend to into infancy.

Prena_tal Stress and Childhood and Adolescent Outcomes. Unfortunately the
majority of the studies that have examined PS and later child outcomes are conducted
using a retrospective design. The impact of prenatal stress is also present in later
childhood. For example, Laucht, Esser, Baving, Gerhold, Hoesch, Ihle, Steigleider et al.
(2000), examined later child development in 8 year olds and found that mothers exposed
to psychosocial stress during pregnancy had children who experienced a higher number
of attentional difficulties than other mothers. McIntosh, Mulkins, and Dean (1995) found
similar results. Specifically, mothers of children diagnosed with Attention Deficit
Hyperactivity Disorder (ADHD) experienced more psychological stress during pregnancy
than mothers of children without ADHD. Notably this study was conducted using survey

data from a retrospective report, which by its nature has many biases.

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These findings also extend to older children. O’Connor et al. (2003) (using the
same analysis format as previously stated), found that high levels of maternal PS and
maternal prenatal anxiety levels, predicted parent reported inattention and hyperactivity
in boys, conduct problems in girls, and behavior/emotional difficulties in both boys and
girls, up to age six years. Using the same sample, O’Connor (2005) also found that
prenatal anxiety predicted behavior difficulties in pre-adolescent children. In 14-15 year
old children, van den Bergh et al. (2005) used a prospective design and reported that
children of mothers who had high prenatal stress at 12 to 22 weeks displayed more
impulsivity on cognitive tasks at age 14-15 years than children without prenatal stress
exposure. Overall, these studies provide evidence that the emotional state of the mother
significantly contributes to infant and later child development.

Prenatal Stress and Adult Outcomes. There is a growing body of literature that
attributes prenatal stress in humans to later adult development. One of the key studies on
this topic utilized a retrospective design to associate prenatal famine with later affective
disorders in adults (Brown, Van Os, Driessens, Hoek, & Susser, 2000; Van Os & Selten,
1998). Based on a cohort that was exposed to the Dutch famine, the researchers found
that individuals exposed during the second and third trimester of pregnancy were more
likely to develop affective disorders than non-exposed individuals or those exposed
during the first trimester. The major limitation of these studies is that they each employ a
retrospective design. Although there are many issues associated with retrospective
designs, one significant drawback is that “a significant correlation between life events
and birth outcomes may indicate merely that adverse birth outcomes cause increased

reporting of life events” (Lobel, 1993, p 234). In addition, the results may be a function

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of famine rather than stress per se. Nonetheless, these studies provide some evidence
(albeit weak at best) that stress experienced by the mother during pregnancy also affects
the child. This now raises the question of how psychosocial stress experienced by the
mother is transmitted to the baby.

Stress and the HPA in humans

Since PS has been linked to problems with emotional and attention regulation in
infancy (de Weerth et 1a., 2003; Dunkel-Schetter, 1998; Huizink et al., 2002; Lou et a1.,
1994; Meijier, 1985; Mohler, Parzer, Brunner, Wiebel, & Resch,, 2006; O’Connor et al., 2002;
Paarlberg et al., 1999), childhood (Brouwers et al., 2001; Laucht et. Al., 200; McIntosh et
al., 1995; O’Connor et al., 2005) adolescence (O’Connor et al., 2003; 2005; van den
Bergh et al., 2005) and in adulthood (Brown et a1, 2000; Van Os et al., 1998), the areas
responsible for this behavior and therefore, most likely to be impacted by cortisol is the
limbic system.

The limbic system holds among other structures, the amygdala, hippocampus and
hypothalamus (Campbell, Mitchell, & Reece, 1997; Elliot, 1999; Shaffer, 1999,
Weinstock, 2001). It works in emotional regulation, attention, and memory. As
previously mentioned, GC receptors are located within various brain structures (Korte,
2002; Maccari et a1., 2003; Mastorakos & Ilias, 2003; Ratka et al., 1989; Ruel & De
Kloet, 1985; Vazquez, 1998; Weinstock, 2001), but the highest concentration is in the
hypothalamus, hippocampus, and pituitary (Korte, 2002; Maccari et a1., 2003;
Mastorakos & Hias, 2003; Ratka et al., 1989; Rue1& De Kloet, 1985; Vazquez, 1998). In
the animal literature, there have been documented associations between decreased GC

receptors in the amygdala and hippocampus and prenatal corticosterone exposure (Korte,

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2002; Francis et al., 1996; Francis & Meaney, 1999; Maccari et al., 2003; Mastorakos &
Ilias, 2003; Meaney et al., 1996; Owen et al., 2005; Tsigos & Chrousos, 2002;Vazquez,
1998; Weinstock, 2001). At present, there are no published comparable studies to
demonstrate this reduction in the human fetus. So an alternate way to assess this
possibility, is by examining the rate of fetal brain development in animals as compared to
humans.

The development of the fetal rat brain is similar to a developing human fetal brain
up to days 22-23 in the rat and weeks 16-17 (late 1St and early 2“d trimester) for a human
(Bayer, Altman, Russo, & Zhang, 1993). In the rat brain, the hypothalamus,
hippocampus, and amygdala are structurally formed from day 13 to 19 (Bayer et al.,
1993; Weinstock, 2001). In humans however, these areas are structurally developed from
week 5 to 19. However, refinement of these structures (i.e. development of dentate
granule cells of the hippocampus) is not completed until week 32 (mid 3rd trimester). By
the 7th month, most cell migration and differentiation has occurred (Bush, Lou, & Posner,
2000; Paus, 2001; Bourgeois, 1997; Levitt, Reinoso, & Jones, 1998; Rakic, 2002;
Weaver, la Plante, Weaver, Parent, Sharrna, Diorio et al., 2001). Afterwards mylenation
and synaptic development of the cells continues into adolescence. So depending on the
timing of exposure, cortisol can alter the development of early structural components of
the fetus, the development of more refined imbedded structures, or the mylenation
process. However, continued exposure to stress could impact all of these areas. So the
published reports of difficulties with attention and emotional regulation in infancy and
into adolescence following PS (Brouwers et al., 2001; de Weerth et a1., 2003; Dunkel-

Schetter, 1998; Huizink et al., 2002; Laucht et. al., 2000; Lou et al., 1994; McIntosh et

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al., 1995; Meijier, 1985; O’Connor et al., 2002; 2003;2005; van den Bergh et a1., 2005),
is likely mediated by prenatal stress hormone exposure to these parts of the fetal brain.

As previously mentioned, research in animals has documented that the experience
of stress is associated with the arousal of the HPA axis (Barbazanges et al.,1996; Korte,
2002; Schneider, Coes, & Lubach, 1992; Sapolsky, 1997; Weinstock et al., 1992). This
has also been documented in pregnant women as well. For example, Wadhwa, Dunekl-
Schetter, Chicz-DeMet, Porto, and Sandman (1996) examined the association between
HPA activity and stress in a sample of pregnant women. Using the multidimensional
approach to stress discussed earlier, researchers recruited pregnant women at or before 28
weeks of gestation and assessed life events, perceived stress, chronic stress, daily hassles,
social support, pregnancy anxiety, and personality during their prenatal visit between the
28m and 30‘h week of gestation. In addition, hormonal levels of ACTH and cortisol were
also assessed. Data analysis showed that perceived stress was significantly correlated
with ACTH (r= .44). Multiple regressions (controlling for demographic and personality
variables) that combined the stress and social support variables predicted 36% of the
variance in ACTH and 13% in cortisol. However, when time of blood draw was added,
these variables accounted for 22% of the variance in cortisol. It important to note that
pregnancy and delivery complications were not taken into account in these analyses, and
therefore may be confounds to the results.

PS stress hormones and fetgl development. Using the animal literature as a
model, it is now believed that the HPA axis serves to mediate the relationship between
maternal stress and infant development in humans as well (Dodic et al., 2002; Huznik et

al., 2004; Maccari et al., 2003; Matthews, 2000; Nyirenda & Seckl, 1998; Owen et al.,

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2005; Sapolsky, 1997; Wadhwa et al., 2001). Gitau and Glover (2003) examined the
acute stress caused by intrauterine needling on maternal and fetal CRH concentrations
during gestational age 17 to 38. They found that maternal and fetal levels of CRH were
significantly correlated with each other. Other work by Gitau et al. (1998) also found a
linear relationship between maternal and fetal cortisol. In fact, maternal cortisol in this
sample accounted for 40% of the variance in fetal concentrations.

As discussed previously, the presence of CRH during pregnancy serves two main
functions. One function is its role in the stress response feedback loop (Majzoub &
Karalis, 1999; Challis et al., 1995). It also firnctions as a natural process that assists with
the timing of delivery (Korte, 2002; Lockwood, 1999; Majzoub & Karalis, 1999;
Mastorakos & Ilias, 2003; Owen et al., 2005; Petraglia et a1., 1992; Sandman et a1., 2002;
Smith, 1999; van den Bergh, 2005). Specifically, levels of cortisol gradually rise across
pregnancy and eventually peak during the third trimester in preparation for parturition.
Although there are many benefits to this natural rise in cortisol, one of its functions is to
initiate lung maturation of the fetus (Haram, Mortensen, & Wollen, 2003). The
importance of this process is most easily seen in women at risk for preterm delivery.

Women who are between 23 and 34 weeks of gestation and at risk for preterm
delivery are typically given 2 doses of 12mg betarnethasone or 6mg dexamethasone (a
synthetic stress hormone) to help facilitate fetal lung development and prevent respiratory
distress syndrome (RDS) (Haram et al., 2003). However as seen in other research where
high levels of stress hormones are related to neuronal deficits in animals (Barbazanges et
a1., 1996; Korte, 2002; Schneider et al., 1992; Weinstock et al., 1992), too much

dexamethasone can result in marked atrophy of hippocampal cells (Uno et al., 1994) as

34

 

 

well as decreased birth weight and head circumference in newborns (French, Hagan,
Evans, Godfrey, & Newnharn, 1999).

Given its influence on delivery, it is not surprising that high CRH levels during
gestation are also correlated with an increased risk of preterm delivery (Glynn, Wadhwa,
& Sandman, 2000; Mastorakos & Ilias, 2003; Ruiz, Fullerton, Brown, & Dudley, 2002;
Smith, 1999; Wadhwa et al., 1996; Welber & Seckl, 2001). For example, Wadhwa et al.
(1998) examined CRH of women who were between 28 and 30 weeks of gestation.
Results demonstrated a significant negative relationship between CRH and gestation
length. In addition, CRH was positively correlated to preterm delivery (r=.48). Hobel et
al. (1999) also examined CRH during pregnancy. They focused on CRH, cortisol, and
ACTH levels between 3 time periods: 18 to 20, 28 to 30, and 36 to 38 weeks of gestation.
In addition, researchers also included self report measures of perceived stress and
anxiety. Women with high CRH and ACTH levels across all three time periods were
more likely to experience preterm delivery than women who did not. Cortisol at 18 to 20
weeks and 28 to 30 weeks was also related to preterm delivery. Analyses also revealed
that maternal stress at 18 to 20 weeks of gestation accounted for a significant amount of
variance in CRH levels at 28 to 30 weeks of gestation.

Prenatal stress hormones and infant development. Stress hormones during
pregnancy also affect fetal and infant development as well. Sandman et al. (1998)
examined CRH concentrations in mothers and their fetuses between the 31St and 32nd
week of gestation. Results showed that fetuses of mothers with high concentrations of
CRH did not respond to a novel stimulus repeated over time. According to the

researchers, the “dishabituated response” of the fetus to the stimulus implies that CRH

35

 

.7“:
'1'.)
(1:1

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has a direct influence on learning and memory associated with the parahippocampal
region of the brain. There is also some evidence that this carries over into infancy and
childhood as well.

Ponirakis, Susman, and Stiftler (1996) examined morning salivary cortisol during
pregnancy and infant outcomes in a sample of adolescent women. Researchers assessed
the women at 16 weeks of gestation, at 32-34 weeks of gestation, 24 hours after birth, and
at 4 weeks postpartum. Data analysis revealed that women with overall higher levels of
cortisol during pregnancy delivered infants who were more likely to need resuscitation at
delivery. However, only maternal cortisol during early pregnancy (16 weeks gestation)
was a significant predictor of lower infant APGAR scores at l and 5 minutes. de Weerth
et al. (2003) also examined maternal cortisol during pregnancy. Infant temperament was
assessed across postnatal week 1 through 20 using videotaped bathing sessions;
temperament questionnaires were also completed during weeks 7 and 18. Mothers were
divided into high and low cortisol groups based on a prenatal assessment conducted at 36
weeks of gestation. Mothers in the high cortisol group were more likely to deliver early
as well as have infants who displayed more crying, fussing, and negative facial
expressions than mothers in the low cortisol group. Obel et al. (2005) examined life
stress and cortisol during early, mid, and late pregnancy. Results showed that evening
cortisol levels of women with more than one life stressor were 27% higher than women
without one life stressor.

Psycholog'cal stress, hormones. and infant outcomes. Other researchers have also
included measures of maternal psychological stress and hormones in their analysis. For

example, Lundy et al. (1999) examined depression with a clinical structured interview

36

 

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and cortisol using urine in a sample of pregnant women. They found that depressed
mothers not only had higher cortisol levels (average: 400.05ng/mg depressed vs
269.17ng/mg non-depressed) but their full term newborn infants also exhibited high
cortisol levels (average: 562.07ng/mg vs 348.20ng/mg) as well. Further analysis of the
infants also revealed that infants of depressed mothers, compared to those without
depressed mothers, were more withdrawn, had more abnormal reflexes, and more
difficulty orienting to new objects. Field, Diego, Dieter, Hernandez-Reif, Schanberg,
Kuhn et al. (2001) compared nondepressed mothers with withdrawn or intrusive mothers
on their prenatal cortisol, dopamine levels, and on neonatal outcomes in full term infants.
Results showed that compared to non-depressed mothers, withdrawn mothers had higher
cortisol levels during pregnancy and their newborns also had higher cortisol levels and
the most asymmetrical EEG patterns. Newborns of depressed mothers also had lower
scores on the Brazelton infant development scale.

Other researchers have examined the relationship between anxiety and hormones
on infant development. For example, Vaughn, Bradley, J offe, Seifer, and Barglow
(1987) examined anxiety and maternal hormones during pregnancy and infant
temperament at 4 months. Unlike the previous studies, investigators found that ACTH
measured during the 3lrd trimester was not related to later infant temperament. However,
anxiety during pregnancy was significantly correlated with difficult infant temperament
at 4 months.

Field, Diego, Hernandez-Reif, Scanber, Kuhn, Yando, and Bendell (2003)

examined anxiety and comorbid depression in addition to urinary hormonal levels during

the second trimester in a sample of women with self-report and observer data. They

37

 

 

watt.

‘5‘

Pm"-
\

found that women who reported high anxiety also experienced high levels of depression.
Results also showed that compared to fetuses of low anxious mothers, high anxious
mothers were significantly more active and had smaller abdominal circumferences.
Mothers with high anxiety also had high norepinephrine and low dopamine levels during
pregnancy, there were no significant differences in cortisol. Their newborns had
significantly low vagal tone and levels of dopamine and serotonin but no differences in
cortisol. A sleep assessment, demonstrated that these infants also spent more time in
deep sleep and less time in quiet and alert states. Given the occurrence of prenatal of
stress, it stands to reason that these stressors may continue into the postnatal period, also
affecting infant development. Unfortunately these studies did not consider the possible
confound of the postnatal environment on infant development.
Postnatal Stress in Humans

Research has shown that postnatal emotional stress experienced by the caregiver
significantly contributes to infant and child development (Field, 1998; Shaw, Vondra,
Homrnerding, & Keenan, 1994; Weissman, Prusoff, Gammon, 1984; Lyons-Ruth, Wolfe,
& Lyubchick, 2000). One of the earliest studies on this topic examined 8 month old
infants of anxious mothers (Davids, Holden, & Gray, 1963). Using the Bayley Scales of
Infant Development, they found that infants of highly anxious mothers were more likely
to have lower scores on the Bayley than low anxious mothers. Other studies have
extended these findings. Specifically, infants of anxious women are more likely to be
irritable, sleep poorly, be more active, and be less responsive than infants of mothers with
low anxiety (Farber, Vaughn, & Egeland, 1981; Warren, Gunnar, Kagan, Anders,

Simmens, Rones et al., 2003; Ferriera, 1960). Observational studies of infants of

38

 

 

 

 

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bl

depressed mothers have documented that at 3 months these infants display fewer facial
expressions, cry less, display fewer head orientations towards stimuli, and are more fussy
than infants of nondepressed mothers (Martinez, Malphrus, Field, Pickens, Yando,
Bendell et al., 1997).

Emotional stress can also occur with other types of stressors to affect the infant as
well. For example, Righetti-Veltema, Conne-Perreard, Bosquet, and Manzano (2002)

examined postpartum depression and interactions between mothers and their 3 month old

infants. Depressed mothers experienced more negative life events, more professional and

financial restrictions, and overall had more worries since the birth of their infant. Infants

 

of depressed mothers cried more and had increased difficulty with eating and sleeping
and had fewer vocalizations than infants of nondepressed mothers. In addition, the
depressed mothers also reported less positive feelings about their infant. Based on the
caregiver experience of postnatal stress, it may be that his/her parenting behavior is also
compromised.
Parenting and Postnatal Stress

As discussed in the animal models, one of the mechanisms thought to mediate
postnatal stress is parenting behavior. Ideally, parenting behavior is the exchange of
interactions between the mother and the child. When babies cry, receptive mothers tend
to respond by feeding, changing, or soothing the child. Problems arise when the mother
is not responsive. In this case, when a mother does not respond to her child’s crying, the
child is unable to regulate his/her system (Hofer, 1987). Unlike the prenatal literature,
most of the research on postnatal stress and parenting focuses on maternal depression.

According to McFarland and Sanders (2003), the children of depressed mothers

39

__;—4k_gA

 

are exposed to a different parenting environment than those of nondepressed mothers.
Specifically, the environment these children experience is “characterized by lack of
responsiveness, higher levels of negative affect, and poor supervision” (p 41). Research
has shown that depressed mothers tend to have either a withdrawn or intrusive interaction
style (Cohn, Matias, Tronick, Connell, & Lyons-Ruth, 1986; Field, 1986; Tronick &
Field, 1986). One explanation for the restrictive parenting of depressed mothers may be
their inability to tolerate excessive activity (Cohn et al., 1986). There are many studies
that have supported this idea. For example, Martinez et al. (1997) reported that depressed
mothers demonstrated fewer facial expressions and a lower interaction rating regardless
of whether or not they were interacting with their own infant or an infant of a
nondepressed woman. Fleming, Ruble, Flett, and Shaul (1988) reported that depressed
mothers were less inclined to respond to their infant’s vocalizing than nondepressed
mothers. One of the seminal studies conducted in this area was carried out by Field
(1984). In this study, depressed and nondepressed women were recruited at the time of
delivery and followed up 3 months later with their infants. The researcher used a
“depressed” interaction where the mother pretended to be depressed and then a reunion
where normal affect was restored to examine how this simulation affected depressed and
nondepressed dyads. Results showed that across interactions, infants of nondepressed
mothers displayed more positive facial expressions, fewer negative expressions, more
vocalizations, and protesting than infants of depressed mothers. In addition, unlike
nondepressed mothers, the behavior of the depressed mothers in the interactions did not
change. These results suggest that the infants of depressed mothers are accustomed to the

depressive behavior of their mother and therefore do not react in an otherwise anxiety-

40

 

 

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provoking situation.

Unlike the previous studies, that only examined depression, recently some studies
have begun to examine parenting in other stressful states as well. Assel, Landry, Swank,
Steelrnan, Miller-Loncar, and Smith (2002) used a combined emotional stress score
(depression, anxiety, and anger) to assess emotional stress and parenting in 3 year old
children. Analysis showed that mothers who experienced higher levels of stress were less
warm and flexible in their interactions with their children. Interestingly, this study also
found that mild levels of emotional stress also affected parental sensitivity to their
children’s needs.

Warren et al. (2003) examined the infants of mothers with panic disorder. Based
on two samples of infants at 4 months and at 14 months, researchers examined parenting
behaviors, cortisol, infant sleep, and infant temperament. They found that the infants of
mothers with panic disorder did not show more reactivity, behavioral inhibition, or
ambivalent attachment. Instead they found that these infants exhibited higher cortisol
levels and more disturbed sleep compared to infants of non-panic disorder mothers.
Panic disorder mothers were also less sensitive to their infants than non-panic disorder
mothers. Together these studies show that both high and low levels of maternal
psychological stress can impact parenting and child behavior and physiology.

Prenatal stress. hormones and later outcomes.

 

To date there are only a handful of studies that have examined PS, maternal
physiology, and infant development while considering the postnatal environment.
Huizink et al. (2003) examined prenatal stress in early, mid, and late gestation in a

sample of healthy term infants and assessed infant development up at 3 and 8 months.

41

 

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They found that after controlling for postnatal depression and perceived stress, high
levels of pregnancy anxiety predicted lower mental and motor development among 8-
month-old infants. They also found that daily hassles in early pregnancy were related to
lower mental development scores on the Bayley at 8 months. This study also assessed
the influence of maternal physiology. Specifically, prenatal maternal salivary cortisol in
late pregnancy displayed an inverse relationship with motor and mental development
scores at 3 months. Guitteling, de Weerth, & Buitelaar (2004) using the same sample as
Huizink (2003), found that 4 to 6 year old children who were exposed to high levels of
morning cortisol had higher levels of cortisol after vaccination than other children.
Unfortunately these studies did not consider parenting behaviors that, as previously
mentioned, do influence infant outcomes.

Susman, Schmeelk, Ponirakis, and Gariepy (2001) conducted a longitudinal study
examining prenatal stress, postnatal stress, concurrent stress, physiology, and parenting
among 3-year-old children. They found that the children of women who experienced low
levels of hormones (cortisol, testosterone, and estradiol) during pregnancy, displayed
more verbal and nonverbal aggression than children of mothers in the high group.
Unfortunately this study did not individually distinguish between the hormones so it is
difficult to determine how they may independently impact later child deve10pment.
Another limitation of this study is that the influence of the postnatal environment was not
controlled in the analyses for PS. Therefore, these results should be interpreted with
caution, because they are confounded with the influence of either the pre or postnatal
enviromnent.

Rationale for the Present Study

42

 

 

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The purpose of this dissertation is to examine maternal cortisol as a mediator of
the relationship between PS experienced by the mother and infant regulation
development at 3 months. Over the past decades many researchers have speculated and
found support for the idea that maternal experience of stress during pregnancy can have a
lasting impact on infant development (de Weerth et a1., 2003; Dunkel-Schetter, 1998;
Huizink et al., 2002; Lou et al., 1994; Meijier, 1985; Paarlberg et al., 1999). Only
recently though have researchers identified the mechanism that may be responsible for
the transmission of maternal stress during pregnancy to the infant (Gitau et al., 1998;
Stewart et al., 1995).

According to the animal literature, the theorized mechanism is the maternal HPA
axis. Specifically, it is the maternal experience of stress and the subsequent arousal of
the HPA system that mediates the relationship between PS and offspring development
(Barbazanges et a1., 1996; Clark et al., 1997; Mastorakos et al., 2003; Schneider et al.,
1992; Weinstock, 1997). Although work with animals does not directly overlap with
human development, it does provide a solid basis for extrapolating the same model to
humans. Researchers have documented a possible direct relationship between maternal
cortisol during pregnancy and the fetus, infant birth outcomes and a relationship between
cortisol at delivery (French et al., 1999; Gitau et a1., 2001;Glynn et al., 2000; Haram et
al., 2003; Wadhwa et a1., 1996; Wadhwa et al., 2001) and later infant developmental
outcomes as well (de Weerth et a1., 2003; Field et al., 2001 & 2003; Huizink et al., 2002;
Lundy et al., 1999; O’Connor et al., 2004; Ponirakis et al., 1996; Sandman et al., 1998).
A relationship between maternal stress hormones and maternal stress has also been

identified (Arishima et al., 1977; Zarrow et al., 1970). Given the relationship among

43

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these variables and what is already known in the animal literature, it seems logical that
the maternal HPA axis may also mediate the relationship between maternal psychosocial
stress during pregnancy and infant outcomes (Dodic et al., 2002; Huznik et al., 2004;
Maccari et al., 2003; Matthews, 2000; Nyirenda & Seckl, 1998; Sapolsky, 1997; Wadhwa
et al., 2001). Unfortunately, the mediational role of the HPA axis has yet to be examined
within humans. In addition, most extant studies suffer from methodological problems.
For example, they often do not specify what times of the day cortisol was collected. This
is important because cortisol fluctuates based on a diurnal pattern where peak levels
occur in the morning. So depending on the time, the ability to detect significant
observable levels may vary.

Another important consideration is the postnatal environment. Research has
shown that postnatal stress experienced by the caregiver significantly contributes to
infant and child development (Davids et a1., 1963; Farber et al., 1981; Field et a1., 1998;
Lyons-Ruth et al., 2000; Shaw et al., 1994; Weissman et al., 1984; Warren et a1, 2003).
In addition, postnatal parenting behaviors can also be compromised by caregiver stress
(Hofer, 1987). This in turn can lead to dysregulation in infant regulatory behaviors (Field,
1984; Warren et al., 2003). Therefore considering the contribution of these variables in
the context of prenatal stress and infant regulation is essential.

The majority of work in the area of PS omitted the HPA component and focused
primarily on maternal stress during pregnancy or how stress during pregnancy influenced
delivery outcomes. Further, very few studies have gone beyond assessing delivery
outcomes to examine the lasting effects of PS on later infant development. The handful

of studies that have extended beyond this time frame are typically retrospective and

 

 

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correlational--methodologies which have inherent limitations. Therefore a critical
analysis of the maternal HPA axis as a mediator of PS and infant regulation development
is essential.

Another difficulty in this research is the multiple and imprecise definitions of
stress employed. In animal studies, the stressors are easily operationalized and examined.
Stress in humans, however, is harder to define. Stress has been defined as the occurrence
of external events such as life events or daily hassles or as internal events such as
perception of stress or emotional distress. However, given the complex multidimensional
nature of humans, stress does not consist of just one type of stressor, rather stress is the
combination of many individual events or states that a person deems or perceives to be
stressfiil (Lazarus & Folkman, 1984). The perception of stress is the pivotal factor
influencing transmission of mental stress to physical stress and the HPA axis. It is not
the occurrence of an event that produces a physiological reaction, rather it is how a
person perceives the event that matters (Kalat, 1998; Korte, 2001).

Overall, there appears to be several gaps in the current literature on the
mediational role of the HPA axis on PS and infant regulation. To address these gaps, the
purpose of this dissertation is to further the literature by examining PS and infant
regulation at 3 months examining maternal cortisol during pregnancy as a mediator.
Because cortisol is highest during the last trimester of pregnancy (Huizink et al., 2004;
Korte, 2002; Mastorakos & Ilias, 2003; Smith, 1999) and since this time period is thought
to be the most predictive of infant outcomes (Obel, Hedegaard, Henriksen, Secher, Olsen,
& Levine, 2005), women between 30 and 35 weeks of pregnancy will be examined.

The 3 month assessment of infant regulation was chosen for two primary reasons.

45

 

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For infants the time between 2 and 4 months is referred to as the “first biobehavioral
shift” (Emde, Gaensbaurer, & Harmon, 1976) because this is when changes in sleep
pattern, attention, and irritability emerge (see Barr, 1990; Berg & Berg, 1987).
Specifically, adult circadian rhythms emerge between 8 and 10 weeks of age (Castro,
Elias, Martinelli, Antonini, Santiago, & Moreira, 2000; Hanna, Jett, Laird, Mandel,
LaFranchi, & Reynolds, 1997; Jett, Samuels, McDaniel, Benda, LaFranchi, Reynolds, &
Hanna, 1997; Riad-Fahmy, Read, & Walker, 1983; Rokicki, Forest, Loras, Bonner, &
Bertrand, 1990). Therefore, infant regulation will be measured by infant temperament (to
assess irritability and attention) and infant sleep patterns. In addition, this study will
examine the diurnal pattern of maternal cortisol.

To this end, the present study used a prospective design to examine pregnant .
women in the last trimester of pregnancy and assessed how maternal cortisol mediates the
relationship between high versus low PS and infant temperament and sleep development
at 3 months. In addition, to clarify the nature of this relationship, the influence of
postnatal stress and parenting were also considered.

Hypotheses:

a. PS will have a direct effect on infant regulation.

b. PS will have a direct effect on cortisol.

l. Cortisol examination using A.M. and P.M. values will be viewed as
exploratory in nature so specific hypotheses are not provided.

0. Cortisol will have a direct effect on infant regulation.

(1. Cortisol will mediate PS and infant regulation.

e. PS have a direct effect on postnatal stress.

46

Postnatal maternal stress will have a direct effect on infant regulation.
Postnatal maternal stress will have a direct effect on parenting competency.
Parenting competency will have a direct effect on infant regulation.
Parenting competency will mediate postnatal maternal stress and infant

regulation.

47

 

SD=1

diff)

nerce

METHOD
Participants

At time 1, participants were 92 women ranging in age from 18 to 39 (M=26,
SD=5.3) and between 27 and 36 weeks of gestation (M=33, SD=1.89) at the time of
interview. Fifty-eight percent of the sample was single never married and forty-two
percent was married or divorced. F ifiy percent of women were White, 29% were Black,
8% of women were Latina, and the remaining 13% of women were Native American,
Asian/Pacific Islander, or Multi-racial. The median monthly income was $2,036 and
ranged from $0 to $8,000. Eighty-two percent of women were at least high school
educated. Twenty percent of women smoked during pregnancy. The average level of
A.M. salivary cortisol was 12.22 nmol/L (SD 7.78) with a range of .00 to 36.14 nmol/L.
The average P.M. salivary cortisol was 7.95 nmol/L (SD 7.43) with a range of 1.10 to
65.11 nmol/L. See Table l for details.

At time 2 when the infants were 3 months, seventy-one percent or a total of 65
participants returned for the study. The average age of the infant at the interview was 3.9
months ranging from 2.1 to 7.3 months (corrected for prematurity). Forty-nine percent of
infants were boys and fifty-one percent were girls. Twenty-eight percent of children
were Black, 34% were Caucasian, 27% were bi-racial, 4% were multi-racial, and the
remaining 4% were Asian and Latino. The average age of gestation at delivery was 39
weeks (range: 26-42). The average weight at birth was 7lbs. 9oz., ranging from 4lbs.
1402. to IOlbs. 9ozs. Ninety-one percent of births were considered full-term (37 to 42
weeks), 13% (N=8) were considered moderately premature (between 32 and 36 weeks),

and 2% (N =1) were considered extremely premature (before 28 weeks). There was an

48

 

 

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average of 4 health risk factors during pregnancy (i.e., diabetes, HIV, cancer, smoking,
etc). See Table 2 for details of the sample at T1 and T2 and procedures section for
details of the recruitment.

Measures

Demographics. A 22 item demographic questionnaire assessing ethnicity, marital

 

status, family income, occupation, and participant education was administered during
pregnancy. See Appendix A for a copy of the measure.

Maternal Health. Adapted from Bogat and Levendosky (1999), this is a 35-item
health questionnaire that assesses various chronic health conditions as well as pregnancy—
related health conditions. This measure was administered during pregnancy. For

661,,

example, participants are asked to answer with yes or no “2” if they “have ever been
diagnosed by a medical professional” with HIV, cancer, or gestational diabetes. See
Appendix B for a copy of the measure.

Physical Health Symptomatology (Cohen & Hoberman, 1983). This is a modified
version of the Cohen-Hoberman Inventory of Physical Symptoms. This l9-item
questionnaire assesses physical symptoms such as fatigue, coughing, muscle, or sleep
problems related to stress. This measure was administered during pregnancy to assess
physical health before and during pregnancy and postnatally to assess symptoms not
accounted for in the last month of pregnancy and postnatal symptoms. Each statement is
answered on a 5 point scale ranging from 0 “never” to 4 “3 or more times a week.” The
scale was modified to assess symptoms before, during and after pregnancy. Scores were

summed and can range from 0 to 76, the reported reliability of this scale .92. The

reliability for this sample was .90 at T1 and T2. See Appendix C for a copy of this

49

 

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measure.

Center for Epidemiolgical Studies Depression Scale (CES-D; Radloff, 1977).
The CES-D is a 20 item scale that is used to measure symptoms of depression during the
past week. Symptoms that are assessed in this questionnaire include guilty feelings,
hopelessness, changes in appetite, or sleep disturbances. This measure was administered
both pre and postnatally. Participants are asked to rate statements of how they have felt
during the past week. Examples of statements include “I felt depressed” or “I thought my
life had been a failure.” Each statement is ranked on a 4 point scale from 1 “Rarely or
none” to 4 “Most or all the time.” The results are then summed. Scores were summed
and can range from 0 to 60 the reported reliability of this scale was .95. The reliability
for the current sample was .80 at T1 and .79 at T2. See Appendix D for a copy of the
measure.

State-Trait Anxiety Inventory (STAI; Spielberger, Grousch, & Lushene, 1970).
The STAI is a 40-item inventory used to assess symptoms of state and trait anxiety. This
measure was administered both pre and postnatally. The scale has 2 subscales: state and
trait anxiety. The state anxiety scale measures transient anxiety at the time of
administration. The trait anxiety subscale measures stable anxiety. Examples of items
include “I feel nervous” and “I am calm.” Participants are asked to rate the intensity of
their anxiety on a scale from 1 “Not at All” to 4 “Very Much so.” Scores were summed
and can range fi'om 40 to 160, the reported reliability for this scale was .90. The
reliability for this sample was .95 at T1 and .93 at T2. See Appendix E.

Perceived Stress Scale (PSS; Cohen, Kamark, & Merrnelstein, 1983). The PSS is

a 13-item scale used to measure the degree of stressfulness of events in the last month.

50

 

 

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This measure was administered both pre and postnatally. This scale is designed to
measure how unpredictable, uncontrollable, and overwhelming daily events are to the
individual. Examples of items include “How often have you felt confident about your
ability to handle personal problems” and “How often have you been upset because of
something unexpected happening?” Participants are asked to rate these items on a 5-
point scale ranging from “never” to “very often.” Scores were summed and can range
from 13 to 52. The reported reliability for this scale is .94. The reliability for this sample
was 61 at T1 and .63 at T2. See Appendix F for a copy of the measure.

Life Experiences Survey (LES: Sarason. Johnson. & Siegel. 1978; This is an
adapted version of the original 49-item measure of life events. Items related to males,
becoming pregnant, or having an abortion were omitted in prenatal administration.
Becoming pregnant and having an abortion were included in the postnatal administration.
Participants are asked to indicate the time period in which the event occurred and then
rate the stressfulness of the event on their life. Examples of life experiences include
“divorce,” “death of close family member,” and “new job.” Participants are asked to rate
the impact of the event on a 4-point scale -3 “extremely negative” to 0 “no impact.”
Scores of stress were summed and can range from 0 to 60; the reported reliability
coefficient for the scale is .63. The reliability for this scale was .70 at T1 and T2. See
Appendix G.

DmlLHassles Questionnaire (DHQ: DeLongis, Coyne, Dakof, Folkman, &
Lazarus, 1982). This is an adapted version of the original 117-item scale that assesses
daily stressors. This measure was administered both pre and postnatally. Items related to

becoming pregnant were omitted for T1. Participants are asked to indicate daily hassles

51

such as “concerns about job security” or “not enough money for food” that have occurred
in the last month. They are then asked to rate the severity of the stressor from 0 “No
Impact” to 3 “Extremely Severe.” Scores are summed and can range from 0 to 342. The
reported reliability coefficient for the scale was .98. The reliability obtained from this
sample was .93 at T1 and .98 at T2. See Appendix H.

Birth. gegnancy. and delivery questionnaire (Bogat & Levendosky, 1998;
Spencer & Coe, 1999). This 39-item questionnaire was adapted from the original scales
and asks questions about chronic health conditions diagnosed in the last weeks of
pregnancy, delivery complications, and child health at 3 months. Women answer
questions that inquire about chronic health conditions in the mother during the last weeks
of pregnancy, length of delivery, and current child health with a yes or no. See Appendix
1.

Infant Care Scale (ICS: Frotman & Owen, 1989). The ICS is a 52-item scale that
measures maternal perception of efficacy regarding caring for their infant. Participants
are asked about knowledge of infant health, diet, and safety. Participants are asked to
rate their confidence in each item on a 5-point scale ranging from 1 “very little” to 5
“quite a lot.” Scores were summed and range from 52 to 260, the reported reliability of
this scale is .98. The reliability of the scale for this sample was .96. See Appendix J.

Infant Behavior Questionngire (IBQ; Rothbart, 1981), The IBQ is a 94-item
measure of infant temperament. The scale consists of 6 subscales: soothability, activity
level, distress to limitations, duration of orienting (attention), distress and latency to
approach, and smiling and laughter. Example of items include “during sleep how often

does your baby toss about in the crib” or “when face was washed how often did the baby

52

its or
"N81 Ci
reifa'nil

of the 5

lien] 01
Time:
3011ch
an. 13,
Q} of 1

fuss or cry.” Participants were asked to rate items on a 7 point scale ranging from 1
“Never” to 7 “Always.” Reported reliability for this scale ranges from .72 to .85. The
reliability of the 6 subscales for this sample ranged from .16 to .80. Since the reliability
of the soothability scale was .49 and the reliability of the distress and latency to approach
scale was .16 they were omitted from all analyses. This includes the following items: 9,
10, 11, 30, 33, 35, 42, 44, 45, 46, 50, 54, 61, 75, 76, 77, 79, 83, 84, 86, 88, 89, 90, 94).
See Appendix K.

Cortisol. During the prenatal period, two saliva samples (one morning and one
afternoon) were obtained from the women in one 24-hour period. Each participant was
instructed not to eat or drink 20 minutes before providing the sample. The time of saliva
collection was recorded for each sample. The first saliva sample was provided
individually by the woman 20 minutes after awakening in the morning on the scheduled
day of the interview. The second sample was obtained 20 minutes after the afternoon
interview began between the hours of 3:30 P.M. and 6:00 P.M.

Participants were asked to chew on the end of a straw or chew Trident gum for 1
minute to stimulate saliva flow. Using a straw, women dispensed a volume of 0.5 -1.0ml
of saliva into a container. Morning samples were refiigerated until the afternoon
interview. Both samples were then frozen at (-20°C) in a locked freezer and then
analyzed in duplicate using standard assay procedures discussed by Salimetrics, Inc.
(Pennsylvania State University) at Michigan State University. (See Appendix L for
instructions).

Infant Sleep (IS; Jones, 2004). This is a measure of infant regulation designed to

 

assess the most typical sleeping patterns of infants. Participants are asked to think about

53

the most recent and typical 24—hour period of sleep for their infant. Then, based on l-hour
time blocks over a 24-hour period, participants are asked to report whether their infant
was asleep or awake during a given block. Infants between 10 and 12 weeks of age (3
months) can be expected to sleep on average for 14 hours a day with 5 consecutive hours
occurring at night (Mayoclinic Staff, 2006). Therefore, sleep was defined based on total
consecutive night sleep from 7 pm. to 7 am. So each consecutive hour of sleep was
totaled to obtain one score for total consecutive night sleep from 7PM to 7AM.was
obtained (See Appendix M).

Procedure

A total of 92 women were interviewed during the 3rd trimester of their pregnancy
(T1), and 64 women returned for a second interview conducted when the infant was 3
months old (T2).

Recruitment Participants were recruited for the study through referral and fliers
placed at local OB/GYN offices, health department prenatal clinics, and other places that
offer pregnancy services. (See Appendix N). Women who were interested in
participating in the study were screened over the telephone for week of gestation during
pregnancy, health, and experience of domestic violence. (See Appendix N). Women
were excluded from the study if they were not singleton pregnancies, not between the
ages of 18 and 40, if they occasionally or often smoked or used other substances during
pregnancy, if they had health conditions that could negatively affect pregnancy, if they
experienced severe domestic violence, or if they had limited knowledge of the English
language. After meeting criteria and if she agreed to participate in the study, an interview

date and time were scheduled for the 1St interview. At this time, each woman was

54

 

 

pnnii
sample
A: the
rice Aj

up“ ,'
11.311

\- .K

'10 IOCEI

.v hut”-
“ 14.1.

till-UM.

assigned a subject number, which was kept separate from her identifying information.
The day before the scheduled interview at T1, women were contacted and personally
provided with a saliva sample collection packet. At this time, instructions regarding
sample collection were reviewed (See Appendix 0) and any questions were addressed.
At the time of the scheduled afternoon interview, each woman was given a consent form
(See Appendix P). Women were also asked for recontact information for the Time 2
interview (See Appendix Q). Recontact people were individuals who would know where
to locate the participant if she could not be located directly by the researcher. This
information was also kept in a separate locked file cabinet.

Cortisol samples were stored in a locked freezer and, upon analysis, the samples
were destroyed and the information obtained from the analysis was stored in a locked file
cabinet identified only by subject number. The assays were carried out in three runs using
reagents from the same lot. For each run the instrument was calibrated according to the
manufacturer’s instructions. Commercially prepared high, medium and low controls were
included in each run. The interrun Coefficients of Variability (CV’s) for the controls were
as follows: for the low control, 6.5%, for the medium control, 3.9%, and for the high
control, 6.8%. A single assay was performed on each sample and control since the
intrarun assay CV’s on this machine are reported by the manufacturer to be less than 5%.
All the samples had values within the reportable range and in terms of absolute.

Approximately, one week after the reported due date, participants were contacted
to confirm each infant’s date of birth, weight, length, and head circumference.
Participants were then contacted 11 weeks after the due date to schedule an interview for

the 2“‘1 assessment. The second assessment took place in the 3rd month postpartum

55

.
“r“
I".

k .

between weeks 12 and 16. Four attempts were made to reach each participant at the
initial postnatal contact and for the 2nd interview at 3 months. If these attempts were
unsuccessfiil within 1 week, a letter was sent to the woman’s home requesting her to
contact the office to set up an appointment. If participants could not be reached within
the 2nd week, the recontact people were contacted either by phone or letter to reach the
participant.

Data Collection and Data Entry. Ten undergraduates were trained to administer
both interviews. Each interviewer underwent 3 weeks of training to become competent
and reliable in interview procedures and troubleshooting through role-playing, shadowing
interviews, and other techniques. In addition, after training, each interviewer attended a
weekly meeting to address any concerns or problems experienced during interviews.
Each interviewer received Independent Study credits in exchange for their participation.

The above criteria also applied to the 3 undergraduates trained in data entry. Data
was double entered and each undergraduate maintained an average of 98% reliability on
data entry. Data was then correlated to check for any inconsistencies and data was
cleaned to 100% accuracy.

RESULTS
Initial Data Construction

Imputation. All data analysis was conducted on SPSS version 14. Participants
were 92 women in their 3rd trimester of pregnancy. Due to 30% subject attrition at T2
(N =27 participants were missing) data imputation using the Hot Deck method (LISREL;
J oreskog & Sorbom, 2001) was utilized to estimate data. [The hot deck method of

imputation identifies the participants that most closely match the subjects with missing

56

 

.716?

IN‘
1311‘;

er ‘

hill

data and estimates the missing data based on the responses of the non-missing
participants] All missing scores were imputed using the information obtained during Tl
data collection such as: demographic information, weeks pregnant, total stress, total
mental health, or perceived stress. To ensure consistency between imputed and non-
imputed data, t-tests were used to determine sample differences. There were no
significant differences across the imputed variables. See Table 2 for details.

Variable Construction. Cortisol was evaluated by examining concentrations in
the A.M. and P.M.

Pregnancy risk factors were calculated based on the initial screen and Maternal
Health During Pregnancy questionnaire. One point was assigned to each risk factor such
as smoking and alcohol usage (from the screen), or health conditions such as pre-
eclampsia or anemia occurring during pregnancy (items 3-28 from the maternal health
questionnaire. These items were summed to produce total pregnancy risk factors. The
average number of risk factors was 4.03 (SD: 3.06; range: 0 to 14).

Stress during pregnancy was defined based on the Lazarus and F olkman (1984)
transactional theory that emphasizes stress perception. Specifically, depression, anxiety,
the perception of stressfirlness of daily hassles and life events, and overall perceived
stress are each combined to form one indicator of stress. To construct these predictor
variables, all stress measures (perceived stress, depression, anxiety, life event stress, and
daily hassles stress) were correlated to determine if they could be collapsed into one
variable. Correlations for T1 revealed that depression and anxiety were moderately
correlated r = .53, p<.01. Life event stress and daily hassles were also moderately

correlated r = .51, p<.01. However perceived stress was not substantially correlated to

57

 

other \‘2

srbstan:

till. I]

E;
IT.
C4.
C‘

term he

19 form ‘

mental 5
3:4th L
he: st;

“.3635 it

I’D

other variables so it was analyzed alone. Depression and anxiety did not have a
substantial correlation with either life stress or daily hassles. This pattern was replicated
with T2 data as well. See Table 5 for details.

Next, to assure an unbiased combination of the measures, T-scores for each
individual scale were computed. T—scores for depression and anxiety were combined to
form the scale “mental stress.” T-scores for life events and daily hassles were combined
to form the “life stress” scale.

To further support using combined scales, factor analyses were conducted with
the mental stress and life stress variables. Given the low occurrence of daily hassles and
life events, a factor analysis was not performed on this data. The factor analysis for
mental stress using maximum likelihood extraction was not able to converge when
rotated using varimax rotation. Problems like this are associated with data colinearity
(Neil Schmitt, personal communication, 2007). Thus, using a combined measure of
depression and anxiety as supported by the correlations, was warranted.

Preliminary Data Analysis. The above correlations of variables revealed that
outcome infant IBQ variables and predictor variables were weakly intercorrelated at best.
Therefore, each was treated as an independent predictor or dependent variable. Due to
this, all analyses were conducted using Hierarchical Linear Regression.

To determine covariates, a MANOVA was conducted with all possible covariates
predicting each outcome variable. This includes the following predictors: income,
education, delivery complications, risk factors during pregnancy (smoking, drinking,
alcohol consumption, or health risks), and corrected age of infant. Results showed that

only age of baby and pregnancy risk factors were significant predictors so they were used

58

 

 

 

15 C0)

+‘:P:'

ib‘l C0:

‘vn
.

EC”. 5..

as covariates in all analyses.

A separate MANOVA was conducted using time of cortisol sample as a predictor
for cortisol concentration. Results demonstrate that cortisol sample collection times were
not significant predictors of cortisol concentration so they were omitted from all analyses.

In addition, based on personal communication from Salimetrics (2006), it was
possible that the cortisol values obtained for the study were not accurate due to a change
in the Trident Gum formula. According to Salimetrics in 2006, Trident was “no longer
recommended as a method of saliva stimulation.” In addition, since Salimetrics has no
established norms for cortisol during pregnancy (personal communication, 2007), no
correction formula is available. So to address this the following procedure was
performed. Initial study supplies were purchased in mid-late 2004 (when Trident was still
considered an acceptable form of saliva collection) and were approximately enough
supplies to cover the first half of participants. The serial numbers of gum packages were
not available to analyze for time of purchase and thereby serve as a control. Therefore
the sample was split in half to assess the possible confound of Trident on the assay of
cortisol. The first half represented the early participants or group 1 (N =46) and the
second half represented the later participants or group 2 (N =46). Since the variables were
not normally distributed, they were transformed with rank transformation. Next, using
ANOVA, the groups were compared across AM and PM cortisol concentrations. There
were no significant differences across groups in AM cortisol (p= n.s.; Group 1 M = 13.4
nmol/L and Group 2 M = 11.0 nmol/L) or in PM cortisol (p= .05; Group 1 M = 8.12
nmol/L and Group 2 M = 6.5 nmol/L).

In other published studies that used various methods of collection, differing times

59

 

orsrnplc

30 Sitinn

indies ra
I'll}; GUI

n

EPICS l

of sample collection assay techniques, and time of gestation cortisol ranged to 0.5 nmol/L
to 50.5nmol/L (Buckwalter et al., 1999; de Weerth & Buitelaar, 2005; Guettling et al.,
2004; Huizink et al., 2003; Paoletti et al., 2005; O’Connor et al., 2005, Obel et al., 2005;
Wadwa et al., 1996). However when these studies were examined based on gestation
(women between 28 to 37 weeks), method of collection (salivary), and time (A.M. versus
P.M.), and varying assay methods, the AM cortisol concentration this current study are
within the reported values (de Weerth et al., 2004; Huzink et al., 2003; Guetteling et al.,
2004; O’Connor et al., 2005; Paoletti et al., 2005). Specifically morning cortisol for these
studies ranged from .75nmol/L to 50.5nmol/L (de Weerth et al., 2004; Huzink et al.,
2003; Guetteling et al., 2004; O’Connor et al., 2005; Paoletti et al., 2005) and morning
samples for this study for the whole sample ranged from 0.0 to 36.14 nmol/L. However,
the afternoon concentrations were not within reported ranges. Reported afternoon
cortisol ranged from .50nmol/L to 10.3nmol/L (de Weerth et al., 2004; O’Connor et al.,
2005) and aftemoon cortisol of the whole sample of the present study ranged from 1.1
nmol/L to 27.31 nmol/L. Though, given the small comparison group and differences in
assay methods for the afternoon concentrations, it’s likely that these data are within
acceptable limits. Especially since they are within the overall non-differentiated reported
values of 0.5 nmol/L to 50.5nmol/L (Buckwalter et al., 1999; de Weerth & Buitelaar,
2005; Guettling et al., 2004; Huizink et al., 2003; Paoletti et al., 2005; O’Connor et al.,
2005, Obel et al., 2005; Wadwa et al., 1996). However, these data should still be
interpreted with caution.

Hierarchical Linear Regression was utilized in all analyses. In the first step,

maternal risk factors during pregnancy, corrected age of infant, and T2 stress (for T1

60

 

miyseSlOle 5er
enlined in the 8.110:
mediator was identit
unable (pre or pusti
if! if the independcn
parenting competent
iflie path bem'ecn tl
isignitieant with the
tornpleted separatel}

and for each IBQ seal

 

 

analyses) or T1 stress (for T2 analyses) were used as covariates. Afterwards, the steps
outlined in the Baron and Kenny (1986) method of mediation were used. Specifically, a
mediator was identified as significant based on several criteria: (1) If the independent
variable (pre or postnatal stress) predicts the dependent variable (infant regulation) (a),
(2) if the independent variable predicts the mediator (cortisol [am and pm separately] or
parenting competency) (b), (3) if the mediator predicts the outcome variable (c), (4) and
if the path between the independent variable and dependent variable becomes
insignificant with the addition of the mediator ((1). See Figure 1. These analyses were
completed separately based on type of pre or postnatal stress, time of cortisol collection,

and for each IBQ scale and infant sleep.

61

 

 

l l

Figure 1

Mediator Model

 

 

 

 

 

Independent Variable

 

(Pre or Postnatal Stress)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Mediator
(Cortisol or Parenting
Competency)

 

 

 

62

V V

 

Dependant Variable
(Infant Regulation)

 

 

 

 

 

 

 

 

rere nom
perhnnet

Q
relationsl.
mental sti
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Win

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Al

Frequency analysis. Frequency analysis of variables revealed that all variables
were normally distributed except income and cortisol. Rank transformations were
performed on income and cortisol variables to ensure normal distribution.

Correlations of all variables. Correlations of variables demonstrated significant
relationships between T1 life stress, pregnancy risk, and delivery complications. Tl
mental stress was also correlated with pregnancy risk. T1 perceived stress was not
correlated with any covariate or outcome variables. T2 life stress was correlated with
infant activity. T2 mental stress was correlated with parenting competency and delivery
complications. T2 perceived stress was correlated with P.M. cortisol and infant duration
of orienting. See Table 6 for more details.

Hypothesis A: PS will have a direct effect on infant regulation

Mental Stress and infant regulation. In most cases mental stress was not a
significant predictor of infant regulation (distress to limitations: beta = -.03, p= n.s.;
smiling: beta = .12, p=n.s.; duration of orienting: -.09, p=n.s.; consecutive sleep (beta =
.04, p<. 05.). However mental stress had a significant main effect for activity (beta = -
2.40, p<.05). See Tables 6 to 10 for details.

Life Stress and infant regylation. Life stress as a significant predictor of infant
regulation was not significant for the following: activity: beta = -.08, p=n.s.; distress to
limitations: beta = .14, p= n.s.; smiling: beta = -.02 p=n.s.; duration of orienting: beta = -
.19, p<.05; consecutive sleep: beta = -.20, p=n.s. See Tables 11 to 15 for details.

Perceived stress and infant regulation. Perceived stress was not significant in any

condition (activity: beta = -.19, p=n.s.; distress to limitations: beta = .03, p= n.s.; smiling:

63

5’35). 5

ii- - .L _ .
“.If'l/‘rlu’s

beta = .22, p=n.s.; duration of orienting: beta = .04, p=n.s.; consecutive sleep: beta= -.06,
p= us). See Tables 16 to 20 for details.
Hypothesis B: PS will have a direct effect on cortisol.

Stress and A.M. cortisol. Stress was not a significant predictor of A.M. cortisol:
mental stress: beta= -.09, p=n.s.; life stress: beta = .07, p=n.s.; perceived stress: beta =
.12, p=n.s. See Tables 21 to 23 for details.

Stress and P.M. cortisol. Stress was not a significant predictor of A.M. cortisol:
mental stress: beta= -.18, p=n.s.; life stress: beta = -.16, p=n.s.; perceived stress: beta =
.12, p=n.s . Life stress was a significant predictor of morning cortisol (beta = -.11,
p=.05). See Tables 24 to 25 for details.

Hypothesis C: Cortisol will have a direct effect on infant regulation

A.M. Cortisol and infant regulation. This hypothesis was not supported for any
outcome (activity: beta = .09, p=n.s., distress to limitations: beta = .08; smiling: beta =
-.02, p=n.s.; duration of orienting: beta = .08, p=n.s; consecutive sleep: beta = -.13,
p=n.s). See Tables 26 to 30 for details

P.M. Cortisol and infant regrlation. This hypothesis_was not supported for any
outcome (activity: beta = .14, p=n.s., distress to limitations: beta = .06; smiling: beta =
.03, p=n.s.; duration of orienting: beta = .07, p=n.s; consecutive sleep: beta = -.00,
p=n.s). See Tables 31 to 35 for details.

Hypothesis D: Cortisol will mediate PS and infant regulation

A.M. Cortisol was not a significant mediator for any stress condition and any

infant outcome. P.M. Cortisol was also not a mediator. See Tables 36 to 68 for details

Hypothesis E: PS will have a direct eflect on postnatal stress

 

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Prenatal mental stress was a significant predictor of postnatal mental stress (beta =
.37, p<.05). Prenatal life stress predicted postnatal life stress (beta = .30, p<.05). Prenatal
perceived stress also predicted postnatal perceived stress (beta = .52, p<.05). These
results demonstrate that prenatal stress does predict postnatal stress. See Tables 69 to 71
for details.

Hypothesis F: Postnatal maternal stress will have a direct effect on infant regulation

Mental stress and infant regulation. Mental stress was not a significant predictor
for activity (beta= .04, p=n.s.), distress to limitations (beta=.08, p=n.s.), smiling (beta=
.05, p=n.s.), duration of orienting (beta= -.02, p=n.s.), sleep (beta=.23, p=n.s.). See
Tables 72 to 76 for details.

Life stress and infant regulation. Life distress was not a significant predictor for:
distress to limitations (beta= -.14, p=n.s.), smiling (beta= .03, p=n.s.), duration of
orienting (beta= .07, p=n.s.), (beta=.08, p=n.s). It was significant for sleep (beta= .23,
p=n.s.) and activity (beta= .30, p<.05). See Tables 77 to 81 for details.

Perceived stress and infant regulation. Perceived distress was not a significant
predictor for activity (beta= -.19, p=n.s.), distress to limitations (beta=.04,
p=n.s. ), smiling (beta= -.04, p=n.s.), sleep (beta=-.09, p=n.s). It was significant for
duration of orienting (beta= -.26, p=n.s.). See Tables 82 to 86 for details.

Hypothesis G: Postnatal maternal stress will have a direct effect on parenting
competency.

Mental stress was a significant predictor for parenting competency (beta=-.35,
p<.05.). Life stress (beta= .04, p=n.s.) and perceived stress (beta= -.07, p=n.s.) were not

significant predictors of parenting competency. See Tables 87 to 89 for details

65

 

 

Hipjtht’sis H: Pd r t I

Parenting Ct
p=n.s.). distress to
then=.23. p=n.s.). '1
Tables 90 to 94 for t
hirpotltt‘sis l.‘ Parci:
regulation

Parenting CU

Lie stress or percei \

 

 

 

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predicts infant outco

Rini et al.. 1999. Sat
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Mattress. 2000 X\
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Hypothesis H: Parenting competency will have a direct effect on infant regulation

Parenting competency was not a significant predictor for activity Greta: -.07,
p=n.s.), distress to limitations (beta=-.15, p=n.s.), smiling (beta= .17, p=n.s.), sleep
(beta=.23, p=n.s.). It was significant for duration of orienting (beta= .24, p<.05). See
Tables 90 to 94 for details
Hypothesis 1: Parenting competency will mediate postnatal maternal stress and infant
regulation

Parenting competency was not a significant mediator for postnatal mental stress,
life stress or perceived stress and infant regulation. See Tables 95 to 109 for details.

DISCUSSION

Early researchers demonstrated that maternal experience of prenatal stress
predicts infant outcomes (Abrams et al.; 1995, Field, l995; Hernandez-Reif et a1., 2002;
Rini et al., 1999, Sable & Wilkinson, 2000; Wadhwa et al., 1993). Prenatal maternal
stress hormones, such as cortisol, have been shown to be related to infant outcomes as
well (de Weerth et a1., 2003; Field et al., 2001 & 2003; Huizink et al., 2002; Lundy et a1.,
1999; Mohler, Parzer, Brunner, Wiebel, Resch, 2006; O’Connor et al., 2004; Ponirakis et
al., 1996; Sandman et al., 1998). Based on animal research, it seems likely that stress
hormones would also mediate the relationship between prenatal maternal stress and infant
outcomes in humans (Dodic et al., 2002; Huznik et al., 2004; Maccari et al., 2003;
Matthews, 2000; Nyirenda & Seckl, 1998; Sapolsky, 1997; Wadhwa et al., 2001).
Unfortunately to date, there are no known studies in humans that examine cortisol as a
mediator of PS and infant regulation. Therefore, the purpose of this study was to examine

prenatal maternal cortisol was a mediator of maternal experience of stress during

66

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PS till .13
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pregnancy and infant regulation development at 3 months. It was hypothesized that (a)
PS will have a direct effect on cortisol (b) cortisol will have a direct effect on infant
regulation (0) cortisol will mediate PS and infant regulation ((1) PS have a direct effect on
postnatal stress (e) postnatal maternal stress will have a direct effect on infant regulation.
Given the possible postnatal environmental contributions on infant regulation the
following was also hypothesized: (f) PS have a direct effect on postnatal stress (g)
postnatal maternal stress will have a direct effect on parenting competency (h) parenting
competency will have a direct effect on infant regulation (i) Parenting competency will
mediate postnatal maternal stress and infant regulation.

Results for both mediation hypotheses were not supported due to insignificance in
supporting analyses. However there was some support for PS as a predictor of infant
regulation even after controlling for the postnatal environment. This was also found for
postnatal stress after controlling for the prenatal environment. Results are discussed
below.

Prenatal cortisol was not related to PS or infant regulation. Thereby it was not a
significant mediator for any measure of PS and infant regulation. At first glance these
results are a departure from the literature regarding cortisol. First, unlike this study, other
research has found prenatal cortisol to be a significant predictor of infant regulation (de
Weerth et al., 2003; Lundy et al., 1999; Field et al., 2001; Huizink et al., 2003; Vaughn et
al., 1987). One explanation for the insignificant results for cortisol might be related to
the complications surrounding cortisol collection in the present study. Before providing
cortisol samples, women were instructed (per instructions from Salimetrics, 2004) to

chew sugarless Trident gum if they had difficulty generating a saliva sample.

67

 

 

 

 

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Unfortunately unbeknownst to the researcher, Trident changed their formula at some
point during 2005, and according to Salimetrics in 2006 (personal communication, 2006),
Trident was “no longer recommended as a method of saliva stimulation.” Due to this
change, according to Salimetrics, “it is impossible to determine if this impacted the
sample collection and if so, to what degree the sample collection was altered.” This may
also explain why cortisol at both time collections was not significantly correlated to
predictor or outcome variables.

Even with possible sample contamination, the values of cortisol are reasonably
within the reported values. However, there is still the complication that most studies that
examine cortisol during pregnancy are often devoid of information regarding the time of
cortisol collection. Further, studies also vary based on their method of stress hormone
collection. Some researchers examined blood serum, CRH or ACTH, and still others
salivary cortisol. Although each of these methods of collection, especially blood and
serum, are highly correlated (Lightman & Everitt, 1986), differences across
methodologies still exist and therein make it difficult to draw comparisons across studies.

Another complication is that each study uses a different methodology to examine
infant regulation. Some use maternal report, observer data, or a combination of both.
There are no standards for examining infant outcomes. The limited number of studies to
use as a comparison and the use of maternal report in this study further complicate this
issue and provide more support for the lack of findings for cortisol. It may be that this
relationship exists only within certain measures of infant regulation. As a further
complication, maternal report may be biased and therefore, not the most accurate

reflection of infant behavior.

68

 

 

 

Iii

€1.11

Even with this, the possibility cannot be overlooked that cortisol may not mediate
the relationship of PS and infant regulation. It may be some other factor that can account
for the transmission. One possibility is the placenta. It may be that placental function is
likely the most accurate assessment of actual cortisol exposure from the mother to the
fetus. Since the firnctioning of 1 lBHDSZ varies by placenta (Welber, Seckl, & Holmes,
2001), this enzyme may the regulator of stress hormone transmission in humans. So
examining women with high and low llBHDSZ functioning in comparison to maternal
circulating cortisol and fetal cortisol may prove to be a better method of examining
cortisol as a mediator of maternal stress and infant outcomes.

Another possibility may be that other stress hormones are better indicators of
mediation since they occur earlier in the stress hormone cycle. Specifically, CRH or
ACTH, have been documented across a variety of study methodologies (unlike cortisol)
to predict fetal and early infant outcomes (Glynn, Wadhwa, & Sandman, 2000;
Mastorakos & Ilias, 2003; Ruiz, Fullerton, Brown, & Dudley, 2002; Smith, 1999;
Wadhwa et a1., 1996; Welber & Seckl, 2001). They have also been shown to have a
relationship with PS (Hobel et al., 1999; Sandman et al., 1998; Wadwa et al., 1996).
Given this, these variables should be thoroughly examined as possible mediators.

The possibility also exists that this relationship may be driven by genetics rather
than environment. Young and colleagues (2006) examined salivary cortisol in a sample
of children with one depressed parent. Children of currently depressed parents did not
experience depression individually, but did have elevated levels of cortisol that were
highly correlated to their parent’s levels. They suggest that there is a possible genetic and

environmental effect on child cortisol. Unfortunately only one published study has

69

 

 

ermine
fond th
ill'tdtti
genetics
the ten
Cirrel. .‘
Sherri. (
based up
lttC‘JRitf
illiesses
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5131511“

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t‘tt- .-

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examined maternal personality variables within a prospective prenatal design. They
found that even with controlling for personality, PS still impacted infant outcomes

(W adwa et al., 1996). Parenting control? With that aside, it still seems unlikely that
genetics drives this relationship. For example, it is documented that fetal exposure to
toxic teratogens can alter fetal and infant development (Elliot, 1999; Bercovici, 2005;
Ginzel, Maritz, Neuberger, Pauly, et al., 2007; Huzinik & Mulder, 2006; Mancinetti,
Binetti, Ceccanti, 2007; Schroeder, 1987). These effects are not genetically driven but
based upon the noxious exposure to the toxin. Since prolonged stress exposure has been
documented to predict cardio-vascular difficulties, exacerbate the course of some
illnesses, and lead to some neurological deficits (Hassan, York, Li, Li, & Sheps, 2007;
Mchwen & Sapolsky, 1995; Meyer et al., 2001; Meaney 1996; Neilson, Strandberg,
Gronbeck, Schnohr, & Zhang, 2007) stress too, can be considered a toxin after prolonged
exposure. So, prenatal exposure to stress may be separate from any genetic contribution.
However, there is a paucity of research to account for this so further examination of this
is necessary.

Although prenatal cortisol was not a significant predictor, PS did predict
decreased infant regulation. Specifically mental stress predicted infant activity. This
finding is consistent with previous reports of maternal stress impacting infant regulation
(Brouwers et al., 2001; Huizink, 2002; O’Connor et al., 2003; van den Bergh, 1990).
Notably, unlike other studies, this study also extends the impact of PS to nighttime infant
sleep.

Specifically, results demonstrated no effect for infant sleep. This is different from

other reports of the newborns of high anxiety mothers (Field, Diego, Hernandez-Reif,

70

 

Sehrnbet
etperient
mien-e
;ttsst'hle
monitors
re more
signifies
he doeu:
pthlishe.

did 0(th

mites t}
illltt (in
mint re

Schanberg, Kuhn,Yando, et al., 2003). Researchers found that these newborns
experienced increased deep sleep, cried less, and were quieter and less active than low
anxiety-exposed newborns. Although the sample in the current study is older, it is
possible that a more in-depth analysis of infant sleep (i.e. using sleep journals or
monitors) may yield similar findings. Especially since these methods of data collection
are more likely to be accurate descriptions of infant sleeping patterns.

Interestingly, unlike mental stress, life stress and perceived stress were not a
significant predictors for infant regulation in this study. This is actually a departure from
the documented reports. Close examination of the literature demonstrates that in most
published studies, perceived stress accounted for more variance in infant regulation than
did other stressors (Buitelaar et al., 2003; Huizink et al., 2002).

One possible explanation for this finding is that there are a limited number of
studies that prospectively examine PS and infant regulation. Within these studies, they
differ on the actual methods of data collection of infant regulation. Some studies examine
infant regulation using the Bayley for motor and performance measures (de Weerth et al.,
2003). Other researchers measure regulation using cardiac vagal tone (Ponirakis et al.,
1998), primarily use outside observers to assess temperament and motor activity
(Browers, 2001; Field, 1985), primarily use maternal report to assess temperament and
activity (Vaughn, 1987), or with they use a combination of maternal and observer report
to obtain data about regulation (Huizink et al., 2002, 2003; Van den Bergh, 1990, 1992).
Given the variety of methodologies of data collection, generalizing across these studies is
difficult. In addition, it is notable that a vast majority of studies published in this area are

from one foreign sample population. Unique aspects of that sample such as location,

71

 

 

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dial

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inch
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than
news
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A11

cultural values, access to healthcare, or other variables may not overlap completely with
other US. based samples.

Results regarding the postnatal mediation hypothesis were not significant.
However, postnatal life stress was positively related to nighttime sleep and activity.
Perceived stress on the other hand, was negatively related to duration of orienting. Life
stress involved everyday tasks or events that occur. If a mom is experiencing higher
levels of these stressors, it may take a more active infant to elicit her attention and more
care. This in turn may increase their sleep at night. Perceived stress is different because it
is how a woman generally views her world. She may feel more overwhelmed and may be
more subdued in her interactions with her infant. This in turn may lead to decreased
infant attention to particular stimuli. Either way, it seems that stress has some impact on
infant behavior.

Based upon the findings of this study, it is puzzling why prenatal mental stress
predicted infant outcomes, but prenatal life stress and perceived stress did not. Further, it
is also puzzling why the findings were not replicated in the postnatal period. As
predicted, prenatal stress predicted postnatal stress. Also correlations showed that T1
stress variables were significantly correlated to corresponding T2 stress variables.
Therefore, it would seem logical that what is significant prenatally, would also be
significant postnatally as well. But this was not shown in this study. One possible
explanation is that certain stressors may be more salient during pregnancy and vice versa.
A pregnant woman may be more susceptible to particular stressors during this time
simply as a function of the bodily changes and hormonal changes that occur. Due to the

growing baby, she may find it harder to complete daily tasks such as cleaning or picking

72

 

tp sim
tonne
inner:
.iliitl‘.
more g
in: yr
'he let
deptes

up.

Infin-

up simple objects. She may also have stopped working and thereby have few social
contacts or experience decreased outlets for recreation due to fatigue. Hormonally, rapid
increases in the natural hormones that prepare for birth may also alter her sense of self.
Although many of these stressors are present after the birth of the baby, they may become
more global in nature. So feeling stressed in general or feeling like there is less time or
that you unable to control important aspects of life may be more salient at this time. With
the demands of a new baby, a woman may not “have time” to reflect on feelings of
depression but may actually feel stressed in general, or have feelings that things are piling
up.

Interestingly, only mental stress predicted parenting competency. Specifically as
mental stress increased parenting competency decreased. This makes sense. As a mother
is more stressed, her parenting suffers and she feels less unsure about her caretaking
abilities. It’s possible that mental stress may be more taxing since it directly affects an
individual’s sense of self. Thereby it may impact an individual’s perception of their
parenting skills in a more direct manner than perceived or life stress.

It should be noted that there are several limitations to the present study. As
mentioned earlier possible sample contamination, methodological differences in cortisol
collection as compared to other studies, sample, and data collection may impact the
ability of this study to generalize to larger populations. For example, there are only a
handful of studies in this area, and most are based on non-U.S. populations and come
from higher SES backgrounds. This aspect alone may alter the ability of this study to
compare to those populations. Also, given that this study is based on a primarily lower

income population, there may be other contributory factors that women may be

73

expefien
or p-C‘Or It
533011315 5""
3mg713 Si.
tmderstandi
primarily 0“
some of the r
01cm.
infant develop
study. this doe:
transmission of
to understand tht
to have in infant.
In additio.
detetorment. Th.
mEdiator model. I
that lfany relatit:

Finally, sin

   
  
 

later childhood ant
Ct al., 1995; O'C 01
identification and “
lderttifsing pregnz:

experiencing related to economics (such as: access to healthcare, unsafe neighborhoods,
or poor nutrition) which may also impact the generalizability of the results. Future studies
should examine other protective factors such as social support, spirituality, or other
stressors such as neighborhood location, racism or domestic violence to help gain a better
understanding of the role of PS on infant development. Lastly, this study was based
primarily on maternal report so the possible confound of rater bias may have impacted
some of the results as well.

Overall this study highlights the need for further research on PS, cortisol, and
infant development. Although the role of cortisol may have been compromised in this
study, this does not diminish the possibility that cortisol may hold a significant role in the
transmission of stress from mother to child. A broader examination of possible sources
to understand the transmission of stress is essential given the impact PS has been shown
to have in infant, child and adolescent development.

In addition, to date there is a paucity of published studies of PS and infant sleep
development. This study provides the first look at these variables within the context of a
mediator model. Future studies should include this in their analysis to help determine
what, if any relationship PS and cortisol have on the developing sleep patterns of infants.

Finally, since studies are beginning to demonstrate that PS has a lasting impact on
later childhood and adolescent behavior (Allen et al., 1998; Laucht et al., 2000; McIntosh
et al., 1995; O’Connor et al., 2002; 2003; 2005; van den Bergh et al., 2005), early
identification and interventions may attenuate the later effects on child development.
Identifying pregnant mothers at high risk for experiencing stressors, could greatly reduce

the detrimental effects that PS have on infants’ social, emotional, physiological and brain

74

deelopment. There-ti
;ssessrnents of prcgn
farms of stress red uct
ojtfisol during pregn;
identifying high corti

:tientifying women at

ended-tilt health and j

 

 

development. Therefore, physicians and clinicians should include inquiries of PS in their
assessments of pregnant women and aid them in establishing and integrating healthy
forms of stress reduction in their lives. Lastly, there are no established norms for levels of
cortisol during pregnancy. More research is needed to determine specific criteria for
identifying high cortisol during pregnancy. A simple saliva swab could also aid in
identifying women at risk and help prevent related future infant, childhood, adolescent,

and adult health and psychological complications.

75

 

 

.ts

(.11
C11

(,1:

REFERENCES

Abrams, 8., Field, T., Scafidi, F., & Prodromidis, M. (1995). Maternal depression effects
on infants’ brazelton scale performance. Infant Mental Health Journal, 16, 231-
235.

Aldwin, C. (1994). Stress, Coping, and Development: An Integrative Perspective. New
York: The Guilford Press.

Allen, N., Casolini, P., Patacchioli, F., & Angelucci, L. (1998). Prenatal and perinatal
influences on risk for psychopathology in childhood and adolescence.
Development and Psychopathology, 10, 513-529.

Altman, J ., & Bayer, S. (1990). Migration and distribution of two populations of
hippocampla granule cell precursors during the preinatal and postnatal periods.
Journal of Camp Neurology, 301, 365-381.

Anderson, S.L. (2003). Trajectories of brain development: point of vulnerability or
window of opportunity? Neuroscience and Biobehavioral Reviews, 27, 3-18.

Amsten, A. (2000). Stress impairs prefrontal cortical function in rats and monekys: role
of dopamine D1 and norepinephrine alpha-l receptor mechanisms. Progress in
Brain Research, 126, 183-192.

Arishima, K., Nakama, S., Morikawa, Y, Hashimoto, Y, & Eguchi, Y. (1977). Changes
in placental permeability to corticosterone and estradiol-17 beta toward the end of
gestation in the rat. Experientia, 34, 262-263.

Assesl, M.A., Landry, S.H., Swank, P.R., Steelman, L., Miller-Loncar, C., & Smith, KB.
(2002). How do mothers’ childrearing histories, stress and parenting affect
children’s behavioral outcomes? Child: care, Health & Development, 28, 359-
368.

Barbazanges, A., Piazza, P., Le Moal, M., & Maccari, S. (19960. Maternal
glucocorticoid secretion mediates long-term effects of prenatal stress. Journal of
Neuroscience, 16, 3943-3949.

Barrett, G., Smith, S.C., & Wellings, K. (2004). Conceptualisation, development, and
evaluation of a measure of unplanned pregnancy. Journal of Epidemiology
Community Health, 58, 426-433.

Bayer, S. (1980). Quantitative 3-H thymidine radiographic analyses of neurogenesis in
the rat Clorticot. Journal of Comparative Neurology, [94, 845-875.

Bell, R; Nitschke, W; Gorry, T; Zachrnan, T (1970). Infantile Stimulation and Ultrasonic
Signaling: A Possible Mediator of Early Handling Phenomena. Developmental

76

Beet CT. (ZOOl ). Pl

to. 5. 3753“

and Researt i:

Bltonlicld. F.H.. Ol
P.D.. Challis.

for noninfect: -

, .. I

Britt L. 8; \ielscn.
working with
Environment'-

  
  
   
    
   
  
   
  

Brenner ID. 8; Ben
biological cor.

Brenner ID. & Yen
biological cor:

Bttno. J.P.: Bless. E..
Weanling Alh
Developments

Broth A.S.. ran 08.

evidence of re
American Jou

Bitters. E.P.\1 ya
pregnancy and
24. 95-106.

 

Ettda‘Mana‘L. PL‘tl
mm)? C ont
lock of agar

Brett ML; Razzoli
(2007).R0pea
rat mothers. P
Buttoalterd G St
. . a;
Rankin, KP I
Steroid ho -»
24,69-84rmor

Pchhobiology, 4, (2) 181-191.

Beck, CT. (2001). Predictors of postpartum depression: an update. Nursing Research,
50, 5, 275-285.

Benes, F. (2000). Emerging principles of alterd neural circuitry in schizophrenia. Brain
and Research Reviews, 3, 2-3), 251-269.

Bloomfield, F .H., Oliver, M.H., Hawkins, R, Campbell, M., Phillips, D.J., Gluckman,
P.D., Challis, J .R., & Harding, J .E. (2003). A periconceptional nutritional origin
for noninfectious preterm birth. Science, 300, 606.

Brandt, L. & Nielsen, CV. (1990). Congenital malformations among children of women
working with video display terminals. Scandinavian-Journal—of Work,-
Environment-and-Health, 16,5, 329-333

Brernner, J .D. & Bennetten, E. (2001). Stress and development: behavioral and
biological consequences. Development and psychopathology, 13, 473-489.

Bremner, J .D. & Verrnetten, E. (2001). Stress and development: behavioral and
biological consequences. Development and Psychopathology, 13, 473-489.

Bruno, J .P.; Blass, E.M; Amin, F. (1983). Determinants of Suckling versus Drinking in
Weanling Albino Rats: Influence of Hydrational State and Maternal Contact.
Developmental Psychobiology, 16, 177-184.

Brown, A.S., van Os, J ., Driessesn, C., Howk, H.W., & Susser, ES. (2000). Further
evidence of relation between prenatal famine and major affective disorder.
American Journal Psychiatry, 15 7, 2, 190-195.

Brouwers, E.P.M., van Baar, A.L., & Pop, V.J.M. (2001). Maternal anxiety during
pregnancy and subsequent infant development. Infant Behavior & Development,
24, 95-106.

Boccia,-Maria-L; Pedersen,-Cort-A. (2001). Brief vs. long maternal separations in
infancy: Contrasting relationships with adult maternal behavior and lactation
levels of aggression and anxiety. Psychoneuroendocrinology, 26(7), 657-672.

Boccia, ML; Razzoli, M; Vadlamudi, SP; Trumbull, Whit; Caleffie, C; Pedersen,-CA.
(2007). Repeated long separations from pups produce depression-like behavior in
rat mothers. Psychoneuroendocrinology 32(1), 65-71.

Buckwalter, J .G., Stanczyk, F.Z., McCleary, C.A., Bluestein, B.W., Buckwalter, D.K.,
Rankin, K.P., Chang, L., & Goodwin, M. (1999). Pregnancy, the postpartum, and
steroid hormones: effects on cognition and mood. Psychoneuroendocrinology,
24, 69-84.

77

Chapillon. P.. Pa:
postnatal .\
rodents: a

 

Citing J. 8: Newttl
in pregnar.
Stauber. .\7
Springer-\

Christopher. S.E..
support ant-
intensit'e c

Ciechetti. D. (:01 i '
consequent

|
Cicchetti. D. 8; R1
maltreated

Cicehetti. D. & Rt.
PSYChOPJtl‘.
Poetopah;

Cintlli. F.. Berry. :1
relationshi pl
Neuroscien

Wt. F; Capone.

enrichment
antiohtic d
rain-Reset

airlift. A & Schnt‘

 

IESPOHSCS to
21257269
Clarke. A 8., Wittu
penatal str
eve/0pm

Coe '
CEKr er.
L003). Pret
esus 1710th

Cohen,

 

Chapillon, P., Patin, V., Roy, V., Vincent, A., & Caston, J. (2002). Effects of pre and
postnatal stimulation on developmental, emotional, and cognitive aspects in
rodents: a review. Developmental Psychobiology, 41, 373-387.

Ching, J. & Newton, N. (1982). A prospective study of psychological and social factors
in pregnancy related to preterm and low birth-weight deliveries. In Prill, H]. and
Stauber, M. (eds.) Advances in Psychosomatic Obstetrics and Gynecology,
Springer-Verlang, New York.

Christopher, S.E., Bauman, K.E., & Veness-Meehan, K. (2000). Perceived stress, social
support and affectionate behaviors of adolectent mothers with infants in neonatal
intensive care. Journal of Pediatric Health Care, 14, 288-296.

Cicchetti, D. (2001). Editorial: stress and development: biological and psychological
consequences. Development and Psychopathology, 13, 413-418.

Cicchetti, D. & Rogosch, F.A. (2001a). Diverse patterns of neuroendocrine activity in
maltreated children. Development and Psychopathology, 13, 677-693.

Cicchetti, D. & Rogosch, F.A. (2001a). The impact of child maltreatment and
psychopathology on neuroendocrine functioning. Development and
Psychopathology, 13, 783-804.

Cirulli, F., Berry, A., & Alleva, E. (2003). Early disruption of the mother-infant
relationship: effects on brain plasticity and implications for psychopathology.
Neuroscience and Biobehavioral Reviews, 27, 73-82.

Cirulli, F; Capone, F; Bonsignore, LT; Aloe, L; Alleva, Enrico. (2007). Early behavioural
enrichment in the form of handling renders mouse pups unresponsive to
anxiolytic drugs and increases NGF levels in the hippocampus. Behavioural-
Brain-Research, 1 78(2), 208-215

Clarke, A. & Schneider, M. (1993). Prenatal stress has long-term effects on behavioral
responses to stress in juvenile rhesus monkeys. Developmental Psychobiology,
27, 257-269.

Clarke, A.S., Wittwer, D., Abbott,D., Schneider, M. (1994). Long-term effects of
prenatal stress on HPA axis activity in juvenile rhesus monkeys.
Developmental Psychobiology, 27, 5, 257-69.

Coe, C.L., Kramer, M., Czeh, B., Gould, E., Reeves, A.J., Kirschbaum, C., & Fuchs, E.
(2003). Prenatal stress diminishes neurogenesis in the dentate gyrus of juvenile
rhesus monkeys. Biological Psychiatry, 54, 1025-1034.

Cohen, S., Kamarck, T., & Merrnelstein, R. (1983). A global measure of perceived

78

Colin J., Campbell
postpartum
Dew/apart ‘r

Collins. XL. Dun}

support in l
depression.

Costa D.D.. Larou
over the cor.
anxiety. ant
609-621.

  
   
 
  

Come. J.C.. Aldu: I
episodes. J.

Da Costa. D.. Brent
psychosoeia
Psrchosomt.

 

Da Costa. 0.. Late

Prepartum a
31-40.

Dahlofi L, Hard. E
developmen

Damaudm.‘ M., Di
during gesta
Bt’hat'1'0ra1 ‘

Di‘hfittdery. XI K(
Eflrly and la
.\€urOSC.I-(,n(

D. .

roan, " CreVeuil.

A' 13002). l

a
b0r, A me,

Be _ .
Bellis. M. (2001
of maltreate

PIOP’NC’M

stress. Journal of Health and Social Behavior, 24, 385-96.

Cohn, J ., Campbell, 8., Matias, R.,& Hopkins, J. (1990). Face to face interactions of
postpartum depressed and nondepressed mother infant pairs at 2 months.
Developmental Psychology, 26, 1, 15-23.

Collins, N.L., Dunkel-Schetter, C., Lobel, M., & Scrimshaw, S.C.M. (1993). Social

support in pregnancy: psychosocial correlates of birth outcomes and postpartum
depression. Journal of Personality and Social Psychology, 65, 6, 1243-1258.

Costa, D.D., Larouche, J ., Drista, M., & Brender, W. (1999). Variations in stress levels
over the course of pregnancy: factors associated with elevated hassles, state

anxiety, and pregnancy specific stress. Journal of Psychosomatic Research, 4 7, 6,
609-621.

Coyne, J .C., Aldwin, C., & Lazarus, RS. (1981). Depression and coping in stressful
episodes. Journal of Abnormal Psychology, 90, 5, 439-447.

Da Costa, D., Brender, W., & Larouche, J. (1998). A prospective study of the impact of
psychosocial and lifestyle variables on pregnancy complications. Journal of
Psychosomatic Obstetrics and Gynaecology, 3 7, 28-37.

Da Costa, D., Larouche, J., Drista, M., & Brender, W. (2000). Psychosocial correlates of
prepartum and postpartum depressed mood. Journal of Aflective Disorders, 59,
31-40.

Dahlof, L., Hard, E., & Larsson, K. (1978). Influence of maternal stress on the
development of the feotal genital system. Physiological Behavior, 20, 193-195.

Darnaudery, M., Dutriez,1., Viltart, O., Morley-Fletcher, S., Maccari, S. (2004). Stress
during gestation induces lasting effects on emotional reactivity of the dam rat.
Behavioral Brain Research, 153,], 211-6

Darnaudery, M., Koehl, M., Barbazanges, A., Cabib,S., Le-Moal, M., Maccari,S. (2004).
Early and later adoptions differently modify mother-pup interactions. Behavioral
Neuroscience, [18, 3, 590-6.

Dayan, J ., Creveuil, C., Herlicoviez, M., Herbel, C., Baranger, E., Savoye, c., & Thouin,
A. (2002). Role of anxiety and depression in the onset of spontaneous preterm
labor. American Journal of Epidemiology, 155, 293-301.

De Bellis, M. (2001). Developmental traumatology: the psychobiological development

of maltreated children and its implications for research, treatment, and policy.
Development and Psychopathology, 13, 539-564.

79

   

Demoet, R. (19‘
Front Net

De Quen'ain. D.. I
impair ret'

Delnes. AC. (3‘ I
pituitary-u

De Weerth. C .. \‘o
infant belt. I
151.

Detongis. A., C0}
and major

Derniniere. 1.. Pia.
(19921.1111
amphetamt
Research, .‘

 

 

 

Derogatis. L. UPI‘
measure of
Measurcmt
Pharmaco;

lhego. M.A.. Diett

Largie. 8..

stimulatior

sychobio.

DtPietro. JA. (2Q

13. 2. 71-7
DiPietro. IA. C0
maternal s
Dottie. 31.. Hantzi

Programm
10126.

D .
Un€hl~SChEIIEr .

De Kloet, R. (1991). Brain corticosteroid receptor balance and homeostatic control.
Front Neuroendocrinology, 12, 95-104.

De Quervain, D., Roozendaal, B., & McGaugh, J. (1998). Stress and glucocorticoids
impair retrieval of long term spatial memory. Nature, 394, 787-790.

DeVries, AC. (2002). Interaction among social environment, the hypothalamic-
pituitary-adrenal axis, and behavior. Hormones and Behavior, 41 , 405-413.

De Weerth, C., van Hees, Y., & Buitelaar, J. (2003). Prenatal maternal cortisol levels and
infant behavior during the first 5 months. Early Human Development, 74, 139-
1 51 .

DeLongis, A., Coyne, J ., Dakof, G. et al. (1982). Relationships of daily hassles, uplifts,
and major life events to health status. Health Psychology, 1, 119-136.

Derniniere, J ., Piazza, P., Guegant, G., Abrous, N., Maccari, Le Moal, M., & Simon, H.
(1992). Increased locomotor response to novelty and propensity to intravenous
amphetamine self-administration in adult offspring of stressed mothers. Brain
Research, 586, 135-139.

Derogatis, L., Lipman, R., Rickels, et a1. (1974). The Hopkins symptom checklist: A
measure of primary symptom dimensions. In Pichot P (ed), Psychological
Measurements in Psychopharmacology: Modern Problems in
Pharmacopsychiatry, vol 7. Base]: Karger.

Diego, M.A., Dieter, J .N., Field, F., Lecanuet, J .P., Hernandez-Reif, M., Beutler, J .,
Largie, S., Redzepi, M., & Salman, FA. (2002). Fetal activity following
stimulation of the mother’s abdomen, feet and hands. Developmental
Psychobiology, 41, 396-406.

DiPietro, J .A. (2004). The role of prenatal maternal stress in child development.
13, 2, 71-78.

DiPietro, J .A., Costigan, K.A., & Gurewitsch, ED. (2003). Fetal response to induced
maternal stress. Early Human Development, 74, 125-138.

Dodic, M., Hantzis, V., Duncan, J ., Rees, S., Koukoulas, 1., Johnson, K., et al. (2002).
Programming effects of short prenatal exposure to cortisol. FAEB J, 16, 1017-
10126.

Dole, N., Savitz, D.A., Hertz-Picciotto, I., Siega-Riz, McMahon, M.J., & Buekens, P.
(2003). Maternal stress and preterm birth. American Journal of Epidemiology,
I57, 1, 14-24.

Dunekl-Schetter, C., Wadhwa, P., & Stanton, AL. (2000). Stress and reproduction:

8O

introdUCllf”

felitnan. P.1.. Dur-

support pre.
Psrthosonz.

Fielil.11995)- 1‘

13.

field. T. (1908 ). .\
Preventive

field. I. (30031. E
mothers. 1i;

field 1.. Diego. .\1
I

R.. & Bendt

their fetusesli

|

Field 1.. Diego. .\1
mothers wh.
intrusive. It

field 1.. Diego. .‘\1.
Bendell. D.
effects on t1“.

Fieneira A. (1965)
modem. .4.

 

 

firming. A. Ruble.
time mother;

interaction.

flaming, A.S., Stein
responsit'ent

fogc1.C.1& Belyea
challenge for

mm“: 3- & Laza

10mm] ofxl l

introduction to the special section. Health Psychology, 19, 6, 507—509.

F eldman, P.J., Dunekl-Schetter, C., Sandman, C. & Wadhwa, P. (2000). Maternal social
support predicts birth weight and fetal growth in human pregnancy.
Psychosomatic Medicine, 62, 5, 715-725.

Field, T. (1995). Infants of depressed mothers. Infant Behavior and Development, 18, 1-
13.

Field, T. (1998). Maternal depression effects on infants and early interventions.
Preventive Medicine, 2 7, ZOO-203.

Field, T. (2002). Early interaction between infants and their postpartum depressed
mothers. Infant Behavior & Development, 25, 25-29.

Field, T., Diego, M.A., Dieter, J ., Hernandez-Reif, M., Schanberg, S., Kuhn, C, Yando,
R., & Bendell, D. (2001). Depressed withdrawn and intrusive mothers’ effects on
their fetuses and neonates. Infant Behavior & Development, 24, 27-39.

Field, T., Diego, M., Hernandez-Reif, M., Schanberg, S., & Kuh, C. (2003). Depressed
mothers who are good interaction partners versus those who are withdrawn or
intrusive. Infant Behavior & Development, 26, 23 8-252.

Field, T., Diego, M., Hernandez-Reif, M., Schanberg, S., Kuhn, C., Yando, R., &
Bendell, D. (2003). Pregnancy anxiety and comorbid depression and anger:
effects on the fetus and neonate. Depression and Anxiety, 1 7, 140-151.

Fierreira, A. (1965). The pregnant woman’s emotional attitudes and its reflection on the
newborn. American Journal of Orthopsychiatry, 30, 553-561.

Fleming, A., Ruble, D., Flett, G., & Shaul, D. (1988). Postpartum adjustment in first-
time mothers: relations between mood, maternal attitudes and mother infant
interaction. Curr. Opin. Pediatirics, 24, 77-81.

Fleming, A.S., Steiner, M., & Corter, C. (1997). Cortisol, hedonics, and maternal
responsiveness in human mothers, Hormones, and Behavior, 32, , 85-98.

Fogel, C.I & Belyea, M. (2001). Psychosocial risk factors in pregnant inmates: a
challenge for nursing. American Journal of Maternal/Child Nursing, 26, 1 , 10-16.

Folkman, S. & Lazarus, RS. (1985). Stress processes and depressive symptomatology.
Journal of Abnormal Psychology, 95, 2, 107-113.

Francis, D. & Meaney, M. (1999). Maternal care and the development of stress
responses. Neurobiology, 9, 128-134.

81

lran-cis. D.. Dione
reverses th.
neuroscicn

French MHz-1113“-
antenatal er
Journal 0} t

Fride. E.. Dany. Y.
maternal be
receptors.

Fade. E. 8.; \Veinstt
unpredictab
PSl‘C'hODl-Olt

 

 

 

Froman. RD 3; On
Nursing Pro

ltjiolra T.. Fujjiok
(2001). .\'lil
rat Offspring

(imam. 3- & Hen
preterm bin

Gitau R" cameron
cortisoL La

Gitau R., Fisk. N}
releasing he
89. 1:29-1:31

Francis, D., Diorio, J ., Plotsky, P., & Meaney, M. (2002). Environmental enrichment
reverses the effects of maternal separation on stress reactivity. The Journal of
neuroscience, 22, 18, 7840-7843.

French, N., Hagan, R., Evans, S., Godfrey, M., & Newnham, J. (1999). Repeated
antenatal corticosteroids: size at birth and subsequent development. American
Journal of Obstetrics and Gynecology, 180, 114-121.

Fride, E., Dany, Y, Gavish, M., & Weinstock, M. (1985). Prenatal stress impairs
maternal behavior in a conflict situation and reduces hippocampal benzodiazepine
receptors. Life Science, 36, 2103-2109.

Fride, E. & Weinstock, M. (1984). The effects of prenatal exposure to predictable or
unpredictable stress on early development in the rat. Developmental
Psychobiology, I 7, 651-660.

Froman, R.D & Owen, S.V. (1989). Infant care self-efficacy. Scholarly Inquiry for
Nursing Practice: An International Journal, 3, 3, 199-211.

Fujioka, T., Fujjioka, A., Chowdhury, G.M.I., Mouri, H., Sakata, Y., & Nakamura, S.
(2001). Mild prenatal stress enhances learning performance in the non-adopted
rat offspring. Neuroscience, 2, 301-30 7.

Gennaro, S. & Hennessy, D. (2003). Psychological and physiological stress: impact on
preterm birth. JOGNN, 32, 5, 668- 675.

Gitau, R., Cameron, A., Fisk, N., & Glover, V. (19980. Fetal exposure to maternal
cortisol. Lancet, 352, 707-708.

Gitau, R., Fisk, N.M., & Glover, V. (2004). Human fetal and maternal corticotrophin
releasing hormone responses to acute stress. Arch Dis Child Fetal Neonatal Ed,
89, F29—F 32.

Gitau, R., Fisk, N., Teixeira, J ., Cameron, A., & Glover, V. (2001). Fetal hypothalamic-
pituitary-adrenal stress responses to invasive procedures are independent of
maternal responses. The Journal of Clinical Endocrinology & Metabolism, 86, 1,
104-109.

Glynn, L.M., Pathik, W.D., & Sandman, C. (2000). The influence of Elorticotrophin-
releasing hormone on human fetal development and parturition. Journal of

Prenatal and Perinatal Psychology and Health, 14, 3-4, 243-257.

Gould, E. & Tanapat, P. (1999). Stress and hippocampal neurogenesis. Biological
Psychiatry, 46, 1472-1479.

Gould, E., Tanapat, P., McEwen, B., Flugge, G., & Fuchs, E. Proliferation of granule

82

cell precur‘
proceedin -.

 

Granger. D.A.. Ho.
DCVClOme
and inhibit

0mm. \" 8; Freid
[he behaVit'

l

Guillory. \".J.. Sanil
birth outcot‘

and L'ndcn

Gunnar. .\1.R., Mor
lCVClS in ch:
Psychopar/z.

Hahn'eeh. C. An ie
Depression .

llram. K., Morten.-
Acta Obslcrz

Hart. 5.. Field. T., 8
neonates bel"

 

Hassan .\1;York. K
myocardial i
dysfunction.

liedegaard, M., Hen
distress in pr

delegaard, N1. Hen
str4essful lit}
pzdemiolog

Helm. C.

cell precursors in the dentate gyrus of adult monkeys is diminished by stress.
Proceedings of the National Academy of Sciences, USA, 95 , 3168-3171.

Granger, D.A., Hood, K.E., Dreschel, N.A., Sergeant, E., & Lilos, A. (2001).
Developmental effects of early immune stress on aggressive, socially reactive,

and inhibited behaviors. Development and Psychopathology, 13, 599-610.

Grimm, V & Freider, B. (1987). The effects of mild maternal stress during pregnancy on
the behavior of rat pups. International Journal of Neuroscience, 35, 65-72.

Guillory, V.J., Samules, M.B., Probst, J .C., & Sharp, G. (2003). Prenatal care and infant
birth outcomes among Medicaid recipients. Journal of Health Care for the Poor
and Underserved, 14, 2, 272-289.

Gunnar, M.R., Morison, S.J., Chisholm, K., & Schuder, M. (2001). Salivary cortisol
levels in children adopted from Romanian orphanages. Development and
Psychopathology, I3, 61 1-628.

Halbriech, U. Anxiety disorders in women: a developmental and lifecycle perspective.
Depression and Anxiety, 1 7, 107-110.

Haram, K., Mortensen, J .H., & Wollen, AL. (2003). Preterm delivery: an overview.
Acta Obstetrics Gynecology Scandanivia, 82, 687-704.

Hart, S., Field, T., & Roitfarb, M. (1999). Depressed mothers’ assessments of their
neonates behaviors. Infant Mental Health Journal, 20, 2, 200-210.

Hassan, M; York, K.M.; Li, H; Li, Q; Sheps, D S. (2007). Mental stress-induced
myocardial ischemia in coronary artery disease patients with left ventricular
dysfunction. Journal of Nucleus Cardiology, 14(3): 308-13

Hedegaard, M., Henriksen, T.B., Sabroe, S., & Secher, NJ. (1993). Psychological
distress in pregnancy and preterm delivery. BMJ, 307, 234-239.

Hedegaard, M., Henriksen, T.B., Secher, N.J., Hatch, M.C., & Sabroe, S. (1995). Do
str4essful life events affect duration of gestation and risk of preterm delivery.
Epidemiology, 7, 339-345.

Heim, C., & Nerneroff, CB. (1999). The impact of early adverse experiences on brain
systems involve din the pathophysiology of anxiey and affective disorders.
Biological Psychiatry, 46, 1509-1522.

Hennessy, M.B., Davis, H.N., McCrea, A.A., Harvey, A.T., & Williams, M.T. (2001).

Short and long term consequences of Clorticotrophin releasing factor in early
development. Annals New York Academy of Sciences.

83

llemessy. M.B.. .\
unfamiliar
adrenocort
42-52.

1

Herriksen. T.B.. \1
preterm an.I
Epidemic/l

llerrandez-Reif. 3"
nett'bOmS 5
Mental m“

Herrenlrohl. L. (19'

561177159- 3 I

Herrenltohl. L 8- lit
behavior. 111
17, 1019-1"

Hob-e101. Dunkel
Maternal pl.
\t'eeks' gest'
Obstetrics ul

Holtrnan. S. & Hulk
evidence for
social class i

Hitler. MA. (1996).
Psrchoneurr .

literal-1A: Brunell;

poor to separl
i euroscienct

Hague. CJ.R.. Hofli‘

conceptual f
3(140. it

 

 

Hennessy, M.B., Maken, D.S., & Graves, F .C. (2002). Presence of mother and
unfamiliar female alters levels of testosterone, progesterone, cortisol,

adrenocorticoropin, and behavior in guinea pigs. Hormones and Behavior, 42,
42-52.

Henriksen, T.B., Wilcox, A.J., Hedegaard, M., & Secher, NJ. (1995). Bias in studies of
preterm and postterm delivery due to ultrasound assessment of gestational age.
Epidemiology, 6, 5, 533-537.

Hernandez-Reif, M., Field, T., Diego, M., & Largie, S. (2002). Depressed mothers’
newborns show longer habituation and fail to show face/voice preference. Infant
Mental Health Journal, 23, 6, 643-653.

Herrenkohl, L. (1979). Prentatl stress reduces fertility and fecundity in female offspring.
Science, 206, 1097-1099.

Herrenkohl, L. & Whitney, J. (1976). Effects of prepartal stress on postpartal nursing
behavior, litter development, and adult sexual behavior. Physiology & Behavior,
17, 1019-1021.

Hobel, C.J., Dunkel-Schetter, C., Roesch, S.C., Castro, L.C., & Arora, GP. (1999).
Maternal plasma Elorticotrophin-releasing hormone associated with stress at 20
weeks’ gestation in pregnancies ending in preterm delivery. American Journal of
Obstetrics and Gynecology, 180,1, S257-S263.

Hoffman, S. & Hatch, MC. (2000). Depressive symptomatology during pregnancy:
evidence for an association with decreased fetal growth in pregnancies of lower
social class women. Health Psychology, 19, 6, 535-543.

Hofer, M.A. (1996). Multiple regulators of ultrasonic vocalization in the infant rat.
Psychoneuroendocrinology, 21, 2, 203-217.

Hofer,_MA; Brunelli, SA; Masmela,_.lenny; Shair,_HN. (1996). Maternal interactions
prior to separation potentiate isolation-induced calling in rat pups. Behavioral-
Neuroscience, 110(5) Oct 1996, 1 158-1 167.

Hogue, C.J.R., Hoffman, S., & Hatch, M. (2001). Stress and preterm delivery: a
conceptual framework. Paediatric and Perinatal Epidemiology, 15 (Suppl. 2),
3040.

Holmes, T. & Rahe, R. (1967). The social readjustment rating scale. Journal of
Psychosomatic Research, 11, 213-8.

Holzman, C., Bullen, 8., Fisher, R., Paneth, N., Reuss, & the Prematurity Study Group.
(2001). Pregnancy outcomes and community health: the pouch study of preterm
delivery. Paediatric and Perinatal Epidemiology, 15, Suppl. 2, 136-158.

84

Hueston. WJ. 8; 1
normal pre

Huizink. A.. de M
during purl
ofChi/d Pi

 

loltnston. C. 8; M;-.
Journal of .

lines. NA. Field. '
of mothers
Behavior d

lanes. .\'.A.. Field.

perceptions
mothers. 12:

Kaufmm J. 8; Chat
function: in
maltreatmcn

 

lessler. R.C.. .\1cG
1.15.14). Lifetime an
anal states: Resul
Pri'cliiatrt', 51; 8-19
Killingsworth, R E

Psychologie;

StTeSS. and St
when. 0. (2002)
ehavioral d

Mote-11;”, HESe—A-
COHditioninu

g...
ediarrics (g

(2003
010720] 0f.\'

Hueston, W.J. & Kasik-Miller, S. (1998). Changes in functional health status during
normal pregnancy. The Journal of Family Practice, 4 7, 3, 209-212.

Huizink, A., de Medina, P.G.R., Mulder, B., Visser, G, & Buitelaar, J. (2003). Stress
during pregnancy is associated with developmental outcome in infancy. Journal
of Child Psychology and Psychiatry, 44, 6, 810-818.

Johnston, C. & Mash, E.J. (1989). A measure of parenting satisfaction and efficacy.
Journal of Clinical Child Psychology, 18, 2, 167-175.

Jones, N.A., Field, T., Fox, N.A., Davalos, M., Lundy, B., & Hart, S. (1998). Newborns
of mothers with depressive symptoms are physiologically less developed. Infant
Behavior & Development, 21, 3, 537-541.

Jones, N.A., Field, T., Hart, S., Lundy, B., & Davalos, M. (2001). Maternal self-
perceptions and reactions to crying among intrusive and withdrawn depressed
mothers. Infant Mental Health Journal, 22, 5, 576-586.

Kaufinan, J. & Charney, D. (2001). Effects of early stress on brain structure and
function: implications for understanding the relationship between child
maltreatment and depression. Development and Psychopathology, 13, 451-471.

Kessler, R.C., McGonagle, K.A., Zhao, S., Nelson, C.B., Hughes, M., Eshleman, S. et al.,
(1994). Lifetime and 12-month prevalence of DSM-IIIR psychiatric disorders in the
united states: Results from the national comorbidity survey. Archives of General
Psychiatry, 51; 8-19.

Killingsworth, R., Dunkel-Schetter, C., Sandman, C., & Wadhwa, P. (1999).
Psychological adaptation and birth outcomes: the role of personal resources,
stress, and sociocultural context in pregnancy. Health Psychology, 18, 333-345.

Kofman, O. (2002). The role of prenatal stress in the etiology of developmental
behavioral disorders. Neuroscience and Biobehavioral Reviews, 26, 457-470.

Kosten,-Therese-A; Lee,-Hongioo-J; Kim,-Jeansok-J (2006). Early life stress impairs fear
conditioning in adult male and female rats. Brain Research, 1087(1), 142-150.

Kramer, MS. (1987). Intrauterine growth and gestational duration determinants.
Pediatrics, 80, 502-511.

Kramer, MS. (2003). The epidemiology of adverse pregnancy outcomes: an overview.
Journal of Nutrition, 133, 15928-15968.

Kramer, M.S., Goulet, L., Lydon, J ., Seguin, L., Mcnamara, H., Dassa, C., Platt, R.W., et

al. (2001). Socio-economic disparities in preterm birth: causal pathways and
mechanisms. Paediatric and Perinatal Epidemiology, 15, (Suppl 2), 104-123.

85

 

Lerner. .\l.S.. Mi
& \t'en. s]
grottth ant

Kurstiens. S. 8; \\ I
derelopme
Pst'cholog;

lembert. KG. K1:
Prenatal str
and Beirut.

Larson. .\l.C.. \l'h;
cortisol res;l
sleep. circa.
P SIC/101(11):?

Laucht. Essen B m
det'elopmcn
malemal 10>
300.

Wis. R.S. (1974
[mentationa

mi R-S- (1991,

l u
4335mm, J" Zhlm]
Stressors imp

.etine. S. (1960). St

 

Kramer, M.S., Morin, 1., Yang, H., Platt, R.W., Usher, R., McNamara, H., Joseph, K.S.,
& Wen, SW. (2002). Why are babies getting bigger? Temporal trends in fetal
growth and its determinants. The Journal of Pediatrics, 141, 4, 538-542.

Kurstjens, S. & Wolke, D. (2001). Effects of maternal depression on cognitive
development of children over the first 7 years of life. Journal of Child
Psychological Psychiatry, 42, 5, 623-636.

Lambert, K.G., Kinsley, C.H., Jones, H.E., Klein, S.L. et a]. ( 1995).
Prenatal stress attenuates ulceration in the activity stress paradigm. Physiology
and Behavior, 57, 5, 989-994

Larson, M.C., White, B.P., Donzella, B., & Gunnar, M. (1998). Dampening of the
cortisol response to handling at 3 months in humans infants and its relationship to
sleep, circadian cortisol activity, and behavioral distress. Developmental
Psycholobiology, 33, 327-337.

Laucht, Esser, Baving, Gerhold, Hoesch, Ihle, Steigleider, et al. (2000). Differential
development of infants at risk for psychopathology: The moderating role of early
maternal responsivity. Developmental Medicine and Child Neurology, 43, 5, 292-
300.

Lazarus, R.S. (1974). Psychological stress and coping in adaptation and illness.
International Journal of Psychiatry Medicine, 5, 4, 321-333.

Lazarus, R.S. (1991). Theory-based stress management. Psychological Inquiry, 1, 3-13.
Lazarus, R. & Folkman, S. (1984). Stress, appraisal, and coping. New York: Springer.

Lesserman, J ., Zhiming, L., Yuming, J.E., Douglas, D. (1998). How multiple types of
stressors impact on health. Psychosomatic Medicine, 60, 175-181.

Levine, S (1957). Infantile experience and resistance to physiological stress. Science,
126, 32-70.

Levine, S. (1960). Stimulation in infancy. Scientific American, 202, 80-86.

Levine, S (1967). Maternal and Environmental Influences on the Adrenocortical
Response to Stress in Weaning Rats. Science, 156, 258-260.

Levine, S and Broadhurst, P. (1963). Genetic and Ontogenetic Determinants of Adult
Behavior in the Rat. Journal of Comparative and Physiological Psychology, 56,
423-428.

Levine, S; Haltmeyer, G.C; Karas, G; and Denenberg, V.H (1966). Physiological and

86

Behaviour
leiine. S.: Mulliri
Rats. Sch

lint-an. E, Behan.
binding pr.
placental bl
.lletabolisn

lit D. Tannenbat
Plotsky. P..'
receptors. ;1‘
1659-1662.

label. )1. (19941.
Stress on bi."

Label. 11.. DeVint-t
I

maternal str
1151' women.

label. 11.. Dunkel‘
prematurit} :
Health Pstt ,.

hclt'ood. C ..l . ( 1 till
releasing 1101
8364-8266.

t., '

41111.8" Patin. V“
pregnant {31>
Oilspring. It:

ltit'q‘oy, CM, Grac
and parenting

it
.11.. C. & Halfon.

141D, Diono, J_ T.
Matemal care“
adrenal l espr ll

 

Limb}, .L., Jones! ‘\

 

Behavioral Effects of Infantile Stimulation. Physiology and Behavior, 2, 55-59.

Levine, S.; Mullins, R. (1966). Hormonal Influences on Brain Organization in Infant
Rats. Science, 52, 1585-1592.

Linton, E., Behan, D., & Saphier, P. (1990). Corticotropin releasing hormone (CRH)-
binding protein: reduction in the adrenocorticotropin-releasing activity of
placental but not hypothalamic CRH. Journal of Clinical Endocrinology
Metabolism, 70, 1574-1580.

Lin, B., Tannenbaum, B., Caldji, C., Francis, D., Freedman, A., Sharma, S., Pearson, D.,
Plotsky, P., & Meaney, M. (1997). Maternal care, hippocampal glucocorticoid
receptors, and hypothalamic-pituitary-adrenal responses to stress. Science, 277,
1659-1662.

Lobel, M. (1994). Conceptualizations, measurement, and effects of prenatal maternal
stress on birth outcomes. Journal of Behavioral Medicine, 1 7, 3, 225-272.

Lobel, M., DeVincent, C.J., Kaminer, A., & Meyer, BA. (2000). The impact of prenatal
maternal stress and optimistic disposition on birth outcomes in medically high-
risk women. Health Psychology, 19, 544-553.

Lobel, M., Dunkel-Schetter, C., & Scrimshaw, S. (1992). Prenatal maternal stress and
prematurity: A prospective study of socioeconomically disadvantaged women.
Health Psychology, 11, 32-40.

Lockwood, C.J. (1999). Stress-associated preterm delivery: the role of Elorticotrophin
releasing hormone. American Journal of Obstetrics and Gynecology, 180, 1,
$264-$266.

Lordi, B., Patin, V., Protais, P., Mellier, D., & Caston, J. (2000). Chronic stress in
pregnant rats: effects on growth rate, anxiety, and memory capabilities of the
offspring. International Journal of Psychopathology, 37, 195-205.

Lovejoy, C.M., Graczk, P.A., O’Hare, B., & Neuman, G. (2000). Maternal depression
and parenting behavior. Clinical Psychology Review.

Lu, M., C. & Halfon, N. (2003). Racial and ethnic disparities in birth outcomes: a life-
course perspective. Maternal and Child Health Journal, 7, I, 13-30.

Lui, D., Diorio, J ., Tannenbaum, B., Caldji, C., Francis, D., Freedman, A., et al. (1997).
Maternal care, hippocampal glucocorticoid receptors, and hypothalamic-pituitary-
adrenal responses to stress. Science, 2 77, 1659-1662.

Lundy, B.L., Jones, N.A., Field, T., Nearing, G., Davalos, M., Pietro, P.A., Schanberg,

87

S., & Kuhn, C. (1999). Prenatal depression effects on neonates. Infant Behavior
& Development, 22, I, 119-129.

Lyons-Ruth, K., Wolfe, R., Lyubchik, A. (2000). Depression and the modulation of
pituitary-adrenal activity in rat pups after early stimulation. Harvard Review of
Psychiatry, 8, 148-153.

MacCallum, R.C., Browne, M.W., & Sugawara, HM. (1996). Power analysis and
determination of sample size for covariance structure modeling. Psychological
Methods, 1, 2, 130-149.

Maccari, S., Damaudery,M, Morley-Fletcher, S., Zuena, A.R., Cinque, C., Van-Reeth, O.
(2003). Prenatal stress and long-term consequences: implications of

glucocorticoid hormones. Neuroscience-and—Biobehavioral-Reviews, 27, 1-2,
1 19-127.

Maccari, S., Piazza, P., Kabbaj, M., Barbazanges, A., Simon, H., & Le Moal, M. (1995).
Adoption reverses the long-term impairment in glucocorticoid feedback induced
by prenatal stress. Journal of Neuroscience, 15, 110-116.

Majzoub, J .A. & Karalis, KR (1999). Placental Dorticotrophin-releasing hormone:
function and regulation. American Journal of Obstetrics and Gynecology, 180, 1,
$242-$246.

Mastorakos, G. & Ilias, I. (2003). Maternal and fetal hypothalamic-pituitary-
adrenal axes during pregnancy and postpartum. Annals of New York Academy of
Science, 997, 136-49

Martinez, A., Malphurs, J ., Field, T., Pickens, J ., Bendell, D., DelValle, C., & Messinger,
D. (1996). Depressed mothers and their infants interactions with non-depressed
partners. Infant Mental Health Journal, I 7, 152-160.

McEwen, B. (1991). Nongenomic and genomic effects of steroids on neural activity.
Trends in Pharmacological Sciences, 12, 141 -147.

Matthews, S,G. (2000). Antenatal glucocorticoids and programming of the developing
CNS. Pediatric Research, 47, 3, 291-300

McEwen, B., Magarinos, A.& Regan, L. (2002). Studies of hormone action in the
hippocampal formation possible relevance to depression and diabetes. Journal of

Psychosomatic Research, 53, 883-890.

McEwen, B. & Sapolsky, R. (1995). Stress and cognitive function. Current Opinions in
Neurobiology, 5, 235-245.

McFarland, M.L. & Sanders, MR. (2003). The effects of mothers’ depression on the

88

behavioral assessment of disruptive child behavior. Child & Family Behavior
Therapy, 25, 3, 39-63.

McIntosh,-D-E; Mulkins,-R-S; Dean,-R-S. (1995). Utilization of maternal perinatal risk
indicators in the differential diagnosis of ADHD and UADD children.
International Journal of Neuroscience, 81, 1-2, 35-46

Meaney, M., Diorio, J ., Widdowson, J ., LaPlante, P., Caldji, C., Sharma, S., Seckl, J ., &
Plotsky, P. (1996). Early environmental regulation of forebrain glucocorticoid
receptor gene expression: implications for adrenocortical response to stress.
Developmental Neuroscience, 18, 40-72.

Meek, L.R., Burda, K.M., & Paster, E. Effects of prenatal stress on development in mice:
maturation and learning. Physiology & Behavior, 71, 543-549.

Mertesaker, B., Bade, U., Haverkock, A., & Pauli-Pott, U. (2004). Predicting maternal
reactivity/sensitivity: the role of infant emotionality, maternal

depressiveness/anxiety, and social support. Infant Mental Health Journal, 25, 1,
47-61.

Meyer, S.E., Chrousos, G.P., & Gold, P.W. (2001). Major depression and the stress
system: a life span perspective. Development and psychopathology, 13, 565-580.

Meijer, A. (1985). Child psychiatric sequalae of maternal war stress. Acta Psychiatrica
Scandinavia, 72, 505-511.

Monk, C., Fifer, W.P., Myers, M.M., Sloan, R.P., Trien, L., & Hurtado, A. (2000).
Maternal stress responses and anxiety during pregnancy: effects on fetal heart
rate. Developmental Psychobiology, 36, 67-77.

Moutquin, J .M. (2003). Socio-economic and psychosocial factors in management and
prevention of preterm labor. BJOG: an International Journal of Bestetrics and
Gynaecology, 110, Supp 20, 56-

60.

Mutale, T., Creed, F., Maresh, M., & Hunt, L. (1991). Life events and low birthweight
analysis by infants preterm and small for gestational age. British Journal
Obstetrics and Gynecology, 131, 166-172.

Nielsen, NR; Strandberg-Larsen, K; Gronbaek, M; Kristensen, TS; Schnohr, P; Zhang,
ZF (2007). Self-reported stress and risk of endometrial cancer: a prospective
cohort study. Psychosomomatic Medicine, 69(4), 383-9

Newton, R. & Hunt, L. (1984). Psychosocial stress in pregnancy and its relation to low
birth weight. British Medical Journal, 29, 1191-1194.

89

\ettton. F

Newport.
lit

Xiillli‘t‘li.
in

Nyirenda.
di
.11

O'Conno
at

1:

O'Conno

Newton, R., Wevster, P., binu, P., Maskrey, N., & Phillips, A. (1979). Psychosocial
stress in pregnancy and its relation to the onset of premature labor. British
Medical Journal, 2, 411-413.

Nicely, P., Tamis-LeMonda, C.S., & Grolnick, W.S. (1999). Maternal responsiveness to
infant affect: stability and prediction. Infant Behavior & Development, 22, 1,
103-1 17.

Newport, J .D., Wilcox, M.M., & Stowe, Z.N. (2002). Maternal depression: a child’s
first adverse life event. Seminars in Clinical Neuropsychiatry, 7, 2, 113-119.

Norbeck, J .S., Lindsey, A.M., & Carrieri, V.L. (1981). The development of an
instrument to measure social support. Nursing Research, 30(5), 364-269.

Nyirenda, M. & Seckl, J. (1998). Intrauterine events and the programming of adulthood
disease: the role of fetal glucocorticoid exposure. Internal Journal of Molecular
Medicine, 2, 607-614.

O’Connor, T., Heron, J ., Golding, J., & Glover, v. (2003). Maternal antenatal anxiety
and behavioral/emotional problems in children: A test of a programming
hypothesis. Journal of Child Psychology and Psychiatry, 44, 7, 1025-1036.

O’Connor, T., Heron, J ., Golding, J ., Beveridge, M., & Glover, V. (2002). Maternal
antenatal anxiety and children’s behavioral/emotional problems at 4 years.
British Journal of Psychiatry, 180,, 502-508.

Obel, C., Hedegaard, Henriksen, M., Scher, N., & Olsen, J. (2003). Stressful life events
in pregnancy and head circumference at birth. Developmental Medicine & Child
Neurology, 45, 802-806.

Olsson, C. & Nilsson-Wikrnar, L. (2004). Health-related quality of life and physical
ability among pregnant women with and without pain in late pregnancy. Acta
Obstetrics of Gynecology Scandinavia, 83, 351-357.

Paarlberg, K.M., Vingerhoets, J.M., Passchier, J., Dekker, G.A., & van Geijn, H. (1995).
Psychosocial factors and pregnancy outcome: a review with emphasis on
methodological issues. Journal of Psychosomatic Research, 39, 5, 563-595.

Paarlberg, K.M., Vingerhoets, J .M., Passchier, J., Dekker, G.A., & van Geijn, H. (1999).
Psychosocial predictors of low birthweight: a prospective study. British Journal
of Obstetrics and Gynaecology, 106, 834-841.

Page], M., Smilkstein, G., Regen, H., & Montano, D. (1990). Psychosocial influences on

new born outcomes: a controlled prospective study. Social Science and
Medicine, 30, 597-604.

90

Panza P.
dill

Prior. .\1
lnt‘
mi.

Ptialo. .\l.
me-
lo.

Pearlin. 1
DD

Pearlin. 1
So-

Petets. D,
h}
in

Plflrakis
(l
n

Pallet: '

0.9

St

at.
nq‘tfis‘ SL

Palanza, P. (2001). Animal models of anxiety and depressioin: how are females
different? Neuroscience and Biobehavioral Reviews, 25, 219-233.

Pardon, M.C., Gerardin, P., Joubert, C., Perez-Diaz, F., Cohen-Salmon, C. (2000).
Influence of prepartum chronic ultramild stress on maternal pup care behavior in
mice. Society of Biological Psychiatry, 4 7, 858-863.

Pajulo, M., Savonlathi, E., Sourander, A., Piha, J, & Helenius, H. (2001). Prenatal
maternal representations: mothers at psychosocial risk. Infant Mental Health
Journal, 22, 5, 529-544.

Pearlin, L.I., Lieberman, M.A., Menaghan, E.G., & Mullan, J .T. (1981). The stress
process. Journal of Health and Social Behavior, 22; 337-356.

Pearlin, L. & Schooler, C. (1978). The structure of coping. Journal of Health and
Social Behavior, 19, 2-21.

Peters, DA. (1990). Maternal stress increases fetal brain and neonatal cerebral cortex 5-
hydroxytryptamine synthesis in rats: A possible mechanism by which stress
influences brain development. Pharmacology,Biochemistry and Behavior, 35,4,
943-947

Pfeiffer, W.D; Rotundo, R.; Myers, M; Denenberg, V.H. (1976). Stimulation in Infancy:
Unique Effects of Handling. Physiology & Behavior, 1 7, 781-784.

Ponirakis, A., Susman, E.J. & Stifier, CA. (1997). Negative emotionality and cortisol
during adolescent pregnancy and its effects on infant health and autonomic
nervous system reactivity.

Radloff, L. (1977). The CES-D Scale: A self report depression scale for research in the
general population. Journal of Applies Psychological Measures, 1, 385-401.

Raison, C.L. & Miller, AH. (2003). When not enough is too much: the role of
insufficient glucocorticoid signaling in the pathophysiology of stress-related
disorders. American Journal of Psychiatry, 160, 9, 1554-1565.

Ratka, a., Sutanto, W., Bloemers, M., De Kloet, E. (1989). On the role of brain
mineralcorticoid (type I) and glucocorticoid (type 11) receptors in neuroendocrine
regulation. Neuroendocrinology, 50, 2, 117-123.

Redman, C.W. & Sargent, LL. (2003). Pre-eclampsia, the placenta and maternal
systemic inflammatory response-a review. Placenta, 24, Suppl A, Trophoblast

Research, 17, $21-$27.

Rees, SL; Panesar, S; Steiner, M; Fleming, AS (2004). The effects of adrenalectomy and

91

Rinit

- 11161“

Road

Roth

Ruel

Rue

Rut

corticosterone replacement on maternal behavior in the postpartum rat.
Hormones-and-Behavior, 46(4), 411-419.

Rees, SL; Panesar, S; Steiner, M; Fleming, AS (2006). The effects of adrenalectomy and
corticosterone replacement on induction of maternal behavior in the virgin female
rat. Hormones-and-Behavior, 49(3), 337-345.

Righetti-Velterna, M., Conne-Perrard, E., Bousquet, A., & Manzano, J. (2002).
Postpartum depression and mother-infant relationship at 3 months old. Journal of
Aflective Disorders, 70, 291-306.

Rini, C., Wadhwa, P., Sandman, CA. (1999). Psychological adaptation and birth
outcomes: The role of personal resources, stress, and sociocultural context in
pregnancy. Health Psychology, 18, 4, 333-345.

Fug

Q‘A—‘w .' ,‘I'fl

Ritter, C., Hobfoll, S.E., Lavin, J ., Cameron, R.P., & Hulsizer, MR. (2000). Stress,
psychosocial resources, and depressive symjptomatology during pregnangy in
low-income, inner-city women. Health Psychology, 19, 6, 576-585.

 

Rondo, PHC., Ferreira, RR, Riberio, MCN, Lobert, H, & Artes, R. (2003). Maternal 9‘ *
psychological stress and distress as predictors of low birth weight, prematurity
and intrauterine growth retardation. European Journal of Clinical Nutrition, 5 7,
266-272.

Rothbart, M. ( 1981). Measurement of temperament in infancy. Child Development, 64,
569-578.

Ruedi-Bettschen, D; Feldon, J; Pryce, CR (2004). Circadian- and temperature-specific
effects of early deprivation on rat maternal care and pup development: Short-terrn
markers for long-term effects? Developmental-Psychobiology, 45(2), 59-71.

Ruel, J. & De Kloet, R. (1985). Two receptor system for corticosterone in the rat brain:
microdistribution and differential occupation. Endocrinology, 11 7, 25025-2511.

Ruiz, J .R., Fullerton, J ., Brown, C.E.L., & Dudley, D. (2002). Predicting risk of preterm
birth: the roles of stress, clinical risk factors, and Dorticotrophin-releasing
hormone. Biological Research for Nursing, 4, I, 54-64.

Sanchez, M.M., Ladd, C.O., & Plotsky, P.M. (2001). Early adverse experience as a
developmental risk factor for later psychopathology: evidence from rodent and
primate models. Development and Psychopathology, 13, 419-449.

Sandman, C.A., Wadhwa, P.D., Chicz-DeMet, A., Porto, M., & Garite, T.J. (1998).

Maternal Dorticotrophin-releasing hormone and habituation in the human fetus.
Developmental Psychobiology, 34, 163-173.

92

 

Sandman.
(21'

pre

Sapolsly.
l 6

Sarason. 1

de

SmOlllt

Smith.

Slllolh

Smith

Sandman, C.A., Wadhwa, P., Glynn, L., Chicz-Demet, A., Porto, M., & Garite, T.J.
(2000). Corticotropin-releasing hormone and fetal responses in human
pregnancy. Annals New York Academy of Sciences.

Sapolsky, R.M. (1997). The importance of a well groomed child. Science, 277, 1620-
1621.

Sarason, I.G., Johnson, J .H., & Siege], J .M. Assessing the impact of life changes:

development of the life experiences survey. Journal of Co. Clinical, 46, 932-
947.

Sable, M. & Wilkinson, D. (2000). Impact of perceived stress, major life events, and

pregnancy attitudes on low birth weight. Family Planning Perspectives, 32, 288-
294.

Schneider, M. & Moore, C. (2000). Effect of prenatal stress on development: A

nonhuman primate model. In C. Nelson (Ed). Minnesota Symposium on Child
Psychology. New Jersey: Erlbaum.

Schneider, M. & Suomi, S. (1992). Neurobehavioral assessment in rhesus monkey

neonates (macaca mulatta): Developmental changes, behavioral stability, and
early experience. Infant Behavior and Development, 15, 155-177.

Seyle, H. (1956). The Stress of Life. New York: McGraw-Hill.

Shaw, D., Vondra, J., Hommerding, K., & Keenan, K. (1994). Chronic family adversity
and early child behavior problems: a longitudinal study of low income families.

Journal of Child Psychology and Psychiatry and Allied Disciplines, 35, l 109-
l 122.

SITl'l()therrnan, W. (1982). Mother infant interaction and modulation of pituitary-adrenal
activity in rat pups after early stimulation.

Smotherman, W. and Bell, R. (1980). Maternal Mediation of Early Experience.

Maternal Influences and Early Behavior. New York: SP Medical & Scientific
Books.

Sjl"-'1()therman, W. Brown, C., & Levine, S. (1977). Maternal responsiveness following

differential pup treatment and mother-pup interactions. Hormones and Behavior,
8, 242-253.

S’11'1i th, R. (1999). The timing of birth. Scientific American, 409, 68-73.

SI)€=Itcer, N.J. & Coe, C. (1999). Validation of the Warwick Child Health and Morbidity

Profile in routine child health surveillance. Child: Care, Health, and
Development, 26, 4, 323-336.

93

liF—imrn n. _ .e .

51362.

Store-e.

Samar

Sana

lal'lor

ltlc g

liadj,

110m 1

TSIgQ

Spielberger, C. (1983). Manual for the State—Trait Anxiety Inventory. Palo Alto, CA:
Consulting Psychologists Press.

Stancil, T.R., Hertz-Picciotto, 1., Schramm, M., & Watt-Morse, M. (2000). Stress and
pregnancy among African-american women. Paediatric and Perinatal
Epidemiology, 14, 127-13 5.

Stewart, P., Rogerson, F., & Mason, J. (1995). Type 2 ll-beta-Hysdroxysteroid
dehydrogenase messenger ribonuclceic acid and activity in human placenta and
fetal membranes: Its relationship to birth weight and putative role in fetal adrenal

steroidogenesis. Journal of Clinical Endocrinology and Metabolism, 80, 885-
890.

Suarez, L., Cardarelli, K., & Hendricks, K. (2003). Maternal stress, social support, and

risk of neural tube defects among Mexican Americans. Epidemiology, 14, 5, 612-
616.

Suchecki, D. & Neto, RI. (1991). Prentatl stress and emotional response of adult
offspring. Physiology & Behavior, 49, 423-426.

Susman, E.J., Schmeelk, K.H., Ponirakis, A., & Gariepy, J .L. (2001). Maternal prenatal,
postpartum, and concurrent stressors and temperament in 3-year-olds: a person
variable analysis. Development and Psychopathology, 13, 629-652.

SUSman, E.J., Schmeelk, K.H., Worrall, B., Granger, D., Ponirakis, A., & Chrousos, GP.
(1999). Corticotropin-releasing hormone and cortisol: longitudinal associations
with depression and antisocial behavior and pregnant adolescents. Journal of the
American Academy of Child & Adolescent Psychiatry, 38, 4, 460-467.

Tab/l or, R.J. (1986). Receipt of social support among black Americans: Demographic
and familial differences. Journal of Marriage and Family, 48; 67-77.

Tei Cher, M.H., Andersen, S.L., Polcari, A., Anderson, C.M., Navalta, C.P., & Kim, D.M.
(2003). The neurobiological consequences of early stress and childhood
maltreatment. Neuroscience and Biobehavioral Reviews, 27, 33-44.

Tiedje, LB. (2003). Psychological pathways to prematurity: changing our thinking
toward a lifecourse and community approach. JOGNN, 32, 5, 650-658.

Tro trick, E. & Field, T. (Eds). Maternal Depression and Infant Disturbance. San
Francisco: Josey-Bass, Inc.

T Sigos, C. & Chrousos, G. P. (2002). Hypothalamic-pituitary-adrenal axis,

neuroendocrine factors and stress. Journal of Psychosomatic Research, 53, 865-
87 1.

94

mun-nu.
l'

mefifti.f t v.1

lrrtier. R.J.
1C.
Next

ltanpson.
1315
1m

1m. ll. Ei
.\'et
Eli.

lat den 8
ant
linl
Rt"

in 05. 0

scl

1'3;th 1
ch
dil
Ps

Turner, R.J. & Turner, J.B. (1999). Social integration and support. In C.S. Aneshensel &
J .C. Phelan (Eds), Handbook of the Sociology of Mental Health. (pp 301-319)
New York: Kluwer/Plenum Publishers.

Thompson, W. (1976). Influence of prenatal maternal anxiety on emotionality in young
rats. In Advances In The Study of Behavior Vol 6. Academic Press Inc., New
York.

Uno, H., Eisele, S., Saki, A., Shelton, S., Baker, E., DeJesus, O, et al. (1994).
Neurotoxicity of glucocorticoids in the primate brain. Hormones and Behavior,
28, 336-348.

Van den Bergh, B.H; Mulder, E.J., Mennes, M., & Glover, V. (2005). Antenatal maternal
anxiety and stress and the neurobehavioural development of the fetus and child:

links and possible mechanisms. A review. Neuroscience and Biobehavioral
Reviews, 29, 237-258.

Van Os, 0. & Selten, J. (1998). Prenatal exposure to maternal stress and subsequent
schizophrenia. British journal of Psychiatry, 1 72, 324-326.

Vaughn, B., Bradley, C., Joffe, L., Seifer, R., & Barglow, P. (1987). Maternal
characteristics measured prenatally are predictive of ratings of temperamental
difficulty on the Carey Infant Temperament questionnaire. Developmental
Psychology, 23, 152-161.

Vanuez, D.M. (1998). Stress and the developmeing limbic-hypothalamic-pituitary-
adrenal axis. Psychoneuroendocrinology, 23, 7, 663-700.

Wadhwa, P.D., Culhane, J.F., Rauh, V., Brave, S.S., Hogan, V., Sandman, C.A., Hobel,
C]. et al. (2001). Stess, infection and preterm birth: a biobehavioural
perspective. Paediatric and Perinatal Epidemiology, 15, Suppl. 2, 17-29.

Wadhwa, P., Dunekl-Schetter, c., Chicz-DeMet, A., Porto, M., & Sandman, c. (1996).
Prenatal psychosocial factor and the neuroendocrine axis in human pregnancy.
Psychosomatic Medicine, 58, 432-446.

Wadhwa, P., Porto, M., Garite, T., Chicz-DeMet, A., & Sandman, C. (1998). Maternal
Dorticotrophin-releasing hormone levels in the early third trimmest predict level

of gestation in human pregnancy. American Journal of Obstetrics and
Gyencology, 179, 1079-1085.

Wadhwa, P, Sandman, c, Proto, M., Dunekl-Schetter, c., & Garite, T.J. (1993). The
association between prenatal stress and infant birth weight and gestational age at
birth: a prospective investigation. American Journal of Obstetrics and

Gynecology, 169, 4, 858-865.

95

 

ll’rl'ter

ll'a'ren

lleiss

Walker, E.F., Walder, D.J., & Reynolds, F. (2001). Developmental changes in cortisol
secretion in normal and at risk youth. Development and Psychopathology, 13,
721-732.

Warren, S., Gunnar, M., Kagan, J ., Anders, T., Simmens, S., Rones, M., Wease, S., et al.
(2003). Maternal panic disorder: Infant temperament, neurophysiology, and
parenting behaviors. Journal of American Child and Adolescent Psychiatry, 42,
7, 814-825.

Welber, L.A.M. & Seckl, J .R. (2001). Prenatal stress, glucocorticoids and the
programming of the brain. Journal of Neuroendocrinology, I3, 1 13-128.

Weinstock, M. (1997). Does prenatal stress impair coping and regulation of

hypothalamic-pituitary-adrenal axis? Neuroscience and Biobehavioral Reviews,
21, 1-10.

Weinstock, M. (2001). Alterations induced by gestational stress in brain morphology and
behavior of the offspring. Progress in Neurobiology. 65, 427-451.

Weinstock, M., Matlina, E., Maor, g., Rosen, H, & McEwen, B. (19920. Prenatal stress
selectively alters the reactivity of the hypothalamic-pituitary-adrenal system in the
female rat. Brain Research, 595, 195-200.

Weissman, M.M., Bruce, M.L., Leaf, P.J., Florio, L.P., & Holzer, C.ll. (1991). Affective
disorders. In Robins, L.N. & Regier, D.A. (Eds). Psychiatric Disorders in
America: The Epidemiologic Catchment Area Study. (pp 53-80) New York: The
Free Press.

Wei ssman, M., Prusoff, B., Gammon, G. (1984). Psychopathology in the children (ages
6-18) of depressed and normal parents. Journal of American Academy of Child
Psychology, 23, 78-84.

Wheaton, B. (1999). Social Stress. In C.S. Aneshensel & J .C. Phelan (Eds), Handbook
of the Sociology of Mental Health. (pp 301-319) New York: Kluwer/Plenum
Publishers.
Wi 1 liams, D.I (1970). Differences in home-cage emergence in the rat in relation to
infantile handling. Psychological Science, 18, 168-169.
Yal i, A.M. & Lobel, M. (2002). Stress resistance resources and coping in pregnancy.
Anxiety, Stress, and Coping, 15, 3, 289-309.

Young, EA; Vazquez, D; Jiang, H; Pfeffer, CR. (2006). Saliva Cortisol and Response to
Dexarnethasone in Children of Depressed Parents. Biological-Psychiatry, 60(8),

96

 

831-836.

Zarrow, M., Philpott, J ., & Denenberg, V. (1970). Passage of the C4 corticosterone from
the rat mother to the feotus and neonate. Nature, 226, 1058-1059.

Zuckerman, B., Amaro, H., Bauchner, H., & Cabral, H. (1989). Depressive symptoms

during pregnancy: relationship to poor health behaviors. American Journal of
Obstetrics and Gynecology, 160, 1107-1011.

97

 

 

APPEX

APPENDICES

Appendix A: Demographics

98

 

Subject #
Date of Interview
Name of interviewer

 

Pregnancy Interview
Demographic Questionnaire

1. What is your date of birth: _ _ /_ _ /_ _
("10) (W) (W)

2. How many weeks are you in your pregnancy?

 

3. What is your baby’s due date: _ _ /_ __ /V_ _
(m0) (dy) (yr)

4. How many biological children do you currently have?

 

5. How many people, including yourself, live in your household?
(If participant is living in a shelter, questions 7 8r 8 refer to household composition before moving into
shelter.)

 

3. Please list these: (Write in specific relationship to mother. Be specific—is the person (for ex.) a husband,
stepfather. biological child, foster child, or partner's child?)

 

 

 

 

 

 

 

 

 

 

7- Choose the one that best describes your current marital/relationship status (choose only one):

(a) single, never married

(b) married bb) For how long? _ (in months)

I separated cc) For how long? __ (in months)

((1) divorced dd) For how long? __ (in months)

(e) widowed ee) For how long? _ (in months)

If (a) is circled: Are you currently in a relationship? YES NO

If NO, were you in a relationship that lasted at least
6 weeks during your current pregnancy? YES NO

First name of your current partner or the partner you were with for at least 6 weeks during your

 

pregnancy:

Are you currently living with your partner? YES NO
~ Is your partner the father of your baby? YES NO
- lf no, what is your current relationship with the father of your baby? (Circle one)

1 = spouse

2 = ex-spouse

3 = partner

4 = ex-partner

5 = friend

6 = acquaintance
7 = stranger

8 = other Please specify:

 

99

12. What is your racial or ethnic group?
1 = Native American
2 = Asian American/Pacific Islander
3 = Black, Afi‘ican American
4 = Latino, Hispanic, Chicano
5 = Biracial (mixed): Specify

 

6 = Caucasian, White
7 = Other:

 

13. What is the baby’s father’s racial or ethnic group?
I = Native American
2 = Asian American/Pacific Islander
3 = Black, African American
4 = Latino, Hispanic, Chicano
5 = Biracial (mixed): Specify

 

6 = Caucasian, White
7 = Other:

 

14. What is the highest level of education you have completed? (Circle one)
I = grades I, 2, 3, 4, 5, 6, 7, 8. 9. 10, l l, 12, GED (circle specific grade)

2 = trade school

3 = some college

4 = AA degree

5 = BN33

6 = some grad school

7 = graduate degree such as MA, Ph.D., Law, or MD?

1 5 - Do you currently work outside the home? YES NO

If NO, did you work outside the home during the last year?

YES NO

 

1 6- If YES to either part of Question 18, what is/was your occupation?

1 9- If yes to Question 18, what is his/her occupation?

 

20- What is your total family income per month (estimate)?

2 l - Do you currently receive services from . . . ?

a. W1C ............................................... YES
b. TANF (formerly AFDC) ........................ YES
c. Protective Services .............................. YES
d. Food Stamps ..................................... YES
e. Medicaid ........................................... YES
f. SS1 (Disability) .................................. YES
g. F IA cash assistance/grant ...................... YES
b. Any child related programs (e.g., 0-3;

Mother-Infant Program; Head Start)? ............... YES

NO
NO
NO
NO
NO

NO

NO

NO

(Please be specific)

3. Are you currently residing in homeless shelter or a shelter for battered women?

# days in shelter?

100

YES NO

Appendix B: Maternal Health

101

MATERNAL HEALTH

1) In general would you say that your health is excellent, very good, good, fair, or poor?

3. In what month of your pregnancy did you receive prenatal care?

2a. 1 2 3 4 5 6 7 8 9 (circle one)
2b. How many visits did you have with the doctor or midwife during your pregnancy?
VISIIS
3) During your pregnancy are you excessively tired? ................ YES NO
4) During your pregnancy have you experienced bleeding? ......... YES NO
5) During your pregnancy have you been on bed rest? ............... YES NO

Have you ever been diagnosed by a health professional with any of the following health conditions during your

pregnancy?

Before you were pregnant While you were pregnant

 

6 High blood pressure (hypertension) Yes No Don’t know Yes No Don’t know
7 Asthma Yes No Don’t know Yes No Don’t know
8 Allergies Yes No Don’t know Yes No Don’t know
9 Sickle Cell disease Yes No Don’t know Yes No Don’t know
10 Diabetes Yes No Don’t know Yes No Don’t know
1 ] Epilepsy Yes No Don’t know Yes No Don’t know
12 Anemia Yes No Don’t know Yes No Don’t know
I3 Migraines Yes No Don’t know Yes No Don’t know
14 Heart disease Yes No Don’t know Yes No Don’t know
l5 High Cholesterol Yes No Don’t know Yes No Don’t know
16 AIDS Yes No Don’t know Yes No Don’t know
17 Hepatitis Yes No Don’t know Yes No Don’t know
18 Herpes Yes No Don’t know Yes No Don’t know
19 Cancer Yes No Don’t know Yes No Don’t know
20 Thyroid disease Yes No Don’t know Yes No Don’t know
21 Menstrual irregularities Yes No Don’t know Yes No Don’t know
22 Albumin or protein in your urine Yes No Don’t know Yes No Don’t know
23 Toxemia Yes No Don’t know Yes No Don’t know
24

25 Influenza or the flu Yes No Don’t know
26 Other conditions? (please specify) Yes No Don’t know
27 What kind of medicine?

 

During what month of pregnancy did you take it?

 

102

28
29
3O
31
32

Have you been pregnant before?
Have you ever had a miscarriage?
Have you ever delivered still born?
Have you ever had an abortion?

Have you ever delivered prematurely?

103

No
No
No
No
No

Appendix C: Physical Health Symptoms

104

Physical Health Symptoms

Now I have a list of specific symptoms and would like you to answer how much you have
experienced these.

 

 

 

 

 

 

 

 

 

0 1 2 3 4
NEVER Once a month 2-3 times a Once or twice 3 or more times a
or less month a week week
pregnancy? Before you became pregnant?
1. Sleep problems (can’t fall asleep, wake up / /

 

 

in the middle of the night or early in
the morning)

2. Back pain

3. F aintness

4. Constant fatigue

5. Headache

6. Nausea and/or vomiting

7. Acid stomach or indigestion

8. Stomach pain

9. Hands trembling

10. Heart pounding or racing

1 1. Poor appetite

12. Feeling weak all over —__/
13. Feeling low in energy
14. Muscle tension or soreness
15. Severe aches and pains
16- Constant coughing
17. Heavy chest cold
18- Trouble breathing or shortness of breath
19- Pain or tightness in chest

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

\\\\\\\\\\

 

 

 

 

 

 

 

 

 

 

 

\\\\\\\\\\\\\\\\

 

 

\

 

 

\\\\\\\

\

 

 

105

Appendix D: Center for Epidemiological Studies Demession Scale

106

CES—D

 

We would like to know about your feelings during the past week. For each of the following statements
please consider how often you have felt this way.

 

Answer Key

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

0 Rarely or none of the timgless than 1 day)
l = Some or a little of the timfil-Z days)
2 = Occasional or a moderate amount of time (3-4 days)
3 = Most or all of the time (5-7 days)
I. I was bothered by things that usually don’t bother me. O 1 2 3
2. I did not feel like eating; my appetite was poor. 0 l 2 3
3. I felt that I could not shake off the blues even with help from family. 0 I 2 3
4. I felt that I was just as good as other people. 0 l 2 3
5. I had trouble keeping my mind on what I was doing. 0 1 2 3
6. I felt depressed. O l 2 3
7. I felt that everything I did was an effort. 0 l 2 3
8. I felt hopefiJl about the fiiture. 0 1 2 3
9. I thought my life had been a failure. 0 1 2 3
10. I felt fearful O 1 2 3
11. My sleep was restless 0 1 2 3
12. I was happy. 0 1 2 3
I3. I talked less than usual 0 1 2 3
I4. I felt lonely O 1 2 3
15. People were unfriendly 0 1 2 3
16. Ienjoyed life 0 1 2 3
l7. 1 had crying spells O 1 2 3
Ta. I felt sad 0 1 2 3
19. I felt that people disliked me O l 2 3
20. I could not get “going.” 0 1 2 3

 

 

107

 

Appendix E: State-Trait Anxiety Inventog

108

 

STAI Y-l

A number of statements which people have used to describe themselves are given below. Read
each statement and indicate how you feel right now, that is at this moment. There are no right or
wrong answers. Do not spend too much time on any one statement but give the best answer
which seems to describe your present feelings best

 

 

 

 

 

 

Not at all Somewhat Moderately So Very Much So
1 2 3 4

1. I feel calm ...................................................................... 1 2 3 4
2. I am secure ..................................................................... 1 2 3 4
3. I am tense ...................................................................... 1 2 3 4
4. I feel strained .................................................................. 1 2 3 4
5. I feel at ease ................................................................... 1 2 3 4
6. I feel upset ..................................................................... 1 2 3 4
7. I am presently worrying over possible misfortunes ..................... 1 2 3 4
8. I feel satisfied .................................................................. l 2 3 4
9. I feel frightened ............................................................... 1 2 3 4
10. I feel comfortable ............................................................ 1 2 3 4
1 l . I feel self confident .......................................................... 1 2 3 4
12. I feel nervous .................................................................. 1 2 3 4
13 . I am jittery ..................................................................... 1 2 3 4
14. I feel indecisive ............................................................... 1 2 3 4
15. I am relaxed .................................................................. 1 2 3 4
16. I feel content ................................................................. 1 2 3 4
17. I am worried .................................................................. 1 2 3 4
18. I feel confused ................................................................ l 2 3 4
19. I feel steady ................................................................... 1 2 3 4
20. I feel pleasant ................................................................. 1 2 3 4

109

 

STA] Y-2

A number of statements which people have used to describe themselves are given below. Read
each statement and indicate how you generally feel. There are no right or wrong answers. Do
not spend too much time on any one statement but give the best answer which seems to describe
your present feelings best

 

 

 

 

 

 

 

Not at all Somewhat Moderately So Very Much So
1 2 3 4

21. I feel pleasant ................................................................. 1 2 3 4
22. I feel nervous and restless .................................................. l 2 3 4
23. I feel satisfied with myself ................................................. l 2 3 4
24. I wish I could be as happy as other seem to be .......................... 1 2 3 4
25. I feel like a failure ........................................................... 1 2 3 4
26. I feel rested ................................................................... 1 2 3 4
27. I am “calm, cool, and collected” .......................................... l 2 3 4
28. I feel that difficulties are piling up so that I cannot overcome them... 1 2 3 4
29. I won'y too much over something that really doesn’t matter ........... 1 2 3 4
30. I am happy .................................................................... 1 2 3 4
3 1 . I have disturbing thoughts .................................................. 1 2 3 4
32. I lack self confidence ........................................................ 1 2 3 4
33. I feel secure ................................................................... 1 2 3 4
34. I make decisions easily ...................................................... 1 2 3 4
35. I feel inadequate ............................................................. 1 2 3 4
36. I am content .................................................................. 1 2 3 4
37. Some unimportant thought runs through my mind and bothers me... 1 2 3 4
38. I take disappointments so keenly that I can’t put them out of my mind 1 2 3 4
39. I am a steady person ........................................................... 1 2 3 4

40. I get in a state of tension or turmoil as I think over my recent

concerns and interests ......................................................... 1 2 3

110

 

Appendix F: Perceived Stress Scale

 

lll

PSS

Sometimes when people are stressed they can feel upset while others do not. In the last month
how often have you had these feelings?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Answer Key
0 = Never
1 = Once or twice
2 == Several Times
3 = Often
4 = VerLOften
1. How often have you been upset because of something that happened 1 2 3 4
unexpectedly?
2. How often have you felt that you were unable to control the important 1 2 3 4
things in your life?
3. How often have you felt nervous and “stressed?” 1 2 3 4
4. How often have you dealt successfully with irritating life hassles? l 2 3 4
5. How often have you felt confident about your ability to handle your 1 2 3 4
personal problems?
6. How often have you felt that things were going your way? 1 2 3 4

 

7. How often have you found that you could not cope with all the things that 1 2 3 4

 

 

you had to do?
8. How often have you been able to control irritation in your life? 1 2 3 4
9. How often have you felt that you were on top of things? 1 2 3 4

 

10. How often have you been angered because of things that happened that 1 2 3 4

were outside of your control?

 

11. How often have you found yourself thinking about things that you have to 1 2 3 4

accomplish?

 

12. How often have you been able to control the way you spend your time? 1 2 3 4

 

 

13. How often have you felt difficulties were piling up so high that you could I 2 3 4

not overcome them?

 

 

112

 

Appendix G: Life Experiences Survey

113

LES
Listed below are a number of events that sometimes bring about change in the lives of those who experience them.
Please check those events that you have experienced since you were pregnant and indicate the time period during which
they happened. Be sure that all check marks are directly across from the items they correspond to.

Also, for each item checked below, please indicate whether you viewed the event as having a positive or negative
impact on your life at the time it occurred. A rating of -3 would indicate an extremely negative impact. A rating of 0
suggests no impact either positive or negative. A rating of +3 would indicate an extremelv positive impact. Check NA
if the event did not happen to you in the last year.

 

NA During Extremely Moderately Somewhat

 

 

pregnancy negative negative negative

I. Marriage -3 -2 -1

2. Detention in jail or comparable -3 -2 -I

institution

3. Death of a spouse/partner -3 -2 -l

4. Major change in sleeping habits -3 -2 -1

(much more or much less sleep)

5. Death of close family member -3 -2 -I
a. mother -3 -2 -1
b. father -3 -2 -l
c. brother -3 -2 -l
d. sister -3 -2 -I
e. grandmother -3 -2 -I
f. grandfather -3 -2 -l
g. spouse/partner -3 -2 -l
h. child -3 -2 -1
3. other (specify) -3 -2 -l

6. Major change in eating habits -3 -2 -I

(eating much more or much less food)

7. Foreclosure on mortgage or loan -3 -2 -I

8. Death of close friend -3 -2 -1

9. Outstanding personal achievement -3 -2 -I

10. Minor law violations (traffic -3 -2 -1

tickets, disturbing the peace, etc.)

1 1. Pregnancy -3 -2 -I

12. Changed work situation (different -3 -2 -1

work responsibility, major change in

working conditions, working hours,

etc.)

I3. New job -3 -2 -l

114

NA During
pregnancy

14. Serious illness or injury of close
family member

a. mother

b. father

c. brother

(I. sister

e. grandmother

f. grandfather

g. spouse/partner

h. child in study

i. other child

j. other (specify)

 

15. Sexual difficulties

16. Trouble with employer (for
example, in danger of losing job, being
suspended, demoted, etc.)

17. Trouble with in-Iaws or partner’s
family

18. Major change in financial status (a
lot better off or a lot worse off)

19. Major change in closeness of
family members (a lot more close or a
lot less close)

20. Gaining a new family member
(through birth, adoption, family
member moving in, etc.)

21. Change of residence

22. Marital separation (due to conflict)

23. Major change in church activities
(increased or decreased attendance)
24. Marital reconciliation

25. Major change in number of
arguments with spouse/partner (a lot
more or a lot less arguments)

26. Change in spouse/partner’s work
(loss of job, beginning new job,
retirement, etc.)

27. Major change in usual type and/or
amount of recreation

28. Borrowing more than $10,000
(buying home, business, etc)

29. Borrowing less than $10,000
(buying car, TV, getting school loan,
etc.)

30. Being fired from job

115

Extremely
negative

-3
-3

-3

-3

-3

-3

-3

-3

-3

Moderately
negative

—2
-2

-2

-2

-2

-2

-2

-2

-2

-2

Somewhat
negative

NA During

pregnancy
31. Having abortion

32. Major personal illness or injury

33. Major change in social activities,
e.g., parties, movies, visiting
(increased or decreased participation)
34. Major change in living conditions
of family (building new home,
remodeling, deterioration of home,
neighborhood, etc.)

35. Divorce

36. Serious injury or illness of close
friend
37. Retirement from work

38. Son or daughter leaving home (due
to marriage, college, etc.)
39. Ending of formal schooling

40. Separation from spouse/partner
(due to work, travel, etc.)
41. Engagement

42. Breaking up with
boyfriend/girlfriend

43. Leaving home for the first time
44. Reconciliation with

boyfriend/girlfriend

Other recent experiences which have
had an impact on your life. List and
rate

47.

48.

49.

116

Extremely
negative

-3

-3

-3

-3
-3
-3
-3

-3

Moderately
negative
-2
-2

-2

-2

-2
-2
-2
-2
-2
-2
-2
-2
-2

—2

Somewhat
negative
- I

Appendix H: Daily Hassles Questionnaire

117

0:00 EOm

 

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. a 95 u 9:9 emu—h doom 2&8: an... 8.3!— 053
.3 83:9:— 629-5 :9“ 2:3— 2: he Eu: 2: :0 33:5: 2: “a 32 :2: 55”: ans near—uhuuomfimhduauofifiefiwnuua — 9... onus.— .. «a5 a a. 9:. 3.3:
. . 3 do . E .859. .— E
95 .533 $39.: .35: 55:. .5 .58 .53: = m2: £355 .5 a «30.. w E. E do n. 5... I

118

 

119

Appendix 1: Birth. plegnanq, and delivery questionnaire

120

Birth, Pregnancy, and Delivery Questionnaire

The first questions I want to ask you concern your health during your pregnancy as well as
the birth and delivery of your baby.

I. What is your baby’s name?

 

2. What date was your baby born?
Month Day Year

 

3. Is your baby a (circle one) Boy or Girl?

These next questions are about your health the last weeks of pregnancy and since your delivery

Last weeks of pregnancy

4 High blood pressure Yes No Don’t know
(hypertension)
5 Asthma Yes No Don’t know
6 Allergies Yes No Don’t know
7 Sickle Cell disease Yes No Don’t know
8 Diabetes Yes No Don’t know
9 Epilepsy Yes No Don’t know
10 Anemia Yes No Don’t know
11 Migraines Yes No Don’t know
12 Heart disease Yes No Don’t know
13 High Cholesterol Yes No Don’t know
14 AIDS Yes No Don’t know
15 Hepatitis Yes No Don’t know
16 Herpes Yes No Don’t know
17 Cancer Yes No Don’t know
I8 Thyroid disease Yes No Don’t know
19 Menstrual irregularities Yes No Don’t know
20 Albumin or protein in your urine Yes No Don’t know
2| Toxemia Yes No Don’t know

22 What kind of medicine?
During what month of pregnancy did you take it?

 

 

121

 

 

 

23 Rh or other blood group incompatibility Yes No Don’t know
24 Influenza or the flu Yes No Don’t know
25 Other conditions? (please specify) Yes No Don’t know
26 Have you taken any over the counter or prescribed Yes No Don’t know
medication during your pregnancy?
these conditions since delivery Yes No
a. IF yes, which ones (list # of condition above)
The next questions are about your delivery
28. Where was your baby delivered? (Check one)
Hospital
Home
Other (Please specify: J
29. How long was your labor? hours
Was it a vaginal or caesarean birth? (Check one)
Vaginal
Caesarean
31. Was it a breech (bottom first) delivery? YES NO
32. Were you given anaesthetic for the delivery (e.g., an epidural or spinal?) YES NO
33. How many weeks pregnant were you when you delivered your baby? weeks
34. What was your baby’s birth weight? (lbs.) (023.)
35. What was your baby’s birth length? (inches)
36. What was your baby’s APGAR score at 1 minute 5 minutes?
37. After delivery, did you stay in the hospital because of health problems? YES NO
If YES, how many days? days
38. After delivery, did the baby stay in the hospital because of health problems? YES NO

If YES, how many days? days

Did your baby have any of the following complications during delivery or shortly after delivery?

 

39a. Bleeding? YES NO
39c. Poor feeding/suckin g? YES NO
39d. Seizures? YES NO
3%. Cord around neck? YES NO
39f. Infection? YES NO
39g. Low blood sugar? YES NO
39h. Trouble keeping a constant temperature? YES NO
39i. Alcohol or drug withdrawal? YES NO
39j. Heart problems? YES NO
39k. Birth defects? YES NO
(What were they? )
39!. Injured during birth? YES NO
(How?

 

122

27.
Were
you
diagno
sed
with
any of

These new questions are about your baby ’s health now

3. Which of the following best describes your infant’s overall state of health?

may Healthy Healthy DNot very healthy 1:1Unhealthy

4) Has your child had any serious illnesses or health problems since birth that have required active medical treatment?

 

 

 

 

YES
NO
If yes can you please specify the illness
a) Are there any lasting problems?
b) Please circle one ofthe following:
Doubtful (as to full recovery or lasting problems)
Yes, full recovery
Yes, with persistent problems
5) Has your child been admitted to the hospital for one night or more. at any time since birth?
YES NO
a) If yes, how many times 1 time 2 times 3 or more times
c) What was the reason for the admission?
6) Does your child have any long standing illnesses, disabilities, or health problems? YES NO
7 Does your child breast feed? YES NO
8 About how long in minutes does your baby suck?
9 Does your child use a bottle? YES NO
10 About how much does your baby take at one time? ounces
II On average, how many times a day does your child eat?
12 How often does your baby feed? Every __ hours
14 How many weeks old was your baby when s/he was l_as_t
measured? __ weeks
15 How much did your baby weigh at the last measurement? _(lbs.)_(ozs.)
16 What was your baby’s length at the last measurement? inches

17 How big around was your baby’s head (head circumference) at

the last measurement? inches

123

Appendix J: Infant Care Scale

124

ICS

How much confidence do you have about doing each of the behaviors listed below.
There are no right or wrong answers.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Very Little (- -) Quite A Lot
A f B l C l r) T E
1 Knowing immunization schedules 27 Knowing what articles are safe to leave
with your baby in the crib or baby seat
2 Knowing schedule for physical exam 28 Treating diagr rash
3 Recognizing signs of an ear infection 29 Burping your baby
4 Identifying diaper rash 30 Weighing your baby
5 Knowing when to get help from the 31 Taking your baby’s temperature
clinic, emergency room, or doctor
6 Recognizing teething 32 Changing a diaper
7 Knowing regular breathing sounds of 33 Relieving pain from teething
babies
8 Recognizing cwestion 34 Relieving congestion
9 Recognizing an allergic response 35 Giving your baby a liquid medication
10 Recognizing a croup 36 Relievigg croup
11 Knowing expected weight gain patterns 37 Treating constipation
for an infant
12 Recognizing constipation 38 Treatigg diarrhea
13 Recognizing diarrhea 39 Relieving gas pains
14 Recognizing gas pains 40 Establishing a sensible sleeping
schedule
15 Knowing normal growth and 41 Soothing your crying baby
development gttems
16 Knowing how much to feed your baby 42 Breast or bottle feeding your biby
l7 Selecting the best formula 43 Spoon feeding your baby
18 Selecting baby foods 44 Preparing baby food
19 Flaming a balanced diet for your baby 45 Introducing new food into baby’s diet
20 Knowing how to use a baby bottle 46 Establishing a sensible feeding
schedule
21 Identifying safety hazards in the house 47 Holding your baby
22 Choosing safe baby toys 48 Demonstrating a tonic neck reflex
23 Choosing safe baby furniture 49 Bathing your baby
24 Choosing safe baby clothes 50 Using a car seat
25 Knowing which medications are 51 Walking while holding your baby
dangerous
26 Knowing safe positions for a baby after Playing with your baby
feedirg

 

 

 

 

125

 

 

Appendix K: Infant Behavior Questionnaire

126

IBQ

INSTRUCTIONS: Please road ogrgfully before starting:
As you read each description of the baby’s behavior below, please indicate how often the baby did this during the LAST WEEK (the

past seven days) by circling one of the numbers in the left column. These numbers indicate how often you observed the behavior

described during the last week.
(I) (2) (4) (5) (6) (7) 00
Never Very Less Than About Half More Than Almost Always Does Not
Rarely Half the Time the Time Half the Time Always Apply

The “Does Not Apply” (X) column is used when you did not see the baby in the situation described during the last week. For
example, if the situation mentions the baby having to wait for food or liquids and there was no time during the last week when the
baby had to wait, circle the (X) column. “Does Not Apply” is different from "Never" (1). “Never” is used when you saw the baby in
the situation, but the baby never engaged in the behavior listed during the last week. For example. if the baby did have to wait for
food or liquids at least once but never cried loudly while waiting, circle the (l ) column.

Please be sure to circle a number for evm item.

Feeding

When having to wait for food or liquids during the last weele how often did the brim

During fgging, how often (Ed tho baby:

I34 7X ...... (4)
134 7

X ...... (5)

0‘05

2 5
2 5

Dugng feeding, how often did the baby:

 

I 2 3 4 5 6 7 X ...... (l) seemnotbothered?
I 2 3 4 5 6 7 X ...... (2) show mild fussing?
I 2 3 4 5 6 7 X ...... (3) cryloudly?

lie or sit quietly?
squirm or kick?

I 2 3 4 5 6 7 X ...... (6) wavearrns?
l 2 3 4 5 6 7 X ...... (7) fussorcrywhens/hehadenoughtoeat?
I 2 3 4 5 6 7 X ...... (8) fuss orcry when givenadisliked food?

When giveb a new food or liquid, how ofton did the baby:

1 2 3 4 5 6 7 X ...... (9) accept it immediately?

I 2 3 4 5 6 7 X ...... (10) reject it byspittingout, closingmouth, etc.?

I 2 3 4 5 6 7 X ...... (ll) notacceptitno matterhow manytimes offered?
Slegping

Befor fallin a lo atni h min thel tw h w i the '

1234567X ...... (12)

During sleep, how often did tho baby:

Ailey sloeoing, how often did tho baby:

show no fussing or crying?

I 2 3 4 5 6 7 X ...... (l3) tossaboutinthecrib?
1 2 3 4 5 6 7 X ...... (14) move fromthemiddletotheendofthecn'b?
l 2 3 4 5 6 7 X ...... (15) sleepinoneposition only?

I 2 3 4 5 6 7 X ...... (l6) fussorcryimmediately?
l 2 3 4 5 6 7 X ...... (l7) playquietlyinthecn'b?
l 2 3 4 5 6 7 X ...... (18) coo and vocalize forperiods of 5 minutes or longer?
I 2 3 4 5 6 7 X ...... (l9) cry if someone doesn’t come withinafew minutes?
w 'd b b :
l 2 3 4 5 6 7 X ...... (20)seem angry (crying and fussing) when you left her/himinthecrib?

127

l 2 3 4 5 6 7 X ...... (2|) seem contented when left in thecrib?
1 2 3 4 5 6 7 X ...... (22) cry or fuss before going to sleep for naps?
Batbing and Drossing

When being dressed or undressgl during the last week. how often did the baby:

I 2 3 4 5 6 7 X ...... (23) waveher/hisarmsandkick?
l 2 3 4 5 6 7 X ...... (24) squinnand/ortrytoroll away?
1 2 3 4 5 6 7 X ...... (25) smileorlaugh?

When put into the bath water. how often did the bziiy:

l 2 3 4 5 6 7 X ...... (26) stanle(gasps, throws out arms: stiffens body, etc)?
I 2 3 4 5 6 7 X ...... (27) smile?

I 2 3 4 5 6 7 X ...... (28) laugh?

1 2 3 4 5 6 7 X ...... (29) haveasurprised expression?

I 2 3 4 5 6 7 X ...... (30) splash orkick?

l 2 3 4 5 6 7 X ...... (31) turn bodyand/orsquirm?

When face was washed. how often did the bafl

X ...... (32) smile or laugh?

1234567
1234567X ...... (33) fussorcry?

When hair was washed. how often did the baby:

 

 

I 2 3 4 5 6 7 X ...... (34) smileorlaugh?
I 2 3 4 5 6 7 X ...... (35) fussorcry?
Play
How often during the last week did the baby:
I 2 3 4 5 6 7 X ...... (36)look at pictures in books and/or magazines for 2-5 minutes atatime?
l 2 3 4 5 6 7 X ...... (37)]ook at pictures in books and/or magazines forSminutes or longer atatime?
I 2 3 4 5 6 7 X ...... (38)stare atamobile, crib bumper or picture forSminutes or longer?
I 2 3 4 5 6 7 X ...... (39)play with onetoyorobject for 5-10 minutes?
I 2 3 4 S 6 7 X ...... (40)play with one toy or object for 10 minutes or longer?
I 2 3 4 5 6 7 X ...... (41)spend time just looking at playthings?
l 2 3 4 5 6 7 X ...... (42)repeat the same sounds over and over again?
1 2 3 4 5 6 7 X ...... (43)laugh aloudinplay?
I 2 3 4 5 6 7 X ...... (44)smileorlaugh when tickled?
l 2 3 4 5 6 7 X ...... (45)cryorshow distress when tickled?
l 2 3 4 5 6 7 X ...... (46)repeat the same movement withanobject for2minutes or longer(e.g.. puttingablock inacup,

kicking or hitting a mobile)?

When methin th ba w la'n withha tobe mv hw

I 2 3 4 5 6 7 X ...... (47) cryorshowdistress foratime?
I 2 3 4 5 6 7 X ...... (48) cry or show distress for several minutes for longer?
I 2 3 4 5 6 7 X ...... (49) seem notbothered?
t arun 1 full h w ftendidthe b:
I 2 3 4 5 6 7 X ...... (50) smile?
I 2 3 4 5 6 7 X ...... (51) laugh?

During a oeekaboo game. how often did th; baby:

12345
12345

005

7 X ...... (52) smile?
7 X ...... (53) laugh?

128

Daily Activities

How often during the last_week did the baby:

I 2 3 4 5 6 7 X ...... (54)cry or show distress at a loud sound (blender, vacuum cleaner, etc)?
I 2 3 4 5 6 7 X ...... (55)cry or show distress at a change in parents’ appearance (glasses off, shower cap on, etc.)?
I 2 3 4 5 6 7 X ...... (56)when in a position to see the television set, look at it for 2 to 5 minutes at a time?
I 2 3 4 5 6 7 X ...... (57)when in a position to see the television set, look at it for 5 minutes or longer?
1 2 3 4 5 6 7 X ...... (58)protest being put in a confining place (infant seat, play pen, car seat, etc)?
I 2 3 4 5 6 7 X ...... (59)stattle at a sudden change in body position (for example, when moved suddenly)?
I 2 3 4 5 6 7 X ...... (60)startle to a loud or sudden noise?
I 2 3 4 5 6 7 X ...... (6l)cry after startling?

When beingheld. how often did the baby;
I 2 3 4 5 6 7 X ...... (62) squirm. pull away, or kick?

When pl_a_ced on hisrher back; how often did the baby:

I 2 3 4 S 6 7 X ...... (63) fussorprotest?

l 2 3 4 5 6 7 X ...... (64) smileorlaugh?

I 2 3 4 5 6 7 X ...... (65) liequietly?

l 2 3 4 5 6 7 X ...... (66) waveannsandkick?

l 2 3 4 5 6 7 X ...... (67) squirmand/ortum body?

Whon the baby wanted something, how often did s/he:

X ...... (68) become upset when s/he could not get what s/he wanted?

3 4 5
3 4 5 X ...... (69 )have tantrums (crying, screaming, face red, etc.) when she did not get what s/he wanted?

OO\

2 7
2 7

When placed in go infant seat or gar seat. how often did the baby;

 

l 2 3 4 5 6 7 X ...... (70) waveannsandkick?

I 2 3 4 5 6 7 X ...... (71) squinnandtumbody?

l 2 3 4 5 6 7 X ...... (72) lieorsit quietly?

l 2 3 4 5 6 7 X ...... (73) show distressat first; then quiet down?

When you returned from having been aw; amithe babywas awake. how often dfil she:
I 2 3 4 5 6 7 X ...... (74) smile or laugh?

When introduced to a strange person. how often did the baby:

I 2 3 4 5 6 7 X ...... (75) clingtoaparent?

l 2 3 4 5 6 7 X ...... (76) refusetogotoastranger?

I 2 3 4 5 6 7 X ...... (77) hang back from thestranger?

I 2 3 4 5 6 7 X ...... (78) never “warm up" to the stranger?
l 2 3 4 5 6 7 X ...... (79) approach the stranger at once?

I 2 3 4 5 6 7 X ...... (80) smileorlaugh?

When introduced to a dog (neat. how often did the baby;

I 2 3 4 5 6 7 X ...... (81) cryorshowdistress?
l 2 3 4 5 6 7 X ...... (82) smileorlaugh?
l 2 3 4 5 6 7 X ...... (83) approach at once?

mum

Have you tried any of the following soothing techniques in the last two weeks? If so, how often did the method soothe the baby?
Circle (X) if you did not try the technique during the LAST TWO WEEKS.

l 2 3 4 5 6 7 X ...... (84) rocking?

I 2 3 4 5 6 7 X ...... (85) holding?

I 2 3 4 5 6 7 X ...... (86) singingortalking?

l 2 3 4 5 6 7 X ...... (87) walking with the baby?

I 2 3 4 5 6 7 X ...... (88) givingthebabyatoy?

l 2 3 4 5 6 7 X ...... (89) showing the baby something to look at?

I 2 3 4 5 6 7 X ...... (90) patting or gently rubbing some parts of the baby‘s body?
I 2 3 4 5 6 7 X ...... (9i) offering food or liquid?

1 2 3 4 5 6 7 X ...... (92) offering baby her/his securityobject?

1 2 3 4 5 6 7 X ...... (93) changingbaby’s position?

129

I 2 3 4 5 6 7 X ...... (94) other(pleasespecify)

 

130

Appendix L: Cortisol

131

Directions fir Saliva Sample
Before You Take Your Saliva Sample Remember:

0 Please take this sample as soon as you wake up in the morning and write down the time on the line
below.

0 Please do oo_t eat or drink anything before taking this sample.

To Take Sample

. With the straw inside the collection tube, drool into the straw until the 1.0 mL line is reached. Be
careful to no have “Spit bubbles” at the top. The sample should be clear without bubbles.

o If you have trouble producing saliva, you can:

0 chew on the end of the straw
e or chew the piece of gum enclosed to help stimulate the flow.

0 When you are finished, place the sample in your refrigerator until your afternoon interview

Thank you so much for participating in the Pregnancy Stress Studyllll If you have any questions please
call us at 432-3825.

Time of Sample

132

Appendix M: Infant Sleep

133

E
Please use the chart below to describe your infant’s sleep pattern in the last 24 hours. If

this was not a typical 24-hr period please describe the most typical pattern.

A= awake S= sleep

 

 

134

Appendix N: Fliers

135

 

 

ARE YOU PREGNANT?
———————IJ______—___I

YOU MAY BE ELIGIBLE TO PARTICIPATE IN A
STUDY ABOUT
Maternal Stress During Pregnancy

!! $10.00 !!

 

 

 

 

 

 

We are looking for pregnant women between 30 and 34
weeks to participate in a research study at Michigan State
University. You will be asked about experiences and
feelings during pregnancy, perceptions of your infants, and
recent life events.

- Interview can be done at MSU or at your home.
- You will be paid $10.00 in cash.
- All information is kept completely confidential.

 

 

!! $10.00 !!
If you are interested or would like more information,
please call 432-3825 and ask for

The Pregnancy Stress Study

   

 

 

I36

Appendix 0: Screen

137

 

l

ll".

SCREEN

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

]. How far along in weeks are you in your pregnancy?
3. Was this verified by a doctor? YES NO
2. Are you pregnant with more than one baby? YES NO
3. About how many prenatal visits have you had?
4. Have you been diagnosed with any fetal abnormalities? YES NO
a. If yes, what kind of abnormalities?
5. During this pregnancy did you drink alcoholic beverages? YES NO
a. About how often did you drink (rarely, sometimes, often)?
6. During this pregnancy did you use marijuana, crack cocaine, heroin, or other YES NO
substances?
3. About how often did you use these substances (rarely, sometimes,
ofien)?
7. During this pregnancy did you smoke cigarettes? YES NO
a. About how ofien did you smoke (rarely, sometimes, often)?
8. Did you take prescription medicine during this pregnancy? 1 YES NO
a. If yes please specify what kind and when
9. Did you take over the counter medicine during this pregnancy I YES NO
3. lfyes please specify what kind and when
10. Have you been diagnosed with hypertension, diabetes, or any other health YES NO
condition during this pregnancy?
a. If yes please specify?
1 l. Wergyou diagposed with any of these conditions before you were pregnant? YES NO
12. Have you ever been diagnosed with a chronic disease such as sickle cell, cancer, YES NO
or thyroid disease during this pregnancy?
13. Before this pregnancy? YES NO
12. Have you been diagnosed with an STD such as herpes or HIV during this YES NO
regnancy?
[3. Before this megnancy? YES NO
14. Have you ever been punched, kicked, or beaten up by a romantic partner during YES NO
this pregnancy?

 

 

 

138

Appendix P: Consent Forms

139

Pregnancy and Stress Study
Consent Form — Time 1

This study is part of a survey of women in Michigan, some of whom may be stress during their
pregnancy. We hope to learn about the types of stressors you may have faced during your pregnancy, how
stressful they are to you, the strengths that you bring to your situation, your feelings, your perceptions of
your child, and your relationships with others, including partners and friends, as well as how stress effects
the physiology of pregnant women. We hope to use this information to help plan better programs for
pregnant women experiencing stress during pregnancy.

If you decide to take part in the survey today, you will be asked questions about events that have
happened to you in the last year, how you have been feeling recently, and your feelings about your child
and the people in your life who provide support for you. You will also be asked to give a saliva sample to
help us learn more about the biology of stress. However, nothing that we do will be painful or dangerous.
The total interview will take about 1 hour. You will be paid $10 for your participation.

All information that you give us will be kept strictly confidential among the project staff. Your
name or will not be on any questionnaires; an identification number will be put on them instead. All
questionnaires and saliva samples will be kept in locked file cabinets in a locked office. All saliva samples
will be stored in a locked freezer and destroyed after analysis. Your identity will not be revealed in any
reports written about this study. We will summarize information fi'om all study participants and will not
report information about yourself or any individuals. Your privacy will be protected to the maximum extent
allowable by law.

The only exception to full confidentiality is in the case of ongoing child abuse or neglect. If you
indicate that child abuse or neglect is occurring in your household, we are required to make a report to
Child Protective Services. We would inform you if we thought we needed to make such a report.

You have the right to refuse to answer any questions or to withdraw from this study at any point
during the interview with no penalty or negative consequences. Your decision about whether to participate
or not will not affect your relationship with any agencies or Michigan State University. If you have any
questions, please ask us. If you have any questions about the study later, you can contact Dr. Anne Bogat
or Shallimar Jones, M.A. at (517) 432-3825. If you have questions about your rights as a participant in this
research study you may contact Dr. Peter Vasilenko at (517) 355-2180.

We may be interested in recontacting you when your child turns 3 months. At the end of the
interview today, we will ask you to update the contact information that we have for you. Your participation
today does not obligate you to participate in any fiiture interviews.

 

I have read this form and agree to participate.

 

 

 

 

 

Signature of Participant Print Name Date
Witness Date
Anne Bogat, Ph.D. Dr. Peter Vasilenko
Michigan State University 202 Olds Hall
Department of Psychology Michigan StateUniversity
East Lansing, MI 48824 East Lansing, MI 48824

UCHRIS@msu.edu

Shallimar Jones, M.A.
Department of Psychology

East Lansing, MI 48824

140

I“?

 

 

Pregpancy and Stress Study
Consent Form — Time 2

Thank your for participating in the first time period of the Pregnancy and Stress study. This is the
second part of a survey of women in Michigan, some of whom may be stress during their pregnancy. We
hope to learn about the types of stressors you may have faced during your pregnancy, how stressful they are
to you, the strengths that you bring to your situation, your feelings, your child’s development, and your
relationships with others, including partners and friends, as well as how stress effects the physiology of
pregnant women. In addition we are also interested in how stress during pregnancy may impact infants.
We hope to use this information to help plan better programs for pregnant women experiencing stress
during pregnancy.

If you decide to take part in the survey today, you will be asked questions about events that have
happened to you in the last year, how you have been feeling recently, and your feelings about your child,
their development, and the people in your life who provide support for you. Nothing that we do will be
painful or dangerous. The total interview will take about 1 1/2 hours. You will be paid $15 for your
participation.

All information that you give us will be kept strictly confidential among the project staff. Your
name or will not be on any questionnaires; an identification number will be put on them instead. All
questionnaires and will be kept in locked file cabinets in a locked office. Your identity will not be revealed
in any reports written about this study. We will summarize information fi'om all study participants and will
not report information about yourself or any individuals. Your privacy will be protected to the maximum
extent allowable by law.

The only exception to full confidentiality is in the case of ongoing child abuse or neglect. If you
indicate that child abuse or neglect is occurring in your household, we are required to make a report to
Child Protective Services. We would inform you if we thought we needed to make such a report.

You have the right to refuse to answer any questions or to withdraw from this study at any point
during the interview with no penalty or negative consequences. Your decision about whether to participate
or not will not affect your relationship with any agencies or Michigan State University. If you have any
questions, please ask us. If you have any questions about the study later, you can contact Dr. Anne Bogat
or Shallimar Jones, M.A. at (517) 432-3 825. If you have questions about your rights as a participant in this
research study you may contact Dr. Peter Vasilenko at (517) 355-2180.

 

I have read this form and agree to participate.

 

 

 

 

 

Signature of Participant Print Name Date
Witness Date
Anne Bogat, Ph.D. Dr. Peter Vasilenko
Michigan State University 202 Olds Hall
Department of Psychology Michigan State University
East Lansing, MI 48824 East Lansing, MI 48824
UCHRIS@msu.edu

Shallimar Jones, M.A.
Department of Psychology
East Lansing, MI 48824

141

Appendix Q: Recontact Information

142

RECONTACT INFORMATION

We would like permission to stay in contact with you throughout the 6 months. We will contact you after your delivery
date to make sure we have your correct address and telephone number. Then 3 months after your baby is born, we will
call to set up an interview to ask you similar questions and also about the birth as well as your child’s health and
development. Providing us with the following information does not obligate you to talk to us on the telephone or meet
with us for the second visit.

Please list at least three people who will always know where you are, even if you were to move or relocate
unexpectedly.

lSt pgrson:
Name (Relationship to you):

 

Address:

 

 

Phone Number:

 

2"“ Person
Name (Relationship to you):

 

 

Address:

 

 

Phone Number:

 

3"I Person
Name (Relationship to you):

 

Address:

 

 

Phone Number:

 

1. Would you prefer: (circle one)

a) to be contacted directly? OR

b) to be contacted through one of the 3 persons listed on the previous page?
If you would like to be contacted through the above-listed persons, we will call them and ask if we may
call you directly. If we may not, we will send a note to you in care of the contact person.

3. If we or the people on the previous sheet lose contact with you, may we try finding you
through your social security # or driver’s license? YES NO

If yes, social security no.
driver’s license no.

 

 

INTERVIEWER: Have participant sign 3 letters.

Check here when completed

143

TABLES AND FIGURES

144

Table 1

Demographic Description of Sample at T1 (N=92)

 

Variable
Age 25.7 (5.3)
Income (median) $2,036 (1736)

 

Education (percent) --

Weeks pregnant 32.5 (1.89)
No High School 19%
High school, GED 24%
Trade School 26%
Associates 3%
B.A., BS. 21%
Med/Grad/Law 8%
Ethnicity (percent) --
White 50%
Black 29%
Latino 8%
Asian 3%
Native American 2%
Multi-racial 8%
Smoking 20%
Am cortisol nmol/L 12.22 (7.78)
Pm cortisol nmol/L 11.86 (7.43)

 

145

Table 2

Demographic Variables for T2 (N=65)

 

 

Variable Name Mean
Sex _-
Male 49%
Female 51%
Ethnicity --
Black 28%
White 34%
Asian 3%
Latino 1%
Bi-racial 27%
Multi-racial 4%
Gestation at delivery 39
Moderately premature 8(13%)
Extremely premature 1(2%)

Birth weight 7 lbs. 9 oz. (1.30)

Child age at interview 3.9 months (1.1)

(corrected for prematurity)

Type of birth --
Vaginal 80%
Caesarian 20%

Pregnancy Risk Factors 4 (3.01)

 

146

Table 3

Table of Means for Imputed vs. Non-Imputed Data

 

 

Demographic Characteristics N=65 mean N=27 mean
Age of mom (t1) 26 24
Age of child (t2) 3.9 4.1
Gestation (t2) 38 38
Birth weight (t2) 6.8 7.8
Number of bio children (t1) .83 1.2
People in household (T1) 3.1 3.3
Income (T1) 2249 1524
Education (T1) 3.6 2.8
Maternal Health complications during 4.4 4.6
pregnancy (T1)
Marriage 1.55 1.33

Study Variables of interest N=65 mean N=27 mean

Mental health (T1) 147 155
Stress (T1) 89 103
Perceived 35 36
Am cortisol (T1) nmol/L 13.01 10.32
Pm cortisol (T1) nmol/L 8.69 6.15
Mental health (T2) 152 144
Stress (T2) 100 99
Perceived (T2) 34 35
Activity (T2) 56 58
Distress to Limitations (T2) 54 59
Duration of Orienting (T2) 30 3O
Smiling (T2) 65 61
Infant Care (T2) 221 222
Consecutive Sleep (T2) 6.76 6.80

 

(T1. = original non-imputed and all of T2 was imputed)

147

Table 4

Table of Combined Imputed and Non-imputed Data for Study Variables

 

 

Variable Name Mean SD Range
Age ofmom (t1) 25.68 5.32 18-38
Age of child (t2) 4.0 1.11 2.14-7.25
Gestation (t2) 38.75 5.60 26—42
Income (T1) 2036 1736 O-8,000
Pregnancy Risk Factors 4.03 3.01 0-14
T1 Depression 24.02 8.79 0-47
T1 Anxiety 78.11 22.12 44-139
T] Life Events 20.61 12.68 2-60
T1 Daily Hassles 68.92 51.59 0-234
T2 Depression 19.5 7.48 0-42
T2 Anxiety 63.27 14.39 41-105
T2 Life Events 14.58 8.31 1-33
T2 Daily Hassles 51.41 4.26 42-58
Mental health (T1) 100 17.51 75-146
Stress (Tl) 100.00 14.58 0-234
Perceived (T1) 35.63 4.86 16-47
Am cortisol (T1) nmol/L 12.22 7.78 0.00-36.14
Pm cortisol (T1) nmol/L 11.86 4.36 1.10-27.31
Mental health (T2) 100.00 23.68 100-209
Stress (T2) 100.00 6.25 77-131
Perceived (T2) 34.61 4.64 22-47
Parenting Competency (T2) 4.27 .54 2.90-4.96
Activity (T2) 56.6 13.66 25-84
Distress to Limitations (T2) 56.00 14.01 16-94
Duration of Orienting (T2) 30.34 8.44 11-51
Smiling (T2) 64.22 12.53 41-96
Consecutive Sleep (T2) 6.78 2.88 2-12

 

148

8:95 .96. 5.5 v a : 828-3 .82 8.5 v a .

 

 

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8.3 .8. 8.- 3. 8.- 8.- 8.- 8.- 8. 8. 8. S. 8.- 8. 8. 8.- 8:53 2.85
8.3 8. .5. 8. 8.- .5. 8.- 8. 8. 8.. 8. .5. 8.- 8.- 8. 6:882
8.3 8.- :8. 8. :5. 5.- ..8. 8.- 8.- 8. 8. 8.- 5. 8. 355880
8.3 5.- 5.- 8.- 8. 8.- 5. 3. 8. 8.- 8. :5. 8. 8:53 .88
8.3 :8. 8. 8.- 8. 8. 8. 8. 8. 43. 3.- 8. 838.85
8.3 S.- 8. 8.- 8. t. 3.- t. 8. 8.- :8. 3:84.80:
8.3 8. 8. 8.- 5.- 8. 8.- 8.- 5.- 8.- 8:86.88
8.3 8. 8. 8. .8: 8. 8. 3. .8. @8898
8.3 8. 8.- 8.- 8. 3.- 8.- 8. av 80 2a
8.3 8. N3.- 8.- 5. m3.- 8. E too 52
8.3 S. 8. :8. 8. 8.- § 28 8
8.3 8. 8. :8. 8.- A3 .982 5
004 m P. we. we. A3 .83 N...
8.3 .8. E .382 3
8.3 E a: 5
8 t S 8 3 m3 8 3 S 5 m a o m 3. m N 3

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

L

 

 

 

 

asses, =< 8 882.68

m 88

149

Table 6: Hypothesis A: Mental Stress Predicting Infant Activity

 

 

 

 

Step 1 B SE [3 Beta
Age of baby 3.84 1.18 .28”
Pregnancy risk factors 1.37 .43 .31 **
T2 Perceived Stress -.54 .28 -.84
T2 Life Stress .57 .21 .26“
T2 Mental Stress -.OO .06 -.05

Total for Step 1 AR2 .23

Step 2
Age of baby 3.44 1.51 .28**
Pregnancy risk factors 1.74 .45 .39“
T2 Perceived Stress -.56 .27 -.19*
T2 Life Stress .59 .20 .27**
T2 Mental Stress .00 .06 .03
T1 Mental stress -.14 .06 -.25*

Total for Step 2 AR2 .05, F(6,91)= 5.41, p<.01
Notes to table:

 

*p<.05, **p<.01

150

Table 7: Hypothesis A: Mental Stress Predicting Distress To Limitations

 

 

 

 

Step 1 [3 SE [3 Beta
Age ofbaby -1.33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Stgp 1 AR2 = 04

Step 2
Age ofbaby -1 .34 1.36 -.11
Pregnancy risk factors .44 .53 .10
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.22 .24 -.10
T2 Mental Stress .07 .07 .11
T1 Mental Stress -.01 .07 -.03

Total for Step 2 AR2 = .00, F(6,91)= .65, p=n.s.
Notes to table:

*p<.05, **p<.01

151

Table 8: Hypothesis A: T1 Mental Stress Predicting Smiling

 

 

 

Step 1 [3 SE [3 Beta
Age of baby 2.03 1.21 .10
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .03 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age of baby 2.05 1.21 .18
Pregnancy risk factors .18 .47 .04
T2 Perceived Stress .10 .29 .04
T2 Life Stress .05 .21 .00
T2 Mental Stress .04 .06 .01
T1 Mental Stress .06 .06 .12

 

Total for Step 2
Notes to table:
*p<.05, **p<.01

ARZ = .01, F(6,91)= .82, p=n.s.

152

Table 9: Hypothesis A: Mental Stress Predicting Duration of Orienting

 

 

 

Step 1 [3 SE [3 Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .09 .29 .00
T2 Perceived Stress -.42 .19 -.23*
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08

Total for Step 1 AR2 = .07

Step 2
Age of baby -.44 .81 -.06
Pregnancy risk factors .09 031 .32
T2 Perceived Stress -.43 .19 -.24*
T2 Life Stress .01 .14 .01
T2 Mental Stress -.02 .04 -.05
T1 Mental Stress -.03 .04 -.09

 

Total for Step 2 AR2 = .01, F(6,91)= 1.09, p=n.s.

Notes to table:
*p<.05, **p<.01

153

Table 10: Hypothesis A: Mental Stress Predicting Consecutive Sleep

 

 

 

Step 1 [3 SE [3 Beta
Age of baby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .11

Step 2
Age of baby .30 .27 .11
Pregnancy risk factors -.07 .11 -.08
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .18
T2 Mental Stress .02 .01 .16
Mental Stress .00 .02 .04

 

Total for Step 2 AR2 = .00, F(6,91)= 1.65, p=n.s.

Notes to table:
*p<.05, **p<.01

154

Table 11: Hypothesis A: T1 Life Stress Predicting Activity

 

 

 

Step 1 B SE B Beta
Age of baby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.O3 .06 -.05

Total for Step 1 AR2 = .23

Step 2
Age of baby 3.52 1.19 .29**
Pregnancy risk factors 1.40 .47 .35“
T2 Perceived Stress -.51 .29 -.17
T2 Life Stress .61 .22 .28"
T2 Mental Stress -.01 .06 —.03
T1 Life Stress -.06 .10 -.O8

 

Total for Step 2 AR2 = .00, F(4,91)= 4.23, p <.01

Notes to table:
*p<.05, **p<.01

155

Table 12: Hypothesis A: Life Stress Predicting Distress to Limitations

 

Step 1 [3 SE [3 Beta
Age ofbaby -1.13 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

 

Total for Step 1 AR2 = .04

 

 

 

Step 2 ‘3.
Age of baby -1.40 1.35 -.11 '1:
Pregnancy risk factors .17 .54 .04 1;
T2 Perceived Stress .13 .33 .04 -‘
T2 Life Stress -.30 .25 -.13
T2 Mental stress .04 .07 .06
T1 Life Stress .12 .11 .14

Total for Step 2 AR2 = .01, F(6,91)= .84, p=n.s.
Notes to table:

 

*p<.05, **p<.01

156

Table 13: Hypothesis A: Life Stress Predicting Smiling

 

 

 

Step 1 B SE B Beta
Age of baby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .10 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .03 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .10 .29 .03
T2 Life Stress .08 .22 .00
T2 Mental Stress .02 .06 .04
Life Stress -.01 .05 -.02

 

Total for Step 2 AR2 = .00, F(6,91)= .65, p = n.s.

Notes to table:
*p<.05, **p<.01

157

Table 14: Hypothesis A: T1 Life Stress Predicting Duration of Orienting

 

 

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .09 .29 .00
T2 Perceived Stress -.42 .19 -.23*
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08

Total for Step 1 AR2 = .07

Step 2
Age of baby -.37 .80 -.05
Pregnancy risk factors .21 .32 .08
T2 Perceived Stress -.40 .19 -.20
T2 Life Stress .07 .15 .05
T2 Mental Stress -.08 .04 -.02
T1 Life Stress -.10 .07 -.19

Total for Step 2 AR2 = .03, F(6,91)= 1.41 p= n.s-
Notes to table:
*p<.05, **p<.01

158

Table 15: Hypothesis A: T] Life Stress Predicting Consecutive Sleep

 

 

 

Step 1 B SE B Beta
Age of baby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.O7 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .Ol .18

Total for Step 1 AR2 = .11

Step 2
Age of baby .32 .28 .13
Pregnancy risk factors .01 .11 .03
T2 Perceived Stress -.O6 .06 -.09
T2 Life Stress .11 .05 .22*
T2 Mental Stress .03 .01 .24*
T1 Life Stress -.04 .02 -.20

 

Total for Step 2 AR2 = .03, F(6,91)= 2.14 p= n.s-

Notes to table:
*p<.05, **p<.01

159

Table 16: Hypothesis A: T1 Perceived Stress Predicting Activity

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.50 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05

Total for Step 1 AR2 = 23

Step 2
Age ofbaby 3.27 1.18 .27**
Pregnancy risk factors 1.39 .43 .31 **
T2 Perceived Stress -.27 .32 -.09
T2 Life Stress .64 .21 .30**
T2 Mental Stress -.01 .06 -.02
T1 Perceived Stress -.53 .32 -.19

Total for Step 2 AR2 = .02, F(6,91)= 4.76 p<. 05.
Notes to table:
*p<.05, **p<.01

160

Table 17: Hypothesis A: T1 Perceived Stress Predicting Distress to Limitations

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress —.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.30 1.37 -. l 0
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .15 .37 .05
T2 Life Stress -.24 .25 -.10
T2 Mental Stress .06 .07 .10
T1 Perceived Stress .07 .37 .03

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

AR2 = .00, F(6,91)= .65 p=n.s.

161

Table 18: Hypothesis A: T1 Perceived Stress Predicting Smiling

 

 

 

Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age of baby 2.26 1.20 .20
Pregnancy risk factors .32 .43 .08
T2 Perceived Stress -.20 .33 -.07
T2 Life Stress -.06 .22 -.03
T2 Mental Stress .06 .06 .01
T1 Perceived Stress .57 .32 .22

 

Total for Step 2 AR2 = .03, F(6,91)= 1.19 p=n.s.

Notes to table:
*p<.05, **p<.01

162

Table 19: Hypothesis A: T1 Perceived Stress Predicting Duration of Orienting

 

 

 

 

Step 1 SE B Beta
Age of baby .80 -.06
Pregnancy risk factors .29 .00
T2 Perceived Stress .19 -.23*
T2 Life Stress .14 .10
T2 Mental Stress .04 -.08

Total for Step 1

Step 2
Age of baby .81 -.05
Pregnancy risk factors .29 .00
T2 Perceived Stress .22 -.25*
T2 Life Stress .15 .00
T2 Mental Stress .04 -.08
T1 Perceived Stress .22 .04

Total for Step 2 AR2 = .00, F(6,91)= 1.01 p=n.s.

Notes to table:
*p<.05, **p<.01

 

163

Table 20: Hypothesis A: T1 Perceived Stress Predicting Consecutive Sleep

 

 

 

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .10

Step 2
Age of baby .28 .27 .11
Pregnancy risk factors -.06 .10 -.06
T2 Perceived Stress -.06 .07 .10
T2 Life Stress .09 .05 .18
T2 Mental Stress .02 .01 .19
T1 Perceived Stress -.03 .07 -.06

 

Total for Step 2 AR2 = .00, F(6,91)= 1.68 p=n.s.
Notes to table:
*p<.05, **p<.01

 

164

Table 21: Hypothesis B: T1 Mental Stress Predicting A.M. Cortisol

 

 

 

 

Step 1 B SE B Beta
Age of baby .12 2.60 .00
Pregnancy risk factors .24 .94 .03
T2 Perceived Stress .18 .62 .03
T2 Life Stress -.36 .46 -.09
T2 Mental Stress -. 14 .12 -.12

Total for Step 1 AR2

Step 2
Age of baby .09 2.60 .00
Pregnancy risk factors .50 1.00 .06
T2 Perceived Stress .17 .62 .03
T2 Life Stress -.35 .46 -.08
T2 Mental Stress -.10 .13 -.09
T1 Mental Stress -.09 .13 -.09

Total for Step 2 211:2 = .01, F(6,91)= .47 p=n.s.
Notes to table:

 

*p<.05, **p<.01

165

Table 22: Hypothesis B: T1 Life Stress Predicting A.M. Cortisol

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -.37 2.562 -.02
Pregnancy risk factors .14 .94 .07
T2 Perceived Stress .18 .61 .03
T2 Life Stress -.60 .47 -.14
T2 Mental Stress -.21 .18 -.13

Total for Step 1 AR2 = .03

Step 2
Age ofbaby -. 12 2.60 -.01
Pregnancy risk factors .10 .94 .01
T2 Perceived Stress .20 .62 .04
T2 Life Stress -.62 .47 -.14
T2 Mental Stress -.20 .18 -.12
T1 Life Stress .20 .30 .07

Total for Step 2 AR2 = .04, F(6,91)= 1.05 p=n.s.
Notes to table:

 

*p<.05, **p<.01

166

Table 23: Hypothesis B:

Tl Perceived Stress Predicting A.M. Cortisol

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .12 2.60 .01
Pregnancy risk factors .24 .94 .03
T2 Perceived Stress .18 .62 .03
T2 Life Stress -.37 .46 -.09
T2 Mental Stress -.14 .12 -.12

Total for Step 1 AR2 = .03

Step 2
Age of baby .40 2.61 .02
Pregnancy risk factors .22 .94 .03
T2 Perceived Stress -.16 .71 -.03
T2 Life Stress -.45 .47 -.11
T2 Mental Stress -.16 .12 -.14
T1 Perceived Stress .67 .70 .12

Total for Step 2 AR2 = .01, F(6,9l)= .53 p=n.s.
Notes to table:

 

*p<.05, **p<.01

167

Table 24: Hypothesis B: T1 Mental Stress Predicting P.M. Cortisol

 

 

 

Step 1 B SE B Beta
Age of baby 1.95 2.56 .08
Pregnancy risk factors -.07 .93 -.01
T2 Perceived Stress -1.4 .61 -.20
T2 Life Stress -.05 .45 -.01
T2 Mental Stress -.O6 .12 -.05

Total for Step 1 AR2 = .05

Step 2
Age of baby 1.90 2.54 .08
Pregnancy risk factors .45 .99 .05
T2 Perceived Stress -1.l.7 .61 -.20
T2 Life Stress -.O3 .45 -.00
T2 Mental Stress -.00 .13 .01
T1 Mental Stress -.19 .13 -.18

 

Total for Step 2 AR2 = .02, F(6,91)= 1.14; p=n.s.

Notes to table:
*p<.05, **p<.01

168

Table 25: Hypothesis B: T1 Life Stress Predicting P.M. Cortisol

 

 

 

Step 1 B SE B Beta
Age of baby 1.95 2.56 .08
Pregnancy risk factors -.07 .93 -.01
T2 Perceived Stress -1.4 .61 -.20
T2 Life Stress -.05 .45 -.01
T2 Mental Stress —.O6 .12 -.05

Total for Step 1 AR2 = .05

Step 2
Age ofbaby 2.10 2.56 .09
Pregnancy risk factors .47 1.02 .05
T2 Perceived Stress -1.01 .62 -.18
T2 Life Stress .01 .47 .02
T2 Mental Stress -.07 .13 -.01
T1 Life Stress -.25 .21 -.16

 

Total for Step 2

Notes to table:
*p<.05, **p<.Ol

AR2 = .02, F(6,91)= 1.01; p=n.s.

169

Table 26: Hypothesis B: T1 Perceived Stress Predicting P.M. Cortisol

 

 

 

Step 1 B SE B Beta
Age of baby 1.95 2.56 .08
Pregnancy risk factors -.07 .93 -.01
T2 Perceived Stress -1.4 .61 -.20
T2 Life Stress -.05 .45 -.01
T2 Mental Stress -.06 .12 —.05

Total for Step 1 AR2 = .05

Step 2
Age of baby 1.70 2.81 .07
Pregnancy risk factors -.05 .93 -.01
T2 Perceived Stress -.84 .71 -.15
T2 Life Stress .03 .47 .01
T2 Mental Stress -.O3 .12 -.03
T1 Perceived Stress -.6O .70 —.11

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

 

A18 = .01, F(6,91)= .88; p=n.s.

170

Table 27: Hypothesis C: T1 A.M. Cortisol Predicting Activity

 

 

 

 

Step 1 B SE B Beta
Age of baby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05

Total for Step 1 AR2

Step 2
Age ofbaby 3.48 1.18 .28**
Pregnancy risk factors 1.35 .43 .30**
T2 Perceived Stress —.55 .28 -.19
T2 Life Stress .59 .21 .27**
T2 Mental Stress -.02 .06 .04
A.M. Cortisol .05 .05 .09

Total for Step 2 A18 = .01, F(6,91)= 4.37; p<. 05.

Notes to table:
*p<.05, **p<.01

171

Table 28: Hypothesis C: T1 A.M. Cortisol Predicting Distress to Limitations

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.34 1.35 -.11
Pregnancy risk factors .39 .49 .09
T2 Perceived Stress .18 .32 .06
T2 Life Stress -.21 .24 -.09
T2 Mental Stress .06 .06 .11
A.M. Cortisol .04 .06 .08

Total for Step 2 A18 = .01, F(6,91)= .73; p= n.s.
Notes to table:

 

*p<.05, **p<.01

172

Table 29: Hypothesis C: Tl A.M. Cortisol Predicting Distress to Smiling

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age of baby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .04
T2 Life Stress .00 .22 .00
T2 Mental Stress .02 .06 .04
A.M. Cortisol -.01 .05 -.02

Total for Step 2 A18 = .00, F(6,91)= .65; p= n.s.
Notes to table:

 

*p<.05, **p<.01

173

Table 30: Hypothesis C: T] A.M. Cortisol Predicting Duration of Orienting

 

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .01 .29 .00
T2 Perceived Stress -.04 .19 -.23
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08

Total for Step 1 AR2 = .07

Step 2
Age of baby -.43 .81 -.06
Pregnancy risk factors .00 .29 .00
T2 Perceived Stress -.43 .19 -.23
T2 Life Stress .02 .14 .08
T2 Mental Stress -.02 .04 -.07
A.M. Cortisol .03 .03 .08

Total for Step 2 A18 = .01, F(6,91)= 1.10; p= 71.3.
Notes to table:

 

*p<.05, **p<.01

174

Table 31: Hypothesis C: T1 A.M. Cortisol Predicting Consecutive Sleep

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress .08 .06 -.12
T2 Life Stress .08 05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .1 1

Step 2
Age of baby .29 .27 .1 1
Pregnancy risk factors -.06 .10 -.06
T2 Perceived Stress -.07 .06 -.12
T2 Life Stress .07 .05 .16
T2 Mental Stress .02 .01 .16
A.M. Cortisol -.01 .01 -.13

Total for Step 2 A18 = .02, F(6,91)= 1.91; p= n.s.
Notes to table:

 

*p<.05, **p<.01

175

Table 32: Hypothesis C: T1 P .M. Cortisol Predicting Activity

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.19
T2 Life Stress .57 .21 .26
T2 Mental Stress -.31 .06 -.05

Total for Step 1 AR2 = .23

Step 2
Age ofbaby 3.34 1.18 .27
Pregnancy risk factors 1.37 .43 .31
T2 Perceived Stress -.46 .29 -.16
T2 Life Stress .58 .21 .26
T2 Mental Stress -.03 .06 -.05
P.M. Cortisol .07 .05 .14

Total for Step 2 A18 = .02, F(6,91)= 4.62; p<. 05.
Notes to table:

 

*p<.05, **p<.01

176

Table 33: Hypothesis C: T1 P.M. Cortisol Predicting Distress to Limitations

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 A18 = .04

Step 2
Age ofbaby -1.39 1.36 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .23 .33 .08
T2 Life Stress -.22 .24 -.10
T2 Mental Stress .06 .06 .11
P.M. Cortisol .03 .06 .06

Total for Step 2 A18 = .01, F(6,9l)= .69; p= n.s.
Notes to table:

 

*p<.05, **p<.01

177

Table 34: Hypothesis C: T1 P.M. Cortisol Predicting Distress to Smiling

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age of baby 2.00 1.22 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .1 1 .29 .04
T2 Life Stress .01 .22 .01
T2 Mental Stress .03 .06 .05
P.M. Cortisol .02 .05 .03

Total for Step 2 A18 = .00, F(6,91)= .66; p= n.s.
Notes to table:

 

*p<.05, **p<.01

178

Table 35: Hypothesis C: T1 P.M. Cortisol Predicting Duration of Orienting

 

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .01 .29 .00
T2 Perceived Stress -.04 .19 -.23
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08

Total for Step 1 AR2 = .07

Step 2
Age of baby -.67 .81 -.06
Pregnancy risk factors .01 .29 .00
T2 Perceived Stress -.40 .20 -.22
T2 Life Stress .02 .14 .01
T2 Mental Stress -.03 .04 -.07
P.M. Cortisol .02 .03 .07

Total for Step 2 A18 = .01, F(6,91)= 1.06; p= n.s.
Notes to table:

 

*p<.05, **p<.01

179

Table 36: Hypothesis C: T1 P.M. Cortisol Predicting Consecutive Sleep

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress .08 .06 -.12
T2 Life Stress .08 05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .11

Step 2
Age ofbaby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.08 .07 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18
P.M. Cortisol .00 .01 .00

Total for Step 2 A18 = .00, F(6,91)= 1.64; p= n.s.
Notes to table:

 

*p<.05, **p<.01

180

Table 37: Hypothesis D: T] A.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

Activity

Step 1 B SE B Beta
Age of baby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05

Total for Step 1 AR2 = .23

Step 2
Age of baby 3.44 1.15 .28**
Pregnancy risk factors 1.72 .45 .39"
T2 Perceived Stress -.57 .28 -.19*
T2 Life Stress .60 .21 .28**
T2 Mental Stress .02 .06 .04
A.M. Cortisol .04 .05 .08
T1 Mental Stress -.14 .06 -.25*

 

Total for Step 2 A18 = .06, F(6,91)= 4.71 p<. 05.

Notes to table:
*p<.05, **p<.01

181

Table 38: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Life Stress and Activity

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.48 1.18 .28**
Pregnancy risk factors 1 .37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05

Total for Step 1 AR2 = .23

Step 2
Age ofbaby 3.51 1.19 .29**
Pregnancy risk factors 1.45 .18 .33“
T2 Perceived Stress -.52 .29 -.18
T2 Life Stress .62 .22 .28**
T2 Mental Stress -.01 .06 -.03
A.M. Cortisol .04 .05 .08
T1 Life Stress -.05 .10 -.06

Total for Step 2 A18 = .01, F(6,91)= 3.74 p<. 05.
Notes to table:

 

*p<.05, **p<.01

182

Table 39: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and

 

 

 

 

Activity
Step 1 B SE B Beta
Age of baby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05
Total for Step 1 AR2 = .23
Step 2
Age of baby 3.24 1.18 .26**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.27 .32 -.09
T2 Life Stress .67 .21 .31"
T2 Mental Stress -.00 .06 -.01
A.M. Cortisol .06 .05 .1 1
T1 Perceived Stress -.57 .31 -.20
Total for Step 2 A18 = .04, F(6,91)= 4.28, p<. 05.
Notes to table:

 

*p<.05, **p<.01

183

Table 40: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and
Distress to Limitations

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.34 1.36 -.11
Pregnancy risk factors .42 .53 .09
T2 Perceived Stress .18 .32 .06
T2 Life Stress -.22 .24 -.09
T2 Mental Stress .07 .07 .12
A.M. Cortisol .04 .06 .08
T1 Mental Stress -.01 .07 -.02

Total for Step 2 A18 = .01, F(6,91)= .62, p=n.s..
Notes to table:

 

*p<.05, **p<.01

184

Table 41: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Life Stress and Distress
to Limitations

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.42 1.35 -.11
Pregnancy risk factors .11 .54 .02
T2 Perceived Stress .11 .33 .04
T2 Life Stress -.29 .25 -.13
T2 Mental Stress .04 .07 .07
A.M. Cortisol .05 .06 .11
T1 Life Stress .14 .11 .16

Total for Step 2 A18 = .02, F(6,91)= .85, p=n.s..
Notes to table:
‘p<.05, **p<.01

185

Table 42: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and
Distress to Limitations

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -l .33 1.35 -.11
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 A18 = .04

Step 2
Age ofbaby -1.32 1.37 -.10
Pregnancy risk factors .39 .50 .09
T2 Perceived Stress .16 .37 .05
T2 Life Stress -.22 .25 -.10
T2 Mental Stress .06 .07 .11
A.M. Cortisol .04 .06 .08
T1 Perceived Stress .05 .37 .02

Total for Step 2 A18 = .01, F(6,91)= .62, p=n.s..
Notes to table:
‘p<.05, **p<.01

186

 

Table 43: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

 

Smiling
Step 1 B SE B Beta
Age of baby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05
Total for Step 1 AR2 = .04
Step 2
Age ofbaby 2.05 1.21 .18
Pregnancy risk factors .18 .47 .04
T2 Perceived Stress .10 .29 .04
T2 Life Stress .00 .22 .00
T2 Mental Stress .00 .06 .01
A.M. Cortisol -.00 .05 -.02
T1. Mental Stress .06 .06 .12
Total for Step 2 A18 = .01, F(6,91)= .69, p=n.s..
Notes to table:

 

*p<.05, **p<.01

187

Table 44: Hypothesis D:

T] A.M. Cortisol AS A Mediator of T1 Life Stress and Smiling

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05
Total for Step 1 AR2 = .04
Step 2
Age ofbaby 2.13 1.21 .19 F
Pregnancy risk factors .66 .48 .16 ‘
T2 Perceived Stress .18 .29 .07 ‘
T2 Life Stress .09 .22 .05
T2 Mental Stress .05 .06 .10
A.M. Cortisol -.O3 .05 -.O6 3
T1 Life Stress .16 .10 -.21 -
Total for Step 2 A18 = .03, F(6,91)= .92, p=n.s.. -
Notes to table:

 

*p<.05, **p<.01

188

Table 45: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and

 

 

 

 

Smiling
Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .44 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05
Total for Step 1 AR2 = .04
Step 2
Age of baby 2.27 1.21 .20
Pregnancy risk factors .32 .44 .08
T2 Perceived Stress -.20 .33 -.07
T2 Life Stress -.07 .22 -.04
T2 Mental Stress .00 .06 .01
A.M. Cortisol -.02 .05 -.04
T1 Perceived Stress .58 .33 .23
Total for Step 2 A18 = .04, F(6,91)= 1.03, p=n.s..
Notes to table:

 

*p<.05, **p<.01

189

Table 46: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

 

Duration of Orienting
Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .00 .29 .00
T2 Perceived Stress -.42 .19 -.23
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08
Total for Step 1 AR2 = .07
Step 2
Age of baby -.44 .81 -.06
Pregnancy risk factors .08 .31 .03
T2 Perceived Stress -.43 .19 -.24
T2 Life Stress .03 .14 .02
T2 Mental Stress -.01 .04 -.04
A.M. Cortisol .02 .03 .07
T1 Mental Stress -.03 .04 -.08
Total for Step 2 A18 = .01, F(6,91)= .99, p=n.s..
Notes to table:

 

*p<.05, **p<.01

190

 

Table 47 : Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Life Stress and Duration

 

 

 

 

of Orienting
Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .00 .29 .00
T2 Perceived Stress -.42 .19 -.23
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08
Total for Step 1 AR2 = .07
Step 2
Age ofbaby -.37 .80 -.05
Pregnancy risk factors .19 .32 .07
T2 Perceived Stress -.38 .19 -.21
T2 Life Stress .07 .15 .06
T2 Mental Stress -.00 .04 -.02
A.M. Cortisol .02 .03 .05
T1 Life Stress -.09 .07 -.18
Total for Step 2 A18 = .03, F(6,91)= 1.23, p=n.s..
Notes to table:

 

*p<.05, **p<.01

191

Table 48: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and
Duration of Orienting

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .00 .29 .00
T2 Perceived Stress -.42 .19 -.23
T2 Life Stress .01 .14 .01
T2 Mental Stress -.03 .04 -.08

Total for Step 1 AR2 = .07

Step 2
Age of baby -.41 .82 -.05
Pregnancy risk factors .00 .30 .00
T2 Perceived Stress -.45 .22 -.25
T2 Life Stress .02 .15 .01
T2 Mental Stress -.03 .04 -.O7
A.M. Cortisol .02 .03 .08
T1 Perceived Stress .05 .22 .03

 

Total for Step 2 A18 = .01, F(6,91)= .93, p=n.s..

Notes to table:
*p<.05, **p<.01

192

Table 49: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Mental Stress and Sleep

 

 

 

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .11

Step 2
Age of baby .29 .27 .1 1
Pregnancy risk factors -.07 .11 -.08
T2 Perceived Stress -.07 .06 -.12
T2 Life Stress .07 .05 .15
T2 Mental Stress .02 .01 .15
A.M. Cortisol -.01 .01 ~.13
T1 Mental Stress .00 .02 .03

 

Total for Step 2 A18 = .02, F(6,91)= 1.63, p=n.s..

Notes to table:
*p<.05, **p<.01

 

193

Table 50: Hypothesis D: T] A.M. Cortisol As A Mediator of T1 Life Stress and Sleep

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 A18 = .11

Step 2
Age ofbaby .32 .27 .13
Pregnancy risk factors .03 .1 '1 .03
T2 Perceived Stress .05 .06 -.08
T2 Life Stress .10 .05 .21
T2 Mental Stress .03 .01 .23*
A.M. Cortisol -.2 .01 -.16
T1 Life Stress -.04 .02 -.24

Total for Step 2 A18 = .05, F(6,91)= 2.21, p<. 05.
Notes to table:
*p<.05, **p<.01

194

Table 51: Hypothesis D: T1 A.M. Cortisol As A Mediator of T1 Perceived Stress and

 

 

 

 

Sleep
Step 1 B SE B Beta
Age of baby .30 .27 .1 1
Pregnancy risk factors -.06 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18
Total for Step 1 AR2 = .11
Step 2
Age of baby .28 .27 .11
Pregnancy risk factors -.06 .10 -.06
T2 Perceived Stress -.O6 .07 -.10
T2 Life Stress .08 .05 .16
T2 Mental Stress .02 .01 .17
A.M. Cortisol -.01 .01 -.12
T1 Life Stress -.02 .07 -.04
Total for Step 2 A18 = .02, F(6,91)= 1.63, p=n.s..
Notes to table:

 

*p<.05, **p<.01

195

Table 52: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

 

Activity
Step 1 B SE B Beta
Age of baby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05
Total for Step 1 AR2 = .23
Step 2
Age ofbaby 3.33 1.15 .27**
Pregnancy risk factors 1.72 .45 .39“
T2 Perceived Stress -.50 .30 -.17
T2 Life Stress .59 .20 .27**
T2 Mental Stress .02 .06 .03
P.M. Cortisol .06 .05 .11
T1 Mental Stress -.13 .06 -.23**
Total for Step 2 A18 = .06, F(6,91)= 4.83, p<. 05.
Notes to table:

 

*p<.05, **p<.01

196

Table 53: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Life Stress and Activity

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.03 .06 -.05

Total for Step 1 AR2 = .23

Step 2
Age ofbaby 3.38 1.19 .28**
Pregnancy risk factors 1.47 .47 .33**
T2 Perceived Stress -.44 .29 -.15
T2 Life Stress .61 .22 .27**
T2 Mental Stress -.02 .06 -.03
P.M. Cortisol .07 .05 .14
T1 Life Stress -.05 .10 -.06

Total for Step 2 AR2 = .02, F (6,91)= 3.96, p<.05-
Notes to table:

 

*p<.05, **p<.01

197

Table 54: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and

 

 

 

Activity

Step 1 B SE B Beta
Age of baby 3.48 1.18 .28**
Pregnancy risk factors 1.37 .43 .31**
T2 Perceived Stress -.54 .28 -.18
T2 Life Stress .57 .21 .26**
T2 Mental Stress -.O3 .06 -.05

Total for Step 1 A18 = .23

Step 2
Age ofbaby 3.15 1.18 .26**
Pregnancy risk factors 1.39 .42 .31**
T2 Perceived Stress -.22 .32 -.08
T2 Life Stress .65 .21 .29“
T2 Mental Stress -.01 .06 -.20
P.M. Cortisol .07 .05 .13
T1 Perceived Stress -.49 .32 .17

 

Total for Step 2 A18 = .04, F(6,91)= 4.37, p<. 05.

Notes to table:
*p<.05, **p<.01

198

Table 55: Hypothesis D:

Distress to Limitations

T1 P.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.10
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.39 1.37 -.11
Pregnancy risk factors .43 .53 .09
T2 Perceived Stress .23 .33 .07
T2 Life Stress -.22 .24 -10
T2 Mental Stress .07 .07 .11
P.M. Cortisol .03 .06 .06
T1 Mental Stress -.01 .07 -.02

Total for Step 2 A18 = .00, F(6,91)= .59, p<. 05.
Notes to table:

 

*p<.05, **p<.01

199

Table 56: Hypothesis D: T1 P.M. Cortisol AS A Mediator of T1 Life Stress and Distress
to Limitations

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.10
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.49 1.36 -.12
Pregnancy risk factors .15 .54 .03
T2 Perceived Stress .17 .33 .06
T2 Life Stress -.30 .25 -.13
T2 Mental Stress .04 .07 .07
P.M. Cortisol .04 .06 .08
T1 Life Stress .13 .11 .15

Total for Step 2 A18 = .02, F(6,91)= .78, p=n.s.
Notes to table:

 

*p<.05, **p<.01

200

Table 57: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and
Distress to Limitations

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.33 1.35 -.10
Pregnancy risk factors .40 .49 .09
T2 Perceived Stress .19 .32 .06
T2 Life Stress -.23 .24 -.10
T2 Mental Stress .06 .06 .10

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.36 1.37 -.11
Pregnancy risk factors .40 .50 .09
T2 Perceived Stress .18 .38 .06
T2 Life Stress -.24 .25 -.11
T2 Mental Stress .06 .07 .10
P.M. Cortisol .03 .06 .06
T1 Perceived Stress .09 .37 .03

 

Total for Step 2 AR2 = .00, F(6,91)= .60, p=n.s.

Notes to table:
*p<.05, **p<.01

201

Table 58: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

 

Smiling

Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .044 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age ofbaby 2.00 1.21 .18
Pregnancy risk factors .17 .47 .04
T2 Perceived Stress .13 .30 .05
T2 Life Stress .01 .22 .00
T2 Mental Stress .00 .06 .01
P.M. Cortisol .02 .05 .05
T1 Mental Stress .06 .06 .13

Total for Step 2 AR2 = .01, F(6,91)= .72, p=n.s.

Notes to table:

 

*p<.05, **p<.01

202

Table 59: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Life Stress and

 

 

 

 

Smiling

Step 1 B SE B Beta
Age of baby 2.03 1.21 .18
Pregnancy risk factors .34 .044 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05

Total for Step] AR2 = .04

Step 2
Age ofbaby 2.10 1.21 .19
Pregnancy risk factors .63 .48 .15
T2 Perceived Stress .18 .30 .07
T2 Life Stress .10 .22 .05
T2 Mental Stress .05 .06 .10
P.M. Cortisol .01 .05 .01
T1 Life Stress -.15 .10 -.19

Total for Step 2 A18 = .03, F(6,91)= .88, p=n.s.

Notes to table:

 

*p<.05, **p<.01

203

Table 60: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Perceived Stress

 

 

 

 

and Smiling

Step 1 B SE B Beta
Age ofbaby 2.03 1.21 .18
Pregnancy risk factors .34 .044 .08
T2 Perceived Stress .09 .29 .03
T2 Life Stress .01 .21 .01
T2 Mental Stress .02 .06 .05

Total for Step 1 AR2 = .04

Step 2
Age of baby 2.22 1.21 .20
Pregnancy risk factors .32 .44 .08
T2 Perceived Stress -.18 .33 -.07
T2 Life Stress -.07 .22 -.03
T2 Mental Stress .01 .06 .01
P.M. Cortisol .02 .05 .05
T1 Perceived Stress .59 .33 .23

Total for Step 2 A18 = .04, F(6,91)= 1.04, p=n.s.

Notes to table:

 

*p<.05, **p<.01

204

Table 61: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress
and Duration of Orienting

 

 

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .01 .29 .00
T2 Perceived Stress -.42 .19 -.23*
T2 Life Stress .01 .15 .01
T2 Mental Stress -.03 .04 -.07

Total for Step 1 AR2 = .07

Step 2
Age of baby -.47 .81 -.06
Pregnancy risk factors .08 .32 .03
T2 Perceived Stress -.41 .20 -.22
T2 Life Stress .02 .14 .01
T2 Mental Stress -.O2 .04 -.05
P.M. Cortisol .02 .04 .06
T1 Mental Stress -.03 .04 -.08

Total for Step 2 A18 ——- .01, F(6,91)= .96, p=n.s.

Notes to table:

‘p<.05, **p<.01

205

Table 62: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Life Stress and

Duration of Orienting

 

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .01 .29 .00
T2 Perceived Stress -.42 .19 -.23*
T2 Life Stress .01 .15 .01
T2 Mental Stress -.03 .04 -.07

Total for Step 1 AR2 = .07

Step 2
Age of baby -.40 .81 -.05
Pregnancy risk factors .20 .32 .07
T2 Perceived Stress -.35 .20 -.20
T2 Life Stress .07 .15 .05
T2 Mental Stress -.01 .04 -.02
P.M. Cortisol .01 .03 .05
T1 Life Stress -.01 .07 -.18

Total for Step 2 A18 = .03, F(6,91)= 1.22, p=n.s.
Notes to table:

 

*p<.05, **p<.01

206

 

Table 63: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Perceived Stress
and Duration of Orienting

 

 

 

 

Step 1 B SE B Beta
Age of baby -.43 .80 -.06
Pregnancy risk factors .01 .29 .00
T2 Perceived Stress -.42 .19 -.23*
T2 Life Stress .01 .15 .01
T2 Mental Stress -.03 .04 -.07
Total for Step 1 AR2 = .07

Step 2
Age of baby -.44 .82 -.06
Pregnancy risk factors .01 .30 .00
T2 Perceived Stress -.44 .23 -.24
T2 Life Stress .01 .15 .00
T2 Mental Stress -.O3 .04 -.08
P.M. Cortisol .02 .03 .07
T1 Perceived Stress .08 .22 .04
Total for Step 2 A18 = .01, F(6,91)= .91, p=n.s.

Notes to table:

 

*p<.05, **p<.01

207

Ana .2]. WI!

Table 64: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Mental Stress and

 

 

 

 

Sleep

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.61 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .1 1

Step 2
Age of baby .29 .27 .11
Pregnancy risk factors -.07 .1 1 -.08
T2 Perceived Stress -.08 .07 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .16
P.M. Cortisol .00 .01 .01
T1 Mental Stress .00 .05 .04

Total for Step 2 A18 = .00, F(6,91)= 1.40, p=n.s.

Notes to table:

 

*p<.05, **p<.Ol

208

Table 65: Hypothesis D: T] P.M. Cortisol As A Mediator of T1 Life Stress and Sleep

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .30 .27 .11
Pregnancy risk factors -.61 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18

Total for Step 1 AR2 = .11

Step 2
Age of baby .33 .27 .13
Pregnancy risk factors .01 .11 .01
T2 Perceived Stress -.06 .07 -.10
T2 Life Stress .11 .05 .22*
T2 Mental Stress .03 .01 .24*
P.M. Cortisol -.00 .01 -.02
T1 Life Stress -.O3 .02 -.21

Total for Step 2 A18 = .03, F(6,91)= 1.82, p=n.s.
Notes to table:

 

*p<.05, **p<.01

209

Table 66: Hypothesis D: T1 P.M. Cortisol As A Mediator of T1 Perceived Stress and

 

 

 

V'I‘ ‘l

 

 

Sleep
Step 1 B SE B Beta
Age of baby .30 .27 .11
Pregnancy risk factors -.61 .10 -.07
T2 Perceived Stress -.08 .06 -.12
T2 Life Stress .08 .05 .17
T2 Mental Stress .02 .01 .18
Total for Step 1 AR2 = .11
Step 2
Age ofbaby .28 .27 .11
Pregnancy risk factors -.06 .10 -.06
T2 Perceived Stress -.06 .08 -.10
T2 Life Stress .08 .05 .18
T2 Mental Stress .02 .01 .19
P.M. Cortisol -.00 .01 -.00
T1 Perceived Stress -.03 .08 -.06
Total for Step 2 A18 = .00, F(6,91)= 1.42, p=n.s.

Notes to table:
*p<.05, **p<.01

210

Table 67 : Hypothesis E: T1 Mental Stress Predicting T2 Mental Stress

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.16 2.25 .15
Pregnancy risk factors .19 .83 .02
T2 Perceived Stress .31 .54 .06
T2 Life Stress .41 .40 .11
Total for Step 1 AR2 = 04
Step 2
Age ofbaby 2.87 2.12 .14 . _
Pregnancy risk factors -.79 .83 -.10 F
T2 Perceived Stress .31 .51 .06 1.
T2 Life Stress .38 .38 .08 L
T1 Mental Stress .35 .10 .37" lg
Total for Step 2 A18 = .12, F(6,91)= 3.19; p<. 05.
Notes to table:

 

*p<.05, **p<.01

211

 

Table 68: Hypothesis E: T] Life Stress Predicts T2 Life Stress

 

 

 

Step 1 B SE B Beta
Age of baby -.39 .60 -.07
Pregnancy risk factors -.22 .22 -.11
T2 Perceived Stress .00 .14 .00
T2 Mental Stress .03 .03 .11

Total for Step 1 AR2 — 03
Step 2
Age of baby -.43 .59 -.08
Pregnancy risk factors -.44 .23 -.22
T2 Perceived Stress -.O6 .14 -.05
T2 Mental Stress -.00 .03 .01
T1 Life Stress .12 .05 .30**

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .07, F(6,91)= 1.76; p=n.s..

212

 

Table 69: Hypothesis E: T1 Perceived Stress Predicts T2 Perceived Stress

 

 

 

Step 1 B SE B Beta
Age of baby -.06 .45 -.01
Pregnancy risk factors .16 .16 .11
T2 Life Stress .00 .08 .00
T2 Mental Stress .01 .02 .06

Total for Step 1 AR2 = .02

Step 2
Age of baby .16 .39 .04
Pregnancy risk factors .10 .14 .07
T2 Life Stress -.07 .07 -.09
T2 Mental Stress -.00 .02 -.04
T1 Perceived Stress .49 .09 .52**

 

Total for Step 2 A18 = .25, F(6,91)= 6.11

Notes to table:
*p<.05, **p<.Ol

213

Table 70: Hypothesis F: T2 Mental Stress Predicting Activity

 

 

 

Step 1 B SE B Beta
Age of baby 3.09 1.21 .25*
Pregnancy risk factors 1.33 .48 .30"
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .07 .10 .09
T1 Mental Stress -.11 .07 -.20

Total for Step 1 A18 = .19

Step 2
Age ofbaby 3.03 1.23 .25*
Pregnancy risk factors 1.36 .49 .30"
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .07 .10 .08
T1 Mental Stress -.12 .07 -.21
T2 Mental Stress -.02 .06 .04

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .00, F(6,91)= 3.27, p<. 05.

214

Table 71: Hypothesis F: T2 Mental Stress Predicting Distress to Limitations

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.15 1.35 -.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.03 .07 -.06

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.27 1.37 -.10
Pregnancy risk factors .39 .55 .08
T1 Perceived Stress .07 .34 .02
T1 Life Stress .11 .11 .12
T1 Mental Stress -.04 .08 -.08
T2 Mental Stress .05 .07 .08

Total for Step 2 A18 = .01, F(6,91)= .62, p=n.s.
Notes to table:

 

 

*p<.05, **p<.01

215

 

Table 72: Hypothesis F: T2 Mental Stress Predicting Smiling

 

 

 

Step 1 B SE B Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.20 .09 -.26*
T1 Mental Stress .07 .06 .14

Total for Step 1 AR2 = .12

Step 2
Age ofbaby 2.38 1.17 .21*
Pregnancy risk factors .55 .47 .13
T1 Perceived Stress .55 .29 .21
T1 Life Stress -.21 .10 *.27*
T1 Mental Stress .06 .06 .12
T2 Mental Stress .03 .06 .05

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .00, F(6,91)= .07, p=n.s.

216

 

 

Table 73: Hypothesis F: T2 Mental Stress Predicting Duration of Orienting

 

 

 

Step 1 B SE B Beta
Age of baby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.06 .20 -.03
T1 Life Stress -.11 .07 -.21
T1 Mental Stress -.00 .04 -.01

Total for Step 1 AR2 = .05

Step 2
Age of baby -.40 .82 -.05
Pregnancy risk factors .15 .33 .06
T1 Perceived Stress -.06 .21 -.03
T1 Life Stress -.11 .07 -.20
T1 Mental Stress -.00 .05 -.00
T2 Mental Stress -.01 .04 -.02

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .00, F(6,91)= .73, p=n.s.

217

F3.“

 

Table 74: Hypothesis F: T2 Mental Stress Predicting Sleep

 

 

 

Step 1 B SE B Beta
Age ofbaby .31 .28 .12
Pregnancy risk factors -. 12 .11 -.12
T1 Perceived Stress —.04 .07 -.07
T1 Life Stress -.02 .02 -.12
T1 Mental Stress -.03 .02 .21

Total for Step 1 AR2 = .06

Step 2
Age ofbaby .25 .27 .10
Pregnancy risk factors -.08 .1 1 -.08
T1 Perceived Stress -.04 .07 -.07
T1 Life Stress -.03 .02 -.17
T1 Mental Stress .01 .02 .15
T2 Mental Stress .03 .01 .23

 

Total for Step 2

Notes to table:
*p<.05, **p<.Ol

A18 = .03, F(6,91)= 1.41, p=n.s.

218

 

l”

Table 75: Hypothesis F: T2 Life Stress Predicting Activity

 

 

 

Step 1 B SE B Beta
Age of baby 3.09 1.21 .25*
Pregnancy risk factors 1.33 .48 .30**
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .07 .10 .09
T1 Mental Stress -.11 .07 -.20

Total for Step 1 A18 = .19

Step 2
Age ofbaby 3.31 1.16 .27**
Pregnancy risk factors 1.59 .47 .36**
T1 Perceived Stress -.50 .29 -.18
T1 Life Stress .01 .10 .01
T1 Mental Stress -.O9 .06 -.17
T2 Life Stress .65 .22 .30**

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .08, F(6,91)= 5.15, p<. 05.

219

 

Table 76: Hypothesis F: T2 Life Stress Predicting Distress to Limitations

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.15 1.35 -.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.O3 .07 -.06

Total for Step 1 A18 = .04

Step 2
Age ofbaby -1.26 1.35 -.10
Pregnancy risk factors .20 .55 .04
T1 Perceived Stress .13 .34 .05
T1 Life Stress .16 .11 .18
T1 Mental Stress -.04 .07 -.07
T2 Life Stress -.32 .25 -.14

 

Total for Step 2 A18 = .02, F(6,91)= .81, p=n.s.
Notes to table:
*p<.05, **p<.01

220

1”“

——‘l-'.I‘W‘ .'."‘.- ' .

 

Table 77 : Hypothesis F: T2 Life Stress Predicting Smiling

 

 

 

 

Step 1 B SE B Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.20 .09 -.26*
T1 Mental Stress .07 .06 .14

Total for Step 1 AR2 = .12

Step 2
Age ofbaby 2.47 1.16 .22*
Pregnancy risk factors .54 .47 .13
T1 Perceived Stress .55 .30 .21
T1 Life Stress -.21 .10 -.27*
T1 Mental Stress .07 .06 .14
T2 Life Stress .06 .22 .03

Total for Step 2 A18 = .00, F(6,91)= 2.00, p=n.s.

Notes to table:
*p<.05, **p<.01

221

 

 

Table 78: Hypothesis F: T2 Life Stress Predicting Duration of Orienting

 

 

 

Step 1 B SE B Beta
Age of baby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.06 .20 -.03
T1 Life Stress -.11 .07 -.21
T1 Mental Stress -.OO .04 -.01

Total for Step 1 AR2 = .05

Step 2
Age of baby .37 .81 -.05
Pregnancy risk factors .20 .33 .07
T1 Perceived Stress -.08 .21 -.04
T1 Life Stress -.11 .07 -.23
T1 Mental Stress .00 .04 .00
T2 Life Stress .09 .15 .07

 

Total for Step 2

Notes to table:
‘p<.05, **p<.01

A18 = .00, F(6,91)= .78, p=n.s.

222

 

Table 79: Hypothesis F: T2 Life Stress Predicting Sleep

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .31 .28 .12
Pregnancy risk factors -.12 .1 l -.12
T1 Perceived Stress -.04 .07 -.07
T1 Life Stress -.02 .02 -.12
T1 Mental Stress -.O3 .02 .21

Total for Step 1 AR2 = 06

Step 2
Age of baby .36 .27 .14
Pregnancy risk factors -.06 .11 -.07
T1 Perceived Stress -.O6 .07 -.09
T1 Life Stress -.03 .02 -.18
T1 Mental Stress .02 .02 .21
T2 Life Stress .11 .05 .23*

Total for Step 2 A18 = .05, F(6,91)= 1.64, p=n.s.

Notes to table:
*p<.05, **p<.01

223

Table 80: Hypothesis F: T2 Perceived Stress Predicting Activity

 

Step 1

Age of baby
Pregnancy risk factors
T1 Perceived Stress
T1 Life Stress

T1 Mental Stress

 

Total for Step 1

 

Step 2

Age of baby
Pregnancy risk factors
T1 Perceived Stress
T1 Life Stress

T1 Mental Stress

T2 Perceived Stress

B SE B Beta
3.09 1.21 .25*
1.33 .48 .30**
-.39 .31 -.14
.07 .10 .09
-.11 .07 -.20
AR2 = .19
3.19 1.20 .26*
1.44 .48 .32**
-.O9 .35 -.O3
.09 .10 .11
-.14 .07 -.25*
.56 .34 -.19

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .03, F(6,91)= 3.79, p<. 05.

224

 

’ I

Table 81: Hypothesis F: T2 Perceived Stress Predicting Distress to Limitations

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.15 1.35 -.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.03 .07 -.06

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.18 1.36 -.09
Pregnancy risk factors .30 .55 .07
T1 Perceived Stress .00 .40 .00
T1 Life Stress .12 .11 .14
T1 Mental Stress -.03 .08 -.05
T2 Perceived Stress .13 .39 .04

Total for Step 2 A18 = .00, F(6,91)= .56, p=n.s.
Notes to table:
*p<.05, **p<.01

225

 

Table 82: Hypothesis F: T2 Perceived Stress Predicting Smiling

 

 

 

 

 

Step 1 B SE B Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.20 .09 -.26*
T1 Mental Stress .07 .06 .14
Total for Step 1 AR2 = .12
Step 2
Age of baby 2.47 1.16 .21*
Pregnancy risk factors .53 .47 .13
T1 Perceived Stress .61 .34 .24
T1 Life Stress -.20 .10 -.26*
T1 Mental Stress .06 .06 .13
T2 Perceived Stress -.O9 .33 -.04 ~
Total for Step 2 A18 = .00, F(6,91)= 1.96, p=n.s. -
Notes to table: ...1

 

*p<.05, **p<.01

226

Table 83: Hypothesis F: T2 Perceived Stress Predicting Duration of Orienting

 

 

 

 

 

 

Step 1 B SE B Beta
Age of baby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.06 .20 -.03
T1 Life Stress -.11 .07 -.21
T1 Mental Stress -.00 .04 -.01
Total for Step 1 AR2 = .05
Step 2
Age of baby -.33 .80 -.O4 1”“
Pregnancy risk factors .25 .32 .09 E
T1 Perceived Stress .19 .23 .11 3
T1 Life Stress -.09 .07 -.18 1
T1 Mental Stress -.03 .04 -.08
T2 Perceived Stress -.47 .23 -.26*
Total for Step 2 A18 = .05, F(6,91)= 1.50, p=n.s. .
Notes to table: r2
*p<.05, **p<.01

227

 

Table 84: Hypothesis F: T2 Perceived Stress Predicting Sleep

 

 

 

Step 1 B SE B Beta
Age of baby .31 .28 .12
Pregnancy risk factors -.12 .1 1 -. 12
T1 Perceived Stress -.O4 .07 -.07
T1 Life Stress -.O2 .02 -.12
T1 Mental Stress -.O3 .02 .21

Total for Step 1 AR2 = .06

Step 2
Age ofbaby .32 .28 .12
Pregnancy risk factors -.10 .11 -.11
T1 Perceived Stress -.01 .08 -.02
T1 Life Stress -.02 .2 -.11
T1 Mental Stress .02 .02 .19
T2 Perceived Stress -.05 .08 -.O9

 

Total for Step 2

Notes to table:
*p<.05, **p<.01

A18 = .01, F(6,91)= .96, p=n.s.

228

 

1‘
ii.
1‘

Table 85: Hypothesis G: T2 Mental Stress Predicting Parenting Competency

 

 

 

 

 

Step 1 B SE B Beta
Age of baby .01 .05 .03
Pregnancy risk factors .02 .02 .10
T1 Perceived Stress .00 .01 .08
T1 Life Stress .00 .00 .12
T1 Mental Stress -.00 .00 -.04
Total for Step 1 AR2 = .04
Step 2
Age of baby .04 .05 .07 ,
Pregnancy risk factors .00 .02 .04 7
T1 Perceived Stress .01 .01 .09
T1 Life Stress .01 .00 .21 i
T] Mental Stress .01 .00 .05 E
T2 Mental Stress -.01 .00 -.35** '
Total for Step 2 A18 = .10, F(6,91)= 2.22, p<. 05.

 

Notes to table:
*p<.05, **p<.01

229

Table 86: Hypothesis G: T2 Life Stress Predicting Parenting Competency

 

 

 

 

Step 1 B SE B Beta
Age of baby .01 .05 .03
Pregnancy risk factors .02 .02 .10
T1 Perceived Stress .00 .01 .08
T1 Life Stress .00 .00 .12
T1 Mental Stress -.00 .00 -.04

Total for Step 1 A18 = .04

Step 2
Age of baby .01 .05 .03
Pregnancy risk factors .02 .02 .10
T1 Perceived Stress .00 .01 .07
T1 Life Stress .00 .00 .10
T1 Mental Stress -.00 .00 -.04
T2 Life Stress .00 .01 .04

Total for Step 2 A18 = .00, F(6,91)= .54, p=n.s.
Notes to table:

 

*p<.05, **p<.01

230

. .M‘dm-m r95- ...-' hr - j

 

 

Table 87: Hypothesis G: T2 Perceived Stress Predicting Parenting Competency

 

 

 

Step 1 B SE B Beta
Age of baby .01 .05 .03
Pregnancy risk factors .02 .02 .10
T1 Perceived Stress .00 .01 .08
T1 Life Stress .00 .00 .12
T1 Mental Stress -.00 .00 -.04

Total for Step 1 AR2 = .04

Step 2
Age of baby .01 .05 .03
Pregnancy risk factors .01 .02 .10
T1 Perceived Stress .01 .02 .11
T1 Life Stress .00 .00 .12
T1 Mental Stress -.00 .00 -.06
T2 Perceived Stress -.01 .02 -.O7

 

Total for Step 2 A18 = .00, F(6,91)= .57, p=n.s.

Notes to table:
*p<.05, **p<.01

231

Table 88: Hypothesis H: T2 Parenting Competency Predicting Activity

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.01 1.21 .25*
Pregnancy risk factors 1.33 .18 .30*
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .08 .10 .09
T1 Mental Stress -.11 .07 -.20

Total for Step 1 AR2 = .19

Step 2
Age ofbaby 3.11 1.21 .25*
Pregnancy risk factors 1.36 .49 .30*
T1 Perceived Stress -.38 .31 -.13
T1 Life Stress .08 .10 .10
T1 Mental Stress -.11 .07 -.20
T2 Parenting -1.67 2.50 -.07
Competency

 

Total for Step 2 A18 = .00, F(6,91)= 3.33, p<. 05.

Notes to table:
*p<.05, **p<.01

232

 

Table 89: Hypothesis H:

T2 Parenting Competency Predicting Distress to Limitations

 

 

 

 

Step 1 B SE B Beta
Age ofbaby -1.15 1.35 -.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.03 .07 -.06

Total for Step 1 AR2 = .04

Step 2
Age ofbaby -1.01 1.34 -.09
Pregnancy risk factors .39 .54 .09
T1 Perceived Stress .11 .34 .04
T1 Life Stress .14 .11 .16
T1 Mental Stress -.04 .07 -.06
T2 Parenting -3.88 2.76 -.15
Competency

Total for Step 2 A18 = .02, F(6,91)= .88, p=n.s.

Notes to table:

 

*p<.05, **p<.01

233

Table 90: Hypothesis H: T2 Parenting Competency Predicting Smiling

 

 

 

Step 1 B SE B Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.20 .09 -.26*
T1 Mental Stress .07 .06 .14

Total for Step 1 AR2 = .12

Step 2
Age ofbaby 2.93 1.14 .21*
Pregnancy risk factors .45 .46 .11
T1 Perceived Stress .52 .29 .20
T1 Life Stress -.22 .09 -.28*
T1 Mental Stress .07 .06 .14
T2 Parenting 3.85 2.35 .17
Competency

 

Total for Step 2 A18 = .03, F(6,91)= 2.47, p<. 05..

Notes to table:
*p<.05, **p<.01

234

 

Table 91: Hypothesis H: T2 Parenting Competency Predicting Duration of Orienting

 

 

 

 

Step 1 B SE B Beta
Age of baby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.06 .20 -.03
T1 Life Stress -.11 .07 -.21
T1 Mental Stress -.00 .04 -.01

Total for Step 1 AR2 = .05

Step 2
Age of baby -.47 .79 -.06
Pregnancy risk factors .10 .32 .04
T1 Perceived Stress -.09 .20 -.05
T1 Life Stress -.12 .06 -.24
T1 Mental Stress .00 .04 .00
T2 Parenting 3.72 1.63 .24*
Competency

Total for Step 2 A18 = .06, F(6,91)= 1.64, p=n.s..
Notes to table:

 

1‘p<.05, **p<.01

235

Table 92: Hypothesis H: T2 Parenting Competency Predicting Sleep

 

 

 

 

Step 1 B SE B Beta
Age ofbaby .31 .28 .12
Pregnancy risk factors -. 12 .11 -.12
T1 Perceived Stress -.O4 .07 -.07
T1 Life Stress -.02 .02 -.12
T1 Mental Stress .03 .02 .21

Total for Step 1 AR2 = .06

Step 2
Age ofbaby .31 .28 .12
Pregnancy risk factors -.11 .11 -.12
T1 Perceived Stress -.O4 .07 -.07
T1 Life Stress -.02 .02 -.02
T1 Mental Stress .03 .02 .21
T2 Parenting -.03 .57 -.01
Competency

Total for Step 2 A18 = .00, F(6,91)= .88, p=n.s..

Notes to table:
*p<.05, **p<.01

236

Table 93: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Activity

 

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.09 1.21 .25*
Pregnancy risk factors 1.33 .48 .30**
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .08 .10 .09
T1 Mental Stress -.11 .07 -.20

Total for Step 1 AR2 = .19

Step 2
Age of baby 3.09 1.24 .25
Pregnancy risk factors 1.37 .49 .31
T1 Perceived Stress -.38 .31 -.14
T1 Life Stress .08 .10 .10
T1 Mental Stress -.11 .07 -.21
T2 Parenting -1.56 2.67 -.06
Competency
T2 Mental Stress .01 .07 .02

Total for Step 2 A18 = .00, F(6,91)= 2.83, p<. 05.
Notes to table:

 

‘p<.05, **p<.01

237

Table 94: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Distress
to Limitations

 

 

 

 

Step 1 B SE B Beta
Age of baby -1.15 1.34 .-.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.32 .07 -.06

Total for Step 1 AR2 = .04

Step 2
Age of baby -1.14 1.34 -.09
Pregnancy risk factors .41 .55 .09
T1 Perceived Stress .11 .34 .04
T1 Life Stress .13 .11 .15
T1 Mental Stress -.04 .07 -.07
T2 Parenting -3.67 2.94 -.14
Competency
T2 Mental Stress .02 .07 .03

Total for Step 2 A18 = .02, F(6,91)= .76, p=n.s..
Notes to table:

 

*p<.05, **p<.01

238

 

 

Table 95: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Smiling

 

 

 

 

Step 1 B SE B Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.20 .09 -.26*
T1 Mental Stress .07 .06 .14

Total for Step 1 AR2

Step 2
Age ofbaby 2.21 1.12 .20
Pregnancy risk factors .52 .46 .13
T1 Perceived Stress .51 .29 .20
T1 Life Stress -.24 .10 -.32*
T1 Mental Stress .06 .06 .11
T2 Parenting 4.70 2.48 .20
Competency
T2 Mental Stress .07 .06 .12

Total for Step 2 A18 = .04, F(6,91)= 2.28, p<. 05.

Notes to table:
*p<.05, **p<.01

239

 

Table 96: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Duration

 

 

 

 

 

 

of Orienting
Step 1 B SE B Beta
Age of baby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.06 .20 -.03
T1 Life Stress -.11 .07 -.21
T1 Mental Stress -.00 .04 -.01
Total for Step 1 AR2 == .05
Step 2
Age of baby -.54 .80 -.07
Pregnancy risk factors .13 .32 .05
T1 Perceived Stress -.10 .20 -.06 1
T1 Life Stress -.13 .07 -.26 E
T1 Mental Stress -.01 .04 -.02
T2 Parenting 4.07 1.72 .26*
Competency
T2 Mental Stress .03 .04 .08
Total for Step 2 A18 = .06, F(6,91)= 1.45, p=n.s..
Notes to table:

 

*p<.05, **p<.01

240

Table 97: Hypothesis 1: Parenting Competency Mediating T2 Mental Stress and Sleep

 

 

 

 

Step 1 B SE B Beta
Age of baby .31 .28 .12
Pregnancy risk factors -.1 1 .1 1 -.12
T1 Perceived Stress -.04 .07 -.07
T1 Life Stress -.02 .02 -.12
T1 Mental Stress .03 .02 .21

Total for Step 1 AR2 = .06

Step 2
Age of baby .24 .28 .09
Pregnancy risk factors -.08 .12 -.09
T1 Perceived Stress —.O4 .07 -.08
T1 Life Stress -.03 .02 -.18
T1 Mental Stress .01 .02 .14
T2 Parenting .33 .60 .06
Competency
T2 Mental Stress .03 02 .23

Total for Step 2 A18 = .04, F(6,91)= 1.24, p=n.s..
Notes to table:

 

*p<.05, **p<.01

241

Table 98: Hypothesis 1: Parenting Competency Mediating T2 Life Stress and Activity

 

 

 

 

Step 1 B SE B Beta
Age ofbaby 3.09 1.21 .25*
Pregnancy risk factors 1.33 .48 .30**
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .08 .10 .09
T1 Mental Stress -.11 .07 -.20

Total for Step 1 AR2 = .19

Step 2
Age ofbaby 3.34 1.16 .27**
Pregnancy risk factors 1.62 .47 .36**
T1 Perceived Stress -.49 .30 -.17
T1 Life Stress .01 .10 .01
T1 Mental Stress -.10 .06 -.18
T2 Parenting -1.97 2.39 -.08
Competency
T2 Life Stress .66 .22 .30*

Total for Step 2 A18 = .09, F(6,91)= 4.50, p<. 05.
Notes to table:

 

*p<.05, **p<.01

242

 

Table 99: Hypothesis 1:

Parenting Competency Mediating T2 Life Stress and Distress to

 

 

 

 

 

Limitations
Step 1 B SE B Beta
Age of baby -1.15 1.34 .-.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.32 .07 -.06
Total for Step 1 A18 = .04
Step 2
Age ofbaby -1.20 1.34 .10 in
Pregnancy risk factors .27 .55 .06
T1 Perceived Stress .16 .34 .06
T1 Life Stress .17 .11 .20
T1 Mental Stress -.04 .07 -.08
T2 Parenting -3.75 2.76 -.15
Competency E .
T2 Life Stress -.30 .25 -.13
Total for Step 2 A18 = .04, F(6,91)= .97, p=n.s..
Notes to table:

 

*p<.05, **p<.01

243

Table 100: Hypothesis 1: Parenting Competency Mediating T2 Life Stress and Smiling

 

 

 

 

Step 1 B SE [3 Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.2O .09 -.26*
T1 Mental Stress .07 .06 .14

Total for Step 1 AR2 = .12

Step 2
Age ofbaby 2.41 1.15 .21*
Pregnancy risk factors .47 .17 .11
Tl Perceived Stress ..52 .29 .20
T1 Life Stress -.22 .10 -.29
T1 Mental Stress .07 .06 .15
T2 Parenting 3.83 2.37 .17
Competency
T2 Life Stress .05 .21 .02

Total for Step 2 AR2 = .03, F(6,91)= 2.10, p=n.s..
Notes to table:

 

*p<.05, **p<.Ol

244

 

Table 101: Hypothesis 1: Parenting Competency Mediating T2 Life Stress and Duration

 

 

 

 

of Orienting
Step 1 [3 SE [3 Beta
Age of baby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.O6 .20 -.03
T1 Life Stress -.ll .07 -.21
T1 Mental Stress -.00 .04 -.01
Total for Step 1 AR2 = .05
Step 2
Age of baby -.44 .80 -.06
Pregnancy risk factors .13 .32 .05
T1 Perceived Stress -.10 .20 -.06
T1 Life Stress -.13 .07 -.25
T1 Mental Stress .00 .04 .01
T2 Parenting 3.68 1.63 .24*
Competency
T2 Life Stress .08 .15 .06
Total for Step 2 AR2 = .06, F(6,91)= 1.43, p=n.s..
Notes to table:

 

*p<.05, **p<.Ol

245

Table 102: Hypothesis I: Parenting Competency Mediating T2 Life Stress and Sleep

 

 

 

 

Step 1 [3 SE [3 Beta
Age ofbaby .31 .28 .12
Pregnancy risk factors -.11 .11 -.12
T1 Perceived Stress -.04 .07 -.07
T1 Life Stress -.02 .02 -.12
T1 Mental Stress .03 .02 .21

Total for Step 1 AR2 = .06

Step 2
Age of baby .40 .27 .14
Pregnancy risk factors -.06 .11 -.07
T1 Perceived Stress -.05 .07 -.90
T1 Life Stress -.O3 .02 -.18
T1 Mental Stress .02 .02 .21
T2 Parenting -.06 .60 -.01
Competency
T2 Life Stress .11 .05 .30*

Total for Step 2 AR2 = .05, F(6,91)= 1.39, p=n.s..
Notes to table:

 

*p<.05, **p<.01

246

 

Table 103: Hypothesis 1: Parenting Competency Mediating T2 Perceived Stress and

 

 

 

 

Activity
Step 1 B SE B Beta
Age of baby 3.09 1.21 .25*
Pregnancy risk factors 1.33 .48 .30**
T1 Perceived Stress -.39 .31 -.14
T1 Life Stress .08 .10 .09
T1 Mental Stress -.ll .07 -.20
Total for Step 1 AR2 = .19
Step 2
Age of baby 3.22 1.20 .26*
Pregnancy risk factors .147 .49 .33*
T1 Perceived Stress -.O7 .36 -.03
T1 Life Stress .10 .10 .12
T1 Mental Stress -.14 .07 -.26*
T2 Parenting -1.89 2.48 -.08
Competency
T2 Perceived Stress .57 .34 -.1 8
Total for Step 2 AR2 = .03, F(6,91)= 3.32, p<. 05.
Notes to table:

 

*p<.05, **p<.01

247

 

Table 104: Hypothesis 1: Parenting Competency Mediating T2 Perceived Stress and

Distress to Limitations

 

 

 

 

Step 1 B SE B Beta
Age of baby -1 . 1.5 1.34 .-.09
Pregnancy risk factors .33 .54 .07
T1 Perceived Stress .08 .34 .03
T1 Life Stress .12 .11 .14
T1 Mental Stress -.32 .07 -.06

Total for Step 1 AR2 = .04

Step 2
Age of baby -1.'12 1.35 -.09
Pregnancy risk factors .37 .55 .08
T1 Perceived Stress .05 .40 .02
T1 Life Stress .13 .ll .16
T1 Mental Stress -.O3 .08 -.05
T2 Parenting -3.84 2.89 -.15
Competency
T2 Perceive Stress .10 .38 .03

Total for Step 2 AR2 = .02, F(6,91)= .76, p=n.s..
Notes to table:

 

*p<.05, **p<.01

248

 

Table 105: Hypothesis I: Parenting Competency Mediating T2 Perceived Stress and

 

 

 

 

Smiling
Step 1 B SE B Beta
Age of baby 2.45 1.15 .22*
Pregnancy risk factors .51 .46 .13
T1 Perceived Stress .56 .29 .22
T1 Life Stress -.20 .09 -.26*
T1 Mental Stress .07 .06 .14
Total for Step 1 AR2 = .12
Step 2
Age ofbaby 2.41 1.15 .21*
Pregnancy risk factors .46 .17 .11
T1 Perceived Stress .56 .34 .22
T1 Life Stress -.22 .09 -.28*
T1 Mental Stress .07 .06 .14
T2 Parenting 3.82 2.37 .17
Competency
T2 Perceived Stress -.O7 .33 -.02
Total for Step 2 AR2 = .03, F(6,91)= 2.10, p=n.s..
Notes to table:

 

*p<.05, **p<.01

249

 

Table 106: Hypothesis 1: Parenting Competency Mediating T2 Perceived Stress and

 

 

 

 

 

Duration of Orienting
Step 1 B SE B Beta
Age ofbaby -.41 .81 -.06
Pregnancy risk factors .16 .32 .06
T1 Perceived Stress -.06 .20 -.03
T1 Life Stress -.11 .07 -.21
T1 Mental Stress -.00 .04 -.01
Total for Step 1 AR2 = .05
Step 2
Age of baby -.39 .78 -.05
Pregnancy risk factors .19 .31 .07
T1 Perceived Stress .15 .23 .09
T1 Life Stress -.11 .06 -.21
T1 Mental Stress -.02 .04 -.06
T2 Parenting 3.54 1.60 .23*
Competency
T2 Perceived Stress -.45 .22 -.25*
Total for Step 2 AR2 = .09, F(6,91)= 2.05, p<05..
Notes to table:

 

*p<.05, **p<.Ol

250

Table 107: Hypothesis H: Parenting Competency Mediating T2 Perceived Stress and

 

 

 

 

Sleep
Step 1 B SE B Beta
Age of baby .31 .28 .12
Pregnancy risk factors -.11 .11 -.12
T1 Perceived Stress -.04 .07 -.07
T1 Life Stress -.02 .02 -.12
T1 Mental Stress .03 .02 .21
Total for Step 1 AR2 = .06
Step 2
Age of baby .32 .28 .12
Pregnancy risk factors -.10 .11 -.1 1
T1 Perceived Stress -.01 .08 -.02
T1 Life Stress -.02 .02 -.11
T1 Mental Stress -.02 .02 .19
T2 Parenting -.05 .57 -.Ol
Competency
T2 Perceived Stress -.05 .08 -.08
Total for Step 2 AR2 = .01, F(6,91)= .82, p=n.s..
Notes to table:

 

*p<.05, **p<.01

251

   

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