Prenatal depression effects on the fetus and the newborn
Introduction
Recent studies on newborns of depressed mothers suggest that depressive-like behavior emerges as early as birth. Inferior performance has been noted, for example, on the Brazelton Neonatal Behavior Assessment Scale including lower scores on the orienting and motor scales, greater irritability, lower activity levels, less robustness and more depressive-like behavior (Abrams, Field, Scafidi, & Prodromidis, 1995; Lundy, Field, & Pickens, 1996; Zuckerman, Als, Bauchner, Parker, & Cabral, 1990). Other examples include lesser attentiveness and expressivity during a neonatal imitation paradigm (Lundy et al., 1996).
Physiological and biochemical data converge on the behavioral data suggesting that newborns of depressed mothers are different from birth (Field, 1995; Jones, Field, Fox, Lundy, & Hart, 1998; Lundy, Field, Cigales, & Cuadra, 1997). Newborns of depressed mothers, for example, have been noted to have lower vagal tone and greater relative right frontal EEG activation (Jones et al., 1998). Lower vagal tone and greater relative right frontal EEG activation have also been noted in the depressed mothers of these infants (Jones et al., 1998). Greater relative right frontal EEG activation has been observed in chronically depressed adults even during behavioral remission (Henriques & Davidson, 1990; Tomarken, Davidson, & Henriques, 1990), as well as in older infants of depressed mothers (Dawson, Klinger, Panagitotides, Hill, & Spieker, 1992; Field, Fox, Pickens, & Nawrocki, 1995; Jones, Field, Davalos, & Pickens, 1997). Biochemically, elevated norepinephrine and cortisol levels have been noted in depressed pregnant women (Lundy et al., 1999). The depressed mothers prenatal biochemical profiles were later mimicked by their newborns’ biochemical profiles (Lundy et al., 1999).
These data combined suggest that the behavioral, physiological and biochemical differences noted in newborns of depressed mothers may be related to in utero exposure to their mothers different biochemical profiles. In the Lundy et al. (1999) retrospective study, we noted that depressed women had higher cortisol and norepinephrine levels as well as lower dopamine levels during their last trimester of pregnancy. Their newborns subsequently showed the same pattern of elevated cortisol and norepinephrine levels and lower dopamine levels. The same newborns also showed inferior performance on the Brazelton Neonatal Behavior Assessment Scale including the orientation, reflex, excitability and withdrawal clusters. Stepwise regression analyses using the mothers prenatal data revealed that their norepinephrine and dopamine levels during pregnancy significantly predicted their newborns norepinephrine and dopamine levels as well as their Brazelton scores, suggesting a prenatal biochemical influence on neonatal outcome. In the Lundy et al. (1999) study, the mothers elevated norepinephrine levels may have directly affected fetal neurotransmitter/neurohormone levels and/or may have reduced uterine blood flow, indirectly affecting neurobehavioral development.
Very few studies have been conducted on depression effects on fetal development and neonatal outcome. However, those few studies suggest that maternal neurotransmitter/neurohormone levels may affect prenatal development. In studies by Glover and her colleagues, strong relationships have been noted between maternal and fetal cortisol levels (Gitau, Cameron, Fisk, & Glover, 1998; Glover, Teixeira, Gitau, & Fisk, 1999). Maternal norepinephrine on the other is not related to fetal norepinephrine levels but is associated with impaired blood flow, as measured indirectly by elevated uterine artery resistance (Giannakoulopoulos, Teixeira, Fisk, & Glover, 1999). Elevated norepinephrine would be expected to lead to fetal growth deprivation and subsequent low birthweight. Elevated cortisol, on the other hand, would be expected to lead to prematurity, as has been noted by Wadwha, Porto, Garite, Chicz-DeMet, and Sandman (1998). In their study, prematurity was predicted at a 0.98 reliability by elevated corticotropic hormone (a precursor of cortisol) at 28 weeks gestation in the mother.
These prenatal depression neurotransmitter/neurohormone profiles might be expected, then, to alter fetal growth as well as neonatal outcome. Although many fetal behavior studies have been conducted (Lecanuet, Granier-Deferre, & Busnel, 1995), only a few recent ones have explored fetal behaviors in fetuses of depressed mothers (Allister, Lester, Carr, & Liu, 2001; Dieter et al., 2001; Dieter, Emory, & Ansari, 2002; Monk, Fifer, Myers, & Sloan, 2002). In these studies, fetuses of depressed mothers showed hyperactivity (Dieter et al., 2001), elevated heart rates (Allister et al., 2001) and physiological hyper-reactivity (Dieter et al., 2002, Monk et al., 2002).
The present study improved on our previous studies by being a prospective, longitudinal study with the same sample being repeatedly assessed, first on the mothers’ prenatal biochemistry and then on more comprehensive assessments at the neonatal stage that included maternal and neonatal biochemistry, vagal tone, EEG asymmetry and neonatal behavior during sleep and during the Brazelton Neonatal Behavior Assessment Scale. In addition, we wanted to determine in a prospective sample the differential effects of the mother’s prenatal/biochemistry on neonatal outcome (birthweight and gestational age). In a hypothesized model based on the literature (Glover et al., 1999, Lundy et al., 1999, Wadwha et al., 1998) and tested by path analysis, elevated prenatal cortisol levels were expected to contribute to prematurity and elevated norepinephrine to low birthweight. Only cortisol and norepinephrine were entered in the path analysis inasmuch as catecholamines crossing the placenta are quickly metabolized by monoamine oxidase (Glover & Sandler, 1986) and only relationships between maternal cortisol and norepinephrine levels and fetal behavior and development have been reported in the literature. Also, based on the literature, the newborns’ biochemical profiles were expected to be similar to their depressed mothers’ levels during pregnancy, and the newborns’ vagal tone and frontal EEGs were expected to mimic their mothers’ vagal tone and frontal EEG values. Finally, less optimal performance was expected for the newborns of depressed mothers on the Brazelton Neonatal Behavior Assessment Scale.
Section snippets
Participants
Pregnant women were recruited during their second trimester (M=20.1 weeks, R=16–28 weeks) from obstetrician–gynecologists offices. The pregnant women were assigned to a depressed (depressive symptoms) or non-depressed group based on their scores on the Center for Epidemiological Studies Depression Scale (CES-D; Radloff, 1977). The first 70 women who had elevated scores (≥16) were recruited for the depressive symptom group (M CES-D score=24.0), while the first 70 women scoring in the normal
Results
MANOVAs were performed separately for the prenatal variables (self-report and perinatal complications measures), biochemical data, Brazelton scores and sleep/wake and physiological measures (EEG and vagal tone). Any significant MANOVAs were followed by ANOVAs on the individual variables. Based on the literature and our previous studies the following hypotheses were made: (1) prenatally depressed mothers were expected to have elevated cortisol and norepinephrine levels; (2) their neonates were
Discussion
Several findings in this study replicated earlier findings by our group (Abrams et al., 1995, Jones et al., 1998, Lundy et al., 1999). Regarding the mothers’ prenatal biochemistry, the elevated prenatal cortisol levels in the women with depressive symptoms were consistent with the elevated cortisol levels in depressed pregnant women in the Lundy et al. (1999) study. According to Glover et al. (1999) 40% of the mothers’ cortisol crosses the placenta. The depressed serotonin levels in the
Acknowledgements
We would like to thank the mothers and infants who participated in this study. This research was supported by an NIMH Senior Research Scientist Award (MH#00331) and an NIMH merit award (MH#46586) to T.F and funding by Johnson and Johnson.
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