Elsevier

Sleep Medicine

Volume 30, February 2017, Pages 195-203
Sleep Medicine

Original Article
Altered sleep architecture during the first months of life in infants born to depressed mothers

https://doi.org/10.1016/j.sleep.2016.11.018Get rights and content

Highlights

  • Our data confirm in very young infants the findings from older children and adolescents at high risk for depression.

  • The abnormal sleep pattern found in this high risk group of very young infants seems due to a vulnerability to depression.

  • An abnormal sleep pattern could be an early marker of an altered neuroplasticity associated with the risk of depression.

Abstract

Objective

This study investigated sleep architecture in newborn and six-month-old infants who were born to depressed mothers.

Method

Sixty-four healthy full-term infants (32 males and 32 females) participated in the study. Of these, 32 were high-risk infants who were born to mothers diagnosed with depression, and 32 were low-risk infants born to mothers without a personal history of depression. 24-hour polysomnography was recorded at zero and six months of age (M0 and M6). Sleep macro-structural parameters (total sleep time, TST; awake time; non-rapid eye movement, NREM sleep (%); rapid eye movement, REM sleep %; arousal index; and sleep efficiency) were analysed at M0 and M6. Micro-architectural sleep features (slow-wave activity, SWA; delta sleep ratio, DSR; spindle density; and rapid eye movement density) were calculated at M6. The data between high-risk and low-risk groups were compared using Student's t-tests.

Results

At M0 and M6, the high-risk infants showed more awake time and fewer arousals than the low-risk infants. However, the high-risk group had less NREM% at M0 and a shorter TST as well as less REM% at M6 than the low-risk group. At M6, the high-risk group showed higher SWA, higher DSR and lower spindle density in comparison with the low-risk group.

Conclusions

Altered sleep structure was observed during their first months of life in infants born from depressed mothers, thereby suggesting that the prenatal environment could enhance the depression vulnerability of the child and potentially decrease their neuroplasticity.

Introduction

Major depressive disorder (MDD) is a common, globally pervasive disease with a lifetime prevalence of 16.2% [1] that causes a considerable socioeconomic burden [2]. Notably, women are much more commonly affected than men, and 10–16% of women experience major depression during pregnancy and postpartum [3], [4].

A large portion of the literature has reported that depression in children and adolescents is more likely to occur among the offspring of depressed mothers and that more than half of them develop the disease before adulthood [5], [6]. Many mechanisms have been identified, to date, explaining the transmission of risk from mothers to children, thereby reflecting the complexity of its underlying aetiology [7]. Among these, genetic factors and environmental exposure are prevalent [8], [9].

Several studies [10], [11] have found a need to identify early markers of mother-child transmission of depressive disorders, so that mental illness predictors can be evaluated before the development of pathology. In this context, sleep disturbances have recently been proposed to serve as these types of predictors because they are a common feature of mood spectrum disorders. Indeed, alterations at a macro-structural level, including a reduction in rapid eye movement (REM) sleep latency and slow-wave sleep, and an increase in sleep latency, wakefulness and sleep fragmentation have been reported in depressed adults [12], [13], [14], [15], [16].

Although less studied, micro-architectural sleep features are regarded as even more accurate predictive markers of vulnerability to pathology [17], [18]. Micro-architectural sleep studies have reported decreased slow-wave activity and reduced temporal coherence [12], [15], as well as increased rapid eye movements (REMs) density [19] in depressed patients compared with non-depressed individuals. As such, these micro-architectural indices have been considered to be fundamental markers of depression.

Moreover, a micro-structural sleep correlate of depression has been found in the delta sleep ratio, which is typically decreased in depressed individuals [20], [21]. Furthermore, a reduced delta sleep ratio can be regarded as a predictor of early recurrence, mood worsening and negative therapeutic outcome in major depressive disorders [22], [23].

Despite the unquestionable link between sleep disturbances and mood disorders in adults, studies on depressed children and adolescents have produced inconsistent findings [18], [24]. These inconsistencies originate from age-related or sex-related differences in sleep parameters. Indeed, recent studies have found significant sex differences in the sleep macro-architecture of depressed children and adolescents, with the greatest alterations being observed in adolescent males [25], [26], [27]. These alterations comprised lower sleep efficiency [26], reduced N2 sleep and slow-wave sleep (SWS) durations [27].

Furthermore, micro-architectural sleep alterations have been reported in 8–15-year-onset depression, with, in particular, reduced spindle activity [25], inter-hemispheric and intra-hemispheric coherence [26] and a higher REMs density [10] in depressed children and adolescents. Conversely, the delta sleep ratio has not yet been investigated in this age range.

Nonetheless, few studies have investigated sleep disturbances in never-depressed but high-risk children. Yet, the offspring of depressed mothers are likely to develop mood disorders, particularly unipolar depression. In this perspective, early predictors of pathology are relevant to these children, in order to evaluate their actual risk of developing depression.

At a macro-structural level of sleep, Armitage et al. [10] found that infants from depressed mothers exhibited a longer sleep latency, lower sleep efficiency and more sleep bouts (expression of sleep fragmentation) than controls from two weeks to six months of age. Additionally, Bat-Pitault et al. [11] found that wake after sleep onset (WASO) and sleep efficiency were, respectively, increased and reduced in high-risk adolescents relative to controls.

As for the micro-architectural sleep features, low temporal coherence and reduced sleep spindle activity (SPA) were reported in adolescent females who were at high risk of depression [25], [28]. However, because of the genetic susceptibility of depression and the need to establish early programs of prevention, it appears to be important to assess whether infants at high risk of mood disorders exhibit early onset sleep disturbances. It is believed that, to date, no data are available on the micro-architectural characteristics of this population.

Therefore, the aim of the present study was to compare the macro sleep structure between high-risk and low-risk infants at zero and six months of age. Microstructure was only studied at six months of age, which is an age when architectural features, such as spindles, are settled. The first hypothesis was that the sleep structure in the offspring of depressed mothers was already modified at birth due to the prenatal environment. Second, it was postulated that these sleep disturbances in high-risk children would trace those in adolescence and adulthood depression and, if correct, that these alterations would reflect a vulnerability to depressive mood since childhood and, hence, could be considered to be an early vulnerability marker of depression.

Section snippets

Participants

Sixty-four newborn infants (32 males, 32 females) were separated into two groups: a group of high-risk infants born from mothers with a major depressive disorder (MDD, see Diagnostic procedures and Fig. 1) (N = 32) and a group of low-risk infants born from non-MDD mothers (N = 32). Mothers were drawn from the AuBE cohort (Autonomic Baby Evaluation) [29], in which 302 women whose infants were born in the maternity ward of the University Hospital Centre of Saint-Etienne, France, were recruited

Demographic and clinical data

The HAD depression score values, corresponding to the means of HAD depression score at 0, 6, 12, 18 and 24 months, were significantly different between the two groups and were higher in the high-risk group relative to the low-risk group. No significant differences were found in the other clinical or demographic data of quantitative and categorical variables between the high-risk and low-risk groups (see Table 1).

Macro-architectural features of sleep

At M0 and M6, the high-risk infants showed more awake time and fewer arousals than

Discussion

The purpose of the present study was to assess early onset sleep disturbances in infants born from mothers with a history of major depressive disorder, which confers a considerable risk for mood disorder in their offspring [6], [7], [8], [9]. To that purpose, macro- and micro-architectural sleep indices were recorded and compared between high-risk and low-risk infants. The results revealed striking between-group differences at both levels. Because the two groups were matched on the infants' and

Conclusions

In summary, the findings largely confirm, but more importantly characterize, the findings from older children and adolescents at high risk of depression and from depressed young and adult individuals in very young infants. Moreover, the samples were composed of high risk but non-depressed individuals, indicating that the abnormal sleep pattern that was found in these infants is not due to the presence of the pathology, but rather to a vulnerability to depression. Because macro-, and especially

Acknowledgments

This work was supported in part by the French National Research Agency, Contrat ANR n° 08-MNPS-033-01.

The AuBE study was allowed through consecutive grants from the French Ministry of Health: Programmes Hospitaliers de Recherche Clinique – PHRC interrégional, 2009 and AOL 2010.

We especially acknowledge Mrs. Sophie Foucat and all of the parents of the association SA VIE (www.sa-vie.fr; Nantes-France), Dr Elisabeth Briand-Huchet and Mrs. Myriam Morinay, president of the French national

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    These authors contributed equally to this work.

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