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 Table of Contents  
Year : 2022  |  Volume : 6  |  Issue : 1  |  Page : 16-21

Maternal depression and preeclampsia: Effects on the maternal and offspring's mental and physical health

1 School of Medical and Health Sciences, Edith Cowan University, Perth, WA, Australia
2 Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China

Date of Submission12-Jul-2021
Date of Acceptance27-Sep-2021
Date of Web Publication31-Jan-2022

Correspondence Address:
Dr. Yequn Chen
Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/hm.hm_41_21

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Prenatal depression and preeclampsia (PE) are well-known risk factors of maternal and fetal mortality and morbidity. In recent years, there are emerging evidence suggesting that prenatal depression and PE could be environmental risk factors for several neurodevelopment disorders of offspring. Prenatal depression and PE were also found to be risk factors of each other. At present, the mechanism (s) of how prenatal depression and PE affect one another and their roles in the development of maternal and fetal adverse outcomes are uncertain. In this review, we outline the most recent clinical studies on the effects of prenatal depression and PE on the neurodevelopmental outcomes of offspring, as well as the plausible mechanism(s) of how these two maternal conditions affect each other and their roles in the neurodevelopment of offspring, including inflammation, oxidative stress, and maternal immune activation. We postulate that the overproduction of pro-inflammatory cytokines and increased cortisol levels in maternal depression can alter fetal neurodevelopment, and the autonomic nervous system dysfunction caused by maternal depression may accelerate heart rate and elevate blood pressure in mothers. Similarly, in PE, the elevated inflammation and exaggerated oxidative stress in the mothers, placenta, and fetus could negatively affect maternal depression on and impair the neurodevelopment of offspring. Further studies are needed to examine the combined effects of prenatal depression and PE on the health outcomes of mothers and offspring, to explore the mechanism of maternal depression in the development of PE and to investigate their roles in the neurodevelopment of offspring.

Keywords: Inflammation, neurodevelopmental disorder, oxidative stress, preeclampsia, prenatal depression

How to cite this article:
Lin D, Chen Y. Maternal depression and preeclampsia: Effects on the maternal and offspring's mental and physical health. Heart Mind 2022;6:16-21

How to cite this URL:
Lin D, Chen Y. Maternal depression and preeclampsia: Effects on the maternal and offspring's mental and physical health. Heart Mind [serial online] 2022 [cited 2023 Feb 6];6:16-21. Available from: http://www.heartmindjournal.org/text.asp?2022/6/1/16/336889

  Introduction Top

Prenatal depression and preeclampsia (PE) are well-known complications during pregnancy and are associated with severe health issues of maternal and fetal health.[1] Prenatal depression was associated with increased risks of obstetric and fetal complications, including PE,[2] postpartum depression,[3] and fetal psychiatric problems.[4] PE is defined as de novo hypertension present after 20 weeks of gestation combined proteinuria (>300 mg/day), other maternal organ dysfunction, such as renal insufficiency, liver involvement, neurological or hematological complications, uteroplacental dysfunction, or fetal growth restriction.[5] PE causes not only severe hypertension but also dysfunction of other systems, such as eclampsia (convulsions) or hemolysis, elevated liver enzymes, and low platelets syndrome. In addition, PE was also associated with increased risk of psychological disorders.[6] Emerging evidence shows that the combination of both prenatal depression and PE further increases the risk of adverse pregnancy outcomes, including lower birth weight[7] and lower gestational age at birth.[8] Nevertheless, the therapies of PE are currently limited and focus solely on managing symptoms of PE rather than treating the underlying cause.[9]

The association between depression and PE during pregnancy is very complex as they affect one another.[10] It has been shown that pregnant women with depression were at increased risk of developing pregnancy-induced hypertension than those without depression.[2] Similarly, there is evidence indicating that hypertensive pregnant women were more susceptible to experience depression symptoms during pregnancy and/or in the postpartum period than normotensive pregnant women are.[11] Given the increasing prevalence of depression and the poor prognosis of PE, a clarified understanding of the associations between depression and the neurodevelopment of offspring via the cardiovascular pathway is necessary. However, the extent to which these two diseases are causally related to one another and how prenatal depression could affect the neurological functions of mothers and the neurodevelopment of infants remain to be clarified. Against this background, in this review, we aim to discuss the current findings about the effects of prenatal depression and PE on the physical and mental health of mothers and offspring dyads.

  Review of Clinical Studies Top

Association between prenatal depression exposure and neurodevelopmental outcomes in offspring

Prenatal depression has been associated with poor cognitive functioning, behavioral inhibition, as well as mental and physical diseases, of offspring later in life.[12] In addition, women with depression during pregnancy often exhibit depressive symptoms after delivery,[4] leading to poorer cognitive abilities[13] and cardiac function[14] in children. In the following paragraph, we will describe the relationship between maternal depression in pregnancy and their effects on the neurodevelopmental disorders of offspring.

The offspring of women with prenatal depression are at increased risk of psychological disorders. Several studies have shown that maternal depression during pregnancy could predict child depression in adolescence and that child maltreatment is a risk factor for the development of this disorder.[15],[16] A study of the unpredictability of prenatal maternal mood, as measured by entropy values, found that fetal exposure to higher maternal emotional entropy predicted higher levels of negative emotionality in children at 12 months, 24 months, and 7 years of age.[17] In addition, children exposed to higher prenatal maternal emotional entropy showed higher levels of anxiety symptoms at the age of 10 years and higher levels of depressive symptoms at the age of 13 years.[17] Thus, fetal programming is the biological mechanism primarily responsible for the association between maternal prenatal depression exposure in utero and offspring anxiety disorders.

The offspring of mothers with depression are at increased risk of cognitive and emotional impairment. A large prospective cohort study of Finnish mothers and children (the Prediction and Prevention of PE and Intrauterine Growth Restriction Study) showed that the babies of mothers with the most chronic and severe depressive symptoms during and after pregnancy had poorer overall scores in fine and gross motor, communication, problem-solving, and personal/social skills,[4] suggesting that depressive symptoms could affect the fetal cognitive and emotional development.[18]

Prenatal depression is associated with brain alterations in offspring. Maternal depression during pregnancy is also associated with structural brain changes in the fetal prefrontal cortex,[19] frontal and inferior temporal regions,[20] and neural connections between the amygdala and frontal striatal regions.[21] A prospective, longitudinal study[19] of maternal depressive symptoms at 19, 25, and 31 weeks of gestation, with structural magnetic resonance imaging scans of the children, showed that children exposed to prenatal maternal depression had significant cortical thinning mainly in the right frontal lobe. The strongest association was observed at 25 weeks of gestation, suggesting that this gestational interval is the most sensitive period for the fetus, resulting in a broad pattern of cortical thinning.

These findings suggest that, in general, prenatal depression is associated with the enhanced risk for psychological disorders, cognitive and emotional impairment, and brain alterations of the offspring, emphasizing the importance of preventing and timely intervention of prenatal depression for reduced risk of adverse maternal and fetal outcomes.

Association between PE exposure and neurodevelopmental outcomes in offspring

PE is a risk factor known to affect several fetal outcomes. In the following paragraphs, we will describe the relationship between PE and the neurological outcomes of offspring.

Emerging evidence showed a positive association between fetal exposure to PE and neurodevelopmental disorders such as autism spectrum disorders (ASD), attention-deficit/hyperactivity disorder (ADHD), and altered cognitive function in offspring. ASD is a group of neurodevelopmental disorders characterized by social communication deficits and stereotypic behaviors that affect an estimated 1%–1.5% of children,[22] whereas ADHD is characterized by inattention, hyperactivity, and impulsivity, with an estimated prevalence of 1.4%–3%.[23] There are evidence indicating a strong association between PE and offspring neurodevelopmental trajectories in ASD and ADHD. Several cohort studies have demonstrated PE as an independent risk factor for ASD[24] and ADHD.[24] Recent meta-analyses also showed that PE was strongly associated with ASD or ADHD.[25] The evidence suggests that PE may be associated with the risk of common neurodevelopmental disorders (cerebral palsy, schizophrenia, and epilepsy) in offspring, with the effects of PE on cerebral palsy and epilepsy in offspring possibly related to the week of gestation of delivery.[24] Cognitive function is a person's ability to think, learn and remember adequately and is usually measured by a person's performance in the domains of perception, reasoning, intuition, and creativity.[26] Many studies have reported poorer cognitive function in offspring with PE compared to controls.[27] The Helsinki Birth Cohort Study reported that infants exposed to PE had poorer verbal reasoning skills and overall intelligence at the age of 18 years[28] and exhibited an increased rate of cognitive decline at 69 years, suggesting that the effects of PE exposure persist until old age.[29] Taken together, this evidence suggests that PE may be associated with impaired cognitive function in exposed offspring.

Infants of preeclamptic women are at increased risk of developing neuroanatomical alterations. A small pilot cohort study found that changes in regional grey matter volume, white matter structural connectivity, and functional connectivity in PE-exposed children were consistent with the brain anatomical and functional changes seen in neurodevelopmental disorders, which may underlie their increased risk for neurodevelopmental disorders.[30]

These findings showed that PE is associated with increased risk of neurological disorders in offspring exposed to PE, indicating the need of timely preventing and treatment of PE and additional attention on monitoring the health of infants exposed to PE.

Association between maternal depression and preeclampsia

In addition to offspring, PE is also found to be associated with maternal depression during and after pregnancy. In the following paragraphs, we will summarize the studies on the relationship between PE and maternal depression.

In reviewing the literature, the association between PE and postpartum depression has mixed results.[6] Three cross-sectional studies assessing the association of PE and postpartum depression had the following results: (1) compared to women without PE, women with PE have a higher prevalence of postpartum depression and had more severe depressive symptoms; (2) severe PE is associated with poor psychological prognosis such as depression. In 6 cohort studies assessing PE as a risk factor for postpartum depression, 3 cohort studies, of which the sample sizes ranged from 1155 to 400,717, found that PE is a risk factor for depression, while three other cohort studies did not find this association. One reason for these differences may be the relatively low validity of the latter three studies with a total sample size between 20 and 175.

Previous studies reported inconsistent results of the association between PE and depression outside the perinatal period. Two cohort studies demonstrated that women with a history of PE subsequently experienced more depressive symptoms and fatigue compared to controls in a follow-up of up to 14 years.[31],[32] However, two studies did not find an association between women with a history of PE and depression outside the perinatal period.[33],[34]

A recent meta-analysis[2] of over 61.2 million pregnancies across 44 studies showed three main findings: (1) women with clinical symptoms or diagnoses of depression and/or anxiety during pregnancy had a 39% increase in relative risk (RR) for PE diagnosis compared to the unexposed group; (2) subgroup analyses of depression and anxiety at 20 weeks of gestation showed correlations with PE, such that women experiencing depression or anxiety in early pregnancy had an increased RR for late PE diagnosis compared to unexposed pregnant women; (3) when depression and anxiety were investigated separately, they were each independently associated with a greater risk of developing PE compared to the unexposed group. The findings suggest that depression and anxiety may increase the risk of PE development and point to the potential for future studies to focus on depression and anxiety in people at risk for PE.

In overall, the associations of PE and maternal depression during and after pregnancy are inconsistent across studies. Further research is required to confirm the findings.

  Possible Mechanism Top

In the following paragraphs, we will discuss the possible mechanisms underlying the association between maternal depression, PE, and their effects on the offspring's neurodevelopment [Figure 1].
Figure 1: Relationship between maternal depression, preeclampsia and the neurodevelopment of their offspring

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Effect of anxiety and depression on fetus

Anxiety and depression during pregnancy have been shown to induce pro-inflammatory responses in women, which may affect the developing fetus and lead to negative effects on later behavioral and cognitive functioning.[35] The physiological trajectory of fetal brain development requires a balance of pro- and anti-inflammatory cytokines in the maternal and fetal environment. In maternal depression, maternal overproduction of pro-inflammatory cytokines can be transported to the fetal blood–brain barrier (BBB) via the placenta, leading to altered fetal neurodevelopment.[36] In addition to the key role of the pro-inflammatory state, maternal depression during pregnancy is associated with higher cortisol levels, some of which may be transported to the fetus via the placenta. In addition, the presence of stress and depression may reduce placental 11β-hydroxysteroid dehydrogenases-2 activity and expression,[37] and may also expose the fetus to detrimentally high cortisol levels, which are associated with low fetal weight and high-stress response in the offspring.[37]

Effect of anxiety and depression on preeclampsia

Anxiety and depression may cause autonomic nervous system dysfunction, hyperactive sympathetic nervous system, as well as increased secretion of catecholamines, resulting in accelerated heart rate and elevated blood pressure.[10],[38],[39],[40] Hypothalamic dysfunction in patients with anxiety and depression can increase the excitability of the pituitary-adrenocortical axis and secrete large amounts of glucocorticoids, causing metabolic disorders, and the retention of water and sodium, resulting in increased blood pressure.[41] Behavioral risk factors associated with depression and anxiety, including decreased physical activity,[42] increased appetite,[43] and poor sleep quality,[44],[45] may also increase the risk of PE.

Effect of preeclampsia on maternal outcome

Dysregulated immune activation is a well-recognized feature of PE.[46] Compared with normotensive women, patients with PE have higher circulating concentrations of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), IL-8, IL-16, c-reactive protein,[47] and pro-inflammatory T-cells (T-helper 1 [Th1] cells and Th17 cells),[48] as well as lower concentrations of the anti-inflammatory cytokines transforming growth factor β and IL-101[49] and anti-inflammatory T-cells (Th2 and Treg cells),[48] leading to neurovascular endothelial dysfunction. Neurovascular endothelial dysfunction could elevate the permeability of the BBB[50] via exacerbating cerebral hyperperfusion impaired by cerebral blood flow autoregulation, inevitably inducing neuroinflammation.[51] In addition, placental injury induced through ischemia-reperfusion injury increases placental oxidative stress in PE patients. This triggers a series of trophoblast damage, including syncytial trophoblast apoptosis, DNA fragmentation, localized membrane damage, and dysregulation of the levels of placental growth factor,[52] vascular endothelial growth factor, and tyrosine kinase-1 (sFlt-1)[53] released by trophoblast cells into the maternal circulation, followed by systemic endothelial vascular damage and dysfunction,[54],[55] leading to BBB damage.

PE is known to cause neurovascular dysfunction manifested by endothelial dysfunction,[56] white matter lesions, stroke, and accompanied by behavioral changes such as cognitive, emotional, and mood alterations.[50],[54],[57] A major mechanism of neurovascular dysfunction caused by PE is through impairment of cerebral blood flow autoregulation. Impairment of cerebral autoregulation in PE exacerbates hyperperfusion of the brain, leading to cerebral vascular damage and elevated BBB permeability,[50] inevitably inducing neuroinflammation.[51]

Effect of preeclampsia on fetal outcome

Similarly, maternal immune activation (MIA) exposed to PE can lead to alterations in structural and functional brain connectivity of infants.[14] A potential mechanism for this association is the effect of MIA on microglia in the offspring. Alterations in microglia have been linked to the pathogenesis of neurodevelopmental disorders such as ASD. On the other hand, placental oxidative stress exposed to PE causes a relative increase in intracellular reactive oxygen species (ROS) production and a decrease in antioxidant levels. Neurodevelopmental alterations may result from excessive ROS levels in the fetal brain.[58] High concentrations of ROS regulate many neurodevelopmental processes, including proliferation and differentiation of neural precursor cells, apoptosis, dendritic growth, and axonal guidance,[59],[60] suggesting that oxidative stress may lead to suboptimal neurodevelopmental trajectories through the direct effects of excessive ROS concentrations on neurodevelopmental processes. In addition, placental oxidative stress may indirectly affect fetal neurodevelopment by inducing the placenta to secrete a variety of factors that can cross the BBB, such as TNF-α, IL-1 beta, and IL-6, into the fetal circulation.

Taken together, although PE and prenatal depression alone are associated with similar underlying mechanisms and adverse effects on the offspring, only a few studies have explained the presence of these two pregnancy complications and their impact on mental and metabolic disorders in the offspring. The proportion of women with comorbid hypertension and depression during pregnancy is increasing in the last years, but there are no follow-up studies to investigate the impact and timing of these two comorbid disorders on the health of their offspring during their lifetime. Indeed, this would greatly contribute to the understanding of the relationship between maternal hypertension and depression during pregnancy and to identify the molecular mechanisms and biological targets of alterations that play a key role in the transmission of disease susceptibility across generations.

  Conclusions Top

This review sheds a light on the relationship of prenatal depression and PE with the mental and physical health of mother and offspring dyads. Maternal oxidative stress and inflammation could potentially play important roles in the neurodevelopment of infants in the intrauterine environment. These comorbid conditions increase the risk for adverse maternal and neonatal outcomes and may enhance the long-term susceptibility for several psychological disorders in mothers and their descendants. The precise mechanism of prenatal depression in the development of PE remains to be elucidated. Further experimental studies need to be carried out to examine the biological pathways of depression and PE. Considerably more studies are needed to examine the combined effects of depression and PE on maternal and fetal outcomes. Promptly diagnosis and treatment of maternal depression and anxiety in pregnancy have the potential to not only reduce the risk of developing PE but may also minimize the psychological and neurological impact of PE. Depressed and preeclamptic women require more attention and more public initiatives to improve their health conditions and those of their offspring.

Ethical approval

Ethical Statement is not applicable for this article.

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Conflicts of interest

There are no conflicts of interest.

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