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Postpartum depression (PPD) is a potentially debilitating disorder that develops in a significant percentage of women during the first year after giving birth. Women afflicted with PPD experience long-term consequences, including sadness, guilt, and despair. Offspring may be affected as well. Several investigators have tested psychosocial risk factors for the development of PPD; however, substantial amounts of variance in PPD have gone unexplained with regression on psychosocial variables alone. Likewise, interventions for PPD that have focused on psychosocial risk factors alone have been largely unsuccessful. The unexplained variance and disappointing treatment success could well be due to investigators' failure to address relevant biological changes occurring during the postpartum period. Two biological systems that are affected significantly and remain in flux during the postpartum period are the innate immune system and the hypothalamic-pituitary-adrenal (HPA) axis. Bidirectional interactions between these two systems are well established, and it is generally acknowledged that dysfunction in either system can lead to depression in nonpregnant, nonpostpartum populations. To date, little research has pursued the contribution of these interacting systems to the development of PPD. The purpose of this paper is to review the psychoneuroimmunology of PPD. The central hypothesis presented is that dysregulation in either system individually or in their bidirectional interaction is associated with the development of PPD.
Content may be subject to copyright.
Volume 17, Number 9, 2008
© Mary Ann Liebert, Inc.
DOI: 10.1089/jwh.2007.0725
The Psychoneuroimmunology of Postpartum Depression
Elizabeth J. Corwin, Ph.D., and Kathleen Pajer, M.D., M.P.H.
Postpartum depression (PPD) is a potentially debilitating disorder that develops in a significant percentage of
women during the first year after giving birth. Women afflicted with PPD experience long-term consequences,
including sadness, guilt, and despair. Offspring may be affected as well. Several investigators have tested psy-
chosocial risk factors for the development of PPD; however, substantial amounts of variance in PPD have gone
unexplained with regression on psychosocial variables alone. Likewise, interventions for PPD that have focused
on psychosocial risk factors alone have been largely unsuccessful. The unexplained variance and disappoint-
ing treatment success could well be due to investigators’ failure to address relevant biological changes occur-
ring during the postpartum period. Two biological systems that are affected significantly and remain in flux
during the postpartum period are the innate immune system and the hypothalamic-pituitary-adrenal (HPA)
axis. Bidirectional interactions between these two systems are well established, and it is generally acknowl-
edged that dysfunction in either system can lead to depression in nonpregnant, nonpostpartum populations.
To date, little research has pursued the contribution of these interacting systems to the development of PPD.
The purpose of this paper is to review the psychoneuroimmunology of PPD. The central hypothesis presented
is that dysregulation in either system individually or in their bidirectional interaction is associated with the de-
velopment of PPD.
(PPD) is a debilitating disorder
that develops in new mothers during the first year after
giving birth. Long-term sequelae, including maternal sad-
ness, guilt, and despair, may occur, as may consequences for
Despite much research, the mechanisms under-
lying PPD remain elusive. Psychosocial variables are insuf-
ficient as the sole explanatory variables, and interventions
focused on altering psychosocial risk factors alone have
yielded disappointing results.
Biological mechanisms have
also been explored, but research on the role of gonadal hor-
mone fluxes, thyroid dysregulation, and abnormal neuro-
transmitter levels likewise have been inconclusive.
The purpose of this paper is to review the psychoneu-
roimmunology of PPD, wherein the contributions of two
other, interconnected biological systems, both significantly
altered during pregnancy and childbirth, are reviewed in re-
gard to the development of PPD. Specifically, we review how
pregnancy-related changes in the innate immune system and
the hypothalamic-pituitary-adrenal (HPA) axis may contrib-
ute to the development of PPD if they do not return to nor-
mal function after delivery. This perspective is an extrapo-
lation of data indicating that overstimulation of the innate
immune system and HPA axis dysregulation are both asso-
ciated with depression in adults who are not in the post-
partum state.
First, a brief overview of the epidemiological, clinical, and
physiological characteristics of PPD is presented. The next
two sections review data in support of innate immune sys-
tem dysfunction and HPA axis dysregulation as possible eti-
ological factors in the development of PPD. The paper con-
cludes with recommendations for future research to clarify
these associations. Our goal throughout is to highlight the
significance of these two systems in postpartum women in
light of their known relationships with depression, in order
to encourage future research to improve the health of post-
partum women.
Overview of Postpartum Depression
The birth of a child is usually a time of great joy. For some
women, however, the stressors of the postpartum period
combine to reduce the ability of a new mother to meet her
The Ohio State University, Columbus, Ohio.
The authors deny any conflict of interest or financial arrangement with any companies or institutions that may benefit from the find-
ings presented in this paper.
role demands. Of particular concern is the development of
PPD, which occurs in 15%–20% of women during the first
year after giving birth.
PPD is a moderate to severe mood disorder comparable
to a major depressive episode in the DSM-IV-TR. PPD car-
ries significant and dangerous implications for a new
mother’s health and the health of her infant.
It may in-
terfere with maternal role development and mother-infant
bonding and may cause physical risk to mother and child
alike. The effects on children may include behavioral, de-
velopmental, and cognitive delay and may last years beyond
The development of PPD is often insidious, with symptoms
including sadness, an inability to take pleasure in most ac-
tivities, anxiety, irritability, fatigue, poor sleep, and recurrent
thoughts of suicide or death, beginning as early as 2 weeks
to as late as several months after delivery.
PPD is diag-
nosed by careful history and physical examination followed
by application of one of many screening tools; women who
score at high risk may receive a follow-up interview to con-
firm the diagnosis.
Major psychosocial risk factors for PPD
include prenatal depression, previous history of depression,
low self-esteem, inadequate social support, child care stress,
a fussy infant, and life stressors.
Financial hardship more
than triples the risk of PPD, partially explaining the higher
prevalence of PPD in black and Hispanic mothers.
Physiological risk factors for PPD have been proposed as
well, including hypothyroidism and acute change in repro-
ductive hormone levels.
Although depressed mood is
common in those suffering a thyroid abnormality, most
women with PPD have thyroid hormone levels in the nor-
mal range. Similarly, although acute changes in estrogen lev-
els may precipitate PPD, this appears to affect only a sub-
population of women with a history of depression.
A possible biological mechanism that has received little
attention to date is the bidirectional innate immune system-
HPA axis association. This is surprising, given the profound
changes that occur within these systems during pregnancy
and delivery and their associations with depression in other
Innate Immune System
The innate immune response is stimulated by infection,
injury, malignancy, autoimmune disease, and stress. It is
rapid in onset and serves to acutely limit tissue damage and
the spread of infection. It is orchestrated by the synthesis and
release of proinflammatory and anti-inflammatory cyto-
kines. Proinflammatory cytokines, including interleukin-1-
beta (IL-1), IL-2, IL-6, tumor necrosis factor-alpha (TNF-),
interferon-alpha (IFN-), and interferon-gamma (IFN-), are
proteins released from activated white blood cells in re-
sponse to the conditions noted.
Release of proinflamma-
tory cytokines initiates a systemic inflammatory response
characterized by fever, increased sleep, reduction in activity,
increased fatigue, decreased food intake, decreased explo-
ration, diminished sexual activity, and, in humans, de-
pressed mood.
Because of the potential for unabated inflammation to
cause undesirable side effects in the host, the proinflamma-
tory response normally is kept in check through the recip-
rocal production of anti-inflammatory cytokines, including
IL-4 and IL-10, which inhibit the production of proinflam-
matory cytokines.
Occasionally, the balance between
proinflammatory and anti-inflammatory cytokines shifts,
impacting an individual’s mental health.
Inflammation and depression
Research suggests that prolonged or excessive activation
of the proinflammatory immune response may be a mecha-
nism for depression.
Administration of even nanomolar
concentrations of proinflammatory cytokines to patients
with cancer, hepatitis C, or other diseases induces symptoms
of depression.
In individuals already suffering from de-
pression, proinflammatory cytokines, including IL-1, IL-6,
and TNF-, are elevated.
HPA Axis
The HPA axis has far-reaching effects on immunity, me-
tabolism, and reproduction. These are accomplished through
frequent pulsatile secretion of cortisol, accompanied by large
surges of the same hormone in response to changes or threats
in the environment. The secretion of cortisol is the final prod-
uct in a secretory pathway initiated by the release of corti-
cotrophin-releasing hormone (CRH) from the hypothalamus.
CRH stimulates the secretion of adrenocorticotrophic hor-
mone (ACTH) from the anterior pituitary, which serves as
the stimulus for adrenal cortisol secretion. HPA axis func-
tion is predominantly regulated by a negative feedback loop.
Control of HPA axis activity is essential in protecting the or-
ganism from the catabolic, lipogenic, antireproductive, and
immunosuppressive effects of prolonged exposure to gluco-
When exposed to changes in the environment perceived
to be threatening or those which are physically stressful, the
HPA axis secretes a larger amount of cortisol than the fre-
quent pulses that comprise the basal circadian rhythm.
stress response produces an increase in alertness and pro-
vides additional energy through gluconeogenesis, accompa-
nied by suppression of nearly all components of the immune
response, including all the key steps of proinflammatory cy-
tokine production and secretion.
The system usually re-
turns to baseline within a few hours after stress exposure,
but if chronic exposure continues, the system can become
dysregulated, manifest by various patterns of hyperactivity
or hypoactivity.
HPA axis dysfunction and depression
Chrousos and Gold
originally hypothesized that dys-
regulation in HPA axis function is best characterized by a U-
shaped curve. With HPA axis function on either end of the
curve, depression, dysphoria, suicidal ideation, and all the
neurovegetative symptoms of depression are possible.
Clinically, hyperactivation of the stress response is associ-
ated with melancholic depression, anorexia nervosa, attach-
ment disorder of infancy, and childhood maltreatment.
Hypoactivation of the HPA, in turn, has been linked to sea-
sonal and atypical depression, rheumatoid arthritis, fi-
bromyalgia, and chronic fatigue syndrome.
cluded in this group depression that develops during the
postpartum period, as described later.
Innate System and HPA Axis Function
There is a well-documented bidirectional association be-
tween the innate immune response and the HPA axis.
IL-1, IL-2, IL-6, and TNF-stimulate cortisol secretion, di-
rectly by acting on the cells of the adrenal cortex and indi-
rectly via stimulation of CRH from the hypothalamus and
ACTH from the anterior pituitary.
IL-2 is a more potent
known stimulator of ACTH release than CRH on a molar-
to-molar basis. Chronically elevated proinflammatory cyto-
kines appear to induce a decrease in central nervous system
(CNS) glucocorticoid receptor function, decreasing the sen-
sitivity of hypothalamic CRH-secreting cells to rising corti-
sol and blunting the normal negative feedback response of
the hypothalamus to cortisol.
HPA activation, in turn, has profound inhibitory effects
on the immune/inflammatory response, acting to block vir-
tually each step of the proinflammatory process.
The glu-
cocorticoids, of which cortisol is the primary type in humans,
inhibit the production of proinflammatory cytokines at the
level of the DNA by blocking the genes responsible for their
production and by inducing the production of NFkB, a pro-
tein that binds to and neutralizes important cytokine tran-
scription factors. Cytokines known to be downregulated by
cortisol and other glucocorticoids include IL-1, IL-2, TNF-,
and IFN-. Moreover, glucocorticoids favor the production
of the anti-inflammatory cytokines,
especially at low con-
centrations of glucocorticoids.
Innate Immune System, HPA Axis Function, and PPD
The implication that dysregulation in the immune system
or the HPA axis or both may contribute to the development
of PPD is conceptually based on the psychoneuroimmunol-
ogy model originally suggested by Chrousos and Gold as
early as 1992
and expanded upon more recently.
impact of the innate immune response and HPA axis function
on postpartum emotional regulation is depicted as occurring
both independently and via their bidirectional relationships.
In Figure 1, normal immune and HPA axis responses are pro-
posed, which individually and together contribute to post-
partum emotional regulation. In Figure 2, dysfunction in ei-
ther system alone or in their bidirectional interactions is shown
to destabilize emotional regulation and contribute to PPD.
Innate Immunity, HPA Axis Function, and Pregnancy
Pregnancy presents a unique immunological challenge to
the body. To carry a pregnancy to term, a woman must not
reject her developing fetus despite its antigenic incompati-
bility. At the same time, she must maintain her own im-
munocompetence. Studies suggest that maternal anti-in-
flammatory cytokines favorable for immunosuppression and
pregnancy maintenance are elevated during pregnancy
and proinflammatory cytokines are downregulated.
With the cessation of pregnancy and delivery of the in-
fant and placenta, the anti-inflammatory mileu abruptly,
that is, within hours, shifts to a proinflammatory state.
This occurs for several reasons: (1) a woman who has given
birth often has experienced significant perineal tissue in-
(2) uterine involution occurs in all postpartum
women and is characterized by ischemia, autolysis, and
phagocytosis, processes that in animal and human studies
are shown to involve significant inflammation and cytokine
and (3) pain, physical exertion, and emo-
tional stress—all hallmarks of childbirth—stimulate the
proinflammatory response.
Several studies have described an increase in proinflam-
matory cytokines in healthy women with the onset of labor
and lasting at least for the first 72 hours after delivery.
There are, however, only a few reports, often conflicting, that
follow cytokine changes beyond the first few days after par-
turition. In our laboratory, we found that IL-1levels are el-
evated within 24 hours after giving birth and remain signif-
icantly elevated throughout the first month postpartum
compared with levels measured in control, nonpregnant,
nonpostpartum women.
Other authors variously report a
decrease in anti-inflammatory cytokines in the first several
weeks postpartum,
an increase in proinflammatory cyto-
kines from 2 to 11 months postpartum with an overlapping
increase in IL-4 after 6 months,
and an increase in both anti-
inflammatory and proinflammatory cytokines at 3 months
postpartum compared with levels immediately after infant
The conflicting nature of these results may be at
least partially explained by the fact that two of the studies
fail to exclude or identify women with such pregnancy-as-
sociated complications as hemorrhage, surgery, and infec-
Moreover, none collected data on immunizations or
antibiotic use, both of which affect cytokines.
Significant changes in HPA axis function also occur dur-
ing pregnancy and delivery. Maternal levels of CRH, ACTH,
and cortisol increase dramatically during parturition, at-
taining peak levels in the third trimester.
After delivery,
HPA axis hormones drop within the first 3 days, with cen-
HPA Axis
Innate Immune
FIG. 1. Conceptual framework depicting normal relation-
ship between the inflammatory response and the HPA axis.
HPA Axis Activity
Chronic Elevation
in Innate Immune
FIG. 2. Conceptual framework for the proposed study, de-
picting dysregulated relationships among the HPA axis, the
inflammatory response, and PPD.
tral axis suppression similar to that occurring after abrupt
discontinuation of exogenous steroids.
The fetal adrenal gland is critical in understanding HPA
axis physiology during pregnancy and the perinatal period.
It secretes significant amounts of cortisol, which under the
influence of progesterone, stimulates cells of the trophoblast
and placenta to increase (not decrease) their production of
Placental CRH is required for successful implanta-
tion and maintenance of early pregnancy and may play a
role in initiating parturition.
Production of CRH by the pla-
centa leads to a self-propagating cycle wherein elevated CRH
stimulates further fetal cortisol production, causing contin-
ued CRH secretion. Importantly, although fetal cortisol stim-
ulates placental CRH secretion, it suppresses maternal CRH
secretion. Maternal CRH suppression continues after deliv-
ery of the infant.
Maternal HPA axis suppression may last
for several weeks in healthy postpartum women.
In synthesizing these two lines of research, we propose
that for some women, PPD might be a psychoneuroim-
munological disorder. In healthy postpartum women, the in-
nate immune response is stimulated by labor and delivery
and causes an increase in the production of proinflamma-
tory cytokines. Over the next weeks to months, a woman re-
covers from childbirth, and inflammation regresses. HPA
axis function, although elevated early on, is suppressed, and
the cytokines do not stimulate the secretion of HPA axis hor-
mones. Focusing on the HPA axis, following delivery of an
infant and the placenta, a woman’s levels of CRH, ACTH,
and cortisol drop from pregnancy levels, and the axis be-
comes hyporesponsive, normalizing by about 12 weeks.
With recovery, the HPA axis hormones return and assist in
limiting inflammation. Together, these steps assure normal
postpartum emotional regulation.
For women who develop PPD, however, we suggest that
the inflammatory response after labor and delivery is exag-
gerated, the HPA axis function is not adequately suppressed,
or both conditions occur. With an exaggerated proinflam-
matory response, the systemic inflammatory response syn-
drome would occur, characterized by fatigue, poor sleep,
poor appetite, and depressed mood. HPA axis hyperactivity
would be associated with agitation, dysphoria, insomnia,
and anorexia. One would expect an exaggerated inflamma-
tory or stress response after prolonged or difficult labor, ex-
cessive blood loss, perineal damage, clinical or subclinical in-
fection, surgery, or a negative emotional delivery.
There are some data to support this hypothesis. Increased
IL-6 levels have been reported in women with PPD early in
the perinatal period and in women with past histories of de-
In addition, one study has examined both cyto-
kines and cortisol, although the authors did not address this
This study was cross-sectional, involving women vis-
ited in their homes once between postpartum weeks 4 and 6.
Serum IFN-, IL-10, and cortisol were measured and evalu-
ated in light of perceived stress and dysphoric mood. Find-
ings suggested that depressed mothers had significantly lower
salivary but not serum cortisol concentrations and a lower
serum ratio of IFN-/IL-10. IL-6 levels, in contrast, were non-
significantly higher by 3-fold in depressed women. This study
suggests that hypoactivation rather than hyperactivation of
the HPA axis might contribute to PPD and supports a mixed
role for the proinflammatory immune response. It should be
noted, however, that depression was determined using a non-
specific measure (the Profile of Mood States) and was not val-
idated clinically. Also, women who delivered vaginally or sur-
gically were included, perhaps impacting cytokine and stress
hormone levels, and the women scoring as depressed were
significantly more likely to smoke, again potentially impact-
ing cytokine levels
and postpartum depression.
Hyperactivity of the HPA axis has been reported in
women with PPD by some researchers,
although others
have failed to replicate these findings.
Still others have
found a correlation between low cortisol levels and PPD.
It is important to note that few of the studies of either sys-
tem controlled for demographic factors, breastfeeding status,
hormonal contraception, resumption of menses, vaginal vs.
surgical delivery, or season, all of which will affect cytokine
levels and HPA axis function. Very few collected data on past
psychiatric history, which may be an indicator of chronic dys-
regulation of the immune system, the HPA axis, or both.
Future Studies
Additional research controlling for a number of external
variables needs to be performed to clarify the psychoneu-
roimmunology of PPD. These studies should involve, at first,
only women delivering vaginally, without complications,
and without antibiotic or antidepressant therapy. Circadian
function will need to be evaluated, as it may be that very
subtle derangements in cytokines or HPA axis hormones are
at play. Both proinflammatory and antiinflammatory cyto-
kines will need to be measured, as the balance between these
is the variable of most significance. Likewise, measuring cor-
tisol alone tells less about the HPA axis feedback than in-
cluding CRH and ACTH in analysis, as well as diurnal vari-
ation. And finally, women screened as depressed must be
clinically diagnosed as well.
If dysregulation of the bidirectional interactions between
the innate immune system and the HPA axis does play a role
in the development of PPD, we would expect that studies such
as those outlined here would demonstrate that women clini-
cally diagnosed with PPD have a higher ratio of proinflam-
matory cytokines/anti-inflammatory cytokines prior to and
during their episodes of depression compared with women
who do not develop PPD. We would also expect that women
diagnosed with PPD have higher levels of CRH, ACTH, and
cortisol prior to and during their episodes of depression com-
pared with women who do not develop PPD. Finally, we
would expect that women diagnosed with PPD will demon-
strate a cytokine-driven hyperactivity of the HPA axis com-
pared with women who do not develop PPD, as indicated by
significant differences in the slopes of the relationships be-
tween cytokines and HPA axis hormones in nondepressed
women compared with women diagnosed with PPD.
PPD is a significant problem for a substantial number of
women and families. By investigating reciprocal changes in
cytokine and HPA axis functioning over time in nonde-
pressed and depressed postpartum women, researchers will
have the opportunity to address an etiology for PPD not pre-
viously studied. Insights gained from such research will sig-
nificantly influence the prevention, diagnosis, and treatment
of depression afflicting women during this vulnerable and
important time of their lives.
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... Postpartum-onset depression has been suggested to be, at least in some cases, a psychoneuroimmune disorder (Corwin and Pajer, 2008) and it is likely that the experience of childbirth itself has an important role to play in its pathogenesis. For example, there is some suggestion that inflammatory markers may mediate the relationship between perineal injury during childbirth and postnatal depressive symptoms (Dunn et al., 2015) Additionally, obstetric pain at various times throughout the perineal period is independently associated with depressive symptom severity at 6 weeks postpartum (Lim et al., 2020). ...
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The role of inflammation in the pathogenesis of depression is becoming increasingly apparent, but its role in perinatal depression is less well-studied. Pregnancy and the postpartum are characterised by distinct and changing inflammatory profiles throughout, which makes the study of depression-related alterations in this period complex. This review presents literature discussing a role for the immune system in both antenatal and postnatal depression. Furthermore, literature investigating the role of the maternal immune system on breast milk composition and offspring immunological and behavioural outcomes is discussed, before concluding with suggestions for future work as this developing field grows.
... Abnormality in the functioning of hypothalamopituitary-adrenal (HPA) axis has been proposed as a major etiological factor in the development of major depressive disorder and perinatal depression. 15 Among susceptible women, estrogen and progesterone have profound interactions with HPA axis and trigger abnormal behaviour. The trigger for HPA is genetically determined however, life events can also contribute to the abnormal behaviour. ...
Motherhood is challenging both physically and emotionally. Depression and anxiety are common women. Perinatal depression is a major depressive episode happening during or after the pregnancy. It is very often ignored leading to a negative impact on the quality of life of the woman, child and the partner. Obstetricians need to be alert and be aware of the associated risk factors and how to screen for perinatal depression. Undiagnosed or untreated perinatal depression can lead to devastating complications both in the mother and the child. Cognitive behavioural therapy and medications are to be prescribed considering the risks to the mother and the unborn child.
... Others include alteration in cytokines and HPA axis hormones, and altered fatty acid, oxytocin, and arginine vasopressin levels. [11]. ...
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Aims: Various studies have shown that Psychological morbidities of various types occur frequently during pregnancy and after delivery. The main aim of this study was to determine the prevalence as well as correlates of depression among postpartum women attending the postnatal clinic of a tertiary health centre. Study Design: Descriptive cross sectional study. Place and Duration of Study: The study was done at the Post natal clinic of Ekiti State University Teaching Hospital (EKSUTH), Ado-Ekiti, southwest Nigeria over a period of 3 months. Methodology: Women attending the postnatal clinic of the centre were interviewed with a sociodemographic questionnaire and the Edinburgh postnatal depression scale using a cut off value of 9 as suggested by various studies among post partum women in this environment. Results:A total of 287 respondents were recruited in the study. The mean age of the participants Original Research Article Dada et al.; AJPCB, 4(2): 38-43, 2021; Article no.AJPCB.70103 39 was 30.81 ±4.28. The proportion of respondents with post partum depression was 20.4%.It was observed that unbooked patients, respondents with lower education, patients with difficulty in breastfeeding and patients who had suicidal thought had statistically significant higher mean scores on the EPDS (p< .05). Conclusion: PPD is a common psychiatric morbidity. Encouraging pregnant women to seek proper care during pregnancy/child birth will help in reducing postpartum depression; thereby ensuring good maternal and child health.
Serotonin modulates vascular, immune, and neurophysiology and is dysregulated in preeclampsia. Despite biological plausibility that selective serotonin reuptake inhibitors (SSRIs) prevent preeclampsia pathophysiology, observational studies have indicated increased risk and providers may be hesitant. The objective of this meta-analysis and quality assessment was to evaluate the evidence linking SSRI use in pregnancy to preeclampsia/gestational hypertension. PubMed was searched through June 5, 2020 manually and using combinations of terms: “preeclampsia”, “serotonin”, and “SSRI”. This review followed MOOSE guidelines. Inclusion criteria were: 1) Observational cohort or population study, 2) exposure defined as SSRI use during pregnancy, 3) cases defined as preeclampsia or gestational hypertension, and 4) human participants. Studies were selected that addressed the hypothesis that gestational SSRI use modulates preeclampsia and/or gestational hypertension risk. Review Manager Web was used to synthesize study findings. Articles were read and scored (Newcastle-Ottawa Quality Assessment Scale) for quality by two independent reviewers. Publication bias was assessed using a funnel plot and the Egger test. Of 179 screened studies, nine were included. The pooled risk ratio (random effects model) was 1.43 (95% CI: 1.15-1.78, P<0.001; range 0.96-4.86). Two studies were rated as moderate quality (both with total score of 6); others were high quality. Heterogeneity was high (I2=88%) and funnel asymmetry was significant (p<0.00001). Despite evidence for increased preeclampsia risk with SSRIs, shared risk factors and other variables are poorly controlled. Depression treatment should not be withheld due to perceived gestational hypertension risk. Mechanistic evidence for serotonin modulation in preeclampsia demonstrates a need for future research.
Obesity is currently one of the most serious health problems, affecting 13% of the world's adult population. Obesity is characterized by persistent low‐grade chronic inflammation that assumes systemic proportions and triggers several associated metabolic diseases. Furthermore, obesity has been associated with an increased occurrence of central disorders such as impaired cognitive function, reward system dysfunction, and depression. In summary, there is a quantitative reduction in the release of neurotransmitters in depression. Postsynaptic cells capture lower concentrations of neurotransmitters, which leads to a functional reduction in the central nervous system (CNS). Globally, approximately 15–65% of women experience depressive symptoms during pregnancy, depending on their location. Depressive symptoms persist in some women, leading to postpartum depression (PPD). Thus, obesity may be considered a risk factor for PPD development. This study aimed to synthesize studies on the impact of obesity‐related neuroinflammation and PPD. We conducted a narrative review of the relevant literature. The search was performed in electronic databases, specifically PubMed, selecting articles in English published from 2014 to 2021 using the narrative review methodology.
Objective To explore the association of psychological distress, including stress, depression, and anxiety, with the development of a hypertensive disorder during pregnancy. Design A secondary data analysis using a 1:3 case control study; cases (n = 29 with a hypertensive disorder) and controls (n = 87 without hypertension) frequency matched on age and parity. Participants Women in the study were older than 14 years of age, Medicaid eligible, with at least one risk factor for preterm birth, and without a current diagnosis of mental illness. Methods Hypertensive disorder status was verified through medical record report. Components of psychological distress were measured with valid instruments. Measures of psychological distress level, including CESD-R-10, PSS-4, and GAD-7, were compared between women with a hypertensive disorder and normotensive women were made in both early and late pregnancy. Components of psychological distress were tested as independent risk factors with the development of a hypertensive disorder as the outcome. Results There were no differences in psychological distress between hypertensive and normotensive women. Furthermore, no changes in psychological distress by time between groups were identified. However, this population did not present with significant symptoms of psychological distress. BMI was the only independent risk factor associated with an increased risk of developing a hypertensive disorder during pregnancy (OR=1.13; 95% CI: 1.04 - 1.23, p = .003). Conclusions These findings indicate psychological distress was not associated with the development of a hypertensive disorder during pregnancy in women with few symptoms of psychological distress. Women with higher BMI were at an increased risk of developing a hypertensive disorder.
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z: 2019 yılında başlayan COVID-19 pandemisi, tüm dünyada etkisini sürdürerek devam etmektedir. Bu küresel salgın normal yaşamı bozmakta ve hayatın her alanını etkilemektedir. Pandemilerde sağlık bakımı, hızlı eylemler ve müdahaleler gerektirmektedir. Anne ve bebek sağlığının daha dikkatli izlenmesi gereken dönemlerin olduğu; gebelik, doğum ve emzirme gibi durumlarda hızlı bakım gereksinimlerine daha fazla ihtiyaç duyulmaktadır. Emzirmenin anne ve çocuk sağlığını koruyucu ve anne-bebek bağlanmasını güçlendirici etkisi pek çok çalışmada ortaya konmuştur. Pandemi dönemlerinde anne sütünün yararları göz önüne alınarak emzirme sürecine ilişkin bir karar verilmesi gerekmektedir. Sınırlı sayıda da olsa literatürde enfekte olan yenidoğanlarda anne sütü bulaş nedeni olarak gösterilmemiştir. Bu nedenle uluslararası kuruluşlar gerekli hijyen koşullarının sağlanması koşulu ile COVID-19 varlığında emzirmeyi önermektedir. Annelerin emziremeyecek kadar hasta olmaları durumunda da sütlerinin sağılarak sağlıklı kişiler tarafından bebeğe verilmesi önerilmektedir. Bu derleme, COVID-19 pandemisi döneminde emzirmenin öneminin vurgulanması amacıyla yazılmıştır. Abstract: The COVID-19 pandemic, which started in 2019, continues to be effective all over the world. This global epidemic disrupts normal life and affects all areas of life. There is more need for fast care needs in cases where pregnancy, birth and breastfeeding, as well as maternal and infant health are in danger. Breastfeeding is an action that protects both mother and child health, strengthens mother-baby attachment, and these effects have been demonstrated at the level of evidence. A decision should be made regarding a breastfeeding process during pandemic periods, considering the benefits of breast milk. Breast milk has not been shown in the literature as a cause of infection in infants who are infected, even though it is limited in number. Thus, international organizations recommend breastfeeding during the COVID-19 process, under the condition that the necessary hygiene conditions are provided. If mothers are too sick to breastfeed, it is suggested that their milk be expressed and given to baby by healthy people. This review was written to emphasize the importance of breastfeeding during the COVID-19 pandemic.
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Background In today's global world, most women are experiencing midlife health problems which can affect their lives and mental status. Most of the diseases occurr after childbirth and during pregnancy or gestation period which can lead to severe problems such as postpartum depression (PPD), postmenopausal depression, perimenopausal depression which ultimately affects the mental health condition and develop various depressive episodes which ultimately lead to depression in women. Objective The review paper gives the information that if there is untreated maternal depression then it can lead to anxiety, fear, negative effect on child development, disruption of the mother-infant relationship, and the occurrence of depressive symptoms in the early life of infants. Hormone levels are changed at the time of pregnancy. Methods The data was collected by studying combination of research and review papers from different databases like PubMed, Medline, and Web of science by using search keywords like “Postpartum depression”, “Postmenopausal depression”, “Risk factors”, “Pathogenesis of PPD”, “Predictors of postpartum depression”. Results This can lead to disrupting the quality of life of menopausal women like deficiency of nutrients, not properly regular physical activities, elevated Body Mass Index (BMI), loss of libido (loss of interest in sexual activities), due to the lack of education, and awareness among the people. Factors like increase in physical activity can naturally help in PPD condition. Mind body therapy, drug therapy and cognitive and mindfulness-based therapies help in hormonal imbalances. Conclusion It was found that low birth weight and congenital abnormalities in babies lead to affect depression after delivery. It is recommended that health care providers and physicians are provided with information regarding factors contributing PPD and postmenopausal depression. Sleep timings and consumptions of nutraceuticals can help in natural healing with depression amongst women suffering from postpartum, postmenopausal and perimenopausal depression.
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The third trimester of human pregnancy is characterized by a hyperactive hypothalamic-pituitary-adrenal axis, possibly driven by progressively increasing circulating levels of placental CRH and gradually decreasing levels of CRH-binding protein. The postpartum period, on the other hand, is characterized by an increased vulnerability to psychiatric manifestations (postpartum "blues," depression, and psychosis), a phenomenon compatible with suppressed hypothalamic CRH secretion. To investigate the hypothesis that the postpartum period is associated with suppression of hypothalamic CRH secretion, we studied prospectively 17 healthy euthymic women (mean +/- SE age, 32.0 +/- 1.1 yr) with no prior history of depression, starting at the 20th week of gestation. Psychometric testing was performed monthly during pregnancy and postpartum on day 2 and weeks 2, 3, 6, 8, 12, 16, and 20, whereas serial ovine (o) CRH tests were performed postpartum at 3, 6, and 12 weeks. While pregnant, all 17 subjects remained euthymic; in the postpartum period, 7 women developed the "blues," and 1 developed depression. Overall, the mean plasma ACTH response to an iv bolus of 1 microgram/kg oCRH was markedly blunted at 3 and 6 weeks, but normal at 12 weeks postpartum, whereas the mean plasma cortisol response was at the upper limit of normal at all 3 times. These data are compatible with a suppressed hypothalamic CRH neuron that gradually returns to normal while hypertropic adrenal cortexes are progressively down-sizing. When the postpartum ACTH responses to oCRH were analyzed separately for the euthymic women and the women who had the "blues" or depression, the blunting of ACTH was significantly more severe and long lasting in the latter group; this was observed at all 3 times of testing. We conclude that there is central suppression of hypothalamic CRH secretion in the postpartum, which might explain the increased vulnerability to the affective disorders observed during this period. The suppressed ACTH response to oCRH might serve as a biochemical marker of the postpartum "blues" or depression.
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Objective. —This article defines stress and related concepts and reviews their historical development. The notion of a stress system as the effector of the stress syndrome is suggested, and its physiologic and pathophysiologic manifestations are described. A new perspective on human disease states associated with dysregulation of the stress system is provided.
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There has been considerable recent clinical and research interest in postpartum depression. This has been largely provoked by the accumulating evidence that postnatal depression is associated with disturbances in child cognitive and emotional development.1 This evidence, which is reviewed below, has renewed concern about the epidemiology of postnatal depression, its aetiology, methods of prediction and detection, and the most appropriate form of management. Summary points Postnatal depression is associated with disturbances in the mother-infant relationship, which in turn have an adverse impact on the course of child cognitive and emotional development Postnatal depression affects 10% of women in the weeks immediately post partum There is little evidence for a biological aetiology; antenatal personal and social factors are more relevant Postnatal depression is commonly missed by primary care teams despite the fact that simple reliable detection procedures have been developed The treatment of choice in most cases of postnatal depression is counselling, which can be effectively delivered by health visitors There is a need to develop preventive intervention strategies Methods This article is based on a review of the recent research concerned with the impact of postnatal depression on child development, and the epidemiology, prediction, detection and management of the disorder. Authoritative recent reviews are cited as well as the most impressive research papers. To supplement our immediate knowledge of the literature we performed literature searches with Medline and PsychLit (1980-97) using the relevant key words (“postnatal/postpartum depression” in conjunction with “infant/child development/outcome, epidemiology, aetiology, prediction, detection and treatment”). Impact on parenting and child outcome There have been several recent prospective studies of samples of women with postnatal depression and their children.1 They indicate a definite association between the maternal mood disorder and impaired infant cognitive development. Thus, in Cambridge a community sample of children of mothers who had had postnatal depression were found to perform significantly less …
Interleukin-10 (IL-10), first recognized for its ability to inhibit activation and effector function of T cells, monocytes, and macrophages, is a multifunctional cytokine with diverse effects on most hemopoietic cell types. The principal routine function of IL-10 appears to be to limit and ultimately terminate inflammatory responses. In addition to these activities, IL-10 regulates growth and/or differentiation of B cells, NK cells, cytotoxic and helper T cells, mast cells, granulocytes, dendritic cells, keratinocytes, and endothelial cells. IL-10 plays a key role in differentiation and function of a newly appreciated type of T cell, the T regulatory cell, which may figure prominently in control of immune responses and tolerance in vivo. Uniquely among hemopoietic cytokines, IL-10 has closely related homologs in several virus genomes, which testify to its crucial role in regulating immune and inflammatory responses. This review highlights findings that have advanced our understanding of IL-10 and its receptor, as well as its in vivo function in health and disease.
During the postpartum period, women frequently report increased fatigue, which, if severe, may interfere with maternal-child bonding, delay a new mother’s return to her activities of daily living, and contribute to depression. Several studies have sought to determine psychosocial contributions to fatigue during the postpartum period, but few evaluate any physiological changes that may contribute to fatigue during this time. The following study was designed to test whether the potent, proinflammatory cytokine interleukin-1beta (IL-1ß), known to be a physiological mediator of fatigue in several clinical and experimental conditions, is elevated in women during the postpartum period and whether it might be related to symptoms of fatigue. Levels of fatigue and the urinary excretion of IL-1ß were measured in 26 women over 4 weeks postpartum. Correlations between fatigue and activation of the inflammatory response were investigated. Results demonstrated a significant elevation in IL-1ß during the postpartum period compared to control participants (p < .05) and a significant, although delayed, correlation between IL-1ß elevation and fatigue (p < .05). These results suggest that activation of the inflammatory response, as reflected by elevation in urinary IL-1ß, occurs in association with postpartum fatigue. Studies to explore further this association and to identify specific mechanisms of action are needed.
To study the production, interrelationships and determinants of maternal and neonatal cytokines (IL-4 and IFN-gamma) in whole blood cultures during labor, after vaginal delivery and at 3 months after delivery. The concentrations of maternal IFN-gamma and IL-4 in peripheral blood were down-regulated at delivery compared with values 3 months postpartum. The concentrations of neonatal IFN-gamma and IL-4 were down-regulated at birth and were still at a low level 3 months later. The concentrations of IFN-gamma in maternal and umbilical cord blood samples correlated at delivery (r=0.43; P<0.03). Maternal IL-4 concentrations correlated immediately after delivery and 3 months later (r=0.46; P<0.02) as did those of IFN-gamma (r=0.57; P<0.002). Neonates who were delivered at less than 40 weeks of gestation had higher IFN-gamma concentrations 3 months after birth than those who were delivered after a longer duration of gestation (341 vs. 157 pg/ml; P<0.01). Broad immune activation, reflected in increased production of IL-4 and IFN-gamma, can be detected in women during the postpartum period. Labor-related factors had little effect on ranking of mothers in terms of their IL-4 or IFN-gamma levels, since maternal production of these cytokines correlated immediately after delivery and 3 months later. In neonates, the production of IFN-gamma 3 months after birth was dependent on gestational age at delivery.