Endocrine factors in the etiology of postpartum depression

Bloch, Miki; Daly, Robert C.; Rubinow, David R.

doi:10.1016/s0010-440x(03)00034-8

Cited by 372 publications

(285 citation statements)

References 112 publications

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“…We did not have sufficient data to link specific symptoms to individual biological or psychosocial factors, but previous research suggests several targets for further study. A natural target for further research is oestrogen and progesterone, which have neuroregulatory effects, including on the central serotonin system (Moses-Kolko et al 2008), and have been implicated in psychological symptoms in the perinatal period (Maccaria et al 2003;Bloch et al 2003). Also, Fan et al (2009) found that rates of anxiety and depression were higher in the first trimester than later in pregnancy and that depression was correlated with changes in estradiol and progesterone level, and anxiety was correlated with total cortisol level.…”

Section: Discussionmentioning

confidence: 99%

Associated symptoms of depression: patterns of change during pregnancy

Castro

Anderman

Glover

et al. 2017

Arch Womens Ment Health

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Little is known about the natural course of depressive symptoms and associated features throughout pregnancy. We examined the course of some psychological and somatic symptoms in each month of pregnancy in a normative sample. A consecutive, unselected sample of women (N = 374) were interviewed retrospectively at 6 weeks postpartum with the Structured Clinical Interview (DSM-IV). Women were asked whether they had experienced each symptom at any time during pregnancy and the occurrence of the symptom for each month of pregnancy. Associated symptoms of depression showed complex changes across pregnancy. Depressed mood (F(df) = 5.15(1); p = 0.02) showed a quadratic pattern with elevations at the beginning and end of pregnancy. Both linear increases ( a ) and quadratic ( b ) changes over time were observed for sensitivity to criticism (F a (df) = 20.9(1), p a = 0.00; F b (df) = 7.02(1), p b = 0.00), lack of concentration (F a (df) = 37.0(1), p a = 0.00; F b (df) = 10.3(1); p b = 0.00), decreased energy (F a (df) = 13.4(1); p a = 0.00; F b (df) = 62.6(1); p b = 0.00) and feelings of heavy limbs (F a (df) = 92.9(1); p a = 0.00; F b (df) = 67.7(1); p b = 0.00). Only guilt (F(df) = 0.00(1); p = 0.93) showed no significant change over pregnancy. Psychological symptoms changed throughout pregnancy as much as somatic symptoms. A linear increase was found for most symptoms, but significant non-linear changes were also found. The discrepancy between the patterns of depressed mood and most somatic and psychological symptoms suggest complex interactions and potentially important implications for assessment and monitoring treatment.

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Section: Discussionmentioning

confidence: 99%

Associated symptoms of depression: patterns of change during pregnancy

Castro

Anderman

Glover

et al. 2017

Arch Womens Ment Health

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“…Several pieces of evidence documented recently show that abnormal function of the HPA axis plays a key role in the etiology of MDD during pregnancy and postpartum [5,6,27,28] . Recent work has demonstrated that the reproductive steroids estrogen and progesterone interact with the HPA axis and may trigger HPA axis abnormalities in susceptible women.…”

Section: Perinatal Depression and The Hpa Axismentioning

confidence: 99%

“…[5,6,27,28] . Recent work has demonstrated that the reproductive steroids estrogen and progesterone interact with the HPA axis and may trigger HPA axis abnormalities in susceptible women.…”

Section: Introductionmentioning

confidence: 99%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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Abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis is an important pathological finding in pregnant women exhibiting major depressive disorder. They show high levels of cortisol proinflammatory cytokines, hypothalamic-pituitary peptide hormones and catecholamines, along with low dehydroepiandrosterone levels in plasma. During pregnancy, the TH2 balance together with the immune system and placental factors play crucial roles in the development of the fetal allograft to full term. These factors, when altered, may generate a persistent dysfunction of the HPA axis that may lead to an overt transfer of cortisol and toxicity to the fetus at the expense of reduced activity of placental 11β-hydroxysteroid dehydrogenase type 2. Epigenetic modifications also may contribute to the dysregulation of the HPA axis. Affective disorders in pregnant women should be taken seriously, and therapies focused on preventing the deleterious effects of stressors should be implemented to promote the welfare of both mother and baby.Keywords: brain; depression; neuroendocrine; pregnancy; stress; glucocorticoids Extensive studies have demonstrated that early life stressors produce changes in behavior and enhance the sensitivity of the stress response systems [1][2][3][4] . Although the genetic background has been implicated in the development of mood-related disorders, and genetic research has identified some chromosomal regions and genes that are involved in susceptibility to mood disorders, the etiology of anxiety and depressive disorders is still not clear in humans, particularly in women with major depressive disorder (MDD) [1] .The pathogenesis of perinatal depression is an emerging field. Although considerable progress has been made in this area in the last few years, there still remain unanswered questions and gaps in our knowledge of the underlying pathogenesis, the long-term impact of perinatal depression on the developing fetus, and the best methods for counseling pregnant women concerning the risks of untreated MDD versus the risks of psychopharmacologic treatment during pregnancy and lactation [5] . Meta-analysis studies have reported that the mean prevalence rate of prenatal depression is ~12% (this varies greatly according to location, mode of assessment, and socioeconomic conditions), and show that a large percentage of pregnant women displaying major depression remain depressed in the postpartum period and/or continuously [6,7] . Anxiety, depressive disorder, and stress during pregnancy are risk Phillipe Leff Gelman, et al. HPA axis in perinatal depression 339 factors for negative outcomes in newborns, like preterm birth or low birth weight; also, insecure attachment and impaired child development could be a consequence of mental disorders during pregnancy [6,[8][9][10] . The mechanisms by which maternal depression impacts fetal and neonatal development are currently under investigation; there is some evidence that depressive symptoms impact the infant's hypothalamic-pituitary-adrenal (HPA) axis, enhancing the ...

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“…Withdrawal from the progesterone derivative allopregnanolone increases both the messenger RNA (mRNA) and protein of GABAAR α4 (GABAARA4), a subunit that is relatively insensitive to benzodiazepines (36,70) and has been reported to be involved in the pathophysiology of PPD and premenstrual syndrome (3). The results of the present study are consistent with these findings and demonstrate that GABAARA4 expression is increased in HSPP-H animals compared with HSP-H. Aquaporin 4 is the predominant water channel in the brain and might be related to the formation of blood-brain barrier (71).…”

Section: Gene Expression Analysismentioning

confidence: 99%

“…Conversely in humans, both estrogen and progesterone increase gradually throughout the pregnancy (11). Progesterone has been shown to alter neurotransmission, indicating a crucial role in the pathophysiology of PPD (3). Thus, novel strategies may be necessary to address the pathophysiology of human PPD.…”

mentioning

confidence: 99%

A Postpartum Model in Rat: Behavioral and Gene Expression Changes Induced by Ovarian Steroid Deprivation

Suda

Segi-Nishida

Newton

et al. 2008

Biological Psychiatry

131

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Background-Postpartum depression (PPD) affects approximately 10% to 20% of women during the first 4 weeks of the postpartum period and is characterized by labile mood with prominent anxiety and irritability, insomnia,and depressive mood. During the postpartum period, elevated ovarian hormones abruptly decrease to the early follicular phase levels that are postulated to play a major role in triggering PPD. However, the underlying neurobiological mechanisms that contribute to PPD have not been determined.

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Endocrine factors in the etiology of postpartum depression

Cited by 372 publications

References 112 publications

Associated symptoms of depression: patterns of change during pregnancy

Associated symptoms of depression: patterns of change during pregnancy

Hypothalamic-pituitary-adrenal axis function during perinatal depression

A Postpartum Model in Rat: Behavioral and Gene Expression Changes Induced by Ovarian Steroid Deprivation

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