Pathogenesis Of Postpartum Depression Research Articles

Antidepressant effects of activation of infralimbic cortex via upregulation of BDNF and β-catenin in an estradiol withdrawal model.

Clinical and preclinical studies have demonstrated that estradiol withdrawal after delivery is one of important factors involved in the pathogenesis of postpartum depression (PPD). The infralimbic cortex (IL) is related to anxiety and mood disorders. Whether IL neurons mediate PPD is still unclear. This study was to observe the antidepressant effect and expression of BDNF and β-catenin in IL by allopregnanolone (ALLO) treatment or the selective activation or inhibition of IL neurons using a chemogenetic approach in a pseudopregnancy model of PPD. Administration of estradiol combined with progesterone and the abrupt withdrawal of estradiol simulated the pregnancy and early postpartum periods to induce depression in ovariectomized rats. The relative expression levels of β-catenin and BDNF were observed by western blotting. Immobility time was significantly increased in the forced swim test and open-arm movement was reduced in the elevated plus maze test in the estradiol-withdrawn rats. After ALLO treatment, the immobility time were lower and open-arm traveling times higher than those of the estradiol-withdrawn rats. Meanwhile, the expression level of BDNF or β-catenin in the IL was reduced significantly in estradiol-withdrawn rats, which was prevented by treatment with ALLO. The hM3Dq chemogenetic activation of pyramidal neurons in the IL reversed the immobility and open-arm travel time trends in the estradiol-withdrawal rat model, but chemogenetic inhibition of IL neurons failed to affect this. Upregulated BDNF and β-catenin expression and increased c-Fos in the basolateral amygdala were found following IL neuron excitation in model rats. Our results demonstrated that pseudopregnancy and estradiol withdrawal produced depressive-like behavior and anxiety. ALLO treatment or specific excitement of IL pyramidal neurons relieved abnormal behaviors and upregulated BDNF and β-catenin expression in the IL in the PPD model, suggesting that hypofunction of IL neurons may be involved in the pathogenesis of PPD.

Capacities for meta-cognition, social cognition, and alexithymia in postpartum depression

Postpartum depression (PPD), a female-specific disorder, is the most common medical complication associated with childbirth (10–20%). The pathological relevance of emotion processing, meta-cognition, alexithymia, and social cognition to PPD is unclear. We tested 25 mothers with PPD (mean age: 30.72 ± 5.76 years) and 25 healthy mothers (mean age: 32.03 ± 3.54 years) for alexithymia (Toronto Alexithymia Scale) and evaluated cognitive empathy (Faux Pas Test), affective empathy (Interpersonal Reactivity Index), meta-cognition (Meta-Cognitions Questionnaire), sociodemographic and clinical-psychometric characteristics and personality dimensions. Mothers with PPD showed higher levels of neuroticism and more anxiety–depressive characteristics. Their metacognitive abilities were significantly altered and they more often had alexithymia. Significant correlations between alexithymia and meta-cognition, trait anxiety, and neuroticism were found. Alexithymia, neurotic personality traits, and dysfunctional meta-cognition appear more frequently in PPD women than healthy women. Social cognition abilities were not significantly altered. Alexithymia and metacognitive distortions play important roles in the pathogenesis of PPD. Dysfunctional meta-cognition, neuroticism, and alexithymia may be risk factors that should be detected early in expectant mothers to prevent the development of PPD.

A novel mouse model of postpartum depression using emotional stress as evaluated by nesting behavior

Postpartum depression is an important mental health issue not only for the mother but also for the child’s development, other family members, and the society. An appropriate animal model is desired to elucidate the pathogenesis of postpartum depression. However, methods for stress loading during pregnancy have not been established. Behavioral experiments to investigate postpartum depression-like behaviors should be conducted without stress because behavioral tests affect rearing behaviors such as lactation. Therefore, we developed a new mouse model of postpartum depression using a psychological stress method. Mating partners were made to witness their partners experiencing social defeat stress and then listen to their cries. Emotional stress loading during pregnancy significantly increased postpartum depression-like behaviors. Postpartum depression also affected nurturing behaviors and caused disturbances in pup care. Furthermore, nesting behavior was impaired in the stressed group, suggesting that the observation of nesting behavior may be useful for assessing social dysfunction in postpartum depression. These results demonstrate the utility of this new mouse model of postpartum depression.

A Detailed Biological Approach on Hormonal Imbalance Causing Depression in Critical Periods (Postpartum, Postmenopausal and Perimenopausal Depression) in Adult Women

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.

Research progress in prediction of postpartum depression.

Postpartum depression is a kind of mental disorder caused by the comprehensive effects of economics, psychosociology, biology, obstetrics and other characteristic factors in the process of female pregnancy. The pathogenesis of postpartum depression is complicated and has not been clarified. With the process pregnancy, the influence of psychosocial and biology factors are also in dynamic change. The postpartum depression predictor among psychosocial factors are antenatal depression, life events and social supports. Among biological factors, the predictors are hypothalamic-pituitary-thyroid axis and serum lipids. Timely and effective prediction can identify the high-risk population and risk factors for postpartum depression.

PPAR and functional foods: Rationale for natural neurosteroid-based interventions for postpartum depression

Allopregnanolone, a GABAergic neurosteroid and progesterone derivative, was recently approved by the Food and Drug Administration for the treatment of postpartum depression (PPD). Several mechanisms appear to be involved in the pathogenesis of PPD, including neuroendocrine dysfunction, neuroinflammation, neurotransmitter alterations, genetic and epigenetic modifications. Recent evidence highlights the higher risk for incidence of PPD in mothers exposed to unhealthy diets that negatively impact the microbiome composition and increase inflammation, all effects that are strongly correlated with mood disorders. Conversely, healthy diets have consistently been reported to decrease the risk of peripartum depression and to protect the body and brain against low-grade systemic chronic inflammation. Several bioactive micronutrients found in the so-called functional foods have been shown to play a relevant role in preventing neuroinflammation and depression, such as vitamins, minerals, omega-3 fatty acids and flavonoids. An intriguing molecular substrate linking functional foods with improvement of mood disorders may be represented by the peroxisome-proliferator activated receptor (PPAR) pathway, which can regulate allopregnanolone biosynthesis and brain-derived neurotropic factor (BDNF) and thereby may reduce inflammation and elevate mood.Herein, we discuss the potential connection between functional foods and PPAR and their role in preventing neuroinflammation and symptoms of PPD through neurosteroid regulation. We suggest that healthy diets by targeting the PPAR-neurosteroid axis and thereby decreasing inflammation may offer a suitable functional strategy to prevent and safely alleviate mood symptoms during the perinatal period.

Gene expression profile in peripheral blood mononuclear cells of postpartum depression patients

Postpartum depression (PPD) is a common mental health problem that causes maternal suffering and various negative consequences for offspring. The pathogenesis of PPD and the causes of consequences for offspring remain largely unknown. Here, we applied RNA sequencing to sequence the whole transcriptomes of peripheral blood mononuclear cells (PBMCs) from PPD patients (Edinburgh Postnatal Depression Scale [EPDS] score ≥13) and control subjects (EPDS = 0). We found that PPD was positively correlated with multiple genes involved in energy metabolism, neurodegenerative diseases and immune response, while negatively correlated with multiple genes in mismatch repair and cancer-related pathways. Remarkably, genes associated with appetite regulation and nutrient response were differentially expressed between PPD and control subjects. Then, we employed a postnatal growth retardation model by repeated immobilization stress (IS) stimulation to maternal mice. The expression of appetite regulation and nutrient response-related genes in the PBMCs of IS mice and in the hypothalamus of their offspring were also affected. In conclusion, this study provides a comprehensive characterization of the PBMCs transcriptome in PPD and suggests that maternal stress may affect appetite regulation and nutrient response in the hypothalamus of offspring mice.

Evaluation of the promoter region polymorphism (5-HTTLPR) in the serotonin transporter gene in females with postpartum depression.

The aim of the present study was to investigate the association between polymorphism in the serotonin transporter (5-HTT) gene-linked polymorphic region (5-HTTLPR) in the promoter region of the 5-HTT gene and the pathogenesis of postpartum depression (PPD). Blood samples were collected from 120 female patients with PPD and 140 age-matched normal controls. Polymerase chain reaction analysis was performed to detect the 5-HTTLPR polymorphism in these subjects, and the genotype and allele frequencies were compared between the two groups. The disease severity was evaluated using the Hamilton Depression Rating Scale (HAMD) score. The results showed that the frequency of the homozygous long/long (L/L) genotype was significantly lower in the PPD group than that in the control group; by contrast, the frequencies of the heterozygous long/short (L/S) and homozygous S/S genotypes were similar for the two groups, without significant differences. No significant differences were observed in the L and S allele frequencies between the two groups. Furthermore, compared with the L/S heterozygous and S/S homozygous genotypes, patients with PPD with the L/L homozygous genotype had a significantly lower HAMD score. The present results suggest that female patients with PPD carrying the homozygous L/L genotype may be less susceptible to depressive symptoms and that the L/L genotype may be associated with the reduced occurrence of PPD. These findings provide a theoretical basis for the clinical diagnosis and treatment of PPD.

Pharmacologic Treatment for Postpartum Depression: A Systematic Review

During the past decade, the medical community has expressed a growing concern over the high prevalence of postpartum depression and the tragic repercussions of untreated illness. However, many questions persist about the pathogenesis of postpartum depression, the natural course of the illness, and the safety and effectiveness of available treatments. To summarize the data on pharmacologic treatments for postpartum depression, we performed a systematic review of four major databases to identify original research published from 1960-September 2009 that featured pharmacologic treatments for depression detected in women during the 12 months after delivery. Pharmacologic treatments included prescription drugs (antidepressants and hormones), herbal remedies, and dietary supplements. Case reports, studies examining the prevention of postpartum depression, and those including diagnosed episodes of depression preceding the postpartum period (i.e., antepartum onset) were excluded. Treatment randomization or the presence of a control group was not required for inclusion in this review. Fourteen investigations met inclusion criteria. Nine studies examined the effects of prescription antidepressants, two investigated hormones, and three featured omega-3 fatty acid supplementation. Significant heterogeneity was evident in study design and prevented a pooled quantitative analysis of treatment effects. The power of most investigations was limited, and numerous confounding biases were evident. Therapeutic effects were documented for prescription antidepressants and hormone supplementation (estrogen derivatives). Tolerability of the interventions in depressed mothers and breastfed infants was not well described. The effectiveness of omega-3 fatty acids was not evident in postpartum depression trials, although significant limitations in study methodology were apparent. Postpartum depression is a common and serious medical problem, but most cases go undetected and untreated. The need to identify safe, effective, and convenient treatments for postpartum depression is urgent, but the current state of the medical literature describing pharmacologic interventions is not impressive. Preliminary evidence documenting the effectiveness of serotonergic antidepressants and hormone supplementation should serve as an impetus for rigorous controlled investigations in the future.