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Abstract Background The incidence of gestational diabetes mellitus (GDM) is increasing worldwide, and has been associated with some changes in the gut microbiota. Studies have shown that the maternal gut microbiota pattern with hyperglycemia can be transmitted to the offspring. The study aimed to evaluate the gut microbiota of obese postpartum women with and without previous GDM and their offspring. Methods We evaluated a total of 84 puerperal women who had (n = 40) or not GDM (n = 44), and their infants were also included. Stool samples were obtained 2–6 months after delivery. The molecular profile of the fecal microbiota was obtained by sequencing V4 region of 16S rRNA gene (Illumina® MiSeq). Results We found that the gut microbiota structures of the puerperal women and their infants were similar. Stratifying according to the type of delivery, the relative abundance of Victivallis genus was higher in women who had natural delivery. Exposure to exclusive breastfeeding was associated with a greater abundance of Bacteroides and Staphylococcus. The differential abundance test showed correlations to clinical and laboratory parameters. This work showed no difference in the microbiota of obese puerperal women with and without GDM and their offspring. However, breastfeeding contributed to the ecological succession of the intestinal microbiota of the offspring. Conclusion This work can contribute to understanding the potential effects of GDM and early life events on the gut microbiome of mothers and their offspring and its possible role in metabolism later in life.

Background: The incidence of gestational diabetes mellitus (GDM) is increasing worldwide, and has been associated with some changes in the gut microbiota. Studies have shown that the maternal gut microbiota pattern with hyperglycemia can be transmitted to the offspring. The study aimed to evaluate the gut microbiota of obese postpartum women with and without previous GDM and their offspring. Methods: We evaluated a total of 84 puerperal women who had (n = 40) or not GDM (n = 44), and their infants were also included. Stool samples were obtained 2–6 months after delivery. The molecular profile of the fecal microbiota was obtained by sequencing V4 region of 16S rRNA gene (Illumina® MiSeq). Results: We found that the gut microbiota structures of the puerperal women and their infants were similar. Stratifying according to the type of delivery, the relative abundance of Victivallis genus was higher in women who had natural delivery. Exposure to exclusive breastfeeding was associated with a greater abundance of Bacteroides and Staphylococcus. The differential abundance test showed correlations to clinical and laboratory parameters. This work showed no difference in the microbiota of obese puerperal women with and without GDM and their offspring. However, breastfeeding contributed to the ecological succession of the intestinal microbiota of the offspring. Conclusion: This work can contribute to understanding the potential effects of GDM and early life events on the gut microbiome of mothers and their offspring and its possible role in metabolism later in life. [ABSTRACT FROM AUTHOR]

In recent decades, a dramatic rise has been observed in the prevalence of obesity in childhood and adolescence, along with an increase in fetal microsomia rates. The increased risk of obesity during this key period in development negatively affects the health of the individual later in life. Immune cells residing and recruited to white adipose tissue have been highlighted as important factors contributing to the pathogenesis of childhood obesity. Immune dysfunction in the context of obesity begins early in childhood, which is different from the pathological characteristics and influencing factors of adipose immunity in adults. Here, we explore the current understanding of the roles of childhood and early life events that result in high risks for obesity by influencing adipose tissue immune dysfunction under the pathological condition of obesity. Such knowledge will help in determining the mechanisms of childhood and early life obesity in efforts to ameliorate chronic inflammation-related metabolic diseases. Overview of influence of adipose tissue immune dysfunction on childhood obesity. Obesity in childhood and early life lies in both genetic predisposition and obesogenic nurturing environment. Initially, unhealthy lifestyles, such as poor dietary patterns, insufficient exercise, and inadequate sleep, are proved to be negative factors for obesity prevention from an early age. Next in importance, the variety of obesity-related genomic alterations is extensive and is still being studied. What's more, there are particularly obvious correlations between adiposity at birth or infancy and the progression of obesity or metabolic diseases across the whole life stages. Maternal obesity, exposure to endocrine disruptors during pregnancy, and insufficient breastfeeding possibly result in dysfunctional adipose tissue and defective immune function during the very early stages of life, and even lasting until adulthood. Finally, dysregulation of gut microbiota is regarded as an early trigger to the development of obesity and related systemic low-grade inflammation. Interactions between gut microbiota alterations and lipid dysmetabolism plays an important role in individual subsequent adipose tissue development and exerting immune or endocrine function. [Display omitted] • Adipose immune function is defined in early stage of life, and its disorder will lead to a series of chronic diseases in adulthood. • Cytokines derived by obese adipose immune cells aggravate insulin resistance and the whitening of brown and beige adipocytes. • Unhealthy lifestyles play key roles in childhood obesity by affecting adipose immunity. [ABSTRACT FROM AUTHOR]

Background: Adverse intrauterine environment—reflected by low birth weight (LBW)—has been linked to insulin resistance and type 2 diabetes later in life. Whether β-cell function reduction and insulin resistance could be detected even in middle-aged adults without overt diabetes is less investigated. We examined the association of LBW with β-cell function and insulin sensitivity in non-diabetic middle-aged adults from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Methods: This is a cross-sectional analysis of 2,634 ELSA-Brasil participants aged between 34 and 59 years, without diabetes. Participants were stratified according to LBW defined as <2.5 kg and their clinical data were compared. HOMA-IR, HOMA-β, HOMA-adiponectin, TyG index, QUICKI and TG/HDL were calculated and their association with LBW were tested using multiple linear regression including adjustments suggested by Directed Acyclic Graphs and propensity score matching was applied. Results: The sample (47.4 ± 6.3 years) was composed of 57.5% of women and 9% had LBW. Subjects with LBW and normal-weight reported similar BMI values at the age of 20 years and current BMI was slightly lower in the LBW group. In average, cardiometabolic risk profile and also indexes of β-cell function and insulin sensitivity were within normal ranges. In regression analysis, log-transformed HOMA-β—but not with the other indexes—was associated with LBW (p = 0.014) independent of sex, skin color, prematurity, and family history of diabetes. After applying propensity-score matching in a well-balanced sample, HOMA-AD and TG/HDL indexes were associated with LBW. Conclusion: The association between LBW and insulin sensitivity markers may occur in healthy middle-aged adults before overt glucose metabolism disturbances. Our data are coherent with the detection of early life events consequent with insulin resistance markers that could contribute to the risk of glucose metabolism disturbances. [ABSTRACT FROM AUTHOR]

BackgroundAdverse intrauterine environment—reflected by low birth weight (LBW)—has been linked to insulin resistance and type 2 diabetes later in life. Whether β-cell function reduction and insulin resistance could be detected even in middle-aged adults without overt diabetes is less investigated. We examined the association of LBW with β-cell function and insulin sensitivity in non-diabetic middle-aged adults from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil).MethodsThis is a cross-sectional analysis of 2,634 ELSA-Brasil participants aged between 34 and 59 years, without diabetes. Participants were stratified according to LBW defined as

Ursini et al reported recently that the liability of schizophrenia explained by a polygenic risk score (PRS) derived from the variants most associated with schizophrenia was increased 5-fold in individuals who experienced complications during pregnancy or birth. Follow-up gene expression analysis showed that the genes mapping to the most associated genetic variants are highly expressed in placental tissues. If confirmed, these findings will have major implications in our understanding of the joint effect of genes and environment in the pathogenesis of schizophrenia. We examined the interplay between PRS and obstetric complications (OCs) in 5 independent samples (effective N = 2110). OCs were assessed with the full or modified Lewis-Murray scale, or with birth weight < 2.5 kg as a proxy. In a large cohort we tested whether the pathways from placenta-relevant variants in the original report were associated with case-control status. Unlike in the original study, we did not find significant effect of PRS on the presence of OCs in cases, nor a substantial difference in the association of PRS with case-control status in samples stratified by the presence of OCs. Furthermore, none of the PRS by OCs interactions were significant, nor were any of the biological pathways, examined in the Swedish cohort. Our study could not support the hypothesis of a mediating effect of placenta biology in the pathway from genes to schizophrenia. Methodology differences, in particular the different scales measuring OCs, as well as power constraints for interaction analyses in both studies, may explain this discrepancy. [ABSTRACT FROM AUTHOR]

The present study reports on a preregistered investigation of the potential mediating role of the triarchic psychopathy components Boldness, Meanness, and Disinhibition for associations between childhood traumatic experiences (CTE) and aggression. Three nonclinical samples (total N = 1,729; 1,176 women, 68.02%) completed self-report instruments of CTE, triarchic psychopathy traits, reactive and proactive aggression (Samples 1 and 2), and general aggression (Sample 3). Cross-sectional path analyses revealed that both Meanness and Disinhibition consistently mediated associations between CTE and aggression. These indirect effects were consistent across gender, even though the direct effect of Meanness on proactive aggression was stronger in men than in women (Samples 1 and 2). Finally, Boldness had weak negative associations with childhood traumatic experiences in all three samples, but no direct association with aggression. Taken together, these correlational findings suggest potential developmental mechanisms linking early traumatic experiences to adult aggression through elevated levels of psychopathic traits. [ABSTRACT FROM AUTHOR]

The gut microbiome is rapidly becoming the focus of interest as a possible factor involved in the pathophysiology of neuropsychiatric disorders. Recent understanding of the pathophysiology of schizophrenia emphasizes the role of systemic components, including immune/inflammatory and metabolic processes, which are influenced by and interacting with the gut microbiome. Here we systematically review the current literature on the gut microbiome in schizophrenia-spectrum disorders and in their animal models. We found that the gut microbiome is altered in psychosis compared to healthy controls. Furthermore, we identified potential factors related to psychosis, which may contribute to the gut microbiome alterations. However, further research is needed to establish the disease-specificity and potential causal relationships between changes of the microbiome and disease pathophysiology. This can open up the possibility of. manipulating the gut microbiome for improved symptom control and for the development of novel therapeutic approaches in schizophrenia and related psychotic disorders.

Abstract Background Research has shown that a history of childhood adversities is common in patients with psychiatric disorders but few studies have investigated links between specific types of adversity and specific psychiatric disorders. Methods We investigated the frequency of early childhood adversities in a sample consisting of 91 patients with diagnosis of schizophrenic spectrum disorders (SSD), 74 patients with bipolar disorder (BD), 83 patients with major depressive disorder (MDD) and 85 healthy controls and sought to identify adverse early childhood life events that predict the development of major psychiatric disorders. The Childhood Experiences of Care and Abuse questionnaire was used to collect data on traumatic experiences occurring before the age of 17 years and comprehensive demographic data were also collected. The data were analyzed with chi-squared tests, t-tests, post-hoc and logistic regression. Results Maternal absence/loss and economic difficulties in the early life were more prevalent in the BD group than other groups. Escape from home, cannabis abuse, psychological abuse, physical abuse and loneliness were more frequent in the SSD group than in other groups. Paternal absence, neglect of core needs, serious familial tension and absence of adult and peer confidants were all less common in the HC group than in the other groups. The regression model confirmed that different types of adversities play a crucial role in the development of the three investigated disorders. Conclusions Our results support that SSD, BD and MDD are associated to different childhood adversities. This suggests that psychosocial interventions that reduce the incidence of these early life adversities might reduce the incidence of severe and disabling psychiatric disorders.

The gut microbiome is rapidly becoming the focus of interest as a possible factor involved in the pathophysiology of neuropsychiatric disorders. Recent understanding of the pathophysiology of schizophrenia emphasizes the role of systemic components, including immune/inflammatory and metabolic processes, which are influenced by and interacting with the gut microbiome. Here we systematically review the current literature on the gut microbiome in schizophrenia-spectrum disorders and in their animal models. We found that the gut microbiome is altered in psychosis compared to healthy controls. Furthermore, we identified potential factors related to psychosis, which may contribute to the gut microbiome alterations. However, further research is needed to establish the disease-specificity and potential causal relationships between changes of the microbiome and disease pathophysiology. This can open up the possibility of. manipulating the gut microbiome for improved symptom control and for the development of novel therapeutic approaches in schizophrenia and related psychotic disorders. [ABSTRACT FROM AUTHOR]

Background: Functional gastrointestinal disorders (FGIDs) are common digestive conditions characterized by chronic or recurrent symptoms in the absence of a clearly recognized gastrointestinal etiology. The biopsychosocial model, the most accepted concept explaining chronic pain conditions, proposes that the interplay of multiple factors such as genetic susceptibility, early life experiences, sociocultural issues, and coping mechanisms affect children at different stages of their lives leading to the development of different pain phenotypes and pain behaviors. Early life events including gastrointestinal inflammation, trauma, and stress may result in maladaptive responses that could lead to the development of chronic pain conditions such as FGIDs. Aims: In this review, we discuss novel findings from studies regarding the long-term effect of early life events and their relationship with childhood chronic abdominal pain and FGIDs. Methods: A bibliographic search of the PubMed database was conducted for articles published over the last 20 years using the keywords: “Functional gastrointestinal disorders”, “chronic abdominal pain”, “chronic pain”, “gastrointestinal inflammation”, and “early life events”. Forty-three articles were chosen for review. Results: Based on the current evidence, events that take place early in life predispose children to the development of chronic abdominal pain and FGIDs. Conditions that have been studied include cow's milk protein hypersensitivity, pyloric stenosis, gastrointestinal infections, and Henoch–Schonlein purpura, among others. Conclusions: Early events may play an important role in the complex pathogenesis of functional gastrointestinal conditions. Timely intervention may have a critical impact on the prevention of this group of chronic incapacitating conditions.

Background: Chronic abdominal pain is the most common cause for gastroenterology consultation and is frequently associated with functional gastrointestinal disorders including irritable bowel syndrome and inflammatory bowel disease. These disorders present similar brain/gut/microbiota trialogue alterations, associated with abnormal intestinal permeability, intestinal dysbiosis and colonic hypersensitivity (CHS). Intestinal dysbiosis can alter colon homeostasis leading to abnormal activation of the innate immunity that promotes CHS, perhaps involving the toll-like receptors (TLRs), which play a central role in innate immunity., Aim: To understand the mechanisms between early life event paradigm on intestinal permeability, fecal microbiota composition and CHS development in mice with TLRs expression in colonocytes., Methods: Maternal separation model (NMS) CHS model, which mimics deleterious events in childhood that can induce a wide range of chronic disorders during adulthood were used. Colonic sensitivity of NMS mice was evaluated by colorectal distension (CRD) coupled with intracolonic pressure variation (IPV) measurement. Fecal microbiota composition was analyzed by 16S rRNA sequencing from weaning to CRD periods. TLR mRNA expression was evaluated in colonocytes. Additionally, the effect of acute intrarectal instillation of the TLR5 agonist flagellin (FliC) on CHS in adult naive wildtype mice was analyzed., Results: Around 50% of NMS mice exhibited increased intestinal permeability and CHS associated with intestinal dysbiosis, characterized by a significant decrease of species richness, an alteration of the core fecal microbiota and a specific increased relative abundance of flagellated bacteria. Only TLR5 mRNA expression was increased in colonocytes of NMS mice with CHS. Acute intrarectal instillation of FliC induced transient increase of IPV, reflecting transient CHS appearance., Conclusion: Altogether, these data suggest a pathophysiological continuum between intestinal dysbiosis and CHS, with a role for TLR5., Competing Interests: Conflict-of-interest statement: All authors have nothing to disclose., (©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.)

Abstract: Objective: The aim of this study was to investigate the association between early life events in women with postpartum major depression and concomitant hypothalamus-pituitary-thyroid axis disturbances (HPTD), thyroid dysfunction or presence of thyroid antibodies. Methods: Serum total tri-iodothyronine (TT3), free thyroxin (FT4), Thyroid-stimulating hormone (TSH), Thyroperoxidasa (TPOAb) and Thyroglobulin (TGAb) autoantibodies was measured in 103 major postpartum depressive women. HPTD was defined as TSH and/or T4 abnormal, presence of thyroid autoantibodies and alterations of TT3. All women were assessed with a psychiatry structured interview for DSM-IV. Early Trauma Inventory Self Report, sociodemographic, reproductive, psychosocial and psychopathological variables were also assessed. Results: Sixty three percent of women had suffered childhood trauma, which was childhood sexual abuse in 27.2%. Childhood sexual abuse in postpartum major depression women increased the risk for thyroid dysfunction (OR=5.018, 95%CI=1.128–22.327), presence of thyroid autoantibodies (OR=2.528; 95%CI=1.00–6.39) and HPTD (OR=2.955; 95%CI=1.191–7.32). Moreover, age over 34 (OR=12.394; 95%CI=1.424–107.910) and previous postpartum depression (OR=8.470; 95%CI=1.20–59.43) increased the risk for thyroid dysfunction in postpartum depression. Limitations: The study design does not allow us to know the direction of the association and there is a lack of previous assessment of current posttraumatic stress disorder. Conclusions: According to the present findings, childhood sexual abuse may represent an important risk factor for the presence of thyroid autoantibodies and HPTD in women with postpartum depression. [Copyright &y& Elsevier]

Abstract: Adult hippocampal neurogenesis, a once unorthodox concept, has changed into one of the most rapidly growing fields in neuroscience. The present report results from the ECNP targeted expert meeting in 2007 during which cellular plasticity changes were addressed in the adult brain, focusing on neurogenesis and apoptosis in hippocampus and frontal cortex. We discuss recent studies investigating factors that regulate neurogenesis with special emphasis on effects of stress, sleep disruption, exercise and inflammation, a group of seemingly unrelated factors that share at least two unifying properties, namely that they all regulate adult hippocampal neurogenesis and have all been implicated in the pathophysiology of mood disorders. We conclude that although neurogenesis has been implicated in cognitive function and is stimulated by antidepressant drugs, its functional impact and contribution to the etiology of depression remains unclear. A lasting reduction in neurogenesis following severe or chronic stress exposure, either in adult or early life, may represent impaired hippocampal plasticity and can contribute to the cognitive symptoms of depression, but is, by itself, unlikely to produce the full mood disorder. Normalization of reductions in neurogenesis appears at least partly, implicated in antidepressant action. [Copyright &y& Elsevier]

Abstract: Objectives: We examined the effects of extremely low birth weight (ELBW<1000g) on adult brain functioning. Methods: We measured baseline regional EEG spectral power and hemispheric coherence in a cohort of 154 (M age=23years) non-impaired young adults who were born at ELBW (n =71; M birth weight=874g, M gestation age=27.5weeks) and in a control group of full-term adults born at normal birth weight (NBW; n =83). Results: ELBW adults exhibited significantly more power in the low EEG frequency bands (delta and theta) and less in the high EEG frequency bands (alpha and beta) than the NBW adults. This relative difference in the amount of high to low-frequency power was especially salient in the frontal regions. ELBW adults also exhibited significantly more short-distance EEG coherence in the right hemisphere compared to the NBW adults. Conclusions: Our results suggest that even among ELBW survivors without impairments, adverse events early in life may result in subtle neurological abnormalities. Significance: This study provides a unique EEG profile of young adult survivors of ELBW showing that maturational delays of the brain may persist into late adolescence and emerging adulthood. [Copyright &y& Elsevier]

The neurochemical correlates of the behavioural consequences of isolation rearing of rats are complex and involve many neurotransmitters, including the serotonergic system. Impaired functioning of the ascending serotonergic system has been implicated in many neuropsychiatric syndromes, including attention deficit hyperactivity disorder and schizophrenia. In the present investigation serotonergic function was assessed using in vitro receptor autoradiography. The 5-hydroxytryptamine2A (5-HT2A) receptor antagonist [3H]ketanserin and the 5-HT1A receptor antagonist, [3H]WAY100, 635 were used to compare 5-HT receptor subtype densities in the forebrains of socially and isolation-reared rats. Regions of highest receptor density were observed in the frontal cortex for 5-HT2A receptors and in the frontal cortex, dorsal hippocampus and lateral septum for 5-HT1A receptors. In isolation-reared rats, 5-HT2A receptor binding site densities were significantly increased by between 36 and 67% in the prelimbic, motor and cingulate cortices compared with socially reared controls. By contrast, 5-HT1A receptor binding site densities were significantly reduced by 22% in the prelimbic cortex, and significantly increased by between 10 and 50% in the motor cortex, somatosensory cortex, dentate gyrus and CA fields of the hippocampus.These data demonstrate that isolation-rearing produces significant effects on forebrain 5-HT1A and 5-HT2A receptor densities in the adult rat. It is hypothesised that altered serotonergic function, particularly in the hippocampus and prefrontal cortex, may underlie some of the behavioural abnormalities associated with isolation-rearing. [Copyright &y& Elsevier]

Abstract The contribution of early experiences towards the onset of personality disorder has often been stressed. However, the contribution to trait personality has received less attention. To examine the impact of early experiences on the development of personality, two subscale scores of the Eysenck Personality Questionnaire (EPQ): neuroticism (N) and extroversion (E), were used to assess a total of 220 residents of a rural city of Japan (aged ≥18 years). After controlling for age and social desirability response bias, the N score of men could be predicted by the experience of relocation; the E score of men by high parental care and low parental overprotection; and the E score of women by the experience of death of a sibling. Personality traits in a non-patient population may be explained by early experiences. [ABSTRACT FROM AUTHOR]

Previous studies have shown that deprivation of the infant rat from maternal care has pronounced effects on the stress system during ontogeny. Here we test the hypothesis that 24 h of maternal deprivation at postnatal day 3 will cause persistent changes in behaviour. Spatial learning and memory of male Brown Norway rats deprived as infants were observed in the Morris water maze at 3, 12, 24 and 30-32 months of age (young, adult, aged, senescent). Their nondeprived mother-reared littermates served as controls. (i) With increasing age, water maze performance declined in deprived and nondeprived groups. However, once the task was learned the animals maintained their good performance during retest at later ages. (ii) Maternal deprivation delayed acquisition until adulthood and caused at every age a higher degree of persistent behaviour as judged from the performance of deprived rats' free swim trials and reversal trials. (iii) At senescence the mean performance in the water maze did not differ between the groups. Instead, the individual performance was strikingly different within each group. Senescent deprived rats were either nonimpaired or impaired with only a few animals showing an intermediate performance. Thus, a large group of animals (≈ 40%) ages successfully as they are resistant to the effect of maternal deprivation. In contrast, the majority of the control animals displayed intermediate performance. Taken together, maternal deprivation has life-long consequences for behaviour and culminates at senescence in amplification of individual differences in learning ability rather than in a generalized deterioration of cognitive functions. [ABSTRACT FROM AUTHOR]

Previous research has indicated that adults with various anxiety disorders, especially social phobia, recall their parents as excessively protective and controlling and as low in socialization. However, it is not clear whether such results would be supported by parents. In the present study subjects with social phobia, panic disorder, and nonclinical subjects and their mothers were given parallel measures of maternal control, socialization, and offspring early introverted behaviors as well as several questions relating to two early major life events and family size. Anxious offspring reported the usual high maternal control and low paternal socialization and mother supported the data on socialization. On control, mothers provided mixed results, disagreeing on a more standard measure, but showing agreement on a more operationalized measure. The data were more consistent for social phobia than for panic disorder. In terms of early life factors, both anxiety disorders were associated with fewer friends and more introverted behaviors, while family size and two major life events did not differentiate groups. [ABSTRACT FROM AUTHOR]

Background: Research has shown that a history of childhood adversities is common in patients with psychiatric disorders but few studies have investigated links between specific types of adversity and specific psychiatric disorders. Methods: We investigated the frequency of early childhood adversities in a sample consisting of 91 patients with diagnosis of schizophrenic spectrum disorders (SSD), 74 patients with bipolar disorder (BD), 83 patients with major depressive disorder (MDD) and 85 healthy controls and sought to identify adverse early childhood life events that predict the development of major psychiatric disorders. The Childhood Experiences of Care and Abuse questionnaire was used to collect data on traumatic experiences occurring before the age of 17 years and comprehensive demographic data were also collected. The data were analyzed with chi-squared tests, t-tests, post-hoc and logistic regression. Results: Maternal absence/loss and economic difficulties in the early life were more prevalent in the BD group than other groups. Escape from home, cannabis abuse, psychological abuse, physical abuse and loneliness were more frequent in the SSD group than in other groups. Paternal absence, neglect of core needs, serious familial tension and absence of adult and peer confidants were all less common in the HC group than in the other groups. The regression model confirmed that different types of adversities play a crucial role in the development of the three investigated disorders. Conclusions: Our results support that SSD, BD and MDD are associated to different childhood adversities. This suggests that psychosocial interventions that reduce the incidence of these early life adversities might reduce the incidence of severe and disabling psychiatric disorders. [ABSTRACT FROM AUTHOR]