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European Journal of Obstetrics,... Sep 2023The risk of adverse perinatal and maternal outcomes increases with gestational age, and although induction of labour may reduce these risks, the optimal timing of... (Meta-Analysis)
Meta-Analysis Review
The risk of adverse perinatal and maternal outcomes increases with gestational age, and although induction of labour may reduce these risks, the optimal timing of induction remains unknown. We carried out a systematic review and meta-analysis, to determine the gestational age at which induction should be offered. We searched Cochrane Central Register of Controlled Trials, Medline, and Embase databases from inception to July 2022, to identify randomised trials comparing induction of labour at or beyond 37' weeks gestation with expectant management or delayed induction, and according to the gestational age at planned induction. We undertook random effects meta-analysis and pooled estimates as odds ratios with 95% confidence intervals. We assessed risk of bias of studies using the Cochrane Risk of Bias tool 2.0. We included 44 trials (23,960 women and 22,191 offspring) from 1,839 citations in our meta-analysis. The odds of perinatal death (odds ratio 0.42, 95% confidence interval 0.22 to 0.81; 26 studies, 20,154 offspring), stillbirth (0.40, 0.16 to 0.98; 25 studies, 19,412 offspring), admission to neonatal intensive care unit (0.86, 0.78 to 0.96; 23 studies, 18,846 offspring), and caesarean section (0.90, 0.83 to 0.98; 40 studies, 23,616 women) were reduced in the induction of labour group compared to expectant management or delayed induction. The odds of admission to neonatal intensive care unit (0.82, 0.70 to 0.96; 6 studies, 9,316 offspring) were lower with induction of labour at 41 weeks compared to induction at or after 42 weeks' gestation, and the odds of caesarean section were reduced with labour induction at 39 weeks' compared to induction at or after 40 weeks' (0.83, 0.74 to 0.93; 8 studies, 7,677 women). There were no significant differences in pregnancy outcomes by method of induction of labour. Induction of labour compared to expectant management or delayed induction reduces the risk of adverse pregnancy outcomes, and the optimal timing may depend on the specific outcome of interest.
Topics: Infant, Newborn; Pregnancy; Female; Humans; Cesarean Section; Watchful Waiting; Labor, Obstetric; Pregnancy Outcome; Labor, Induced
PubMed: 37549509
DOI: 10.1016/j.ejogrb.2023.07.021 -
EMBO Molecular Medicine Apr 2024Communication via biological mediators between mother and fetus are key to reproductive success and offspring's future health. The repertoire of mediators coding signals... (Review)
Review
Communication via biological mediators between mother and fetus are key to reproductive success and offspring's future health. The repertoire of mediators coding signals between mother and fetus is broad and includes soluble factors, membrane-bound particles and immune as well as non-immune cells. Based on the emergence of technological advancements over the last years, considerable progress has been made toward deciphering the "communicatome" between fetus and mother during pregnancy and even after birth. In this context, pregnancy-associated chimerism has sparked the attention among immunologists, since chimeric cells-although low in number-are maintained in the allogeneic host (mother or fetus) for years after birth. Other non-cellular structures of chimerism, e.g. extracellular vesicles (EVs), are increasingly recognized as modulators of pregnancy outcome and offspring's health. We here discuss the origin, distribution and function of pregnancy-acquired microchimerism and chimeric EVs in mother and offspring. We also highlight the pioneering concept of maternal microchimeric cell-derived EVs in offspring. Such insights expand the understanding of pregnancy-associated health or disease risks in mother and offspring.
Topics: Female; Pregnancy; Humans; Chimerism; Fetus; Stem Cells
PubMed: 38467841
DOI: 10.1038/s44321-024-00045-x -
JAMA Network Open Jan 2024Investigations into the association of antepartum maternal infections with the pathogenesis of biliary atresia (BA) in human offspring are insufficient.
IMPORTANCE
Investigations into the association of antepartum maternal infections with the pathogenesis of biliary atresia (BA) in human offspring are insufficient.
OBJECTIVE
To examine the association between prenatal infections in mothers and the development of BA in their offspring.
DESIGN, SETTING, AND PARTICIPANTS
This population-based case-control study obtained administrative data from the Taiwan National Health Insurance Research Database with linkage to the Taiwan Maternal and Child Health Database, capturing demographic and medical information on nearly all 23 million of the Taiwan population. The cohort comprised 2 905 978 singleton live births among mother-infant dyads between January 1, 2004, and December 31, 2020, in Taiwan. The case group of infants with BA was identified from use of International Classification of Diseases diagnostic codes for BA and subsequent Kasai procedure or liver transplant. The control group was randomly selected from infants without BA, representing approximately 1 in 1000 study population. Data analyses were performed from May 1 to October 31, 2023.
EXPOSURE
Prenatal maternal infections, including intestinal infection, influenza, upper airway infection, pneumonia, soft-tissue infection, and genitourinary tract infection.
MAIN OUTCOMES AND MEASURES
The main outcome was exposure to prenatal maternal infections. Inverse probability weighting analysis was performed by building a logistic regression model to estimate the probability of the exposure observed for a particular infant and using the estimated probability as a weight in subsequent analyses. The weighted odds ratio (OR) estimated by logistic regressions was then used to assess the risk of BA in offspring after prenatal maternal infections.
RESULTS
Among the mother-infant dyads included, 447 infants with BA were cases (232 females [51.9%]) and 2912 infants without BA were controls (1514 males [52.0%]). The mean (SD) maternal age at childbirth was 30.7 (4.9) years. Offspring exposed to prenatal intestinal infection (weighted OR, 1.46; 95% CI, 1.17-1.82) and genitourinary tract infection (weighted OR, 1.22; 95% CI, 1.05-1.41) in mothers exhibited a significantly higher risk of BA. Furthermore, maternal intestinal infection (weighted OR, 6.05; 95% CI, 3.80-9.63) and genitourinary tract infection (weighted OR, 1.55; 95% CI, 1.13-2.11) that occurred during the third trimester were associated with an increased risk of BA in offspring.
CONCLUSIONS AND RELEVANCE
Results of this case-control study indicate an association between prenatal intestinal infection and genitourinary tract infection in mothers and BA occurrence in their offspring. Further studies are warranted to explore the underlying mechanisms of this association.
Topics: Adult; Female; Humans; Male; Pregnancy; Biliary Atresia; Case-Control Studies; Logistic Models; Pregnancy Trimester, Third; Infant, Newborn
PubMed: 38170523
DOI: 10.1001/jamanetworkopen.2023.50044 -
JAMA Network Open Oct 2023Corticosteroids and β2-adrenergic agonists are commonly used during pregnancy to treat asthma. However, offspring neurodevelopmental outcomes following in utero...
IMPORTANCE
Corticosteroids and β2-adrenergic agonists are commonly used during pregnancy to treat asthma. However, offspring neurodevelopmental outcomes following in utero exposure to these medications remain unclear.
OBJECTIVE
To investigate the association between timing of in utero exposure to corticosteroids and β2-adrenergic agonists and offspring neurodevelopmental milestones during the first 3 years of life.
DESIGN, SETTING, AND PARTICIPANTS
This cohort study obtained data from the Japan Environment and Children's Study, an ongoing birth cohort study conducted in collaboration with 15 Regional Centers across Japan. Participants were mother-offspring pairs who were recruited between January 1, 2011, and March 31, 2014. Data were analyzed between January and February 2023.
EXPOSURE
Corticosteroids and β2-adrenergic agonists were the exposure of interest. Timing of corticosteroid and β2-adrenergic agonist exposure included early pregnancy (weeks 0-12), mid- to late pregnancy (weeks >12), and both stages of pregnancy.
MAIN OUTCOMES AND MEASURES
Offspring neurodevelopmental milestones (communication, gross motor, fine motor, problem-solving, and personal-social skills) were assessed using the Japanese version of the Ages and Stages Questionnaires, 3rd edition, at 6, 12, 18, 24, 30, and 36 months.
RESULTS
In total, 91 460 mother-offspring pairs were analyzed. Among mothers, the mean (SD) age at delivery was 31.20 (5.05) years. Among offspring, 46 596 (50.9%) were males and 44 864 (49.1%) were females, of whom 66.4% had a gestational age of 39 to 41 weeks. During early, mid- to late, and both stages of pregnancy, 401 (0.4%), 935 (1.0%), and 568 (0.6%) offspring, respectively, were exposed to corticosteroids, whereas 170 (0.2%), 394 (0.4%), and 184 (0.2%), respectively, were exposed to β2-adrenergic agonists. No association of corticosteroid exposure during early, mid- to late, and both stages of pregnancy with all 5 neurodevelopmental milestones was found. Similarly, no association between β2-adrenergic agonist use during early pregnancy and all 5 neurodevelopmental milestones was observed. An association was found between β2-adrenergic agonist exposure during mid- to late pregnancy and delayed personal-social skills (adjusted odds ratio, 1.48; 95% CI, 1.01-2.32; P = .045).
CONCLUSIONS AND RELEVANCE
Results of this study found no association between in utero corticosteroid and β2-adrenergic agonist exposure and offspring neurodevelopmental outcomes, regardless of the timing of exposure. Despite the limitations and low power of the study, the findings suggest that corticosteroids and β2-adrenergic agonists are safe for pregnant individuals with asthma and the neurodevelopment of their offspring.
Topics: Male; Child; Female; Humans; Pregnancy; Adult; Infant; Cohort Studies; Adrenergic Agonists; Prenatal Exposure Delayed Effects; Asthma; Adrenal Cortex Hormones
PubMed: 37874567
DOI: 10.1001/jamanetworkopen.2023.39347 -
World Psychiatry : Official Journal of... Oct 2023The offspring of parents with mental disorders are at increased risk for developing mental disorders themselves. The risk to offspring may extend transdiagnostically to...
The offspring of parents with mental disorders are at increased risk for developing mental disorders themselves. The risk to offspring may extend transdiagnostically to disorders other than those present in the parents. The literature on this topic is vast but mixed. To inform targeted prevention and genetic counseling, we performed a comprehensive, PRISMA 2020-compliant meta-analysis. We systematically searched the literature published up to September 2022 to retrieve original family high-risk and registry studies reporting on the risk of mental disorders in offspring of parents with any type of mental disorder. We performed random-effects meta-analyses of the relative risk (risk ratio, RR) and absolute risk (lifetime, up to the age at assessment) of mental disorders, defined according to the ICD or DSM. Cumulative incidence by offspring age was determined using meta-analytic Kaplan-Meier curves. We measured heterogeneity with the I statistic, and risk of bias with the Quality In Prognosis Studies (QUIPS) tool. Sensitivity analyses addressed the impact of study design (family high-risk vs. registry) and specific vs. transdiagnostic risks. Transdiagnosticity was appraised with the TRANSD criteria. We identified 211 independent studies that reported data on 3,172,115 offspring of parents with psychotic, bipolar, depressive, disruptive, attention-deficit/hyperactivity, anxiety, substance use, eating, obsessive-compulsive, and borderline personality disorders, and 20,428,575 control offspring. The RR and lifetime risk of developing any mental disorder were 3.0 and 55% in offspring of parents with anxiety disorders; 2.6 and 17% in offspring of those with psychosis; 2.1 and 55% in offspring of those with bipolar disorder; 1.9 and 51% in offspring of those with depressive disorders; and 1.5 and 38% in offspring of those with substance use disorders. The offspring's RR and lifetime risk of developing the same mental disorder diagnosed in their parent were 8.4 and 32% for attention-deficit/hyperactivity disorder; 5.8 and 8% for psychosis; 5.1 and 5% for bipolar disorder; 2.8 and 9% for substance use disorders; 2.3 and 14% for depressive disorders; 2.3 and 1% for eating disorders; and 2.2 and 31% for anxiety disorders. There were 37 significant transdiagnostic associations between parental mental disorders and the RR of developing a different mental disorder in the offspring. In offspring of parents with psychosis, bipolar and depressive disorder, the risk of the same disorder onset emerged at 16, 5 and 6 years, and cumulated to 3%, 19% and 24% by age 18; and to 8%, 36% and 46% by age 28. Heterogeneity ranged from 0 to 0.98, and 96% of studies were at high risk of bias. Sensitivity analyses restricted to prospective family high-risk studies confirmed the pattern of findings with similar RR, but with greater absolute risks compared to analyses of all study types. This study demonstrates at a global, meta-analytic level that offspring of affected parents have strongly elevated RR and lifetime risk of developing any mental disorder as well as the same mental disorder diagnosed in the parent. The transdiagnostic risks suggest that offspring of parents with a range of mental disorders should be considered as candidates for targeted primary prevention.
PubMed: 37713573
DOI: 10.1002/wps.21147 -
Acta Pharmaceutica Sinica. B Sep 2023The formation of learning and memory is regulated by synaptic plasticity in hippocampal neurons. Here we explored how gestational exposure to dexamethasone, a synthetic...
The formation of learning and memory is regulated by synaptic plasticity in hippocampal neurons. Here we explored how gestational exposure to dexamethasone, a synthetic glucocorticoid commonly used in clinical practice, has lasting effects on offspring's learning and memory. Adult offspring rats of prenatal dexamethasone exposure (PDE) displayed significant impairments in novelty recognition and spatial learning memory, with some phenotypes maintained transgenerationally. PDE impaired synaptic transmission of hippocampal excitatory neurons in offspring of F1 to F3 generations, and abnormalities of neurotransmitters and receptors would impair synaptic plasticity and lead to impaired learning and memory, but these changes failed to carry over to offspring of F5 and F7 generations. Mechanistically, altered hippocampal -SIRT1-CDK5-NR2B signaling axis in PDE multigeneration caused inhibition of excitatory synaptic transmission, which might be related to oocyte-specific high expression and transmission of . Together, PDE affects hippocampal excitatory synaptic transmission, with lasting consequences across generations, and CDK5 in offspring's peripheral blood might be used as an early-warning marker for fetal-originated learning and memory impairment.
PubMed: 37719378
DOI: 10.1016/j.apsb.2023.05.013 -
Journal of Molecular Endocrinology Nov 2023Suboptimal in utero environments such as poor maternal nutrition and gestational diabetes can impact fetal birth weight and the metabolic health trajectory of the adult...
Suboptimal in utero environments such as poor maternal nutrition and gestational diabetes can impact fetal birth weight and the metabolic health trajectory of the adult offspring. Fetal growth is associated with alterations in placental mechanistic target of rapamycin (mTOR) signaling; it is reduced in fetal growth restriction and increased in fetal overgrowth. We previously reported that when metabolically challenged by a high-fat diet, placental mTORKO (mTORKOpl) adult female offspring develop obesity and insulin resistance, whereas placental TSC2KO (TSC2KOpl) female offspring are protected from diet-induced obesity and maintain proper glucose homeostasis. In the present study, we sought to investigate whether reducing or increasing placental mTOR signaling in utero alters the programming of adult offspring metabolic tissues preceding a metabolic challenge. Adult male and female mTORKOpl, TSC2KOpl, and respective controls on a normal chow diet were subjected to an acute intraperitoneal insulin injection. Upon insulin stimulation, insulin signaling via phosphorylation of Akt and nutrient sensing via phosphorylation of mTOR target ribosomal S6 were evaluated in the offspring liver, white adipose tissue, and skeletal muscle. Among tested tissues, we observed significant changes only in the liver signaling. In the male mTORKOpl adult offspring liver, insulin-stimulated phospho-Akt was enhanced compared to littermate controls. Basal phospho-S6 level was increased in the mTORKOpl female offspring liver compared to littermate controls and did not increase further in response to insulin. RNA sequencing of offspring liver identified placental mTORC1 programming-mediated differentially expressed genes. The expression of major urinary protein 1 (Mup1) was differentially altered in female mTORKOpl and TSC2KOpl offspring livers and we show that MUP1 level is dependent on overnutrition and fasting status. In summary, deletion of placental mTOR nutrient sensing in utero programs hepatic response to insulin action in a sexually dimorphic manner. Additionally, we highlight a possible role for hepatic and circulating MUP1 in glucose homeostasis that warrants further investigation.
Topics: Animals; Female; Male; Mice; Pregnancy; Diabetes, Gestational; Fetal Macrosomia; Glucose; Insulin; Obesity; Placenta; Proto-Oncogene Proteins c-akt; TOR Serine-Threonine Kinases
PubMed: 37855320
DOI: 10.1530/JME-23-0035 -
Appetite Apr 2024The internal (i.e., interoceptive) sensations that characterise hunger vary between people, and this may also be the case for thirst, although it has not been so well...
The internal (i.e., interoceptive) sensations that characterise hunger vary between people, and this may also be the case for thirst, although it has not been so well explored. There are probably both heritable and learning-based causes for this interoceptive variability. Consequently, it would seem plausible that parents and their offspring would have more similar patterns of hunger and thirst than pairs of strangers. We tested this idea, in addition to exploring its potential moderating variables, by studying the similarity of self-reported hunger and thirst sensations in 170 students and their primary caregivers from childhood. Both students and caregivers completed the same online-survey, covering hunger and thirst sensations, beliefs about the causes of hunger and thirst, the Three Factor Eating Questionnaire (revised) and demographic data. We find evidence of robust student-caregiver similarity in interoceptive hunger and thirst sensations (medium effect sizes), with these being moderated by caregiver beliefs about the homeostatic nature of each state (medium effect sizes). This suggests a potential role for caregivers in the development of their offspring's interoceptive cues for hunger and for thirst. In addition, thirst, like hunger, appears to be multidimensional, and varies between people. The implications of these findings are discussed.
Topics: Humans; Child; Hunger; Thirst; Sensation; Learning; Cues
PubMed: 38218415
DOI: 10.1016/j.appet.2024.107208 -
Trauma, Violence & Abuse Jul 2023This systematic review explores the empirical literature addressing the association between parental preconception adversity and offspring physical health in... (Review)
Review
This systematic review explores the empirical literature addressing the association between parental preconception adversity and offspring physical health in African-American families. : We conducted a literature search in PubMed, Web of Science, PsycINFO, CINAHL, and Scopus through June 2021. Articles were included if they: reported data about at least two generations of African-American participants from the same family; measured parental preconception adversity at the individual level; measured at least one offspring physical health outcome; and examined associations between parental adversity and child health. : We identified 701 unique articles; thirty-eight articles representing 30 independent studies met inclusion criteria. Twenty-five studies (83%) reported that parental preconception adversity was associated with child health; six studies (20%) reported that parental preconception adversity was not associated with at least one offspring outcome; several studies reported both. Only six studies (20%) reported an association specific to African Americans. : Empirical evidence linking parental preconception adversity with offspring physical health in African Americans is limited and mixed. In the current literature, very few studies report evidence addressing intergenerational associations between parental preconception adversity and offspring physical health in the African-American population, specifically, and even fewer investigate forms of parental preconception adversity that have been shown to disproportionately affect African Americans (e.g., racism). To better understand root causes of racial health disparities, more rigorous systematic research is needed to address how intergenerational transmission of historical and ongoing race-based trauma may impact offspring health among African Americans.
Topics: Child; Humans; Black or African American; Child Health; Health Status; Health Status Disparities; Historical Trauma; Longitudinal Studies; Parents; Stress, Psychological
PubMed: 35240883
DOI: 10.1177/15248380221074320 -
BioRxiv : the Preprint Server For... Jan 2024Despite substantial costs, biparental sex is the dominant mode of reproduction across plant and animal taxa. The Red Queen hypothesis (RQH) posits that coevolutionary...
Despite substantial costs, biparental sex is the dominant mode of reproduction across plant and animal taxa. The Red Queen hypothesis (RQH) posits that coevolutionary interactions with parasites can favor biparental sex in hosts, despite the costs. In support of the RQH, previous studies found that coevolutionary interactions with virulent bacterial parasites maintained high outcrossing rates in populations of the androdioecious nematode host . Here we test three non-mutually exclusive mechanisms that could explain how coevolving parasites maintain outcrossing rates in hosts: 1) short-term parasite exposure induces plastic increases in the hosts' propensity to outcross, 2) hosts evolve increased outcrossing propensity in response to selection imposed by coevolving parasites, and 3) outcrossed offspring incur less parasite-mediated fitness loss than selfed offspring, increasing host male frequencies and opportunities for outcrossing. We find no evidence that parasites cause plastic or evolved changes in host outcrossing propensity. However, parental outcrossing significantly increases survival of host offspring in the F2 generation when exposed to a coevolving parasite. Hence, coevolving parasites maintain outcrossing in host populations by selecting against selfed offspring, rather than by inducing changes in the propensity to outcross.
PubMed: 38352489
DOI: 10.1101/2024.01.30.578011