Early Life Trauma Has Lifelong Consequences for Sleep And Behavior.
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ABSTRACT:
SUBMITTER: Lewin M
PROVIDER: S-EPMC6853921 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The role of sleep in the relations between early-life trauma and the development of adverse psychological trajectories is relatively unknown and was the primary aim of the present study. Military veterans were evaluated for posttraumatic stress disorder, combat exposure, trauma history, sleep quality, disruptive nocturnal behaviors, and a subsample completed overnight polysomnography that yielded objectively measured sleep parameters. When relevant variables were controlled, increased earlier-life traumatic event exposure was associated with increased rapid-eye-movement sleep (REMs) fragmentation, and increased REMs fragmentation was associated with increased later-life disruptive nocturnal behaviors. REMs fragmentation carried an indirect relation between earlier-life trauma and later-life disruptive nocturnal behaviors. Objectively measured sleep parameters were used to describe REMs fragmentation physiology. The current findings elucidate the important role that earlier-life trauma exposure may have in the development of REM sleep physiology, and how this altered sleep physiology may have dynamic influences on subsequent posttraumatic stress symptoms in adulthood.
| S-EPMC3299844 | biostudies-literature
Project description:ObjectivesAge stereotypes and expectations about one's own aging commence in childhood but most research focuses on predictive associations with midlife health behaviors, later-life chronic conditions, biomarkers, and longevity. Surprisingly little is known about the role of poor childhood health in these associations. This study aims to fill this gap.MethodsUsing data from the Health and Retirement Study (HRS: N = 5,773, aged 50-98), we investigated whether diagnosed chronic illness before age 16 and self-rated childhood health predict late-life self-perceptions of aging (SPA) and proportional subjective age discrepancy (PSAD). We conducted multivariate multiple regression analysis (MMRA) to determine the joint and partial effects of the two indicators of childhood health. Models included controls for childhood family financial status as well as late-life self-rated health, chronic illnesses, memory status, and demographic covariates (age, gender, race/ethnicity, marital status, socioeconomic status) in 2016.ResultsOver and above all covariates and the covariation of the two views of one's own aging, the MMRA models revealed that the number of childhood chronic illnesses predicted SPA but not for PSAD. Self-rated childhood health predicted both SPA and PSAD in the unadjusted models, but not in the adjusted models.DiscussionThis study provides new insight into potential early-life precursors of self-evaluations of aging. In particular, childhood diagnoses of chronic illness enhance negative SPA up to 50 years later. Non-normative experiences related to poor health in childhood are lifelong foundations for socioeconomic status, health, and for self-related beliefs about age and aging.
| S-EPMC8063672 | biostudies-literature
Project description:Early life stress increases risk for depression. Here we establish a "two-hit" stress model in mice wherein stress at a specific postnatal period increases susceptibility to adult social defeat stress and causes long-lasting transcriptional alterations that prime the ventral tegmental area (VTA)-a brain reward region-to be in a depression-like state. We identify a role for the developmental transcription factor orthodenticle homeobox 2 (Otx2) as an upstream mediator of these enduring effects. Transient juvenile-but not adult-knockdown of Otx2 in VTA mimics early life stress by increasing stress susceptibility, whereas its overexpression reverses the effects of early life stress. This work establishes a mechanism by which early life stress encodes lifelong susceptibility to stress via long-lasting transcriptional programming in VTA mediated by Otx2.
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Project description:Modern life involves chronic circadian disruption through artificial light and these disruptions are associated with numerous mental and physical health maladies. Because the developing nervous system is particularly vulnerable to perturbation, we hypothesized that early-life circadian disruption would negatively impact offspring development and adult function. Pregnant mice were subjected to chronic circadian disruption from the time of uterine implantation through weaning. To dissociate in utero from postnatal effects, a subset of litters was cross-fostered at birth from disrupted dams to control dams and vice versa. Postnatal circadian disruption was associated with reduced adult body mass, social avoidance, and hyperactivity. In utero disruption resulted in more pronounced social avoidance and hyperactivity, phenotypes not abrogated by cross-fostering to control mothers. To examine whether circadian disruption affects development by acting as an early life stressor, we examined birthweight, litter size, maternal cannibalism, and epigenetic modifications. None of these variables differed between control and disrupted dams, or resembled patterns seen following early-life stress. Our findings indicate that developmental chronic circadian disruption permanently affects somatic and behavioral development in a stage-of-life-dependent manner, independent of early life stress mechanisms, underscoring the importance of temporal structure during development, both in utero and early postnatal life.
| S-EPMC5468226 | biostudies-literature
Project description:While Δ9-tetrahydrocannabinol (THC) has been widely studied in the realm of developmental and reproductive toxicology, few studies have investigated potential toxicities from a second widely used cannabis constituent, cannabidiol (CBD). CBD is popularized for its therapeutic potential for reducing seizure frequencies in epilepsy. This study investigated developmental origins of health and disease (DOHaD) via multigenerational gene expression patterns, behavior phenotypes, and reproductive fitness of a subsequent F1 following an F0 developmental exposure of zebrafish (Danio rerio) to THC (0.024, 0.12, 0.6 mg/L; 0.08, 0.4, 2 μM) or CBD (0.006, 0.03, 0.15 mg/L; 0.02, 0.1, 0.5 μM). Embryonic exposure at these concentrations did not cause notable morphological abnormalities in either F0 or F1 generations. However, during key developmental stages (14, 24, 48, 72, and 96 h post fertilization) THC and CBD caused differential expression of c-fos, brain-derived neurotrophic factor (bdnf), and deleted-in-azoospermia like (dazl), while in F1 larvae only CBD differentially expressed dazl. Larval photomotor behavior was reduced (F0) or increased (F1) by THC exposure, while CBD had no effect on F0 larvae, but decreased activity in the unexposed F1 larvae. These results support our hypothesis of cannabinoid-related developmental neurotoxicity. As adults, F0 fecundity was reduced, but it was not in F1 adults. Conversely, in the adult open field test there were no significant effects in F0 fish, but a significant reduction in the time in periphery was seen in F1 fish from the highest THC exposure group. The results highlight the need to consider long-term ramifications of early-life exposure to cannabinoids.
| S-EPMC6347400 | biostudies-literature
Project description:Analysis of hippocampal DNA methylation changes that were induced by environmental enrichment and maintained for long-term after withdrawal from the enriched environment.
2020-08-26 | GSE139051 | GEO
Project description:BackgroundThe interaction of organisms with their surrounding microbial communities influences many biological processes, a notable example of which is the shaping of the immune system in early life. In the Pacific oyster, Crassostrea gigas, the role of the environmental microbial community on immune system maturation - and, importantly, protection from infectious disease - is still an open question.ResultsHere, we demonstrate that early life microbial exposure durably improves oyster survival when challenged with the pathogen causing Pacific oyster mortality syndrome (POMS), both in the exposed generation and in the subsequent one. Combining microbiota, transcriptomic, genetic, and epigenetic analyses, we show that the microbial exposure induced changes in epigenetic marks and a reprogramming of immune gene expression leading to long-term and intergenerational immune protection against POMS.ConclusionsWe anticipate that this protection likely extends to additional pathogens and may prove to be an important new strategy for safeguarding oyster aquaculture efforts from infectious disease. tag the videobyte/videoabstract in this section Video Abstract.
| S-EPMC9167547 | biostudies-literature
Project description:BackgroundOriginally studied as a mechanism to understand eclampsia-related deaths during pregnancy, fetal cells in maternal blood have more recently garnered attention as a noninvasive source of fetal material for prenatal testing. In the 21st century, however, intact fetal cells have been largely supplanted by circulating cell-free placental DNA for aneuploidy screening. Instead, interest has pivoted to the ways in which fetal cells influence maternal biology. In parallel, an increasing appreciation of the consequences of maternal cells in the developing fetus has occurred.ContentIn this review, we highlight the potential clinical applications and functional consequences of the bidirectional trafficking of intact cells between a pregnant woman and her fetus. Fetal cells play a potential role in the pathogenesis of maternal disease and tissue repair. Maternal cells play an essential role in educating the fetal immune system and as a factor in transplant acceptance. Naturally occurring maternal microchimerism is also being explored as a source of hematopoietic stem cells for transplant in fetal hematopoietic disorders.SummaryFuture investigations in humans need to include complete pregnancy histories to understand maternal health and transplant success or failure. Animal models are useful to understand the mechanisms underlying fetal wound healing and/or repair associated with maternal injury and inflammation. The lifelong consequences of the exchange of cells between a mother and her child are profound and have many applications in development, health, and disease. This intricate exchange of genetically foreign cells creates a permanent connection that contributes to the survival of both individuals.
| S-EPMC10072000 | biostudies-literature
Project description:BackgroundPatients with autism spectrum disorder (ASD) experience high rates of sleep disruption beginning early in life; however, the developmental consequences of this disruption are not understood. We examined sleep behavior and the consequences of sleep disruption in developing mice bearing C-terminal truncation mutation in the high-confidence ASD risk gene SHANK3 (Shank3ΔC). We hypothesized that sleep disruption may be an early sign of developmental divergence, and that clinically relevant Shank3WT/ΔC mice may be at increased risk of lasting deleterious outcomes following early life sleep disruption.MethodsWe recorded sleep behavior in developing Shank3ΔC/ΔC, Shank3WT/ΔC, and wild-type siblings of both sexes using a noninvasive home-cage monitoring system. Separately, litters of Shank3WT/ΔC and wild-type littermates were exposed to automated mechanical sleep disruption for 7 days prior to weaning (early life sleep disruption: ELSD) or post-adolescence (PASD) or undisturbed control (CON) conditions. All groups underwent standard behavioral testing as adults.ResultsMale and female Shank3ΔC/ΔC mice slept significantly less than wild-type and Shank3WT/ΔC siblings shortly after weaning, with increasing sleep fragmentation in adolescence, indicating that sleep disruption has a developmental onset in this ASD model. ELSD treatment interacted with genetic vulnerability in Shank3WT/ΔC mice, resulting in lasting, sex-specific changes in behavior, whereas wild-type siblings were largely resilient to these effects. Male ELSD Shank3WT/ΔC subjects demonstrated significant changes in sociability, sensory processing, and locomotion, while female ELSD Shank3WT/ΔC subjects had a significant reduction in risk aversion. CON Shank3WT/ΔC mice, PASD mice, and all wild-type mice demonstrated typical behavioral responses in most tests.LimitationsThis study tested the interaction between developmental sleep disruption and genetic vulnerability using a single ASD mouse model: Shank3ΔC (deletion of exon 21). The broader implications of this work should be supported by additional studies using ASD model mice with distinct genetic vulnerabilities.ConclusionOur study shows that sleep disruption during sensitive periods of early life interacts with underlying genetic vulnerability to drive lasting and sex-specific changes in behavior. As individuals progress through maturation, they gain resilience to the lasting effects of sleep disruption. This work highlights developmental sleep disruption as an important vulnerability in ASD susceptibility.
| S-EPMC9425965 | biostudies-literature
Project description:BackgroundPast research has examined the health outcomes of early sexual trauma in reproductive age women, but little is known about potential long-term effects in older age.ObjectiveTo examine associations between early life sexual trauma and later life sexual/genitourinary dysfunction and general functional disability in women.DesignCross-sectional analysis of nationally representative observational data from the National Social Life, Health, and Aging Project (2010-2011) PARTICIPANTS: One thousand seven hundred forty-five US women aged ≥ 50 years MAIN MEASURES: Two forms of early life sexual trauma (childhood sexual abuse and unwanted first sexual experience), sexual/genitourinary dysfunction (pain during sex, lack of pleasure during sex, urinary incontinence, other urinary symptoms), and general functional disability (difficulty performing 7 activities of daily living (ADLs) or 8 instrumental activities of daily living (IADLs)), assessed by interview and questionnaire.Key resultsOf 1745 women, 11% reported a history of childhood sexual abuse and 39% an unwanted first sexual experience. Childhood sexual abuse was associated with later life sexual/genitourinary dysfunction (pain during sex [OR 1.9, 95% CI 1.1-3.3], other urinary problems [OR 1.9, 95% CI 1.2-3.1]), and difficulty with multiple ADLs/IADLs (walking across the room [OR 1.9, 95% CI 1.2-3.1], getting in or out of bed [OR 2.0, 95% CI 1.2-3.3], bathing [OR 2.0, 95% CI 1.2-3.5], prepping meals [OR 2.4, 95% CI 1.5-3.8], shopping for food [OR 1.6, 95% CI 1.0-2.4], and completing light work [OR 1.6, 95% CI 1.0-2.4]), after adjusting for age, race, and education. Unwanted first sexual experience was associated with later life lack of pleasure with sex (OR 1.7, 95% CI 1.1-2.5) and difficulty with ADLs/IADLs (walking one block [OR 1.5, 95% CI 1.1-2.1], completing light work [OR 1.6, 95% CI 1.1-2.1]) in adjusted analyses.ConclusionsEarly sexual trauma may be an under-recognized marker of risk of aging-related functional decline in women. Findings underline the importance of providing trauma-informed care for women across the aging spectrum.
| S-EPMC7661667 | biostudies-literature