Early Life Events Research Articles

Acute postnatal inflammation alters adult microglial responses to LPS that are sex-, region- and timing of postnatal inflammation-dependent

BackgroundAdverse events in early life can have impact lasting into adulthood. We investigated the long-term effects of systemic inflammation during postnatal development on adult microglial responses to lipopolysaccharide (LPS) in two CNS regions (cortex, cervical spinal cord) in male and female rats.MethodsInflammation was induced in Sprague-Dawley rats by LPS (1 mg/kg) administered intraperitoneally during postnatal development at P7, P12 or P18. As adults (12 weeks of age), the rats received a second LPS dose (1 mg/kg). Control rats received saline. Microglia were isolated 3 h post-LPS followed by gene expression analysis via qRT-PCR for pro-inflammatory (IL-6, iNOS, Ptgs2, C/EBPb, CD14, CXCL10), anti-inflammatory (CD68, Arg-1), and homeostatic genes (P2Y12, Tmemm119). CSF-1 and CX3CL1 mRNAs were analyzed in microglia-free homogenates.ResultsBasal gene expression in adult microglia was largely unaffected by postnatal inflammation. Adult cortical microglial pro-inflammatory gene responses to LPS were either unchanged or attenuated in rats exposed to LPS during postnatal development. Ptgs2, C/EBPb, CXCL10 and Arg-1 were the most affected genes, with expression significantly downregulated vs. rats without postnatal LPS. Spinal microglia were affected most by LPS at P18, with mixed and sometimes opposing effects on proinflammatory genes in males vs. females. Overall, male cortical vs. spinal microglia were more affected by postnatal LPS. Females were affected in both cortex and spinal cord, but the effect was dependent on timing of postnatal LPS. Overall, inflammatory challenge at P18 had greater effect on adult microglia vs. challenge at P12 or P7.ConclusionsLong-lasting effects of postnatal inflammation on adult microglia depend on postnatal timing, CNS region and sex.

The prevalence of lifetime trauma and association with physical and psychosocial health among adults at the end of life.

National guidelines recognize lifetime trauma as relevant to clinical care for adults nearing the end of life. We determined the prevalence of early life and cumulative trauma among persons at the end of life by gender and birth cohort, and the association of lifetime trauma with end-of-life physical, mental, and social well-being. We used nationally representative Health and Retirement Study data (2006-2020), including adults age > 50 who died while enrolled (N = 6495). Early life and cumulative traumatic events were measured using an 11-item traumatic events scale (cumulative trauma: 0-5+ events over the lifespan). We included six birth cohorts (born <1924; children of depression [1924-1930]; HRS cohort [1931-1941]; war babies [1942-1947]; early baby-boomers [1948-1953]; mid-baby boomers [1954-1959]). End-of-life outcomes included validated measures of physical (pain, fatigue, dyspnea), mental (depression, life satisfaction), and social (loneliness, social isolation) needs. We report the prevalence of lifetime trauma by gender and birth cohort and the adjusted probability of each end-of-life outcome by trauma using multivariable logistic regression. The mean age at death was 78 years (SD = 11.1) and 52% were female. Lifetime trauma was common (0 events: 19%; 1-2: 47%; 3-4: 25%; 5+: 9%), with variation in individual events (e.g., death of a child, weapons in combat) by gender and birth cohort. After adjustment, increasing cumulative trauma was significantly associated (p-value<0.001) with higher reports of end-of-life moderate-to-severe pain (0 events: 46%; 1-2 events: 50%; 3-4 events: 57%; 5+ events: 60%), fatigue (58%; 60%; 66%; 69%), dyspnea (46%; 51%; 56%; 58%), depression (24%; 33%; 37%; 40%), loneliness (12%; 17%; 19%; 22%), and lower life satisfaction (73%; 63%; 58%; 54%). Older adults in the last years of life report a high prevalence of lifetime traumatic events which are associated with worse end-of-life physical and psychosocial health. A trauma-informed approach to end-of-life care and management of physical and psychosocial needs may improve a patient's quality of life.

Maternal influences on offspring food allergy.

The prevalence of allergies has been globally escalating. While allergies could appear at any age, they often develop in early life. However, the significant knowledge gap in the field is the mechanisms by which allergies affect certain people but not others. Investigating early factors and events in neonatal life that have a lasting impact on determining the susceptibilities of children to develop allergies is a significant area of the investigation as it promotes the understanding of neonatal immune system that mediates tolerance versus allergies. This review focuses on the research over the recent 10 years regarding the potential maternal factors that influence offspring allergies with a view to food allergy, a potentially life-threatening cause of anaphylaxis. The role of breast milk, maternal diet, maternal antibodies, and microbiota that have been suggested as key maternal factors regulating offspring allergies are discussed here. We also suggest future research area to expand our knowledge of maternal-offspring interactions on the pathogenesis of food allergy.

Maternal separation during lactation affects recognition memory, emotional behaviors, hippocampus and gut microbiota composition in C57BL6J adolescent female mice

BackgroundMaternal separation (MS) in rodents is a paradigm of early life events that affects neurological development in depression. Adolescence is a time of dramatic increases in psychological vulnerability, and being female is a depression risk factor. However, data on whether different MS scenarios affect behavioral deficits and the potential mechanisms in adolescent female mice are limited. MethodsC57BL/6 J female pups were exposed to different MS (no MS, NMS; MS for 15 min/day, MS15; or 180 min/day, MS180) from postnatal day (PND)1 to PND21 and subjected for behavioral tests during adolescence. Behavioural tests, specifically the open field test (OFT), novel object recognition test (NOR) test and tail suspension test (TST), were performed. The expression of proinflammatory cytokines, hippocampal neurogenesis, neuroinflammation, and gut microbiota were also assessed. ResultsThe results showed that MS180 induced emotional behavioral deficits and object recognition memory impairment; however, MS15 promoted object recognition memory in adolescent females. MS180 decreased hippocampal neurogenesis of adolescent females, induced an increase in microgliosis, and increased certain inflammatory factors in the hippocampus, including TNF-α, IL-1β, and IL-6. Furthermore, different MS altered gut microbiota diversity, and alpha diversity in the Shannon index was negatively correlated with the peripheral inflammatory factors TNF-α, IL-1β, and IL-6. Species difference analysis showed that the gut microbiota composition of the phyla Desulfobacterota and Proteobacteria was affected by the MS. LimitationsThe sex differences in adolescent animal and causality of hippocampal neurogenesis and gut microbiota under different MS need to be further analyzed in depression. ConclusionThis study indicates different MS affect recognition memory and emotional behaviors in adolescent females, and gut microbiota-neuroinflammation and hippocampal neurogenesis may be a potential site of early neurodevelopmental impairment in depression.

Social Norms and the Impact of Early Life Events on Gender Inequality

Social Norms and the Impact of Early Life Events on Gender Inequality

Role of stress and early-life stress in the pathogeny of inflammatory bowel disease.

Numerous preclinical and clinical studies have shown that stress is one of the main environmental factor playing a significant role in the pathogeny and life-course of bowel diseases. However, stressful events that occur early in life, even during the fetal life, leave different traces within the central nervous system, in area involved in stress response and autonomic network but also in emotion, cognition and memory regulation. Early-life stress can disrupt the prefrontal-amygdala circuit thus favoring an imbalance of the autonomic nervous system and the hypothalamic-pituitary adrenal axis, resulting in anxiety-like behaviors. The down regulation of vagus nerve and cholinergic anti-inflammatory pathway favors pro-inflammatory conditions. Recent data suggest that emotional abuse at early life are aggravating risk factors in inflammatory bowel disease. This review aims to unravel the mechanisms that explain the consequences of early life events and stress in the pathophysiology of inflammatory bowel disease and their mental co-morbidities. A review of therapeutic potential will also be covered.

Early-life gut bacterial community structure predicts disease risk and athletic performance in horses bred for racing

Gut bacterial communities have a profound influence on the health of humans and animals. Early-life gut microbial community structure influences the development of immunological competence and susceptibility to disease. For the Thoroughbred racehorse, the significance of early-life microbial colonisation events on subsequent health and athletic performance is unknown. Here we present data from a three-year cohort study of horses bred for racing designed to explore interactions between early-life gut bacterial community structure, health events in later life and athletic performance on the racetrack. Our data show that gut bacterial community structure in the first months of life predicts the risk of specific diseases and athletic performance up to three years old. Foals with lower faecal bacterial diversity at one month old had a significantly increased risk of respiratory disease in later life which was also associated with higher relative abundance of faecal Pseudomonadaceae. Surprisingly, athletic performance up to three years old, measured by three different metrics, was positively associated with higher faecal bacterial diversity at one month old and with the relative abundance of specific bacterial families. We also present data on the impact of antibiotic exposure of foals during the first month of life. This resulted in significantly lower faecal bacterial diversity at 28 days old, a significantly increased risk of respiratory disease in later life and a significant reduction in average prize money earnings, a proxy for athletic performance. Our study reveals associations between early-life bacterial community profiles and health events in later life and it provides evidence of the detrimental impact of antimicrobial treatment in the first month of life on health and performance outcomes in later life. For the first time, this study demonstrates a relationship between early-life gut bacterial communities and subsequent athletic performance that has implications for athletes of all species including humans.

Assessing the impact of hatching system and body weight on the growth performance, caecal short-chain fatty acids, and microbiota composition and functionality in broilers

BackgroundVariations in body weight (BW) remain a significant challenge within broiler flocks, despite uniform management practices. Chicken growth traits are influenced by gut microbiota, which are in turn shaped by early-life events like different hatching environments and timing of first feeding. Chicks hatched in hatcheries (HH) experience prolonged feed deprivation, which could adversely impact early microbiota colonization. Conversely, hatching on-farm (HOF) allows early feeding, potentially fostering a more favorable gut environment for beneficial microbial establishment. This study investigates whether BW differences among broilers are linked to the disparities in gut microbiota characteristics and whether hatching systems (HS) impact the initial microbial colonization of broilers differing in BW, which in turn affects their growth patterns. Male Ross-308 chicks, either hatched in a hatchery or on-farm, were categorized into low (LBW) and high (HBW) BW groups on day 7, making a two-factorial design (HS × BW). Production parameters were recorded periodically. On days 7, 14, and 38, cecal volatile fatty acid (VFA) and microbiota composition and function (using 16 S rRNA gene sequencing and PICRUSt2) were examined.ResultsHOF chicks had higher day 1 BW, but HH chicks caught up within first week, with no further HS-related performance differences. The HBW chicks remained heavier attributed to higher feed intake rather than improved feed efficiency. HBW group had higher acetate concentration on day 14, while LBW group exhibited higher isocaproate on day 7 and isobutyrate on days 14 and 38. Microbiota analyses revealed diversity and composition were primarily influenced by BW than by HS, with HS having minimal impact on BW-related microbiota. The HBW group on various growth stages was enriched in VFA-producing bacteria like unclassified Lachnospiraceae, Alistipes and Faecalibacterium, while the LBW group had higher abundances of Lactobacillus, Akkermansia and Escherichia-Shigella. HBW microbiota presented higher predicted functional potential compared to the LBW group, with early colonizers exhibiting greater metabolic activity than late colonizers.ConclusionsDespite differences in hatching conditions, the effects of HS on broiler performance were transient, and barely impacting BW-related microbiota. BW variations among broilers are likely linked to differences in feed intake, VFA profiles, and distinct microbiota compositions and functions.

Acute Postnatal Inflammation Alters Adult Microglial Responses to LPS that Are Sex-, Region- and Timing of Postnatal Inflammation-Dependent.

Adverse events in early life can have impact lasting into adulthood. We investigated the long-term effects of systemic inflammation during postnatal development on adult microglial responses to LPS in two CNS regions (cortex, cervical spinal cord) in male and female rats. Inflammation was induced in Sprague-Dawley rats by lipopolysaccharide (LPS, 1 mg/kg) administered intraperitoneally during postnatal development at P7, P12 or P18. As adults (12 weeks of age), the rats received a second LPS dose (1 mg/kg). Control rats received saline. Microglia were isolated 3 hours post-LPS from the cortex and cervical spinal cord. Gene expression was assessed via qRT-PCR for pro-inflammatory (IL-6, iNOS, Ptgs2, C/EBPb, CD14, CXCL10), anti-inflammatory (CD68, Arg-1), and homeostatic genes (P2Y12, Tmemm119). CSF-1 and CX3CL1 mRNA was analyzed in microglia-free homogenates. Basal gene expression in adult microglia was largely unaffected by early life LPS. Changes in adult microglial pro-inflammatory genes in response to LPS were either unchanged or attenuated in rats exposed to LPS during postnatal development. Ptgs2, C/EBPb, CXCL10 and Arg-1 were the genes most affected, with expression levels significantly downregulated vs control rats without postnatal LPS exposure. Cortical microglia were affected more by postnatal inflammation than spinal microglia, and males were more impacted than females. Overall, inflammatory challenge at P18 had the greatest effect on adult microglial gene expression, whereas challenge at P7 had less impact. Microglial homeostatic genes were unaffected by postnatal LPS. Long-lasting effects of postnatal inflammation on adult microglia depend on the timing of postnatal inflammation, CNS region and sex.

Beyond identity and generations: bringing life course theory to studies of older gay men.

The last century's numerous, rapid social changes affecting gay men make studies of gay male aging a ripe topic for life course theory, which views later life as the product of historical grounded interchanges between individual lives, social change, and structural contexts. That identifying as gay can occur at any point in the life course widens some life course theorists' primary focus on early-life events to include those occurring throughout the life course. Yet most historically-attentive research on older gay men focuses on generations and identity development rather than on cohorts - groups who entered a system or context at the same time - or on the cumulative, concrete outcomes of encountering social change at a particular point in the life course. This article argues for gay male aging studies' use of life course theory, specifically, its focus on cohort membership's implications for later life, including cumulative disadvantage, in addition to more generationally-focused investigations. After briefly reviewing scholarship on older gay men, we introduce the life course approach and its critique by queer gerontologists for adopting a heteronormative view of the LGBT life course and eliding its distinctive contours. With particular attention to later-life concrete outcomes rather than identity formation, we explore key historical events in gay men's lives that have produced (in the case of the AIDS epidemic) or could produce (for example, the Marriage Equality Act, the Don't Ask, Don't Tell policy) distinctive gay male cohorts. We then consider intra-cohort variation within gay male cohorts before exploring some the barriers to investigating cohorts and cohort effects among older gay men.

Association between maternal depression symptoms and child telomere length

The biological mechanisms that explain how adverse early life events influence adult disease risk are poorly understood. One proposed mechanism is via the induction of accelerated biological aging, for which telomere length is considered a biomarker. We aimed to determine if maternal depression pre- and post-partum was associated with telomere length in children at 4 years of age (n = 4299). Mothers completed structured questionnaires assessing depression during pregnancy (Edinburgh Depression Scale), at 9 months (Edinburgh Depression Scale), and at 54 months postpartum (Patient Health Questionnaire 9). Regression methods were used to investigate the relationship between telomere length (DNA from saliva) and maternal depression score recorded at each stage. Significant covariates included in the final model were: maternal age at pregnancy; child sex; child ethnicity; gestational age group, and rurality group. Child telomere length was found to be longer if their mother had a higher depression score at both postpartum time points tested (9 months of age; coefficient 0.003, SE = 0.001, P = 0.01, 54 months of age; coefficient 0.003, SE = 0.002, P = 0.02). Although these findings seem paradoxical, increased telomere length may be an adaptive response to early life stressors. We propose several testable hypotheses for these results and to determine if the positive association between depression and telomere length is a developmental adaptation or an indirect consequence of environmental factors.

Paternal use of selective serotonin reuptake inhibitors and adverse health outcomes: A nationwide cohort study on 13,547 exposed children.

The use of selective serotonin reuptake inhibitors (SSRIs) has increased over time. Several studies indicate that paternal use of medication may adversely affect the developing fetus. Only a few studies have investigated the association between preconceptional paternal exposure to SSRIs and the risks of adverse health outcomes in children. This study aimed to assess adverse birth outcomes and adverse early life events in children fathered by men using SSRIs prior to conception. All live-born singleton children born in Denmark from 1997 until 2019 and their parents were included. The exposed cohort comprised all children fathered by men using SSRIs 3 months prior to conception and the unexposed cohort comprised all other children. We estimated the odds ratios for adverse birth outcomes: small for gestational age (SGA), preterm birth, low Apgar score, and major congenital malformations. Furthermore, we estimated the hazard ratios for adverse early life events of infections and hospitalizations within 1 year from birth. We also examined adverse birth outcomes and the adverse early life events according to SSRI subgroups. There was a statistically significantly increased odds ratio 1.15 (confidence interval, CI: 1.06-1.23) for preterm birth. No significant results were found for SGA, low Apgar score, and major congenital malformations. The adjusted hazard ratios for hospitalizations and infections were 1.06 (CI: 1.02-1.11) and 1.02 (CI: 0.97-1.07), respectively. There was a statistically significantly increased odds ratio for preterm birth with respect to the SSRI subgroups citalopram and escitalopram, and for hospitalizations with respect to citalopram. Although the risks of certain adverse birth and adverse early life outcomes were statistically significantly increased, the ratios were small and may have limited clinical importance. Paternal use of SSRI was in general safe in the preconceptual period.

Correction to “Interplay of early negative life events, development of orbitofrontal cortical thickness and depression in young adulthood”

Correction to “Interplay of early negative life events, development of orbitofrontal cortical thickness and depression in young adulthood”

Impact of a group-based, compassion-focused treatment on shame and early life events among male prisoners

Impact of a group-based, compassion-focused treatment on shame and early life events among male prisoners

Main Biological Models of Resilience.

Resilience is a complex process of adaptation to new conditions that would permit a positive outcome after adversities, traumas or other sources of stress. However, despite the growing interest in this topic, there is no universally accepted definition and no comprehensive bio-behavioural model. This systematic review aims to provide an overview of the main biological models that have been theorized to date, with a focus on new alternative theories to improve our understanding of the mechanisms underlying the development and strengthening of resilience, with potential implications for the prevention of some psychopathological disorders. This review was conducted according to PRISMA guidelines and includes 185 studies published in English in PubMed and Embase up to December 2023. Most studies use the stress-related model, which conceptualizes resilience as the absence of symptoms after the stressful event and mainly deal with the differences between stress-prone and resilient phenotypes in animals exposed to stress. However, the results of this search seem to suggest that resilience might be an independent construct with biological bases rooted in the stress system and the social brain, and widely sculptured by individual and environmental factors, especially early life events and affiliation. This work contributes to ongoing efforts to understand the intricate mechanisms of resilience, while highlighting the potential of improving social relationships since our birth to promote coping strategies towards stress and traumas, and even a peaceful world.

Developmental priming of early cerebrovascular ageing: Implications across a lifetime.

Neurological conditions such as Alzheimer's disease and stroke represent a substantial health burden to the world's ageing population. Cerebrovascular dysfunction is a key contributor to these conditions, affecting an individual's risk profile, age of onset, and severity of neurological disease. Recent data shows that early-life events, such as maternal health during pregnancy, birth weight and exposure to environmental toxins can 'prime' the vascular system for later changes. With age, blood vessels can become less flexible and more prone to damage. This can lead to reduced blood flow to the brain, which is associated with cognitive decline and an increased risk of stroke and other cerebrovascular diseases. These in turn increase the risk of vascular dementia and Alzheimer's disease. We aim to explore how early life factors influence cerebrovascular health, ageing and disease. We have reviewed recently published literature from epidemiological studies, clinical cases and basic research which explore mechanisms that contribute to cerebrovascular and blood-brain barrier dysfunction, with a particularly focus on those that assess contribution of early-life events or vascular priming to subsequent injury. Perinatal events have been linked to acute cerebrovascular dysfunction and long-term structural reorganisation. Systemic disease throughout the lifetime that produce inflammatory or oxidative stress may further sensitise the cerebrovasculature to disease and contribute to neurodegeneration. By identifying these early-life determinants and understanding their mechanisms, scientists aim to develop strategies for preventing or mitigating cerebrovascular ageing-related issues.

The long-term effects of childhood circumstances on older individuals: A systematic review.

Childhood experiences are known to shape individuals' development and can influence various aspects of life later on. Understanding the long-term effects is crucial for informing interventions and policies aimed at promoting healthy aging. This review aimed to explore the long-term effects of childhood experiences on older individuals. This systematic review comprised three distinct phases. Firstly, a systematic review was conducted, exploring databases such as Google Scholar, PubMed, EMBASE, PsycINFO, and the Web of Science. Out of the 2116 studies initially identified, 24 studies were selected based on the inclusion criteria. Secondly, these inclusion criteria were applied to ensure that the chosen studies specifically delved into the connection between childhood experiences and outcomes in older individuals. Finally, data extraction and synthesis techniques were employed to analyze findings, facilitating the drawing of conclusions concerning the enduring impacts of childhood experiences on the well-being of older individuals. The review's findings revealed how negative experiences in childhood continue to affect older individuals in various ways. These early-life events have far-reaching consequences, profoundly impacting their physical health, making them more susceptible to chronic diseases and weakening their immune system. Additionally, they affect mental health, leading to conditions like depression, anxiety, and substance abuse. Cognitive function is also affected, resulting in memory problems and cognitive decline. Furthermore, these experiences impact social relationships, affecting trust, emotional control, and social isolation in later life. This review highlighted the enduring influence of childhood circumstances on the health and well-being of older individuals. Policymakers and health care practitioners should consider these findings when developing strategies to support healthy aging and mitigate the long-term effects of adverse childhood experiences.

Emotional repression in patients with chronic inflammatory rheumatism

Background: A person’s psychological background may support and direct the inflammatory evolution of a disease toward a specific type of chronic inflammatory rheumatism (CIR). Aim: This study aimed to identify a particular emotional profile of patients with CIR, particularly rheumatoid arthritis (RA) and spondyloarthritis (SpA), based on psychological profile assessments between patients with and without CIR. Emotional repression, that is, a tendency to inhibit the expression of negative feelings and/or unpleasant thoughts, was particularly studied. Methods: This monocentric observational pilot study included patients from the rheumatology department of a university hospital. These patients were systematically assessed for different psychological parameters by an experienced psychiatrist, and their clinical and biological characteristics were collected accordingly. Data analysis was performed using the Chi-squared test or Fisher’s exact test. Results: Fifty-nine patients were assessed: 47 patients with CIR (i.e., 27 with RA and 20 with SpA) (CIR group) and 12 non-CIR patients (i.e., nine with osteoarthritis, one with viral disease, one with osteoporosis, and one with osteomalacia) (control group). Severe emotional repression and early life events were both significantly higher in the CIR group than in the control group (P = 0.02). In contrast, severe psychological and somatic complaints were significantly higher in the control group than in the CIR group (P &lt; 0.01 and P = 0.01, respectively). Conclusion: Our findings suggested that emotional repression from traumatic life events could aggravate the etiology and/or course of CIR. Therefore, appropriate psychological care should have a relevant place within the current therapeutic options for the clinical management of CIR. Relevance for Patients: The management of CIR should include psychological support as learning coping mechanisms can facilitate the recovery of CIR patients.

Intergenerational protective anti-gut commensal immunoglobulin G originates in early life

Maternal immunoglobulins of the class G (IgGs) protect offspring from enteric infection, but when, where, and how these antibodies are physiologically generated and confer protection remains enigmatic. We found that circulating IgGs in adult mice preferentially bind early-life gut commensal bacteria over their own adult gut commensal bacteria. IgG-secreting plasma cells specific for early-life gut bacteria appear in the intestine soon after weaning, where they remain into adulthood. Manipulating exposure to gut bacteria or plasma cell development before, but not after, weaning reduced IgG-secreting plasma cells targeting early-life gut bacteria throughout life. Further, the development of this anti-gut commensal IgG response coincides with the early-life interval in which goblet cell-associated antigen passages (GAPs) are present in the colon. Offspring of dams "perturbed" by B cell ablation or reduced bacterial exposure in early life were more susceptible to enteric pathogen challenge. In contrast to current concepts, protective maternal IgGs targeted translocating gut commensals in the offspring, not the enteric pathogen. These early-life events affecting anti-commensal IgG production have intergenerational effects for protection of the offspring.

Persistence of fish populations to longer, more intense, and more frequent mass mortality events.

Over the last decades, mass mortality events have become increasingly common across taxa with sometimes devastating effects on population biomass. In the aquatic environment, fish are sensitive to mass mortality events, particularly at the early life stages that are crucial for population dynamics. However, it has recently been shown for fish, that a single mass mortality event in early life typically does not lead to population collapse. Moreover, the frequency and intensity of extreme events that can cause mass mortality, such as marine heatwaves, are increasing. Here, we show that increasing frequency and intensity of mass mortality events may lead to population collapse. Since the drivers of mass mortality events are diverse, and often linked to climate change, it is challenging to predict the frequency and severity of future mass mortality events. As an alternative, we quantify the probability of population collapse depending on the frequency and intensity as well as the duration of mass mortality events. Based on 39 fish species, we show that the probability of collapse typically increases with increasing frequency, intensity, and duration of the mortality events. In addition, we show that the collapse depends on key traits such as natural mortality, recruitment variation, and density dependence. The presented framework provides quantitative estimates of the sensitivity of fish species to these increasingly common extreme events, which paves the way for potential mitigation actions to alleviate adverse impacts on harvested fish populations across the globe.