Troubled childhoods cast long shadows: Childhood adversity and premature all-cause mortality in a Swedish cohort.
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ABSTRACT:
SUBMITTER: Jackisch J
PROVIDER: S-EPMC6838963 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Events causing stress responses during sensitive periods of rapid neurological development in childhood may be early determinants of all-cause premature mortality. Using a British birth cohort study of individuals born in 1958, the relationship between adverse childhood experiences (ACE) and mortality?50 year was examined for men (n=7,816) and women (n=7,405) separately. ACE were measured using prospectively collected reports from parents and the school: no adversities (70%); one adversity (22%), two or more adversities (8%). A Cox regression model was carried out controlling for early life variables and for characteristics at 23 years. In men the risk of death was 57% higher among those who had experienced 2+ ACE compared to those with none (HR 1.57, 95% CI 1.13, 2.18, p=0.007). In women, a graded relationship was observed between ACE and mortality, the risk increasing as ACE accumulated. Women with one ACE had a 66% increased risk of death (HR 1.66, 95% CI 1.19, 2.33, p=0.003) and those with ?2 ACE had an 80% increased risk (HR 1.80, 95% CI 1.10, 2.95, p=0.020) versus those with no ACE. Given the small impact of adult life style factors on the association between ACE and premature mortality, biological embedding during sensitive periods in early development is a plausible explanatory mechanism.
| S-EPMC3787798 | biostudies-other
Project description:When humans perceive the lightness of an object's surface in shadows there is an implicit assumption that cast shadows dim the surface. In two experiments, we investigated whether 5- to 8-month-old infants make this assumption about shadows. According to this shadow assumption, the apparent change in lightness produced by shadows on an object's surface are attributed to blocked light sources. If infants can use the shadow assumption to perceive the object's lightness in shadows, they will also be able to detect unnatural lightness changes in shadows. We compared the infants' looking times to the unnatural and the natural lightness changes in the shadow when an object (duck) goes through the cast shadow. In Experiment 1, we examined whether infants could detect the unnatural lightness changes of the object's surface in shadows. We created computer-graphic movies of unnatural and natural lightness changes to the duck's surface. Our results showed that 7- to 8-month-olds but not 5- to 6-month-olds significantly preferred the movie with the unnatural changes in lightness, indicating that only the older infants could detect these changes. In Experiment 2, we confirmed that the infants' preference was based on the detection of unnatural lightness changes according to the shadow assumption. The natural and the unnatural lightness changes of Experiment 1 were presented without cast shadows. Under these conditions, neither younger nor older infants showed a significant preference. Taken together, the experiments showed that 7- to 8-month-old infants could detect the unnaturalness of a surface's lightness changes produced by shadows. In conclusion, our findings suggest that 7- to 8-month-old infants can perceive an object's lightness in shadows by using an assumption that cast shadows dim the surface of an object.
| S-EPMC5351879 | biostudies-literature
Project description:BACKGROUND:Pediatric obesity is associated with increased risk of premature death from middle age onward, but whether the risk is already increased in young adulthood is unclear. The aim was to investigate whether individuals who had obesity in childhood have an increased mortality risk in young adulthood, compared with a population-based comparison group. METHODS AND FINDINGS:In this prospective cohort study, we linked nationwide registers and collected data on 41,359 individuals. Individuals enrolled at age 3-17.9 years in the Swedish Childhood Obesity Treatment Register (BORIS) and living in Sweden on their 18th birthday (start of follow-up) were included. A comparison group was matched by year of birth, sex, and area of residence. We analyzed all-cause mortality and cause-specific mortality using Cox proportional hazards models, adjusted according to group, sex, Nordic origin, and parental socioeconomic status (SES). Over 190,752 person-years of follow-up (median follow-up time 3.6 years), 104 deaths were recorded. Median (IQR) age at death was 22.0 (20.0-24.5) years. In the childhood obesity cohort, 0.55% (n = 39) died during the follow-up period, compared to 0.19% (n = 65) in the comparison group (p < 0.001). More than a quarter of the deaths among individuals in the childhood obesity cohort had obesity recorded as a primary or contributing cause of death. Male sex and low parental SES were associated with premature all-cause mortality. Suicide and self-harm with undetermined intent were the main cause of death in both groups. The largest difference between the groups lay within endogenous causes of death, where children who had undergone obesity treatment had an adjusted mortality rate ratio of 4.04 (95% CI 2.00-8.17, p < 0.001) compared with the comparison group. The main study limitation was the lack of anthropometric data in the comparison group. CONCLUSIONS:Our study shows that the risk of mortality in early adulthood may be higher for individuals who had obesity in childhood compared to a population-based comparison group.
| S-EPMC7080224 | biostudies-literature
Project description:This study explores whether there is a short-term relationship between intragenerational social mobility and mortality while individuals are working and whether it is widespread across different causes of death. Net of accumulated advantages and disadvantages, social mobility may influence mortality through health selection or changes in well-being. Men and women working in 1996 up to age 65 are observed annually until 2012 in Swedish register data. Time-varying covariates and origin and destination status are controlled for in discrete time event-history analyses. Results show that when men were upwardly mobile, mortality was lower due to cancer, CVD, IHD, and suicide. Upward mobility was only associated with lower odds of suicide for women. When downwardly mobile, cancer mortality was higher for both men and women and smoking-related cancer mortality was higher for men. Social mobility was not linked to deaths related to accidents and poisoning or alcohol-related mortality. The results may support a relationship between social mobility and mortality characterized by health selection: Only in the case of a chronic illness (cancer) was downward mobility associated with higher mortality. The widespread relationship between upward mobility and lower mortality for men may also indicate positive health selection into attaining a higher class and that individuals with poor health may be less likely to search for better positions or receive promotions.
| S-EPMC6368327 | biostudies-literature
Project description:BackgroundMass unemployment in Europe is endemic, especially among the young. Does it cause mortality?MethodsWe analyzed long-term effects of unemployment occurring during the deep Swedish recession 1992-96. Mortality from all and selected causes was examined in the 6-year period after the recession among those employed in 1990 (3.4 million). Direct health selection was analyzed as risk of unemployment by prior medical history based on all hospitalizations 1981-91. Unemployment effects on mortality were estimated with and without adjustment for prior social characteristics and for prior medical history.ResultsA prior circulatory disease history did not predict unemployment; a history of alcohol-related disease or suicide attempts did, in men and women. Unemployment predicted excess male, but not female, mortality from circulatory disease, both ischemic heart disease and stroke, and from all causes combined, after full adjustment. Adjustment for prior social characteristics reduced estimates considerably; additional adjustment for prior medical history did not. Mortality from external and alcohol-related causes was raised in men and women experiencing unemployment, after adjustment for social characteristics and medical history. For the youngest birth cohorts fully adjusted alcohol mortality HRs were substantial (male HR = 4.44; female HR = 5.73). The effect of unemployment on mortality was not uniform across the population; men, those with a low education, low income, unmarried or in urban employment were more vulnerable.ConclusionsDirect selection by medical history explains a modest fraction of any increased mortality risk following unemployment. Mass unemployment imposes long-term mortality risk on a sizeable segment of the population.
| S-EPMC5054271 | biostudies-literature
Project description:ObjectiveTo investigate the association of spontaneous abortion with the risk of all cause and cause specific premature mortality (death before the age of 70).DesignProspective cohort study.SettingThe Nurses' Health Study II (1993-2017), United States.Participants101 681 ever gravid female nurses participating in the Nurses' Health Study II.Main outcomes measuresLifetime occurrence of spontaneous abortion in pregnancies lasting less than 6 months, determined by biennial questionnaires. Hazard ratios and 95% confidence intervals for all cause and cause specific premature death according to the occurrence of spontaneous abortion, estimated with time dependent Cox proportional hazards models.ResultsDuring 24 years of follow-up, 2936 premature deaths were recorded, including 1346 deaths from cancer and 269 from cardiovascular disease. Crude all cause mortality rates were comparable for women with and without a history of spontaneous abortion (1.24 per 1000 person years in both groups) but were higher for women experiencing three or more spontaneous abortions (1.47 per 1000 person years) and for women reporting their first spontaneous abortion before the age of 24 (1.69 per 1000 person years). The corresponding age adjusted hazard ratios for all cause premature death during follow-up were 1.02 (95% confidence interval 0.94 to 1.11), 1.39 (1.03 to 1.86), and 1.27 (1.11 to 1.46), respectively. After adjusting for confounding factors and updated dietary and lifestyle factors, the occurrence of spontaneous abortion was associated with a hazard ratio of 1.19 (95% confidence interval 1.08 to 1.30) for premature mortality during follow-up. The association was stronger for recurrent spontaneous abortions (hazard ratio 1.59, 95% confidence interval 1.17 to 2.15 for three or more spontaneous abortions; 1.23, 1.00 to 1.50 for two; and 1.16, 1.05 to 1.28 for one compared with none), and for spontaneous abortions occurring early in a woman's reproductive life (1.32, 1.14 to 1.53 for age ≤23; 1.16, 1.01 to 1.33 for ages 24-29; and 1.12, 0.98 to 1.28 for age ≥30 compared with none). When cause specific mortality was evaluated, the association of spontaneous abortion with premature death was strongest for deaths from cardiovascular disease (1.48, 1.09 to 1.99). Spontaneous abortion was not related to premature death from cancer (1.08, 0.94 to 1.24).ConclusionsSpontaneous abortion was associated with an increased risk of premature mortality, particularly death from cardiovascular disease.
| S-EPMC7988453 | biostudies-literature
Project description:Here we show that the 5’ end and 3’ end of Malat1 are dependently and independently expressed. Loss of 5’ Malat1 up-regulates Neat1 in cis, while loss of 3’ Malat1 globally regulated gene expression in trans. Furthermore, loss of 3’ Malat1 accelerates premature aging and shortens the lifespan in mice, but loss of 5’ Malat1 produces no phenotypic changes. Mechanistically, 3’ Malat1 exerts a tight regulation of P21 that is drastically up-regulated in brain and retina upon its deletion in mice. This is very likely mediated at two different levels. One is at the mRNA level since Malat1 interacts with hnRNP A1 and hnRNP A2/B1. This is independently of P53 since it is significantly decreased upon 3’ Malat1 KO, probably due to the down-regulation of hnRNP C which has been shown to maintain P53 mRNA stability in our cell line model. The other is at the protein level through NPM, which is significantly up-regulated in 3’ Malat1 KO and which was known to decrease P21 ubiquitination and hence stabilizing of P21. These observations reveal previously unknown functions of 3’ Malat in the brain and indicates the need for more detailed understanding of highly abundant conserved lncRNAs, such as Malat1, and alarms for detailed understanding before therapeutic targeting in the future.
2022-07-02 | GSE130392 | GEO
Project description:ImportanceChildhood adversity (CA) is a powerful determinant of long-term physical and mental health that is associated with elevated risk for chronic disease and psychopathology. However, the degree to which CA contributes to mortality as a preventable driver of ill-health and death is unknown.ObjectiveTo estimate the contribution of CA to health behaviors, including smoking and sedentary behavior, as well as the annual mortality attributable to CA in the US through influences on leading causes of death (eg, cardiovascular disease).Evidence reviewFor this systematic review, the PsycINFO and MEDLINE databases were searched on November 15, 2019. The databases were searched for publications from inception (1806 for PsycINFO, 1946 for MEDLINE) to November 15, 2019. Meta-analyses of the associations between CA and morbidity outcomes were included. The population attributable fraction (PAF) was calculated from these associations along with the estimated US prevalence of CA. The PAF was then applied to the number of annual deaths associated with each cause of death to estimate the number of deaths that are attributable to CA. Additionally, the PAF was applied to the incidence of health behaviors to derive the number of cases attributable to CA. Exposure to 1 or more experiences of adversity before the age of 18 years was analyzed, including abuse, neglect, family violence, and economic adversity.FindingsA total of 19 meta-analyses with 20 654 832 participants were reviewed. Childhood adversity accounted for approximately 439 072 deaths annually in the US, or 15% of the total US mortality in 2019 (2 854 838 deaths), through associations with leading causes of death (including heart disease, cancer, and suicide). In addition, CA was associated with millions of cases of unhealthy behaviors and disease markers, including more than 22 million cases of sexually transmitted infections, 21 million cases of illicit drug use, 19 million cases of elevated inflammation, and more than 10 million cases each of smoking and physical inactivity. The greatest proportion of outcomes attributable to CA were for suicide attempts and sexually transmitted infections, for which adversity accounted for up to 38% and 33%, respectively.Conclusions and relevanceThe results of this systematic review suggest that CA is a leading contributor to morbidity and mortality in the US and may be considered a preventable determinant of mortality. The prevention of CA and the intervention on pathways that link these experiences to elevated disease risk should be considered a critical public health priority.
| S-EPMC9059254 | biostudies-literature
Project description:Adverse childhood experiences (ACEs) encompass negative, stressful, and potentially traumatic events during childhood, impacting physical and mental health outcomes in adulthood. Limited studies suggest ACEs can have short-term effects on children's gut microbiomes and adult cognitive performance under stress. Nevertheless, the long-term effects of ACEs experienced during adulthood remain unexplored. Thus, this study aimed to assess the long-term effects of ACEs on the gut microbiota of adult nursing students. We employed a multidimensional approach, combining 16S rRNA sequencing, bioinformatics tools, and machine learning to predict functional capabilities. High-ACE individuals had an increased abundance of Butyricimonas spp. and Prevotella spp. and decreased levels of Clostridiales, and Lachnospira spp. Prevotella abundance correlated negatively with L-glutamate and L-glutamine biosynthesis, potentially impacting intestinal tissue integrity. While nursing students with high ACE reported increased depression, evidence for a direct gut microbiota-depression relationship was inconclusive. High-ACE individuals also experienced a higher prevalence of diarrhea. These findings highlight the long-lasting impact of ACEs on the gut microbiota and its functions in adulthood, particularly among nursing students. Further research is warranted to develop targeted interventions and strategies for healthcare professionals, optimizing overall health outcomes.
| S-EPMC10815413 | biostudies-literature
Project description:ObjectiveLittle is known concerning the primary cause(s) of mortality in type 1 diabetes responsible for the excess mortality seen in this population.Research design and methodsThe Allegheny County (Pennsylvania) childhood-onset (age < 18 years) type 1 diabetes registry (n = 1,075) with diagnosis from 1965 to 1979 was used to explore patterns in cause-specific mortality. Cause of death was determined by a mortality classification committee of at least three physician epidemiologists, based on the death certificate and additional records surrounding the death.ResultsVital status for 1,043 (97%) participants was ascertained as of 1 January 2008, revealing 279 (26.0%) deaths overall (141 females and 138 males). Within the first 10 years after diagnosis, the leading cause of death was acute diabetes complications (73.6%), while during the next 10 years, deaths were nearly evenly attributed to acute (15%), cardiovascular (22%), renal (20%), or infectious (18%) causes. After 20 years' duration, chronic diabetes complications (cardiovascular, renal, or infectious) accounted for >70% of all deaths, with cardiovascular disease as the leading cause of death (40%). Women (P < 0.05) and African Americans (P < 0.001) have significantly higher diabetes-related mortality rates than men and Caucasians, respectively. Standardized mortality ratios (SMRs) for non-diabetes-related causes do not significantly differ from the general population (violent deaths: SMR 1.2, 95% CI 0.6-1.8; cancer: SMR 1.2, 0.5-2.0).ConclusionsThe excess mortality seen in type 1 diabetes is almost entirely related to diabetes and its comorbidities but varies by duration of diabetes and particularly affects women and African Americans.
| S-EPMC2992785 | biostudies-literature