Type 1 diabetes-early life origins and changing epidemiology.
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ABSTRACT:
SUBMITTER: Norris JM
PROVIDER: S-EPMC7332108 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The origins and neural bases of the current opioid addiction epidemic are unclear. Genetics plays a major role in addiction vulnerability, but cannot account for the recent exponential rise in opioid abuse, so environmental factors must contribute. Individuals with history of early life adversity (ELA) are disproportionately prone to opioid addiction, yet whether ELA interacts with factors such as increased access to opioids to directly influence brain development and function, and cause opioid addiction vulnerability, is unknown. We simulated ELA in female rats and this led to a striking opioid addiction-like phenotype. This was characterized by resistance to extinction, increased relapse-like behavior, and, as in addicted humans, major increases in opioid economic demand. By contrast, seeking of a less salient natural reward was unaffected by ELA, whereas demand for highly palatable treats was augmented. These discoveries provide novel insights into the origins and nature of reward circuit malfunction that may set the stage for addiction.
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Project description:ObjectiveEnvironmental microbial exposures have been implicated to protect against immune-mediated diseases such as type 1 diabetes. Our objective was to study the association of land cover around the early-life dwelling with the development of islet autoimmunity and type 1 diabetes to evaluate the role of environmental microbial biodiversity in the pathogenesis.Research design and methodsAssociation between land cover types and the future risk of type 1 diabetes was studied by analyzing land cover types classified according to Coordination of Information on the Environment (CORINE) 2012 and 2000 data around the dwelling during the first year of life for 10,681 children genotyped for disease associated HLA-DQ alleles and monitored from birth in the Type 1 Diabetes Prediction and Prevention (DIPP) study. Land cover was compared between children who developed type 1 diabetes (n = 271) or multiple diabetes-associated islet autoantibodies (n = 384) and children without diabetes who are negative for diabetes autoantibodies.ResultsAgricultural land cover around the home was inversely associated with diabetes risk (odds ratio 0.37, 95% CI 0.16-0.87, P = 0.02 within a distance of 1,500 m). The association was observed among children with the high-risk HLA-genotype and among those living in the southernmost study region. Snow cover on the ground seemed to block the transfer of the microbial community indoors, leading to reduced bacterial richness and diversity indoors, which might explain the regional difference in the association. In survival models, an agricultural environment was associated with a decreased risk of multiple islet autoantibodies (hazard ratio [HR] 1.60, P = 0.008) and a decreased risk of progression from single to multiple autoantibody positivity (HR 2.07, P = 0.001) compared with an urban environment known to have lower environmental microbial diversity.ConclusionsThe study suggests that exposure to an agricultural environment (comprising nonirrigated arable land, fruit trees and berry plantations, pastures, natural pastures, land principally occupied by agriculture with significant areas of natural vegetation, and agroforestry areas) early in life is inversely associated with the risk of type 1 diabetes. This association may be mediated by early exposure to environmental microbial diversity.
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Project description:CONTEXT:Epidemiology is a discipline which has evolved with the changes taking place in society and the emergence of new diseases and new discipline related to epidemiology. With these evolutions, it is important to understand epidemiology and to analyse the evolution of content of definitions of epidemiology. OBJECTIVES:The main objective of this paper was to identify new definitions of epidemiology available since 1978. Secondary objectives were to analyse the content of these definitions, to compare them with those used by Lilienfeld and to determine whether changes have taken place over the last forty years. METHODS:A review of grey literature and published literature was conducted to find the definitions of epidemiology written between 1978 and 2017. RESULTS:102 definitions of epidemiology were retained. They helped to highlight 20 terms and concepts related to epidemiology. Most of them were already used in the definitions used by Lilienfeld. Five terms were present in more than 50% of definitions from the period 1978 to 2017: "population", "study", "disease", "health" and "distribution". Several developments have occurred: strengthening of the terms "control" and "health" already used, the concept of "disease" was less frequently encountered whereas the concepts "infectious diseases", "mass phenomenon" are no longer used in definitions from 1978 to 2017. CONCLUSION:This evolution of content of definition of epidemiology is absent from books on epidemiology. A thematic analysis of definitions of epidemiology could be conducted in order to improve our understanding of changes observed.
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Project description:Ongoing rapid domestication of Atlantic salmon implies that individuals are subjected to evolutionarily novel stressors encountered under conditions of artificial rearing, requiring new levels and directions of flexibility in physiological and behavioural coping mechanisms. Phenotypic plasticity to environmental changes is particularly evident at early life stages. We investigated the performance of salmon, previously subjected to an unpredictable chronic stress (UCS) treatment at an early age (10 month old parr), over several months and life stages. The UCS fish showed overall higher specific growth rates compared with unstressed controls after smoltification, a particularly challenging life stage, and after seawater transfer. Furthermore, subjecting fish to acute stress at the end of the experiment, we found that UCS groups had an overall lower hypothalamic catecholaminergic and brain stem serotonergic response to stress compared with control groups. In addition, serotonergic activity was negatively correlated with final growth rates, which implies that serotonin responsive individuals have growth disadvantages. Altogether, our results may imply that a subdued monoaminergic response in stressful farming environments may be beneficial, because in such situations individuals may be able to reallocate energy from stress responses into other life processes, such as growth.
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Project description:As adult brain structure is primarily established in early life, genetic and environmental exposures in infancy and childhood influence the risk for Alzheimer disease (AD). In this systematic review, we identified several early life risk factors and discussed the evidence and underlying mechanism for each.Early risk factors for AD may alter brain anatomy, causing vulnerability to AD-related dementia later in life. In the perinatal period, both genes and learning disabilities have been associated with the development of distinct AD phenotypes. During early childhood, education and intellect, as well as body growth, may predispose to AD through alterations in cognitive and brain reserve, though the specific mediators of neural injury are disputed. Childhood socioeconomic status (SES) may predispose to AD by influencing adult SES and cognition. Association of these risk factors with underlying AD pathology (rather than just clinical diagnosis) has not been sufficiently examined.Factors that impede or alter brain growth during early life could render certain brain regions or networks selectively vulnerable to the onset, accumulation or spread of AD-related pathology during later life. Careful life-course epidemiology could provide clues as to why the brain systematically degenerates during AD.
| S-EPMC4679687 | biostudies-literature
Project description:AIM:Diabetic kidney disease is one of the leading complications of Type 1 diabetes, but its prediction remains a challenge. We examined predictors of rapid decline in estimated GFR (eGFR) in two Type 1 diabetes cohorts: the Coronary Artery Calcification in Type 1 Diabetes (CACTI) and the Pittsburgh Epidemiology of Diabetes Complications (EDC). METHODS:A select subset of participants (CACTI: n = 210 and EDC: n = 98) diagnosed before 17 years of age with Type 1 diabetes duration ? 7 years, and follow-up data on eGFR by CKD-EPI creatinine for up to 8 years were included in the analyses. Early renal function decline was defined as annual decline in eGFR ? 3 ml/min/1.73 m2 , and normal age-related decline as eGFR ? 1 ml/min/1.73 m2 . Parallel logistic regression models were constructed in the two cohorts. RESULTS:Early renal function decline incidence was 36% in CACTI and 41% in EDC. In both cohorts, greater baseline eGFR (CACTI: OR 3.12, 95% CI 1.97-5.05; EDC: OR 1.92, 95% CI 1.17-3.15 per 10 ml/min/1.73 m2 ) and log albumin-to-creatinine (ACR) (CACTI: OR 3.24, 95% CI 1.80-5.83; EDC: OR 1.87, 95% CI 1.18-2.96 per 1 unit) predicted greater odds of early renal function decline in fully adjusted models. Conversely, ACE inhibition predicted lower odds of early renal function decline in women in CACTI, but similar relationships were not observed in women in EDC. CONCLUSIONS:A substantial proportion of people with Type 1 diabetes in the EDC and CACTI cohorts experienced early renal function decline over time. ACE inhibition appeared to be protective only in women in CACTI where the prevalence of its use was twofold higher compared with the EDC.
| S-EPMC5647234 | biostudies-literature
Project description:ObjectiveType 2 diabetes develops for many years before diagnosis. We aimed to reveal early metabolic features characterizing liability to adult disease by examining genetic liability to adult type 2 diabetes in relation to metabolomic traits across early life.Research design and methodsUp to 4,761 offspring from the Avon Longitudinal Study of Parents and Children were studied. Linear models were used to examine effects of a genetic risk score (162 variants) for adult type 2 diabetes on 229 metabolomic traits (lipoprotein subclass-specific cholesterol and triglycerides, amino acids, glycoprotein acetyls, and others) measured at age 8 years, 16 years, 18 years, and 25 years. Two-sample Mendelian randomization (MR) was also conducted using genome-wide association study data on metabolomic traits in an independent sample of 24,925 adults.ResultsAt age 8 years, associations were most evident for type 2 diabetes liability (per SD higher) with lower lipids in HDL subtypes (e.g., -0.03 SD [95% CI -0.06, -0.003] for total lipids in very large HDL). At 16 years, associations were stronger with preglycemic traits, including citrate and with glycoprotein acetyls (0.05 SD; 95% CI 0.01, 0.08), and at 18 years, associations were stronger with branched-chain amino acids. At 25 years, associations had strengthened with VLDL lipids and remained consistent with previously altered traits, including HDL lipids. Two-sample MR estimates among adults indicated persistent patterns of effect of disease liability.ConclusionsOur results support perturbed HDL lipid metabolism as one of the earliest features of type 2 diabetes liability, alongside higher branched-chain amino acid and inflammatory levels. Several features are apparent in childhood as early as age 8 years, decades before the clinical onset of disease.
| S-EPMC7305012 | biostudies-literature
Project description:BackgroundInfections in early life have been linked to type 1 diabetes (T1D) risk, but no previous study has comprehensively analysed exposure to antibiotics, acetaminophen and infections during pregnancy and early childhood in relation to offspring risk of T1D.MethodsParticipants in the Norwegian Mother and Child Cohort Study (n = 114 215 children, of whom 403 children were diagnosed with T1D) reported infections and medication use through repeated questionnaires from pregnancy until the children were 18 months old. Adjusted hazard ratios (aHR) for offspring T1D were estimated through Cox regression adjusted for child's sex, maternal age and parity, maternal T1D, smoking in pregnancy, education level, pre-pregnancy body mass index (BMI) and birthweight. Antibiotic use was also analysed in a population-based register cohort of 541 036 children of whom 836 developed T1D.ResultsHospitalization for gastroenteritis during the first 18 months of life was associated with increased risk (aHR 2.27, 95% CI 1.21 - 4.29, P = 0.01) of T1D. Childhood infections not requiring hospitalization, or any kind of maternal infection during pregnancy, did not predict offspring risk of T1D. Antibiotic or acetaminophen use in pregnancy, or child`s use in early childhood, was not associated with risk of T1D.ConclusionsOur study, which is population-based and the largest of its kind, did not find support for general early life infections, infection frequency or use of antibiotics or acetaminophen to play a major role in childhood T1D. Hospital admission for gastroenteritis was associated with T1D risk, but must be interpreted cautiously due to scarcity of cases.
| S-EPMC6208272 | biostudies-literature
Project description:In this ecological study, we used longitudinal data to assess if changes in neighborhood food environments were associated with type 2 diabetes mellitus (T2DM) prevalence, controlling for a host of neighborhood characteristics and spatial error correlation. We found that the population-adjusted prevalence of fast-food and pizza restaurants, grocery stores, and full-service restaurants along with changes in their numbers from 1990 to 2010 were associated with 2015 T2DM prevalence. The results suggested that neighborhoods where fast-food restaurants have increased and neighborhoods where full-service restaurants have decreased over time may be especially important targets for educational campaigns or other public health-related T2DM interventions.
| S-EPMC9860365 | biostudies-literature