The Developmental Origins of Chronic Disease in Later Life

2012 ◽  
pp. 59-83 ◽  
Author(s):  
David J. P. Barker
Keyword(s):  
Chronic Disease ◽  
Later Life ◽  
Developmental Origins

scholarly journals Epigenetics and DOHaD: from basics to birth and beyond

2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne
Keyword(s):  
Dna Methylation ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Early Life ◽  
Later Life ◽  
Metabolic Health ◽  
Number Of Children ◽  
Early Life Environment ◽  
Increased Risk ◽  
Early Life Exposures

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.

scholarly journals Association Between Speed of Multimorbidity Accumulation in Old Age and Life Experiences: A Cohort Study

2019 ◽  
Vol 188 (9) ◽  
pp. 1627-1636 ◽  
Author(s):  
Serhiy Dekhtyar ◽  
Davide Liborio Vetrano ◽  
Alessandra Marengoni ◽  
Hui-Xin Wang ◽  
Kuan-Yu Pan ◽  
...  
Keyword(s):  
Chronic Disease ◽  
Elementary Education ◽  
Chronic Conditions ◽  
Life Experiences ◽  
Laboratory Data ◽  
Later Life ◽  
Adverse Outcomes ◽  
National Study ◽  
Multiple Chronic Conditions ◽  
Medical Histories

Abstract Rapidly accumulating multiple chronic conditions (multimorbidity) during aging are associated with many adverse outcomes. We explored the association between 4 experiences throughout life—childhood socioeconomic circumstances, early-adulthood education, midlife occupational stress, and late-life social network—and the speed of chronic disease accumulation. We followed 2,589 individuals aged ≥60 years from the Swedish National Study on Aging and Care in Kungsholmen for 9 years (2001–2013). Information on life experiences was collected from detailed life-history interviews. Speed of disease accumulation was operationalized as the change in the count of chronic conditions obtained from clinical examinations, medical histories, laboratory data, drug use, and register linkages over 9 years. Linear mixed models were used to analyze the data. Speed of disease accumulation was lower in individuals with more than elementary education (for secondary, β × time = −0.065, 95% CI: −0.126, −0.004; for university, β × time = −0.118, 95% CI: −0.185, −0.050); for active occupations compared with high-strain jobs (β × time = −0.078, 95% CI: −0.138, −0.017); and for richer social networks (for moderate tertile, β × time = −0.102, 95% CI: −0.149, −0.055; for highest tertile, β × time = −0.135, 95% CI: −0.182, −0.088). The association between childhood circumstances and speed of disease accumulation was attenuated by later-life experiences. Diverse experiences throughout life might decelerate chronic disease accumulation during aging.

Searching the web: a survey on the quality of advice on postnatal sequelae of intrauterine growth restriction and the implication of developmental origins of health and disease

2017 ◽  
Vol 8 (5) ◽  
pp. 604-612 ◽  
Author(s):  
S. Perzel ◽  
H. Huebner ◽  
W. Rascher ◽  
C. Menendez-Castro ◽  
A. Hartner ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Later Life ◽  
Growth Restriction ◽  
Developmental Origins ◽  
Intrauterine Growth ◽  
Growing Body ◽  
Health Related ◽  
Health And Disease ◽  
The Individual

Intrauterine growth restriction (IUGR) and fetal growth restriction (FGR) are pregnancy complications associated with morbidity in later life. Despite a growing body of evidence from current research on developmental origins of health and disease (DOHaD), little information is currently provided to parents on long-term metabolic, cardiovascular and neurologic consequences. As parents strongly rely on internet-based health-related information, we examined the quality of information on IUGR/FGR sequelae and DOHaD in webpages used by laypersons. Simulating non-clinicians experience, we entered the terms ‘IUGR consequences’ and ‘FGR consequences’ into Google and Yahoo search engines. The quality of the top search-hits was analyzed with regard to the certification through the Health On the Net Foundation (HON), currentness of cited references, while reliability of information and DOHaD-related consequences were assessed via the DISCERN Plus score (DPS). Overall the citation status was not up-to-date and only a few websites were HON-certified. The results of our analysis showed a dichotomy between the growing body of evidence regarding IUGR/FGR-related sequelae and lack of current guidelines, leaving parents without clear directions. Furthermore, detailed information on the concept of DOHaD is not provided. These findings emphasize the responsibility of the individual physician for providing advice on IUGR/FGR-related sequelae, monitoring and follow-up.

scholarly journals Neighborhoods and Chronic Disease Onset in Later Life

2011 ◽  
Vol 101 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Vicki A. Freedman ◽  
Irina B. Grafova ◽  
Jeannette Rogowski
Keyword(s):  
Chronic Disease ◽  
Disease Onset ◽  
Later Life

scholarly journals Developmental origins of nonalcoholic fatty liver disease as a risk factor for exaggerated metabolic and cardiovascular-renal disease

2018 ◽  
Vol 315 (5) ◽  
pp. E795-E814 ◽  
Author(s):  
Frank T. Spradley ◽  
Jillian A. Smith ◽  
Barbara T. Alexander ◽  
Christopher D. Anderson
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Chronic Disease ◽  
Renal Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Developmental Origins ◽  
Metabolic Dysfunction ◽  
Metabolic Disturbances ◽  
Nonalcoholic Fatty Liver

Intrauterine growth restriction (IUGR) is linked to increased risk for chronic disease. Placental ischemia and insufficiency in the mother are implicated in predisposing IUGR offspring to metabolic dysfunction, including hypertension, insulin resistance, abnormalities in glucose homeostasis, and nonalcoholic fatty liver disease (NAFLD). It is unclear whether these metabolic disturbances contribute to the developmental origins of exaggerated cardiovascular-renal disease (CVRD) risk accompanying IUGR. IUGR impacts the pancreas, adipose tissue, and liver, which are hypothesized to program for hepatic insulin resistance and subsequent NAFLD. NAFLD is projected to become the major cause of chronic liver disease and contributor to uncontrolled type 2 diabetes mellitus, which is a leading cause of chronic kidney disease. While NAFLD is increased in experimental models of IUGR, lacking is a full comprehension of the mechanisms responsible for programming of NAFLD and whether this potentiates susceptibility to liver injury. The use of well-established and clinically relevant rodent models, which mimic the clinical characteristics of IUGR, metabolic disturbances, and increased blood pressure in the offspring, will permit investigation into mechanisms linking adverse influences during early life and later chronic health. The purpose of this review is to propose mechanisms, including those proinflammatory in nature, whereby IUGR exacerbates the pathogenesis of NAFLD and how these adverse programmed outcomes contribute to exaggerated CVRD risk. Understanding the etiology of the developmental origins of chronic disease will allow investigators to uncover treatment strategies to intervene in the mother and her offspring to halt the increasing prevalence of metabolic dysfunction and CVRD.

scholarly journals Developmental Origins of Disease - Crisis Precipitates Change

2016 ◽  
Vol 39 (3) ◽  
pp. 919-938 ◽  
Author(s):  
Christoph Reichetzeder ◽  
Sulistyo Emantoko Dwi Putra ◽  
Jian Li ◽  
Berthold Hocher
Keyword(s):  
Later Life ◽  
Epidemiological Studies ◽  
Developmental Programming ◽  
Noncommunicable Disease ◽  
Developmental Origins ◽  
Comprehensive Overview ◽  
Developmental Origins Of Disease ◽  
Underlying Mechanisms ◽  
Early Life Events ◽  
The Impact

The concept of developmental origins of diseases has gained a huge interest in recent years and is a constantly emerging scientific field. First observations hereof originated from epidemiological studies, linking impaired birth outcomes to adult chronic, noncommunicable disease. By now there is a considerable amount of both epidemiological and experimental evidence highlighting the impact of early life events on later life disease susceptibility. Albeit far from being completely understood, more recent studies managed to elucidate underlying mechanisms, with epigenetics having become almost synonymous with developmental programming. The aim of this review was to give a comprehensive overview of various aspects and mechanisms of developmental origins of diseases. Starting from initial research foci mainly centered on a nutritionally impaired intrauterine environment, more recent findings such as postnatal nutrition, preterm birth, paternal programming and putative interventional approaches are summarized. The review outlines general underlying mechanisms and particularly discusses mechanistic explanations for sexual dimorphism in developmental programming. Furthermore, novel hypotheses are presented emphasizing a non-mendelian impact of parental genes on the offspring's phenotype.

Developmental origins of chronic disease

Public Health ◽  
2012 ◽  
Vol 126 (3) ◽  
pp. 185-189 ◽  
Author(s):  
D.J.P. Barker
Keyword(s):  
Chronic Disease ◽  
Developmental Origins

scholarly journals Developmental origins of health and disease: reducing the burden of chronic disease in the next generation

10.1186/gm135 ◽  
2010 ◽  
Vol 2 (2) ◽  
pp. 14 ◽  
Author(s):  
Peter D Gluckman ◽  
Mark A Hanson ◽  
Murray D Mitchell
Keyword(s):  
Chronic Disease ◽  
Developmental Origins ◽  
Next Generation ◽  
Health And Disease

scholarly journals Health in Transition: Translating developmental origins of health and disease science to improve future health in Africa

2020 ◽  
Keyword(s):  
Public Awareness ◽  
Adult Life ◽  
Later Life ◽  
Research Capacity ◽  
Ageing Population ◽  
Developmental Origins ◽  
Future Health ◽  
Health And Nutrition ◽  
Health And Disease

At STIAS, the ‘Health in Transition’ theme includes a programme to address the epidemic rise in the incidence of non-communicable diseases (NCDs) such as Type 2 diabetes, hypertension, obesity, coronary heart disease and stroke in Africa. The aim is to advance awareness, research capacity and knowledge translation of science related to the Developmental Origins of Health and Disease (DOHaD) as a means of preventing NCDs in future generations. Application of DOHaD science is a promising avenue for prevention, as this field is identifying how health and nutrition from conception through the first 1 000 days of life can dramatically impact a developing individual’s future life course, and specifically predicate whether or not they are programmed in infancy to develop NCDs in later life. Prevention of NCDs is an essential strategy as, if unchecked, the burden of caring for a growing and ageing population with these diseases threatens to consume entire health budgets, as well as negatively impact the quality of life of millions. Africa in particular needs specific, focussed endeavors to realize the maximal preventive potential of DOHaD science, and a means of generating governmental and public awareness about the links between health in infancy and disease in adult life. This volume summarizes the expertise and experience of a leading group of international scientists led by Abdallah Daar brought together at STIAS as part of the ‘Health in Transition’ programme.

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