Developmental origins of health and disease

2018 ◽  
pp. 36-39
Author(s):  
Caroline Fall ◽  
Kalyanaraman Kumaran
Keyword(s):  
Early Life ◽  
Infant Development ◽  
Animal Experiments ◽  
Environmental Pollutants ◽  
Adult Life ◽  
Maternal Diabetes ◽  
Observational Research ◽  
Increased Risk ◽  
Health And Disease ◽  
And Function

Sub-optimal nutrition during foetal and infant development is associated with an increased risk of non-communicable diseases (NCDs) in adult life. Animal experiments show that this results from permanent effects on the structure and function of tissues and hormone systems (‘metabolic programming’), probably mediated by epigenetic changes. NCD risk is increased further by adiposity and/or unhealthy lifestyles in childhood or adulthood. Apart from nutrition, other early life environmental influences can programme later disease, including foetal ‘over-nutrition’ (maternal diabetes or obesity) and exposure to maternal smoking, environmental pollutants, and pregnancy complications. The concept that improving the nutrition and health of mothers pre-conceptionally and during pregnancy could prevent common NCDs has huge public health implications. However, unlike the robust demonstration of programming in experimental animals, the evidence in humans rests mainly on observational research. Intervention studies are ongoing to strengthen the evidence and to identify ways to improve early development and prevent NCDs.

Epigenetics and DOHaD: how translation to predictive testing will require a better public understanding

2021 ◽  
pp. 1-7
Author(s):  
Fiona Lynch ◽  
Sharon Lewis ◽  
Ivan Macciocca ◽  
Jeffrey M. Craig
Keyword(s):  
Health Professionals ◽  
Early Life ◽  
Predictive Testing ◽  
Public Understanding ◽  
Future Research ◽  
Developmental Origins ◽  
Needed Information ◽  
Genes And Environment ◽  
Increased Risk ◽  
Health And Disease

Abstract Epigenetics is likely to play a role in the mediation of the effects of genes and environment in risk for many non-communicable diseases (NCDs). The Developmental Origins of Health and Disease (DOHaD) theory presents unique opportunities regarding the possibility of early life interventions to alter the epigenetic makeup of an individual, thereby modifying their risk for a variety of NCDs. While it is important to determine how we can lower the risk of these NCDs, it is equally important to understand how the public’s knowledge and opinion of DOHaD and epigenetic concepts may influence their willingness to undertake such interventions for themselves and their children. In this review, we provide an overview of epigenetics, DOHaD, NCDs, and the links between them. We explore the issues surrounding using epigenetics to identify those at increased risk of NCDs, including the concept of predictive testing of children. We also outline what is currently understood about the public’s understanding and opinion of epigenetics, DOHaD, and their relation to NCDs. In doing so, we demonstrate that it is essential that future research explores the public’s awareness and understanding of epigenetics and epigenetic concepts. This will provide much-needed information which will prepare health professionals for the introduction of epigenetic testing into future healthcare.

scholarly journals Prevention of overweight and obesity in early life

2018 ◽  
Vol 77 (3) ◽  
pp. 247-256 ◽  
Author(s):  
Julie Lanigan
Keyword(s):  
Risk Factors ◽  
Obesity Prevention ◽  
Early Life ◽  
Complex Interventions ◽  
Adult Life ◽  
Overweight And Obesity ◽  
Childhood Weight ◽  
Increased Risk ◽  
Randomised Controlled ◽  
The Uk

Childhood obesity is a serious challenge for public health. The problem begins early with most excess childhood weight gained before starting school. In 2016, the WHO estimated that 41 million children under 5 were overweight or obese. Once established, obesity is difficult to reverse, likely to persist into adult life and is associated with increased risk of CVD, type 2 diabetes and certain cancers. Preventing obesity is therefore of high importance. However, its development is multi-factorial and prevention is a complex challenge. Modifiable lifestyle behaviours such as diet and physical activity are the most well-known determinants of obesity. More recently, early-life factors have emerged as key influencers of obesity in childhood. Understanding risk factors and how they interact is important to inform interventions that aim to prevent obesity in early childhood. Available evidence supports multi-component interventions as effective in obesity prevention. However, relatively few interventions are available in the UK and only one, TrimTots, has been evaluated in randomised controlled trials and shown to be effective at reducing obesity risk in preschool children (age 1–5 years). BMI was lower in children immediately after completing TrimTots compared with waiting list controls and this effect was sustained at long-term follow-up, 2 years after completion. Developing and evaluating complex interventions for obesity prevention is a challenge for clinicians and researchers. In addition, parents encounter barriers engaging with interventions. This review considers early-life risk factors for obesity, highlights evidence for preventative interventions and discusses barriers and facilitators to their success.

scholarly journals Sex Differences in the Developmental Origins of Cardiovascular Disease

Physiology ◽  
2014 ◽  
Vol 29 (2) ◽  
pp. 122-132 ◽  
Author(s):  
Suttira Intapad ◽  
Norma B. Ojeda ◽  
John Henry Dasinger ◽  
Barbara T. Alexander
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Sex Differences ◽  
Cardiovascular Risk ◽  
Early Life ◽  
Experimental Models ◽  
Developmental Origins ◽  
Proof Of Concept ◽  
Increased Risk ◽  
Health And Disease

The Developmental Origins of Health and Disease (DOHaD) proposes that adverse events during early life program an increased risk for cardiovascular disease. Experimental models provide proof of concept but also indicate that insults during early life program sex differences in adult blood pressure and cardiovascular risk. This review will highlight the potential mechanisms that contribute to the etiology of sex differences in the developmental programming of cardiovascular disease.

scholarly journals Early Life Inflammation and the Developing Hematopoietic and Immune Systems: The Cochlea as a Sensitive Indicator of Disruption

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3596
Author(s):  
Kelly S. Otsuka ◽  
Christopher Nielson ◽  
Matthew A. Firpo ◽  
Albert H. Park ◽  
Anna E. Beaudin
Keyword(s):  
Immune Cells ◽  
Early Life ◽  
Congenital Infection ◽  
Perinatal Infection ◽  
Hematopoietic Stem ◽  
Wide Range ◽  
Infection And Inflammation ◽  
Health And Disease ◽  
And Function ◽  
Future Work

Emerging evidence indicates that perinatal infection and inflammation can influence the developing immune system and may ultimately affect long-term health and disease outcomes in offspring by perturbing tissue and immune homeostasis. We posit that perinatal inflammation influences immune outcomes in offspring by perturbing (1) the development and function of fetal-derived immune cells that regulate tissue development and homeostasis, and (2) the establishment and function of developing hematopoietic stem cells (HSCs) that continually generate immune cells across the lifespan. To disentangle the complexities of these interlinked systems, we propose the cochlea as an ideal model tissue to investigate how perinatal infection affects immune, tissue, and stem cell development. The cochlea contains complex tissue architecture and a rich immune milieu that is established during early life. A wide range of congenital infections cause cochlea dysfunction and sensorineural hearing loss (SNHL), likely attributable to early life inflammation. Furthermore, we show that both immune cells and bone marrow hematopoietic progenitors can be simultaneously analyzed within neonatal cochlear samples. Future work investigating the pathogenesis of SNHL in the context of congenital infection will therefore provide critical information on how perinatal inflammation drives disease susceptibility in offspring.

scholarly journals Intestinal microbiota during early life – impact on health and disease

2014 ◽  
Vol 73 (4) ◽  
pp. 457-469 ◽  
Author(s):  
Lotta Nylund ◽  
Reetta Satokari ◽  
Seppo Salminen ◽  
Willem M. de Vos
Keyword(s):  
Intestinal Microbiota ◽  
Early Life ◽  
Later Life ◽  
Related Factors ◽  
Life Impact ◽  
Health And Disease ◽  
And Function ◽  
The Impact

In the first years after birth, the intestinal microbiota develops rapidly both in diversity and complexity while being relatively stable in healthy adults. Different life-style-related factors as well as medical practices have an influence on the early-life intestinal colonisation. We address the impact of some of these factors on the consecutive microbiota development and later health. An overview is presented of the microbial colonisation steps and the role of the host in that process. Moreover, new early biomarkers are discussed with examples that include the association of microbiota and atopic diseases, the correlation of colic and early development and the impact of the use of antibiotics in early life. Our understanding of the development and function of the intestinal microbiota is constantly improving but the long-term influence of early-life microbiota on later life health deserves careful clinical studies.

scholarly journals Early-Life Nutritional Programming of Health and Disease in The Gambia

2017 ◽  
Vol 70 (3) ◽  
pp. 179-183 ◽  
Author(s):  
Sophie E. Moore
Keyword(s):  
Early Life ◽  
Disease Risk ◽  
Demographic Data ◽  
Nutrition Transition ◽  
Later Life ◽  
Nutritional Deficiencies ◽  
Susceptibility To Infection ◽  
Under Nutrition ◽  
Increased Risk ◽  
Health And Disease

Background: Exposures during early life are increasingly being recognised as factors that play an important role in the aetiology of chronic non-communicable diseases (NCDs). The “Developmental Origins of Health and Disease” (DOHaD) hypothesis asserts that adverse early-life exposures - most notably unbalanced nutrition - leads to an increased risk for a range of NCDs and that disease risk is highest when there is a “mismatch” between the early- and later-life environments. Thus, the DOHaD hypothesis would predict highest risk in settings undergoing a rapid nutrition transition. Summary: We investigated the link between early-life nutritional exposures and long-term health in rural Gambia, West Africa. Using demographic data dating back to the 1940s, the follow-up of randomised controlled trials of nutritional supplementation in pregnancy, and the “experiment of nature” that seasonality in this region provides, we investigated the DOHaD hypothesis in a population with high rates of maternal and infant under-nutrition, a high burden from infectious disease, and an emerging risk of NCDs. Key Messages: Our work in rural Gambia suggests that in populations with high rates of under-nutrition in early life, the immune system may be sensitive to nutritional deficiencies early in life, resulting in a greater susceptibility to infection-related morbidity and mortality.

scholarly journals Nutritional adversity, sex and reproduction: 30 years of DOHaD and what have we learned?

2019 ◽  
Vol 242 (1) ◽  
pp. T51-T68 ◽  
Author(s):  
Patrycja A Jazwiec ◽  
Deborah M Sloboda
Keyword(s):  
Germ Cells ◽  
Early Life ◽  
Disease Risk ◽  
Primordial Germ Cells ◽  
Reproductive Function ◽  
Postnatal Life ◽  
Early Life Adversity ◽  
Increased Risk ◽  
Health And Disease

It is well established that early life environmental signals, including nutrition, set the stage for long-term health and disease risk – effects that span multiple generations. This relationship begins early, in the periconceptional period and extends into embryonic, fetal and early infant phases of life. Now known as the Developmental Origins of Health and Disease (DOHaD), this concept describes the adaptations that a developing organism makes in response to early life cues, resulting in adjustments in homeostatic systems that may prove maladaptive in postnatal life, leading to an increased risk of chronic disease and/or the inheritance of risk factors across generations. Reproductive maturation and function is similarly influenced by early life events. This should not be surprising, since primordial germ cells are established early in life and thus vulnerable to early life adversity. A multitude of ‘modifying’ cues inducing developmental adaptations have been identified that result in changes in reproductive development and impairments in reproductive function. Many types of nutritional challenges including caloric restriction, macronutrient excess and micronutrient insufficiencies have been shown to induce early life adaptations that produce long-term reproductive dysfunction. Many pathways have been suggested to underpin these associations, including epigenetic reprogramming of germ cells. While the mechanisms still remain to be fully investigated, it is clear that a lifecourse approach to understanding lifetime reproductive function is necessary. Furthermore, investigations of the impacts of early life adversity must be extended to include the paternal environment, especially in epidemiological and clinical studies of offspring reproductive function.

scholarly journals Intra-individual methylomics detects the impact of early-life adversity

2018 ◽  
Author(s):  
Shan Jiang ◽  
Noriko Kamei ◽  
Jessica L. Bolton ◽  
Xinyi Ma ◽  
Hal S. Stern ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cell Fate ◽  
Early Life ◽  
Large Scale ◽  
Life Experience ◽  
Early Life Adversity ◽  
Health And Disease ◽  
Genetic And Environmental Factors ◽  
And Function ◽  
The Impact

AbstractGenetic and environmental factors interact during sensitive periods early in life to influence mental health and disease via epigenetic processes such as DNA methylation. However, it is not known if DNA methylation changes outside the brain provide an ‘epigenetic signature’ of early-life experiences. Here, we employed a novel intra-individual approach by testing DNA methylation from buccal cells of individual rats before and immediately after exposure to one week of typical or adverse life experience. We find that whereas inter-individual changes in DNA methylation reflect the effect of age, DNA methylation changes within paired DNA samples from the same individual reflect the impact of diverse neonatal experiences. Genes coding for critical cellular–metabolic enzymes, ion channels and receptors were more methylated in pups exposed to the adverse environment, predictive of their repression. In contrast, the adverse experience was associated with less methylation on genes involved in pathways of death and inflammation as well as cell-fate related transcription factors, indicating their potential upregulation. Thus, intra-individual methylome signatures indicate large-scale transcription-driven alterations of cellular fate, growth and function.

scholarly journals Intra-individual methylomics detects the impact of early-life adversity

2019 ◽  
Vol 2 (2) ◽  
pp. e201800204 ◽  
Author(s):  
Shan Jiang ◽  
Noriko Kamei ◽  
Jessica L Bolton ◽  
Xinyi Ma ◽  
Hal S Stern ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cell Fate ◽  
Early Life ◽  
Large Scale ◽  
Life Experience ◽  
Early Life Adversity ◽  
Health And Disease ◽  
Genetic And Environmental Factors ◽  
And Function ◽  
The Impact

Genetic and environmental factors interact during sensitive periods early in life to influence mental health and disease via epigenetic processes such as DNA methylation. However, it is not known if DNA methylation changes outside the brain provide an “epigenetic signature” of early-life experiences. Here, we used a novel intra-individual approach by testing DNA methylation from buccal cells of individual rats before and immediately after exposure to one week of typical or adverse life experience. We find that whereas inter-individual changes in DNA methylation reflect the effect of age, DNA methylation changes within paired DNA samples from the same individual reflect the impact of diverse neonatal experiences. Genes coding for critical cellular metabolic enzymes, ion channels, and receptors were more methylated in pups exposed to the adverse environment, predictive of their repression. In contrast, the adverse experience was associated with less methylation on genes involved in pathways of death and inflammation as well as cell-fate–related transcription factors, indicating their potential up-regulation. Thus, intra-individual methylome signatures indicate large-scale transcription-driven alterations of cellular fate, growth, and function.

scholarly journals Early Life Factors and Type 2 Diabetes Mellitus

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Xinli Jiang ◽  
Huijie Ma ◽  
Yan Wang ◽  
Yan Liu
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Early Life ◽  
Animal Experiments ◽  
Adult Life ◽  
Later Life ◽  
Negative Effects ◽  
Early Life Factors

Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.

Sign in / Sign up

Export Citation Format

Share Document