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.

scholarly journals Animal models for the study of the developmental origins of health and disease

2009 ◽  
Vol 68 (3) ◽  
pp. 306-320 ◽  
Author(s):  
Sarah McMullen ◽  
Alison Mostyn
Keyword(s):  
Animal Models ◽  
Small Animal ◽  
Later Life ◽  
Epidemiological Studies ◽  
Human Populations ◽  
Developmental Origins ◽  
Advantages And Disadvantages ◽  
Cell Proliferation And Differentiation ◽  
Health And Disease ◽  
Developmental Origins Of Disease

Human epidemiological studies have indicated that the risk of developing non-communicable diseases in later life may be related to exposures during the developmental period. Developmental life is a vulnerable period of the lifespan during which adverse environmental factors have the potential to disturb the processes of cell proliferation and differentiation or to alter patterns of epigenetic remodelling. Animal models have been instrumental in demonstrating the biological plausibility of the associations observed in human populations, providing proof of principle to the theory of the developmental origins of health and disease (DOHaD). A variety of large- and small-animal models have made important contributions to the field, providing strong evidence of a causal relationship between early-life exposures and metabolic risk factors in later life. Studies of animal models are continuing to contribute to improving the understanding of the mechanisms of the developmental origins of disease. All models have their advantages and disadvantages, and the model that is most appropriate for any particular study is hypotheses dependent. The present review aims to briefly summarise the contributions that animal models have made to the DOHaD field, before reviewing the strengths and weaknesses of these animal models. It is proposed that the integration of evidence from a variety of different models is required for the advancement of understanding within the field.

scholarly journals The impact of early nutrition on the ageing trajectory

2014 ◽  
Vol 73 (2) ◽  
pp. 289-301 ◽  
Author(s):  
Jane L. Tarry-Adkins ◽  
Susan E. Ozanne
Keyword(s):  
Animal Models ◽  
Early Life ◽  
Structural Changes ◽  
Molecular Mechanisms ◽  
Later Life ◽  
Epidemiological Studies ◽  
Developmental Programming ◽  
Early Nutrition ◽  
Cellular Ageing ◽  
The Impact

Epidemiological studies, including those in identical twins, and in individualsin uteroduring periods of famine have provided robust evidence of strong correlations between low birth-weight and subsequent risk of disease in later life, including type 2 diabetes (T2D), CVD, and metabolic syndrome. These and studies in animal models have suggested that the early environment, especially early nutrition, plays an important role in mediating these associations. The concept of early life programming is therefore widely accepted; however the molecular mechanisms by which early environmental insults can have long-term effects on a cell and consequently the metabolism of an organism in later life, are relatively unclear. So far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification and microRNA) and permanent changes in cellular ageing. Many of the conditions associated with early-life nutrition are also those which have an age-associated aetiology. Recently, a common molecular mechanism in animal models of developmental programming and epidemiological studies has been development of oxidative stress and macromolecule damage, specifically DNA damage and telomere shortening. These are phenotypes common to accelerated cellular ageing. Thus, this review will encompass epidemiological and animal models of developmental programming with specific emphasis on cellular ageing and how these could lead to potential therapeutic interventions and strategies which could combat the burden of common age-associated disease, such as T2D and CVD.

scholarly journals DIETARY FACTORS AND COGNITIVE DECLINE

2015 ◽  
pp. 1-12
Author(s):  
P.J. Smith ◽  
J.A. Blumenthal
Keyword(s):  
Fatty Acids ◽  
Cognitive Decline ◽  
Randomized Clinical Trials ◽  
Public Health Problem ◽  
Later Life ◽  
Epidemiological Studies ◽  
Dietary Factors ◽  
B Vitamins ◽  
Important Public Health Problem ◽  
The Impact

Cognitive decline is an increasingly important public health problem, with more than 100 million adults worldwide projected to develop dementia by 2050. Accordingly, there has been an increased interest in preventive strategies that diminish this risk. It has been recognized that lifestyle factors including dietary patterns, may be important in the prevention of cognitive decline and dementia in later life. Several dietary components have been examined, including antioxidants, fatty acids, and B vitamins. In addition, whole dietary eating plans, including the Mediterranean diet (MeDi), and the Dietary Approaches to Stop Hypertension (DASH) diet, with and without weight loss, have become areas of increasing interest. Although prospective epidemiological studies have observed that antioxidants, fatty acids, and B vitamins are associated with better cognitive functioning, randomized clinical trials have generally failed to confirm the value of any specific dietary component in improving neurocognition. Several randomized trials have examined the impact of changing ‘whole’ diets on cognitive outcomes. The MeDi and DASH diets offer promising preliminary results, but data are limited and more research in this area is needed.

The impact of maternal obesity on inflammatory processes and consequences for later offspring health outcomes

2017 ◽  
Vol 8 (5) ◽  
pp. 529-540 ◽  
Author(s):  
S. A. Segovia ◽  
M. H. Vickers ◽  
C. M. Reynolds
Keyword(s):  
Maternal Obesity ◽  
Intervention Strategy ◽  
Later Life ◽  
Developmental Programming ◽  
Health Concern ◽  
Low Grade ◽  
Metabolic Complications ◽  
Metabolic Inflammation ◽  
Inflammatory Processes ◽  
The Impact

Obesity is a global epidemic, affecting both developed and developing countries. The related metabolic consequences that arise from being overweight or obese are a paramount global health concern, and represent a significant burden on healthcare systems. Furthermore, being overweight or obese during pregnancy increases the risk of offspring developing obesity and other related metabolic complications in later life, which can therefore perpetuate a transgenerational cycle of obesity. Obesity is associated with a chronic state of low-grade metabolic inflammation. However, the role of maternal obesity-mediated alterations in inflammatory processes as a mechanism underpinning developmental programming in offspring is less understood. Further, the use of anti-inflammatory agents as an intervention strategy to ameliorate or reverse the impact of adverse developmental programming in the setting of maternal obesity has not been well studied. This review will discuss the impact of maternal obesity on key inflammatory pathways, impact on pregnancy and offspring outcomes, potential mechanisms and avenues for intervention.

scholarly journals Developmental Effects of (Pre-)Gestational Diabetes on Offspring: Systematic Screening Using Omics Approaches

Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1991
Author(s):  
Bachuki Shashikadze ◽  
Florian Flenkenthaler ◽  
Jan B. Stöckl ◽  
Libera Valla ◽  
Simone Renner ◽  
...  
Keyword(s):  
Gestational Diabetes ◽  
Biological Fluids ◽  
Later Life ◽  
Maternal Diabetes ◽  
Systematic Screening ◽  
Glucose Levels ◽  
Maternal Metabolism ◽  
Increased Risk ◽  
Underlying Mechanisms ◽  
The Impact

Worldwide, gestational diabetes affects 2–25% of pregnancies. Due to related disturbances of the maternal metabolism during the periconceptional period and pregnancy, children bear an increased risk for future diseases. It is well known that an aberrant intrauterine environment caused by elevated maternal glucose levels is related to elevated risks for increased birth weights and metabolic disorders in later life, such as obesity or type 2 diabetes. The complexity of disturbances induced by maternal diabetes, with multiple underlying mechanisms, makes early diagnosis or prevention a challenging task. Omics technologies allowing holistic quantification of several classes of molecules from biological fluids, cells, or tissues are powerful tools to systematically investigate the effects of maternal diabetes on the offspring in an unbiased manner. Differentially abundant molecules or distinct molecular profiles may serve as diagnostic biomarkers, which may also support the development of preventive and therapeutic strategies. In this review, we summarize key findings from state-of-the-art Omics studies addressing the impact of maternal diabetes on offspring health.

scholarly journals Periconceptional environment and the developmental origins of disease

2019 ◽  
Vol 242 (1) ◽  
pp. T33-T49 ◽  
Author(s):  
Miguel A Velazquez ◽  
Tom P Fleming ◽  
Adam J Watkins
Keyword(s):  
Later Life ◽  
Developmental Origins ◽  
Critical Question ◽  
Physiological Mechanisms ◽  
Maternal Undernutrition ◽  
Increased Risk ◽  
Developmental Origins Of Disease ◽  
Developmental Programme ◽  
And Function ◽  
Maternal Overnutrition

The concept emerging from Professor David Barker’s seminal research on the developmental origins of later-life disease has progressed in many directions since it was first published. One critical question being when during gestation might environment alter the developmental programme with such enduring consequences. Here, we review the growing consensus from clinical and animal research that the period around conception, embracing gamete maturation and early embryogenesis might be the most vulnerable period. We focus on four types of environmental exposure shown to modify periconceptional reproduction and offspring development and health: maternal overnutrition and obesity; maternal undernutrition; paternal diet and health; and assisted reproductive technology. These conditions may act through diverse epigenetic, cellular and physiological mechanisms to alter gene expression and cellular signalling and function in the conceptus affecting offspring growth and metabolism leading to increased risk for cardiometabolic and neurological disease in later life.

130 Early Developmental Exposure to Stress and Programming of Lifelong Gut and Immune Function

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 69-69
Author(s):  
Adam J Moeser
Keyword(s):  
Life Stress ◽  
Disease Risk ◽  
Early Life Stress ◽  
Later Life ◽  
Developmental Programming ◽  
Postnatal Life ◽  
Critical Periods ◽  
Organ Systems ◽  
High Level ◽  
The Impact

Abstract Prenatal and early postnatal life represents critical periods of development across species for many organ systems including immune, nervous, reproductive, and gastrointestinal systems. A high level of plasticity exists during these periods, and thus maternal and environmental cues including stress, immune stimulation, and nutrition, can alter the normal developmental programming of the fetus and neonate and impact the trajectory for disease risk and productivity across the lifespan. This presentation will focus on the impact of and biological mechanisms by which prenatal and early postnatal stressors, including psychological immune and nutritional stressors, alter the normal developmental programming of the immune, gastrointestinal, and neuroendocrine stress axes in the offspring and how this may link to increased disease risk and reduced productivity across the lifespan in animals and humans. Further, specifically how host factors such as biological sex interact with early life stress to shape gut and systemic neuroimmune development and later life disease risk will be discussed.

Sex-specific differences and developmental programming for diseases in later life

2017 ◽  
Vol 29 (11) ◽  
pp. 2085 ◽  
Author(s):  
Deepali P. Sundrani ◽  
Suchitra S. Roy ◽  
Anjali T. Jadhav ◽  
Sadhana R. Joshi
Keyword(s):  
Epidemiological Data ◽  
Later Life ◽  
Developmental Programming ◽  
Fetal Outcome ◽  
Physiological Status ◽  
Developmental Origins ◽  
Placental Development ◽  
Future Studies ◽  
Health And Disease ◽  
And Function

Epidemiological data indicate that developmental programming of various non-communicable diseases (NCDs) occurs as a consequence of altered maternal metabolic and physiological status due to a number of environmental insults during pregnancy. Sex-specific differences have also been reported in most NCDs. Evidence suggests that beginning from conception, the maternal and neonatal metabolic environment, including hormones, contributes to sex-specific placental development. The placenta then regulates the sex-specific differences in NCDs via the epigenetic mechanisms that are further affected by hormones. Male and female embryos have been reported to exhibit sex-specific transcriptional regulation, and it is suggested that their development can be considered as separate processes beginning from conception. This review summarises various animal and human studies examining sex-specific differences in NCDs due to differential placental epigenetic developmental programming. An overview of possible mechanisms underlying this is also discussed. Further, the review describes sex-specific changes in the structure and function of the placenta in pregnancies complicated by fetal growth restriction, pre-eclampsia and preterm birth. Thus, because sex-specific differences are associated with fetal outcome and survival, future studies need to take into consideration the sex of the fetus while explaining the concept of the developmental origins of health and disease.

scholarly journals IMPACT OF KHAT (CATHA EDULIS) CHEWING/USE ON HEART RATE AND BLOOD PRESSURE: A CRITICAL REVIEW

2017 ◽  
Vol 17 (3) ◽  
pp. 76-85 ◽  
Author(s):  
Zhi Xiong Chong ◽  
Mustafa Alshagga ◽  
Khaled Ahmed Saed ◽  
Saba Kassim
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Epidemiological Studies ◽  
Current Evidence ◽  
Active Constituent ◽  
Khat Chewing ◽  
Coronary Syndrome ◽  
Underlying Mechanisms ◽  
Two Parameters ◽  
The Impact

Khat leaves chewing/use, which imparts amphetamine like effects on the user, is widely practiced in parts of Africa, the Arabian Peninsula, and among the diaspora communities from these regions. Basic clinical and epidemiological studies from different settings have reported associations of acute coronary syndrome, heart failure, and cardiomyopathy, with khat chewing /use. This review aims to analyse the current evidence of the impact that khat, or its active constituent, cathinone, has on the cardiovascular system (CVS), particularly in two parameters, heart rate (HR) and blood pressure (BP). Subsequently, the possible mechanism of actions of how khat impacts these cardiovascular parameters is discussed, and different studies’ findings are summarised appropriately. The analysis of literature suggests that khat could influence HR and BP by most likely causing tachycardia and hypertension and the impacts might be dose-dependent and time-dependent. However, most of the studies involved different species and study designs, and had different limitations. Additionally, the underlying mechanisms of khat effects on these CVS parameters remain unclear. Therefore, more studies are needed to further support the current evidence of the impacts that khat has on the CVS parameters of HR and BP.

scholarly journals Early Life Adversity as a Risk Factor for Fibromyalgia in Later Life

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Lucie A. Low ◽  
Petra Schweinhardt
Keyword(s):  
Stress Responses ◽  
Early Life ◽  
Pain Sensitivity ◽  
Later Life ◽  
Early Life Adversity ◽  
Stress Responsivity ◽  
Unclear Etiology ◽  
Epigenetic Modulation ◽  
Early Life Events ◽  
The Impact

The impact of early life events is increasingly becoming apparent, as studies investigate how early childhood can shape long-term physiology and behaviour. Fibromyalgia (FM), which is characterised by increased pain sensitivity and a number of affective co-morbidities, has an unclear etiology. This paper discusses risk factors from early life that may increase the occurrence or severity of FM in later life: pain experience during neonatal life causes long-lasting changes in nociceptive circuitry and increases pain sensitivity in the older organism; premature birth and related stressor exposure cause lasting changes in stress responsivity; maternal deprivation affects anxiety-like behaviours that may be partially mediated by epigenetic modulation of the genome—all these adult phenotypes are strikingly similar to symptoms displayed by FM sufferers. In addition, childhood trauma and exposure to substances of abuse may cause lasting changes in developing neurotransmitter and endocrine circuits that are linked to anxiety and stress responses.

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