Developmental origins of metabolic diseases

Abstract

Almost 2 billion adults in the world are overweight and more than half of them are classified as obese while nearly 1/3 of children globally experience poor growth and development. Given the vast amount of knowledge that has been gleaned from decades of research on growth and development, a number of questions remains as to why the world is now in the midst of a global epidemic of obesity accompanied by the "double burden of malnutrition" where overweight coexists with underweight and micronutrient deficiencies. This challenge to the human condition can be attributed to nutritional and environmental exposures during pregnancy that may program a fetus to have a higher risk of chronic diseases in adulthood. To explore this concept, frequently called the developmental origins of health and disease (DOHaD) or metabolic diseases (DOMD), this review considers a host of factors and physiological mechanisms that drive a fetus or child towards a higher risk of obesity, fatty liver disease, hypertension, and/or type 2 diabetes (T2D). To that end, this review explores the epidemiology of DOHaD with discussions focused on adaptations to human energetics, placental developmental, dysmetabolism, and key environmental exposures that act to promote chronic diseases in adulthood. These areas are complementary and additive in understanding how providing the best conditions for optimal growth can create the best possible conditions for lifelong health. Moreover, understanding both physiological as well as epigenetic and molecular mechanisms for DOMD is vital to most fully address the global issues of obesity and other chronic diseases.

Childhood obesity prevention across borders: The promise of U.S.–Latin American research collaboration

“…The first 1000 days of life (i.e., gestation and the first 2 years of life) represent a highly important window of opportunity for the prevention of the dysregulation in the metabolism of sugars and fats that can lead to childhood obesity and noncommunicable diseases such as type 2 diabetes later in life 28,29 . Hence, to be effective, national childhood obesity programs need to have robust maternal, infant, and young children nutrition and physical activity components.…”

Physiological Reviews: The past, the present, and the future

“…This has increased interest and citations considerably. Examples include the outstanding articles on the following: 1 ) the pathophysiology of migraine ( 2 ); 2 ) mechanisms of insulin action and resistance ( 3 ); 3 ) new insights into the mechanisms of aging; 4 ) the origins of metabolic diseases ( 4 ); and 5 ) mechanisms of insomnia ( 5 ). To highlight the translational and clinical implications at a glance, authors are now requested to include call-out-box-for-clinicians, highlighting why physician scientists, clinicians, and even the public may find a review worthwhile to read.…”

“…The review is highly informative and provides an excellent, in-depth overview of the intracardiac feedforward and feedback loops between electrical and mechanical behavior, its molecular mechanisms, and its impact on cardiac electrical activity and arrhythmogenesis. Importantly, the review also addresses the clinical implications of mechanoelectric coupling for arrhythmia formation in the setting of different diseases and resulting potential therapeutic approaches; 2 ) Hoffman et al ( 4 ) on “Developmental Origins of Metabolic Diseases,” which details the physiological mechanisms that increase the risks of obesity, fatty liver disease, hypertension, and diabetes; and 3 ) Ray et al ( 16 ) on “Precision Medicine in Asthma,” which details how one can integrate omics data with the results of animal experiments and molecular and cellular studies to identify new biomarkers to allow patients with asthma to receive maximum benefits from medical treatment; and the various articles on COVID cited previously.…”

Current Resources for Evidence‐Based Practice, May/June 2021

“…This can influence the developing fetus’ HPA axis, which in turn affects the brain and developing organs. Other byproducts of maternal stress are changes in maternal microbiota and release of catecholamines, cytokines, and reactive oxidative products, which can cause inflammation that can be seen in the placenta, and these too could result in epigenetic modifications in the fetus 2 . A strong association between stress in pregnancy and increased low birth weight has been shown 3 .…”