219 research outputs found
Introduction: the window of opportunity
No full textThe United Nations Standing Committee on Nutrition recently stated that "while undernutrition kills in early life, it also leads to a high risk of disease and death later in life. This double burden of malnutrition has common causes, inadequate fetal and infant and young child nutrition followed by exposure (including through marketing practices) to unhealthy energy dense nutrient poor foods and lack of physical activity. The window of opportunity lies from pre-pregnancy to around 24 mo of a child's age.
Fetal Origins Of Adult Health. Commentary: Developmental origins of raised serum cholesterol
No full textHuman beings are plastic during development, and a single genotype can produce more than one alternative form of structure or physiological state in response to environmental conditions.1 There is now a considerable body of evidence that coronary heart disease (CHD) originates in developmental plasticity.2 That being the case environmental conditions during development should be linked to the major biological risk factors for the disease
The developmental origins of chronic adult disease
No full textLow birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin-dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. Coronary heart disease and the disorders related to it arise through a series of interactions between environmental influences and the pathways of development that preceded them. These diseases are the product of branching pathways of development in which the branchings are triggered by the environment before and after birth
Commentary: Components in the interpretation of the high mortality in the county of Finnmark
No full textThe weather in Northern Norway is severe. Anders Forsdahl describes ‘polar nights, harsh cold and long winters’ that force people to spend much of their time indoors. He himself, however, put his long winters to good use, reflecting on why the adult population of Finnmark, far above the Arctic Circle, has such high death rates. He quickly disposed of smoking and genes as possible explanations. He concluded that since economic and social conditions in Finnmark were similar to those in other parts of Norway, its 25% higher adult mortality rates must be a legacy of its history, of events during the childhood or adolescence of the adult population. This was the first of two platforms on which he developed . .
Developmental origins of adult health and disease
No full textThe aim of this glossary is to define some key terms used in the field of developmental and life course epidemiology
The developmental origins of adult disease
No full textLow birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. A new vision of optimal early human development is emerging which takes account of both short and long-term outcomes
Low birth weight, early growth and chronic disease in later life
No full textLow birth weight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birth weight and depend on lower birth weights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. This is an important finding for pediatric health professionals given that promoting weight gain during infancy is standard practice
A new model for the origins of chronic disease
No full textLiving things are often plastic during their early development and are moulded by the environment. Many human fetuses have to adapt to a limited supply of nutrients, and in doing so they permanently change their physiology and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, stroke, diabetes and hypertension
Fetal and infant origins of adult disease
No full textBackground. Many human fetuses and infants have to adapt to a limited supply of nutrients, and in doing so they permanently change their physiology and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, stroke, diabetes and hypertension.Coronary heart disease. We have become accustomed to the idea that coronary heart disease, the commonest cause of death in the Western world, may result from the “unhealthy” lifestyle that is associated with increasing affluence. The influences of this “unhealthy” lifestyle (e. g. obesity, cigarette smoking, dietary fat, stress), however, go only a small way towards explaining why increasing affluence in the Third world is so regularly followed by epidemics of the disease, or why in the Western world these epidemics have risen steeply to become the commonest cause of death but thereafter have declined. Neither do they explain why the highest rates of coronary heart disease in Western countries occur among the poor?Fetal origins. Answers to these questions may come from an understanding of how the structure of the heart and processes such as blood pressure regulation and the way the body handles sugar and fat are established in the womb. The “fetal origins” hypothesis states that coronary heart disease and the disorders related to it – hypertension, adult-onset diabetes and stroke – originate through adaptations that the fetus makes when it is under-nourished. Unlike adaptations made in adult life those made during early development tend to have permanent effects on the body's structure and function – a phenomenon sometimes referred to as programming. They allow the fetus to survive and continue to grow but at the price of a shortened life.ZusammenfassungHintergrund. Viele Säuglinge und Kinder müssen sich an ein limitiertes Nahrungsangebot anpassen, wobei sie ständig ihre Physiologie und ihren Stoffwechsel verändern. Diese programmierten Änderungen sind möglicherweise der Grund von verschiedenen Erkrankungen des Erwachsenenalters wie koronarer Herzkrankheit, Schlaganfall, Diabetes Typ II und Bluthochdruck.Koronare Herzkrankheit. Allgemein wird angenommen, dass koronare Herzkrankheit, die häufigste Todesursache in der westlichen Welt, eine Folge des “ungesunden” Lebensstils ist, der mit steigendem Wohlstand einhergeht. Die Einflüsse dieses Lebensstils (z. B. Adipositas, Zigarettenrauchen, diätetische Fettaufnahme, Stress) erklären jedoch kaum, warum steigender Wohlstand in der Dritten Welt regelmäßig von Epidemien der koronaren Herzerkrankung gefolgt ist oder warum die Häufigkeit dieser Erkrankung in der westlichen Welt zunächst steil anstieg, bis sie zur häufigsten Todesursache geworden war, nun aber abfällt. Sie erklären auch nicht, warum die höchsten Raten der koronaren Herzkrankheit in der westlichen Welt bei der sozial schwachen Bevölkerung gefunden werden.Ursprünge im fetalen Alter. Antworten auf diese Fragen geben uns möglicherweise Erkenntnisse darüber, wie die Struktur des Herzens und Prozesse wie die Blutdruckregulation und die Verwertung von Zucker und Fett im Körper bereits im Mutterleib festgelegt werden. Die Hypothese des “fetalen Ursprungs” geht davon aus, dass koronare Herzkrankheit und die mit ihr verbundenen Funktionsstörungen – Bluthochdruck, Diabetes Typ II und Schlaganfall – aus Anpassungsvorgängen des Fetus an Unterernährung resultieren. Im Gegensatz zu Anpassungsvorgängen im Erwachsenenalter haben Anpassungsvorgänge der frühen Entwicklung eher permanente Effekte auf die Struktur und Funktion des Körpers, ein Phänomen, das manchmal mit Programmierung umschrieben wird. Diese Anpassungsvorgänge erlauben es dem Fetus, zu überleben und weiter zu wachsen, allerdings um den Preis eines verkürzten Lebens.<br/
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