The Experts below are selected from a list of 270369 Experts worldwide ranked by ideXlab platform
P M Clark - One of the best experts on this subject based on the ideXlab platform.
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programming of the hypothalamo pituitary adrenal axis and the fetal origins of Adult Disease hypothesis
European Journal of Pediatrics, 1998Co-Authors: P M ClarkAbstract:There is now a large body of evidence to support the hypothesis that events in fetal life permanently alter the structure or function of an individual, programming later Adult Disease. Reduced birth weight is associated with higher blood pressure in childhood and Adult life, and thinness at birth with glucose intolerance and non-insulin dependent diabetes mellitus. Programming of the hypothalamo-pituitary-adrenal (HPA) axis is an attractive hypothesis linking fetal experience and later Disease, as an excess of glucocorticoids may be associated with hypertension and glucose intolerance. Moreover, animal data support this hypothesis. Exposing fetal rats to glucocorticoid reduces birth weight and leads to raised blood pressure, as well as to alterations in the HPA axis. Data on the long-term effects of exposure to glucocorticoids in human subjects are limited. Recently, however, reduced size at birth was found to be associated with higher fasting 9 a.m. plasma cortisol concentrations in Adults. Raised plasma cortisol concentrations were, in turn, associated with higher blood pressure, and inversely related to measures of glucose tolerance.
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Programming of the hypothalamo-pituitary-adrenal axis and the fetal origins of Adult Disease hypothesis.
European journal of pediatrics, 1998Co-Authors: P M ClarkAbstract:There is now a large body of evidence to support the hypothesis that events in fetal life permanently alter the structure or function of an individual, programming later Adult Disease. Reduced birth weight is associated with higher blood pressure in childhood and Adult life, and thinness at birth with glucose intolerance and non-insulin dependent diabetes mellitus. Programming of the hypothalamo-pituitary-adrenal (HPA) axis is an attractive hypothesis linking fetal experience and later Disease, as an excess of glucocorticoids may be associated with hypertension and glucose intolerance. Moreover, animal data support this hypothesis. Exposing fetal rats to glucocorticoid reduces birth weight and leads to raised blood pressure, as well as to alterations in the HPA axis. Data on the long-term effects of exposure to glucocorticoids in human subjects are limited. Recently, however, reduced size at birth was found to be associated with higher fasting 9 a.m. plasma cortisol concentrations in Adults. Raised plasma cortisol concentrations were, in turn, associated with higher blood pressure, and inversely related to measures of glucose tolerance. Programming of the HPA axis by events in fetal life may be one of the mechanisms linking reduced size at birth with raised blood pressure and glucose intolerance in later life. Studies of the effects of antenatal and neonatal dexamethasone administration on later blood pressure and glucose tolerance may be warranted.
Djp Barker - One of the best experts on this subject based on the ideXlab platform.
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fetal origins of Adult Disease strength of effects and biological basis
International Journal of Epidemiology, 2002Co-Authors: Djp Barker, Johan G Eriksson, T Forsen, Clive OsmondAbstract:Background Low birthweight has been consistently shown to be associated with coronary heart Disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life-death, hospital treatment and the need for medication. Methods Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924-1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic Disease are documented. Results The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension. Conclusions Coronary heart Disease and type 2 diabetes may originate through two widespread biological phenomena-developmental plasticity and compensatory growth.
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fetal and infant origins of Adult Disease
Monatsschrift Kinderheilkunde, 2001Co-Authors: Djp BarkerAbstract:Background. 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.
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fetal nutrition and Adult Disease
The American Journal of Clinical Nutrition, 2000Co-Authors: Keith M. Godfrey, Djp BarkerAbstract:Recent research suggests that several of the major Diseases of later life, including coronary heart Disease, hypertension, and type 2 diabetes, originate in impaired intrauterine growth and development. These Diseases may be consequences of programming, whereby a stimulus or insult at a critical, sensitive period of early life has permanent effects on structure, physiology, and metabolism. Evidence that coronary heart Disease, hypertension, and diabetes are programmed came from longitudinal studies of 25000 UK men and women in which size at birth was related to the occurrence of the Disease in middle age. People who were small or disproportionate (thin or short) at birth had high rates of coronary heart Disease, high blood pressure, high cholesterol concentrations, and abnormal glucose-insulin metabolism. These relations were independent of the length of gestation, suggesting that cardiovascular Disease is linked to fetal growth restriction rather than to premature birth. Replication of the UK findings has led to wide acceptance that low rates of fetal growth are associated with cardiovascular Disease in later life. Impaired growth and development in utero seem to be widespread in the population, affecting many babies whose birth weights are within the normal range. Although the influences that impair fetal development and program Adult cardiovascular Disease remain to be defined, there are strong pointers to the importance of the fetal adaptations invoked when the maternoplacental nutrient supply fails to match the fetal nutrient demand.
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Conference report: Fetal origins of Adult Disease—report of the first international study group, Sydney, 29—30 October 1994
Placenta, 1995Co-Authors: Djp Barker, Peter D. Gluckman, J. S. RobinsonAbstract:The epidemiological observations that prenatal and perinatal events lead to Adult Disease are now well supported by animal data. The events in the periconceptual period, in early and late pregnancy and in infancy can effect programming of cardiovascular, endocrine and metabolic regulatory systems. However, the mechanisms underlying these pathological changes remain to be elucidated. Until this is addressed in experimental animals, clinical trials in human pregnancy are premature.
Torsten Plosch - One of the best experts on this subject based on the ideXlab platform.
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the liver x receptor gene promoter is hypermethylated in a mouse model of prenatal protein restriction
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2010Co-Authors: Esther M E Van Straten, Vincent W Bloks, Nicolette C A Huijkman, Julius F W Baller, Hester Van Meer, Dieter Lutjohann, Folkert Kuipers, Torsten PloschAbstract:Prenatal nutrition as influenced by the nutritional status of the mother has been identified as a determinant of Adult Disease. Feeding low-protein diets during pregnancy in rodents is a well-estab...
Steven H Abman - One of the best experts on this subject based on the ideXlab platform.
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persistent challenges in pediatric pulmonary hypertension
Chest, 2016Co-Authors: Rachel K Hopper, Steven H AbmanAbstract:Pulmonary hypertension and related pulmonary vascular Diseases cause significant morbidities and high mortality and present many unique challenges toward improving outcomes in neonates, infants, and children. Differences between pediatric and Adult Disease are reflected in controversies regarding etiologies, classification, epidemiology, diagnostic evaluations, and therapeutic interventions. This brief review highlights several key topics reflecting recent advances in the field and identifies persistent gaps in our understanding of clinical pediatric pulmonary hypertension.
Ylva B Almquist - One of the best experts on this subject based on the ideXlab platform.
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peer status in school and Adult Disease risk a 30 year follow up study of Disease specific morbidity in a stockholm cohort
Journal of Epidemiology and Community Health, 2009Co-Authors: Ylva B AlmquistAbstract:Background: Children have a social status position of their own, apart from that of the family, that may have an impact on short-term and long-term health. The aim of the present study was to analyse the associations between childhood social status in school (ie, peer status) and Disease-specific morbidity in Adulthood. Methods: Data were derived from a longitudinal study using a 1953 cohort born in Stockholm, Sweden: The Stockholm Birth Cohort Study (1953–2003). Peer status was sociometrically assessed in sixth grade (1966). Hazard ratios for Adult Disease-specific morbidity based on information on inpatient care (1973–2003) were calculated by peer status category for men and women separately, using Cox regression. Results: The results indicate that the lower the childhood peer status, the higher the overall Adult Disease risk. There were, however, differences in the degree and magnitude to which Disease-specific inpatient care varied with peer status. Some of the steepest gradients were found for mental and behavioural disorders (eg, alcohol abuse and drug dependence), external causes (eg, suicide) and various lifestyle-related Diseases (eg, ischaemic heart Disease and diabetes). The results were not explained by childhood social class. Conclusion: The present study underlines the importance of recognising children’s social position, apart from that of their family, for later health. Not only psychologically related Diseases but also those related to behavioural risk factors demonstrate some of the largest relative differences by peer status, suggesting that health-related behaviour may be one important mechanism in the association between peer status and morbidity.
