Fetal Origin of Adult Disease

2021 ◽  
pp. 167-173
Author(s):  
Johann Craus
Keyword(s):  
Adult Disease ◽  
Fetal Origin

scholarly journals OC076: Fetal origin of adult disease in view of the antenatal ultrasound studies

2003 ◽  
Vol 22 (S1) ◽  
pp. 22-22
Author(s):  
K. Marsal ◽  
J. Brodszki ◽  
H. M. Gardiner ◽  
A. Hellstr�m ◽  
L. Martin ◽  
...  
Keyword(s):  
Ultrasound Studies ◽  
Antenatal Ultrasound ◽  
Adult Disease ◽  
Fetal Origin

scholarly journals FETAL ORIGIN OF ADULT DISEASE

2021 ◽  
Vol 13 (6) ◽  
pp. 1-9
Author(s):  
Khanh Nguyễn Công
Keyword(s):  
Fetal Development ◽  
Disease Risk ◽  
Later Life ◽  
Fetal Origins ◽  
Barker Hypothesis ◽  
Adult Disease ◽  
Fetal Origin ◽  
Increased Risk ◽  
Fetal Nutrition ◽  
Size At Birth

“Fetal origins of adult disease”, often called the “Barker hypothesis” after a large proportion data of Barker and colleagues in Southampton over the last decade, that adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in structure, physiology, metabolism, which result in increased disease risk in adulthood. Many further studies have provided evidence for the hypothesis that size at birth is related to the risk of developing disease in later life. In particular, links are well established between reduced birthweight and increased risk of coronary heart disease, diabetes, hypertension and stroke in adulthood. The most widely accepted mechanisms thought to underlie these relationship are those of altered fetal nutrition, genetic–epigenetic links, fetal programming and fetal excess glucocorticoid exposure. It is suggested that the fetus makes physiological adaption in response to changes in its environment to prepare itself for posnatal life. The “Fetal origin of adult disease” hypothesis is attractive. It suggests that these diseases could be prevented by improving maternal health and fetal development

A Fetal Origin of Adult Disease

Fetal Therapy ◽  
2019 ◽  
pp. 8-19
Author(s):  
Mark Hanson ◽  
Lucy Green
Keyword(s):  
Adult Disease ◽  
Fetal Origin

scholarly journals “Extension of the “Fetal Origin Hypothesis of Barker” towards the “Fetal Origin Hypothesis of Mental Diseases”

2018 ◽  
Vol 2 (3) ◽  
pp. 01-07
Author(s):  
Vincent van Ginneken ◽  
Clemens Löwik
Keyword(s):  
Cardiovascular Diseases ◽  
Disease Risk ◽  
Developmental Origins ◽  
Barker Hypothesis ◽  
Adult Disease ◽  
Intrauterine Life ◽  
Common Information ◽  
Fetal Origin ◽  
Mental Diseases ◽  
Origin Hypothesis

In this editorial we will first describe most common information about the intriguing “traditional” fetal origin hypothesis of Barker for physiological, endocrine and cardiovascular diseases (CVDs). The ‘developmental origins of adult disease’ hypothesis, often called the ‘Barker hypothesis’, states that adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood.

Mitochondria-Based Model for Fetal Origin of Adult Disease and Insulin Resistance

2005 ◽  
Vol 1042 (1) ◽  
pp. 1-18 ◽  
Author(s):  
HONG KYU LEE ◽  
KYONG SOO PARK ◽  
YOUNG MIN CHO ◽  
YUN YONG LEE ◽  
YOUNGMI KIM PAK
Keyword(s):  
Insulin Resistance ◽  
Adult Disease ◽  
Fetal Origin

scholarly journals Fetal Origin of Adult Disease

2014 ◽  
Vol 8 (2) ◽  
pp. 164-177 ◽  
Author(s):  
Rishabh Bora ◽  
Neharika Malhotra Bora
Keyword(s):  
Health Care ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Health Care Professionals ◽  
Disease Risk ◽  
Fetal Origins ◽  
Adult Disease ◽  
Fetal Origin ◽  
Increased Risk ◽  
The Central Nervous System

ABSTRACT Fetal origins of adult disease, a concept first popularized by Dr David Barker, has subsequently led to many studies which have provided the evidence that certain diseases do have links pointing to fetal origins—adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood. Links that are well-established are—reduced birth weight and increased risk of coronary heart disease, hypertension and stroke in adulthood. The concept of a fetal origin of adult disease have been extended well-beyond coronary heart disease and being a risk factor for coronary heart disease, and now includes investigations of the development of the central nervous system, early origins of adult mental health and cognitive function. By understanding fetal origin of adult disease, health care professionals and policy makers will make this issue a high health care priority and implement preventive measures and treatment for those at higher risk for chronic diseases. How to cite this article Malhotra N, Malhotra J, Bora NM, Bora R, Malhotra K. Fetal Origin of Adult Disease. Donald School J Ultrasound Obstet Gynecol 2014;8(2):164-177.

Nutritional programming of adult disease

2005 ◽  
Vol 322 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Alex J. Buckley ◽  
Anne L. Jaquiery ◽  
Jane E. Harding
Keyword(s):  
Adult Disease ◽  
Nutritional Programming

scholarly journals Deep immune profiling of MIS-C demonstrates marked but transient immune activation compared to adult and pediatric COVID-19

2021 ◽  
Vol 6 (57) ◽  
pp. eabf7570
Author(s):  
Laura A. Vella ◽  
Josephine R. Giles ◽  
Amy E. Baxter ◽  
Derek A. Oldridge ◽  
Caroline Diorio ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cd8 T Cells ◽  
Immune Activation ◽  
Cell Activation ◽  
Vascular Complications ◽  
Adult Disease ◽  
Vasoactive Medication ◽  
Inflammatory Syndrome

Pediatric COVID-19 following SARS-CoV-2 infection is associated with fewer hospitalizations and often milder disease than in adults. A subset of children, however, present with Multisystem Inflammatory Syndrome in Children (MIS-C) that can lead to vascular complications and shock, but rarely death. The immune features of MIS-C compared to pediatric COVID-19 or adult disease remain poorly understood. We analyzed peripheral blood immune responses in hospitalized SARS-CoV-2 infected pediatric patients (pediatric COVID-19) and patients with MIS-C. MIS-C patients had patterns of T cell-biased lymphopenia and T cell activation similar to severely ill adults, and all patients with MIS-C had SARS-CoV-2 spike-specific antibodies at admission. A distinct feature of MIS-C patients was robust activation of vascular patrolling CX3CR1+ CD8+ T cells that correlated with the use of vasoactive medication. Finally, whereas pediatric COVID-19 patients with acute respiratory distress syndrome (ARDS) had sustained immune activation, MIS-C patients displayed clinical improvement over time, concomitant with decreasing immune activation. Thus, non-MIS-C versus MIS-C SARS-CoV-2 associated illnesses are characterized by divergent immune signatures that are temporally distinct from one another and implicate CD8+ T cells in the clinical presentation and trajectory of MIS-C.

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