scholarly journals RE: “WHY EVIDENCE FOR THE FETAL ORIGINS OF ADULT DISEASE MIGHT BE A STATISTICAL ARTIFACT: THE ‘REVERSAL PARADOX’ FOR THE RELATION BETWEEN BIRTH WEIGHT AND BLOOD PRESSURE IN LATER LIFE”

2005 ◽  
Vol 162 (3) ◽  
pp. 292-292 ◽  
Author(s):  
Matthew W. Gillman
2018 ◽  
Vol 9 (3) ◽  
pp. 270-280 ◽  
Author(s):  
S. A. Lule ◽  
A. M. Elliott ◽  
L. Smeeth ◽  
E. L. Webb

There is substantial evidence of an inverse association between birth weight and later blood pressure (BP) in populations from high-income countries, but whether this applies in low-income countries, where causes of low birth weight are different, is not certain. Objective: We conducted a review of the evidence on the relationship between birth weight and BP among African children and adolescents. Medline, EMBASE, Global Health and Web of Science databases were searched for publications to October 2016. Papers reporting the relationship between birth weight and BP among African children and adolescents were assessed. Bibliographies were searched for further relevant publications. Selected papers were summarized following the preferred reporting items for systematic review and meta-analysis (PRISMA) guidelines. In total, 16 papers from 13 studies conducted in nine African countries (Nigeria, Republic of Seychelles, Gambia, Democratic Republic of Congo, Cameroon, South Africa, Algeria, Zimbabwe and Angola) were reviewed. Eight studies were cohorts, while five were cross-sectional. The relationship between birth weight and later BP varied with age of the participants. Studies in neonates showed a consistently positive association, while predominantly inverse associations were seen among children, and studies in adolescents were inconsistent. Based on the limited number of studies identified, the relationship between birth weight and later BP may vary with age in African children and adolescents. Not all studies adequately controlled for confounding, notably gender or age. Whether the inverse relationship between birth weight and BP in later life observed in Western settings is also seen in Africa remains unclear.


2007 ◽  
Vol 26 (4) ◽  
pp. 235-240 ◽  
Author(s):  
Joan Nalani Thompson

The fetal-origins-of-adult-disease hypothesis describes an adaptive phenomenon of in utero reprogramming of the undernourished fetus that predisposes the infant to increased morbidity as an adult. Studies have identified a positive association between indicators of fetal undernutrition such as low birth weight and chronic adult diseases like hypertension, diabetes, obesity, and coronary artery disease. Current research is focusing on determining other factors that may contribute to these chronic adult diseases.


2021 ◽  
Vol 13 (6) ◽  
pp. 1-9
Author(s):  
Khanh Nguyễn Công

“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


2013 ◽  
Vol 36 (8) ◽  
pp. 725-735 ◽  
Author(s):  
Yong Zhang ◽  
Hui Li ◽  
Shang-jing Liu ◽  
Guang-jian Fu ◽  
Yong Zhao ◽  
...  

2011 ◽  
Vol 29 (12) ◽  
pp. 2324-2331 ◽  
Author(s):  
Karen L. Miles ◽  
Barry J. McDonnell ◽  
Kaisa M. Maki-Petaja ◽  
Yasmin ◽  
John R. Cockcroft ◽  
...  

2010 ◽  
Vol 1 (2) ◽  
pp. 123-130 ◽  
Author(s):  
D. P. Misra ◽  
C. M. Salafia ◽  
A. K. Charles ◽  
R. K. Miller

We hypothesized that the altered placental proportions that influence birth weight affect childhood body proportions, and that these effects would be independent of birth weight. We also hypothesized that altered placental proportions might affect the fetal cardiovascular system, and may be reflected in variation in childhood blood pressure. By using linear regression with birth weight as the dependent variable, placental variables were entered as predictors. The predicted birth weights based on placental factors were then obtained. The ratio of the actual birth weight to that predicted by placental parameters (observed/expected ratio, OER) was used as the independent variable in analyses of age 7 year body mass index (BMI) and diastolic blood pressure (DBP) in the 15,902 singleton liveborns delivered between 34 and 43 weeks. The standardized residual birth weight was also used as a variable to examine the effects of birth weight that is not consistent with placental parameters. For each unit increase in the OER, BMI at 7 years increased 1 kg/m2 (P < 0.0001). The OER also had a significant effect on DBP (β = 4.52, P < 0.001) at 7 years of age but only among African-American children. Results for the standardized residual birth weight variable were consistent with the OER. All results were adjusted for gestational age, sex, socioeconomic status, African-American race and maternal pre-pregnancy BMI. Being larger or smaller than predicted by one’s placenta affects childhood body composition and blood pressure. The placental measurements provide insight into pathophysiological mechanisms of the developmental origins of adult disease.


Sign in / Sign up

Export Citation Format

Share Document