scholarly journals Kidney Stones: A Fetal Origins Hypothesis

2013 ◽  
Vol 28 (12) ◽  
pp. 2535-2539 ◽  
Author(s):  
Sarah A Howles ◽  
Mark H Edwards ◽  
Cyrus Cooper ◽  
Rajesh V Thakker
Keyword(s):  
Kidney Stones ◽  
Fetal Origins ◽  
Fetal Origins Hypothesis

Twins and fetal origins hypothesis: within-pair analyses

The Lancet ◽  
2002 ◽  
Vol 359 (9324) ◽  
pp. 2205-2206 ◽  
Author(s):  
Terence Dwyer ◽  
Ruth Morley ◽  
Leigh Blizzard
Keyword(s):  
Fetal Origins ◽  
Fetal Origins Hypothesis

scholarly journals Killing Me Softly: The Fetal Origins Hypothesis

2011 ◽  
Vol 25 (3) ◽  
pp. 153-172 ◽  
Author(s):  
Douglas Almond ◽  
Janet Currie
Keyword(s):  
Type 2 Diabetes ◽  
Heart Disease ◽  
Educational Attainment ◽  
Test Scores ◽  
Later Life ◽  
Observational Evidence ◽  
Adult Health ◽  
Fetal Origins ◽  
Fetal Origins Hypothesis

In the epidemiological literature, the fetal origins hypothesis associated with David J. Barker posits that chronic, degenerative conditions of adult health, including heart disease and type 2 diabetes, may be triggered by circumstances decades earlier, particularly, by in utero nutrition. Economists have expanded on this hypothesis, investigating a broader range of fetal shocks and circumstances and have found a wealth of later-life impacts on outcomes including test scores, educational attainment, and income, along with health. In the process, they have provided some of the most credible observational evidence in support of the hypothesis. The magnitude of the impacts is generally large. Thus, the fetal origins hypothesis has not only survived contact with economics, but has flourished.

scholarly journals The fetal origins hypothesis—10 years on

BMJ ◽  
2005 ◽  
Vol 330 (7500) ◽  
pp. 1096-1097 ◽  
Author(s):  
Johan G Eriksson
Keyword(s):  
Fetal Origins ◽  
Fetal Origins Hypothesis

Fetal Growth and the Fetal Origins Hypothesis in Twins — Problems and Perspectives

Twin Research ◽  
2001 ◽  
Vol 4 (5) ◽  
pp. 327-331 ◽  
Author(s):  
David I.W. Phillips ◽  
Michael J. Davies ◽  
Jeffrey S. Robinson
Keyword(s):  
Fetal Growth ◽  
Fetal Origins ◽  
Fetal Origins Hypothesis

scholarly journals Nutritional genomics: a practical approach by early life conditioning with dietary phosphorus

2010 ◽  
Vol 39 (suppl spe) ◽  
pp. 268-278 ◽  
Author(s):  
Christopher M. Ashwell ◽  
Roselina Angel
Keyword(s):  
Early Life ◽  
Metabolic Disorders ◽  
Epidemiological Data ◽  
Dietary Manipulation ◽  
Fetal Origins ◽  
Fetal Origins Hypothesis ◽  
Dietary Phosphorus ◽  
In Utero Environment ◽  
Nutritional Genomics

The recent technologies that have led to the new field of functional genomics (how the genome of an organism regulates homeostasis and responds to stimuli) are providing a clearer understanding of how organisms interact with their environment and in particular their diet. We are beginning to learn how the diet may have long-term influence on performance and health. A form of epigenetic regulation has been recently described called fetal "programming". Fueled by epidemiological data the "fetal origins" hypothesis suggests that a poor in utero environment resulting from maternal dietary or placental insufficiency may "program" susceptibility in the fetus to cardiovascular or metabolic disorders. We have observed similar apparent programming by dietary manipulation in the chicken. When birds are challenged with a diet low in phosphorus (P) for 90 hours post-hatch they obtain the ability to better utilize P later in life. This increased retention of P from the diet can partially be explained by an enduring increase in the expression of the intestine-specific Na/P cotransporter (NaPcoT) gene during programming as well as later in life when fed P restricted diets. The resulting data provide the first evidence for neonatal programming of gene expression in an oviparous species.

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