scholarly journals The Good, the Bad, and the Ugly of Pregnancy Nutrients and Developmental Programming of Adult Disease

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 894 ◽  
Author(s):  
Hsu ◽  
Tain

Maternal nutrition plays a decisive role in developmental programming of many non-communicable diseases (NCDs). A variety of nutritional insults during gestation can cause programming and contribute to the development of adult-onset diseases. Nutritional interventions during pregnancy may serve as reprogramming strategies to reverse programming processes and prevent NCDs. In this review, firstly we summarize epidemiological evidence for nutritional programming of human disease. It will also discuss evidence from animal models, for the common mechanisms underlying nutritional programming, and potential nutritional interventions used as reprogramming strategies.

2009 ◽  
Vol 296 (1) ◽  
pp. F1-F9 ◽  
Author(s):  
Karen M. Moritz ◽  
Reetu R. Singh ◽  
Megan E. Probyn ◽  
Kate M. Denton

The risk of developing many adult-onset diseases, including hypertension, type 2 diabetes, and renal disease, is increased in low-birth-weight individuals. A potential underlying mechanism contributing to the onset of these diseases is the formation of a low nephron endowment during development. Evidence from the human, as well as many experimental animal models, has shown a strong association between low birth weight and a reduced nephron endowment. However, other animal models, particularly those in which the mother is exposed to elevated glucocorticoids for a short period, have shown a 20–40% reduction in nephron endowment without discernible changes in the birth weight of offspring. Such findings emphasize that a low birth weight is one, but certainly not the only, predictor of nephron endowment and suggests reduced nephron endowment and risk of developing adult-onset disease, even among normal-birth-weight individuals. Recognition of the dissociation between birth weight and nephron endowment is important for future studies aimed at elucidating the role of a reduced nephron endowment in the developmental programming of adult disease.


2019 ◽  
Vol 242 (1) ◽  
pp. T81-T94 ◽  
Author(s):  
Clare M Reynolds ◽  
Mark H Vickers

Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.


Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1917 ◽  
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain

Hypertension is a growing global epidemic. Developmental programming resulting in hypertension can begin in early life. Maternal nutrition status has important implications as a double-edged sword in the developmental programming of hypertension. Imbalanced maternal nutrition causes offspring’s hypertension, while specific nutritional interventions during pregnancy and lactation may serve as reprogramming strategies to reverse programming processes and prevent the development of hypertension. In this review, we first summarize the human and animal data supporting the link between maternal nutrition and developmental programming of hypertension. This review also presents common mechanisms underlying nutritional programming-induced hypertension. This will be followed by studies documenting nutritional interventions as reprogramming strategies to protect against hypertension from developmental origins. The identification of ideal nutritional interventions for the prevention of hypertension development that begins early in life will have a lifelong impact, with profound savings in the global burden of hypertension.


Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3278
Author(s):  
Michael D. Thompson ◽  
Brian J. DeBosch

Developmental programming of chronic diseases by perinatal exposures/events is the basic tenet of the developmental origins hypothesis of adult disease (DOHaD). With consumption of fructose becoming more common in the diet, the effect of fructose exposure during pregnancy and lactation is of increasing relevance. Human studies have identified a clear effect of fructose consumption on maternal health, but little is known of the direct or indirect effects on offspring. Animal models have been utilized to evaluate this concept and an association between maternal fructose and offspring chronic disease, including hypertension and metabolic syndrome. This review will address the mechanisms of developmental programming by maternal fructose and potential options for intervention.


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

2014 ◽  
Vol 1 (1) ◽  
pp. 63-76 ◽  
Author(s):  
Christoph Curths ◽  
Sascha Knauf ◽  
Franz-Josef Kaup

2010 ◽  
Vol 23 (1) ◽  
pp. 4-22 ◽  
Author(s):  
Paul Guilloteau ◽  
Romuald Zabielski ◽  
Harald M. Hammon ◽  
Cornelia C. Metges

The consequences of early-life nutritional programming in man and other mammalian species have been studied chiefly at the metabolic level. Very few studies, if any, have been performed in the gastrointestinal tract (GIT) as the target organ, but extensive GIT studies are needed since the GIT plays a key role in nutrient supply and has an impact on functions of the entire organism. The possible deleterious effects of nutritional programming at the metabolic level were discovered following epidemiological studies in human subjects, and confirmed in animal models. Investigating the impact of programming on GIT structure and function would need appropriate animal models due to ethical restrictions in the use of human subjects. The aim of the present review is to discuss the use of pigs as an animal model as a compromise between ethically acceptable animal studies and the requirement of data which can be interpolated to the human situation. In nutritional programming studies, rodents are the most frequently used model for man, but GIT development and digestive function in rodents are considerably different from those in man. In that aspect, the pig GIT is much closer to the human than that of rodents. The swine species is closely comparable with man in many nutritional and digestive aspects, and thus provides ample opportunity to be used in investigations on the consequences of nutritional programming for the GIT. In particular, the ‘sow–piglets’ dyad could be a useful tool to simulate the ‘human mother–infant’ dyad in studies which examine short-, middle- and long-term effects and is suggested as the reference model.


2012 ◽  
Vol 27 (12) ◽  
pp. 2175-2182 ◽  
Author(s):  
Lee O’Sullivan ◽  
Melissa H. Little ◽  
Alexander N. Combes ◽  
Karen M. Moritz

Cephalalgia ◽  
1994 ◽  
Vol 14 (6) ◽  
pp. 411-412 ◽  
Author(s):  
VK Gupta

Facchinetti and colleagues present epidemiological evidence regarding comorbidity between menstrual migraine and premenstrual syndrome, and suggest that premenstural symptoms should be incorporated in the diagnostic criteria for menstrual migraine (1). The crux of the matter, however, should be the concern regarding the nature or biological significance of the common neuroendocrine link of transient and cyclic failure of endogenous opioid activity in both premenstrual syndrome and menstrual migraine patients. Is this a primary event of pathogenetic importance (which would merit inclusion in the definition) or the concomitant side effect of a carefully orchestrated adaptive mechanism?


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