4A-6 Early-onset puberty in offspring after maternal undernutrition is exaggerated by a post-weaning high fat diet: sex specific evidence of nutritional mismatch

Sloboda, D.M.; Howie, Graham; Vickers, Mark H.

doi:10.1016/s0378-3782(07)70115-9

Cited by 7 publications

(7 citation statements)

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“…Thus, an evolutionary argument can be presented to suggest that the tendency to adiposity is to support reproductive fitness. There is experimental evidence for gender-specific effects 55,56,70 supporting such an interpretation. Less experimental and clinical data are available for males, and the preferred life-course strategy in males may depend on the species-specific mating system.…”

Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 96%

“…68 There are also data showing that children who gain weight faster also have earlier puberty; in both humans and rats there is a synergism between impaired early development and pre-pubertal weight gain in accelerating the age of female puberty. 69,70 One interpretation might be that the primary predictive adaptive response to an impaired early environment is to accelerate maturation in an attempt to preserve fitness. However, it can also be interpreted that as pregnancy in a young female without adequate energetic stores is likely to compromise both maternal and offspring health, accelerated maturation must be associated with increased energy stores before first conception.…”

Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 99%

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Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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Although variation in individual lifestyle and genotype are important factors in explaining individual variation in the risk of developing obesity in an obesogenic environment, there is growing evidence that developmentally plastic processes also contribute. These effects are mediated at least in part through epigenetic processes. These developmental pathways do not directly cause obesity but rather alter the risk of an individual developing obesity later in life. At least two classes of developmental pathway are involved. The mismatch pathway involves the evolved adaptive responses of the developing organism to anticipated future adverse environments, which have maladaptive consequences if the environment is mismatched to that predicted. This pathway can be cued by prenatal undernutrition or stresses that lead the organism to forecast an adverse future environment and change its developmental trajectory accordingly. As a result, individuals develop with central and peripheral changes that increase their sensitivity to an obesogenic environment. It provides a model for how obesity emerges in populations in rapid transition, but also operates in developed countries. There is growing experimental evidence that this pathway can be manipulated by, for example, postnatal leptin exposure. Secondly, maternal diabetes, maternal obesity and infant overfeeding are associated with a greater risk of later obesity. Early life offers a potential point for preventative intervention.

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Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 96%

Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 99%

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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“…For example, prolonging prenatal undernutrition into the infant period in the rat may modify some aspects of the resulting metabolic phenotype 60 but not obviate the change in tempo of puberty, whereas a different timing of the nutritional challenge affects both. 61 While many physicians find the concepts of anticipation in developmental biology difficult to grasp, much of biological development is anticipatory (see below). Even bacteria have been reported to show adaptive prediction.…”

Section: The Theoretical Basis Of Dohadmentioning

confidence: 99%

“…It seems probable that fetal growth retardation in humans generally has an adaptive value for the offspring: as shown by data in both humans and rats, those born smaller have earlier onset of puberty. 61,74 This is perhaps the equivalent of the accelerated tempo of maturation seen in the spadefoot toad under adverse environmental conditions, suggesting that if the forecast includes the expectation that life may be shorter, accelerated reproductive maturation ensures a chance for gene flow to the next generation. But perhaps the most compelling argument against Wells' concept comes from the (DOHaD) phenomenon in which long-term effects can be shown independently of any obvious fetal responses.…”

Section: The Theoretical Basis Of Dohadmentioning

confidence: 99%

“…Because the windows of plasticity are not the same for different effector components, the timing of experimental insults can be expected to produce differing outcomes. For example, prolonging prenatal undernutrition into the infant period in the rat may modify some aspects of the resulting metabolic phenotype 60 but not obviate the change in tempo of puberty, whereas a different timing of the nutritional challenge affects both 61 …”

Section: The Theoretical Basis Of Dohadmentioning

confidence: 99%

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A conceptual framework for the developmental origins of health and disease

Gluckman

Hanson

Buklijaš

2009

J Dev Orig Health Dis

448

266

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In the last decades, the developmental origins of health and disease (DOHaD) have emerged as a vigorous field combining experimental, clinical, epidemiological and public health research. Its goal is to understand how events in early life shape later morbidity risk, especially of non-communicable chronic diseases. As these diseases become the major cause of morbidity and mortality worldwide, research arising from DOHaD is likely to gain significance to public health and economic development. But action may be hindered by the lack of a firm mechanistic explanation and of a conceptual basis, especially regarding the evolutionary significance of the DOHaD phenomenon. In this article, we provide a succinct historical review of the research into the relationship between development and later disease, consider the evolutionary and developmental significance and discuss the underlying mechanisms of the DOHaD phenomenon. DOHaD should be viewed as a part of a broader biological mechanism of plasticity by which organisms, in response to cues such as nutrition or hormones, adapt their phenotype to environment. These responses may be divided into those for immediate benefit and those aimed at prediction of a future environment: disease occurs in the mismatch between predicted and realized future. The likely mechanisms that enable plasticity involve epigenetic processes, affecting the expression of genes associated with regulatory pathways. There is now evidence that epigenetic marks may be inherited and so contribute to non-genomic heritable disease risk. We end by discussing the global significance of the DOHaD phenomenon and its potential applications for public health purposes.

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