Early life events and their consequences for later disease: A life history and evolutionary perspective

Abstract

Biomedical science has little considered the relevance of life history theory and evolutionary and ecological developmental biology to clinical medicine. However, the observations that early life influences can alter later disease risk--the "developmental origins of health and disease" (DOHaD) paradigm--have led to a recognition that these perspectives can inform our understanding of human biology. We propose that the DOHaD phenomenon can be considered as a subset of the broader processes of developmental plasticity by which organisms adapt to their environment during their life course. Such adaptive processes allow genotypic variation to be preserved through transient environmental changes. Cues for plasticity operate particularly during early development; they may affect a single organ or system, but generally they induce integrated adjustments in the mature phenotype, a process underpinned by epigenetic mechanisms and influenced by prediction of the mature environment. In mammals, an adverse intrauterine environment results in an integrated suite of responses, suggesting the involvement of a few key regulatory genes, that resets the developmental trajectory in expectation of poor postnatal conditions. Mismatch between the anticipated and the actual mature environment exposes the organism to risk of adverse consequences-the greater the mismatch, the greater the risk. For humans, prediction is inaccurate for many individuals because of changes in the postnatal environment toward energy-dense nutrition and low energy expenditure, contributing to the epidemic of chronic noncommunicable disease. This view of human disease from the perspectives of life history biology and evolutionary theory offers new approaches to prevention, diagnosis and intervention.

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

“…These would include a tendency to prefer a high-fat diet, hyperphagia, less investment in muscle mass and a tendency to visceral adipose stores when excess energy was available. 50,61 These adaptations would be of no adverse consequence in a nutritionally limited environment, as was likely to have been the case for humans in pre-agricultural history, but are likely to lead to mismatch in modern environments. As the likelihood of high-energy environments grows in modern times, the risk of mismatch and thus obesity grows.…”

Impact of growth patterns and early diet on obesity and cardiovascular risk factors in young children from developing countries

“…These changes are associated with permanent changes in physiology and/or structure that will predispose individuals to obesity and other nutrition-related chronic diseases in later life, increasing their susceptibility to chronic diseases directly or by interacting with other risk factors (4) . This hypothesis implicitly suggests that action is needed at all stages of the life course in order to ensure long-term health (6) .…”

Homage to the ‘H’ in developmental origins of health and disease

“…4,[6][7][8][9][10][11][12][13] It is also increasingly becoming apparent that the environmental state of both the mother and father can underpin later diseases in offspring, even those who appear healthy at birth. [14][15][16][17][18][19][20][21][22][23][24][25][26] Such intrinsic and extrinsic factors in animal models and humans include exposure to endocrine disrupting chemicals, such as bisphenol A, phthalates, heavy metals, stress, obesity, high fat/ high caloric diets, metabolic status and starvation conditions to provide a few examples.…”