Trends in Endocrinology & Metabolism
ReviewFetal programming of coronary heart disease
Section snippets
Growth and hypertension and type 2 diabetes
There is now a substantial body of evidence showing that people who were small at birth remain biologically different to people who were larger. The differences include an increased susceptibility to hypertension and type 2 diabetes mellitus (T2DM), two disorders that are closely linked to coronary heart disease 11., 12., 13., 14., 15. and which are associated with the same general pattern of growth as coronary heart disease. The risks for each disease fall with increasing birthweight and rise
Biological mechanisms
The association between altered growth and coronary heart disease has led to the suggestion that the disease might originate in two phenomena associated with development – ‘developmental, or phenotypic plasticity’ and ‘compensatory growth’. Phenotypic plasticity is the phenomenon whereby one genotype gives rise to a range of different physiological or morphological states in response to different environmental conditions during development [17]. Such gene–environment interactions are ubiquitous
Responses to adult living standards
Observations on animals show that the environment during development permanently changes not only the body's structure and function but also its responses to environmental influences encountered in later life [34]. Table 5 shows the effect of low income in adult life on coronary heart disease among men in Helsinki [35]. As expected, men who had a low taxable income had higher rates of the disease 36., 37.. There is no agreed explanation for this and it is a major component of the social
Interactions
New studies, especially those of the two exceptionally well-documented cohorts in Helsinki, increasingly suggest that coronary heart disease and the disorders related to it develop through a series of interactions. The effects of genes are conditioned by fetal growth [20]: the effects of small body size at birth are conditioned by growth during childhood [1], and by living conditions in childhood [16] and adult life [35]. Any one influence, such as low income, does not have a single
Conclusion
The associations between slow fetal, infant and childhood growth and later coronary heart disease are strong and graded. Boys who at birth had a ponderal index above 26 kg m−3 and who at one year of age were above the cohort average for BMI (17.7 kg m−3) and height (76.2 cm) were at half the risk of developing coronary heart disease before the age of 65 years [1]. Such findings confirm the strong effects of early growth on later disease [41].
The principal determinant of growth rates in early
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2022, Developmental Cognitive NeuroscienceCitation Excerpt :Such rapid intrauterine development increases fetal susceptibility to prenatal environmental signals. As proposed by the Fetal or Developmental Origins of Adult Disease Hypothesis, environmental signals can promote or jeopardize fetal development, altering the maturation of physiological systems with lifelong consequences for health and disease (Barker, 1998, 2002; Kwon and Kim, 2017). Poor sleep quality and short sleep duration are public health concerns that may have intergenerational consequences.