Abstract
Low- and middle-income countries (LMICs), particularly those in sub-Saharan Africa, are experiencing rapid increases in the prevalence of non-communicable diseases (NCDs), which may not be fully explained by urbanization and associated traditional risk factors such as tobacco smoking, excessive alcohol consumption, poor diet or physical inactivity. In this commentary, we draw attention to the concept of Developmental Origins of Health and Disease (DOHaD), where environmental insults in early life can contribute to long-term risk of NCDs, the impact of which would be particularly important in LMICs where poverty, malnutrition, poor sanitation and infections are still prevalent.
Highlights
Hypothesis, a rather more recent term for the concept initially proposed and called ‘Fetal Origins of Adult Disease’ in the 1990s,1 postulates that exposure to certain environmental influences during critical periods of development and growth may have significant consequences on an individual’s short- and long-term health.[2]
Some examples of shortterm adaptations the fetus may make in these scenarios include down-regulation of endocrine or metabolic function, and/or specific organ function to slow down its growth rate to match the nutrient supply in the deprived uterine environment.[6]
If the individual grows up in an extra-uterine environment the reverse of that experienced in utero, the ‘mismatch’ and poorer fit, would predispose them to a higher risk of certain non-communicable diseases (NCDs).[3]
Summary
Hypothesis, a rather more recent term for the concept initially proposed and called ‘Fetal Origins of Adult Disease’ in the 1990s,1 postulates that exposure to certain environmental influences during critical periods of development and growth may have significant consequences on an individual’s short- and long-term health.[2]. Studies that looked at undernutrition acting in this early life period (as a result of either maternal undernutrition or protein/calorie restriction),[4] showed that it retarded growth,[10] and induced lifelong changes in hormonal concentrations, and the sensitivity of various tissues to these fetal and placental hormones—alterations that lead to abnormal organ development[11,12] and to diseases such as type-2 diabetes mellitus (T2DM), cardiovascular disease (CVD), kidney disease, obesity, hypertension, osteoporosis and metabolic syndrome in later life.[13,14] These irreversible changes to tissue structure and physiology made to survive the harsh environment encountered in utero have been called ‘programming’, and they are dependent on the nature and point at which exposure to the insult occurs, since tissues mature at different rates and time points.[11,15] This differential effect is well illustrated with undernutrition, to which exposure too soon after conception, for example, slows down fetal growth and leads to low birthweight of the infant. Exposure to various other environmental factors including maternal stress, infections, hypertension, obesity, teratogens, alcohol, drugs, cigarette smoke, over nutrition and paternal malnutrition, within these critical windows of growth and development, have been associated with an increased risk of adult disease.[16,17]
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