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Malnutrition during foetal life and infancy have been linked to the development of coronary heart disease, stroke, Type 2 diabetes, hypertension, osteoporosis and certain cancers, including breast cancer. All of these conditions can originate through the developmental plasticity process of foetal life. Geographical studies led David Barker (2007) to propose the ‘Foetal Origins Hypothesis’, that undernutrition in utero and during infancy permanently changes the body’s structure, physiology and metabolism, causing coronary heart disease and stroke in adult life:

Like other living creatures in their early life human beings are ‘plastic’ and able to adapt to their environment. The development of the sweat glands provides a simple example of this. All humans have similar numbers of sweat glands at birth but none of them function. In the first three years after birth a proportion of the glands become functional, depending on the temperature to which the child is exposed. The hotter the conditions, the greater the number of sweat glands that are programmed to function. After three years the process is complete and the number of sweat glands is fixed. Thereafter, the child who has experienced hot conditions will be better equipped to adapt to similar conditions in later life, because people with more functioning sweat glands cool down faster. This brief description encapsulates the essence of developmental plasticity: a critical period when a system is plastic and sensitive to the environment, followed by loss of plasticity and a fixed functional capacity. For most organs and systems, the critical period occurs in utero. (Barker, 2013: 5)

Figure 3.6 A schematic diagram of DNA pulled from a chromosome, showing the double helix wrapped around histones, and some epigenetic modifications to both the DNA and the histones

Source: Reproduced by permission from Hadas et al. (2017)

Developmental plasticity has been described as the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development (West-Eberhard, 1989). One area in which to explore the developmental origins of chronic disease is cardiovascular disease. Barker’s team had earlier identified groups of men and women in middle or late life whose birth size had been recorded. Their birthweight could be related to the later occurrence of coronary heart disease (CHD). In Hertfordshire, UK, from 1911 onwards, women with babies were attended by a midwife, who recorded the birthweight. After the birth, a health visitor went to the baby’s home at intervals throughout infancy, and the weight at 1 year was recorded. In 10,636 men born between 1911 and 1930, hazard ratios for CHD fell with increasing birthweight. There were stronger trends with weight at 1 year. A later study found a similar trend of decreased hazard ratios for CHD with increasing birthweight among women born during this time but no trend with weight at 1 year. The association between low birthweight and CHD has since been replicated in Europe, North America and India. Because the associations are independent of the duration of gestation, they can be assumed to be the result of slow foetal growth (Barker, 2007). The findings from ecological studies have been confirmed in studies with individuals. Barker (2007: 416) concluded that the ‘orthodox view that cardiovascular disease results from adult lifestyles and genetic inheritance has not provided a secure basis for prevention of these disorders. The developmental model of the origins of chronic disease now offers a new way forward’. If true, Barker’s hypothesis means that the majority of work in public health and in much of health psychology, which is designed to help adults change ‘lifestyles’, is redundant. [Hmmm. No need for this textbook then! However, Barker’s hypothesis is only true to a certain extent. Adults’ behaviours, such as smoking, drinking and unhealthy eating, are all examples of known risk factors for cancers and cardiovascular disease.]

The intrauterine period of development certainly is important in development because it includes stimuli such as nutrients, stress, drugs, trauma and smoking. A healthy intrauterine environment enables the mother to impart a rich ‘maternal forecast’ for her developing foetus, predicting a healthy post-birth environment where resources will be plentiful and negative exposures are expected to be minimal. However, a relatively adverse intrauterine environment may result in a poor maternal forecast for her developing foetus, a so-called ‘thrifty phenotype’ (Hales and Barker, 1992) that becomes a small, low-weight baby, preparing the child to survive in a poor post-birth environment. Maternal forecasts that inaccurately predict the post-birth environment are hypothesized to lead to ill health over the child’s later life, for example an increased risk for metabolic diseases and decreased cognitive functioning in offspring that had received a poor maternal forecast but were born into a rich environment (Knopik et al., 2012).

There can be few times in the lifespan that are more significant than the period of prenatal development. At this time there appear to be ‘critical windows’ where disturbances may alter foetal growth and development, leading to health and behavioural consequences across the life course. Early life programming can have long-term effects on metabolism (Tarry-Adkins and Ozanne, 2011) via mechanisms that include: (1) permanent structural changes resulting from suboptimal concentrations of an important factor during a critical period of development (e.g., the permanent reduction in B cell mass in the endocrine pancreas); (2) persistent alterations in epigenetic modifications that lead to changes in gene expression (e.g., several transcription factors are susceptible to reprogrammed gene expression); and (3) permanent effects on the regulation of cellular ageing (e.g., increases in oxidative stress that lead to macromolecular damage, including that to DNA and specifically to telomeres²). Prevention and intervention to combat the burden of common diseases such as Type 2 diabetes and cardiovascular disease may be developed as a consequence of improved understanding of early life programming.

² A telomere is a region of repetitive nucleotide sequences at each end of a chromosome, which protects the end of the chromosome from deterioration or from fusion with neighbouring chromosomes.