Health Psychology. Michael Murray

      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.

      Intergenerational Transmission, Social Epigenetics and Maternal Stress

      ‘Intergenerational transmission’ occurs when enduring epigenetic changes in parental biological systems in response to maternal exposure are transmitted to the offspring and to the offspring of the offspring. Nutritional status, exposure to toxins and drugs, and the experiences of interacting with varied environments can all modify an individual’s epigenome. Epigenetic programming changes how and when certain genes are turned on or off and triggers temporary or enduring health problems. Research suggests that epigenetic changes occurring in the foetus can be passed on to later generations, affecting children, grandchildren and their descendants. For example, turning on genes that increase cell growth, while at the same time switching off genes that suppress cell growth, can cause cancer. Repetitive, stressful experiences can cause epigenetic changes that alter the biological systems that manage one’s response to adversity later in life. We illustrate these ideas with recent examples of epigenetic research on maternal stress.

      Stress exposures of parents may occur before conception, at the time of conception, at the time of pregnancy, or in the early postnatal period, where the environment of mothers influences the epigenetic patterning of their offspring, which can have a life-long influence on their behaviour, emotions and well-being, both mental and physical. Children of mothers who are exposed to poverty, hunger, poor diet, smoking, stress, war or violence prenatally are prone to epigenetic influences on their offspring’s later well-being.

      Research from Moshe Szyf and colleagues has provided significant findings on the epigenetic influences of prenatal maternal stress. This work has been labelled ‘social epigenetics’ (Szyf, 2013). One study looked at the offspring of mothers exposed to severe ice storms in southern Quebec, Canada, in 1998. For several days freezing rain storms covered everything in layers of ice, resulting in power outages which ranged from a few hours to as long as six weeks for 3 million Québécois. Security forces went door to door to rescue isolated individuals in danger from cold and hypothermia, asphyxiation from unconventional heating devices, and fire due to blocked chimneys.

      The investigators of a research project called ‘Project Ice Storm’ have reported that maternal hardship and subjective distress predicted a variety of developmental outcomes. One focus for the project was the potential influence of prenatal maternal stress (PNMS) on the offspring (Box 3.1).

      Intergenerational transmission to offspring from parental exposures and characteristics can