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Published online by Cambridge University Press: 05 April 2022
The last chapter reviewed the aspirations and thought styles of the various actors involved in the prevention science project. We saw that epigenetic mechanisms are starting to be invoked in the name of prevention, treatment and targeting. It is the latest technology to be brought to bear in the project of fixing people, and this chapter will dig into the epigenetic thought style in depth, by analysing some of the seminal work as well as giving a more general flavour of the mainstream research being undertaken, its methods and direction of travel. The bulk of the experimental research is on animals in laboratory settings, using behavioural paradigms which are intended to serve as meaningful surrogates for the human situation. We have witnessed this style of work before. The chapter introduces our cast of laboratory animals, examining how they are bred and handled experimentally to produce findings which seem to transfer so convincingly from the Perspex cage of the laboratory to the disadvantaged housing estate – from rat mum to your Mum.
In an informative recent review paper, Cunliffe (2015) summarises the epigenetic argument thus: ‘A growing body of evidence indicates that experiences acquired during development, childhood, or adulthood induce changes in gene expression, which impart cumulative, long-lasting effects on health, well-being and vulnerability to disease’ (p 59).
The statement very much captures the progressive aspirations of our times, that environmental impacts can exert profound effects on individual health and welfare, via their influence on epigenetic mechanisms, and that this understanding will provide the foundations for public health programmes of various kinds. In this chapter and the next, we aim to provide a critical examination of key developments in epigenetics, by examining relevant examples of journal science. We will consider animal evidence first, before moving to human studies in the next chapter.
Regarding animal work, the crux of the epigenetic argument is captured in the following extract, again from Cunliffe (2015):
Acutely stressful experiences can leave behind strong memories that intensify responses when similar stimuli are encountered again. The molecular basis of this form of memory is poorly understood, but epigenetic mechanisms play important roles. Classic studies in rodent animal models and humans have demonstrated a close relationship between elevated stress in early life and the appearance of behavioural disorders in later life. (p 59)
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