Differing personalities within groups of children and adolescents are evident as we observe and spend time in their company. Children can be inclined toward being shy or more exuberant;anxious or calm; combative or mild. Research can help us understand how children's earliest personality traits develop into adolescent and adult behaviours shaping important life outcomes and how childhood personality development may determine the appearance of psychological disturbances through life. (Shiner R, Caspi A, 2002). These are important questions as we strive to improve the mental health and well-being of our global population.
Behaviour genetics, attempts to uncover how the development of human behaviour through childhood is driven by the interplay between our ‘nature’ considered as our
genetic make-up and ‘nurture’ how nurturing an environment we are subjected to
growing up. The empirical science of how genes and environments combine to generate behaviour cannot be oversimplified to assume nature and nurture act independently upon the development of specific personality traits (Turkheimer E, 2020). This essay will evaluate the critical influence of epigenetics and Adverse Childhood Experiences (ACE) within the wider discussion of how nature and nurture impact personality development.
Epigenetics and Adverse Childhood Experiences in Personality Development
Epigenetics is the study of changes caused by modification of gene expression rather than genetic code itself. The epigenome represents a dynamic adaptation to environmental conditions and therefore plays an important role whilst we evaluate the interplay between nature and nurture in human development. Regulation of the human genome by the epigenome is a fundamental, hereditary, physiologic process and plays a key role in the manifestation of traits which can influence personality and behaviour.
Epigenetics can be illustrated in animal studies by Champagne, 2008 demonstrating that ‘High licking and grooming’ (HLG) ewes noted as having superior maternal qualities go on to produce the next generation of HLG ewes, a trait which is also linked to increased levels of oestradiol (circulating oestrogen) within the blood. Interestingly, if lambs from mothers not showing such high maternal instincts were adopted by ewes that did, the lambs would grow up to exhibit HLG behaviour, as did the next generation, therefore switching on the particular genetic expression leading to high plasma oestradiol post-partum amongst other factors. However, such studies are not as easily transferable to study in humans, particularly when it comes to personality development due to increased complexities and ethical implications.
Human attachment studies have demonstrated that maternal safety signals can attenuate stress responses, evidenced by measuring oxytocin and cortisol secretions from salivary swabs throughout childhood, even in children that are reared in high-stress environments. It is thought that biological and behavioural aspects of attachment combine over time to buffer stress in human children as they grow. (Yirmiya K, Motsan S, Zagoory-Sharon O, Feldman R, 2020). There is growing evidence that early life events can affect long term mental health trajectories in humans by influencing the epigenetic pattern and therefore output from the genome leading to the genesis of personality traits and disorders (PD). (Gescher D, Kahl K, Hillemacher T, Frieling H, Kuhn J and Frodl T, 2018) This would suggest that personality and precursors for PDs can be shaped by early life events including stressful experiences and potentially mediated by the presence of maternal safety signals.
Early childhood experiences have long-term effects on development, including increased probability for the development of psychiatric disorders. Research examining the biologic origins of these associations revealed the impact of childhood mistreatment on the stress response system and activity of the hypothalamic pituitary adrenal (HPA) axis. Several studies have revealed that early adversity is linked to abnormalities in HPA axis function in both children and adults (Tyrka A, Ridout K, Parade S, 2016). A growing body of literature supports the hypothesis that environmental exposures mediate their biological effects via epigenetic mechanisms such as methylation, a chemical process involving modification to DNA code. Methylation, which is thought to be the most stable form of epigenetic change, is a likely mechanism by which early life exposures to adverse experiences has lasting effects. However, the complexity of analysing the epigenetic genesis of behavioural traits confounds definitive results. Differing methylation patterns within selected PD could point to subgroups of patients
that would benefit from patient-centred therapeutic modifications to allow early therapeutic intervention and help prevent severe dysfunctional behaviour traits or full-blown personality disorder in at-risk children and adolescents. (Gescher D, Kahl K, Hillemacher T, Frieling H, Kuhn J and Frodl T, 2018). Identifying cognitive based; compassion based; meditative or other therapies that can definitively show a positive influence on methylation patterning could help reduce the incidence of dysfunctional personality behaviours, especially in children and adolescents who have experienced a high ACE score with transgenerational implications.
Behavioural genetics has demonstrated that both genes and the environment are crucial for the development of psychological traits. As our scientific sophistication evolves, so too do the core questions of the influence of nature and nurture upon personality development. How personality development shapes adolescent and adult lives and may influence the appearance of psychopathology through life can be further assessed by the review of epigenetic research has been evaluated, alongside some complexities involved in research. Early childhood experiences have long-term effects on development, including increased incidence of personality disorders through direct physiological impact upon the epigenome. A growing body of literature supports the theory that environmental exposures illicit their effects via epigenetic