Our class on violence recently explored ideas within developmental psychology that understanding the contexts within which the child develops is crucial for studying child development. The child develops in multiple embedded systems, each of which is unique and incredibly complex. These range from immediate contexts (family life, within a neighborhood and community) to secondarily related (the parent’s work environment, schools) and finally to broader economic, political and historical contexts. The child exists, navigates and acts within all of these spheres simultaneously. Recent research has demonstrated that environmental events within each of these spheres can permanently alter an individuals ‘epigenetic code.’1 This further highlights that a child’s environment can leave a lasting and permanent effect at the level of biology and behavior.
Modern epigenetics can be defined as ‘the structural adaptation of chromosomal regions so as to register, signal or perpetuate altered activity states’2. The most prominent epigenetic mechanisms include DNA methylation (modification of the DNA through the addition of a methyl group) and histone acetylation (modifications of adding an acetyl group to the protein histones, in which the DNA is usually wrapped). Generally, methylation switches genes off and acetylation switches them on. Factors within the environment can influence these mechanisms, which together can change the way genes are turned on or off. In addition to altering the epigenetic code in ways that affect an individual across the lifespan, recent evidence has demonstrated that the epigenetic code acquired throughout life may be inherited – theoretically providing an adaptive advantage for the offspring in preparing them for their future interactions with the world.
Thus in addition to the broader social contexts initially discussed we must also consider 1) post-natal behavioral and social interactions between the parent and the offspring that can impact the epigenetic code, 2) prenatal life involving fetal programming (environmental factors during pregnancy that may influence the fetus and affect its development) and finally, 3) pre-conception contexts (the impact of the parental and grand-parental environment that may be inherited through the epigenetic code). At all three of these levels the epigenetic code may be altered.
While post-natal behavioral and social interactions and fetal programming have received much attention in recent years, the idea that a ‘pre-conception’ environment may influence the health and susceptibility to disease of the offspring has received less attention. A recent study in rodent animal models investigated the intergenerational effects of nicotine and found that in pregnant rats exposed to nicotine, the offspring and the ‘grand-offspring’ develop the same asthma induced by nicotine3. Studies in humans related to nutrition and diet have found that grand-parental food supply is associated with mortality risk, cardiovascular disease and diabetes in the grand-children (even if the grand-children and their parents had a healthy diet and nutrition)4. Diet, environmental toxicants, drugs and particularly stress have the ability to severely impact an individual, and now it seems, to also impact their offspring and grand-offspring.
Stressful conditions and negative environmental factors such as exposure to traumatic or violent events can affect brain functions and mental health throughout life, and we are only beginning to understand how the impacts of these stressors may be transgenerationally passed on to future generations. These data all highlight the critical need for understanding the multiple and complex contexts (both immediate and indirect) within which a child develops.
1Franklin TB, Mansuy IM (2010). Epigenetic Inheritance in mammals: evidence for the impact of adverse environmental effects. Neurobiology of disease 39(1):61-65.
2Bird A (2007). Perceptions of epigenetics. Nature 447: 396-398.
4Pembrey ME, Bygren LO, Kaati G, Edvinsson S, Northstone K, Sjostrom M et al (2006). Sex-specific, male-line transgenerational responses in humans. Eur J Hum Genet 14: 159-166.