Evocative genotype-environment correlation refers to how the social environment reacts to individuals based on their inherited characteristics. For example, whether one has a more outgoing or shy temperament will affect how they are treated by others.
Active genotype-environment correlation occurs when individuals seek out environments that support their genetic tendencies. This is also referred to as niche picking. For example, children who are musically inclined seek out music instruction and opportunities that facilitate their natural musical ability.
Conversely, genotype-environment interactions involve genetic susceptibility to the environment. Adoption studies provide evidence for genotype-environment interactions. For example, the Early Growth and Development Study (Leve, Neiderhiser, Scaramella, and Reiss, 2010) followed 360 adopted children and their adopted and biological parents in a longitudinal study. Results showed that children whose biological parents exhibited psychopathology had significantly fewer behavioural problems when their adoptive parents used more structured parenting than unstructured. Additionally, elevated psychopathology in adoptive parents increased the risk for the children’s development of behavioural problems, but only when the biological parents’ psychopathology was high. Consequently, the results show how environmental effects on behaviour differ based on the genotype, in particular the effects of stressful environments on genetically at-risk children.
Lastly, epigenetics studies modifications in DNA that affect gene expression and are passed on when the cells divide. Environmental factors, such as nutrition, stress, and teratogens are thought to change gene expression by switching genes on and off. These gene changes can then be inherited by daughter cells. This would explain why monozygotic or identical twins may increasingly differ in gene expression with age. For example, Fraga et al. (2005) found that when examining differences in DNA, a group of monozygotic twins were indistinguishable during the early years. However, when the twins were older there were significant discrepancies in their gene expression, most likely due to different experiences. These differences included susceptibilities to disease and a range of personal characteristics.
Box 2.2 The Human Genome ProjectIn 1990 the Human Genome Project (HGP), an international scientific endeavour, began the task of sequencing the three billion base pairs that make up the human genome. In April of 2003, more than two years ahead of schedule, scientists gave us the genetic blueprint for building a human. Since this time, using the information from the HGP, researchers have discovered the genes involved in over 1,800 diseases. In 2005 the HGP amassed a large database called HapMap that catalogs the genetic variations in eleven global populations. Data on genetic variation can improve our understanding of differential risk for disease and reactions to medical treatments, such as drugs. Pharmacogenomic researchers have already developed tests to determine whether a patient will respond favourably to certain drugs used in the treatment of breast cancer or HIV by using information from HapMap (NIH, 2015). Future directions for the HGP include identifying the genetic markers for all fifty major forms of cancer (The Cancer Genome Atlas), continued use of the HapMap for creating more effective drugs for the treatment of disease, and examining the legal, social, and ethical implications of genetic knowledge (NIH, 2015). From the outset, the HGP made ethical issues one of their main concerns. Part of the HGP’s budget supports research and holds workshops that address these concerns. Who owns this information, and how the availability of genetic information may influence healthcare and its impact on individuals, their families, and the greater community are just some of the many questions being addressed (NIH, 2015). |
