Causality in Philosophy; Philosophy in Psychology

Abstract

The phenomenon of Genetic × Environmental (G × E) interaction illustrates not only the genetic revolution but also the environmental one. Neither genes nor environment are considered as separate and additive causal factors in development. Rather, now they are each considered multifactorial, as is their interaction. The current chapter especially presents a detailed literature review of the effects of G × E on behavior. Some of the polymorphisms involved include those related to MAOA, 5-HTTLPR, OXTR (oxytocin receptor), CRHR1 (corticotropin releasing hormone receptor 1), BDNF (brain-derived neurotrophic factor), NET (norepinephrine transporter; SLC6A2; solute carrier family 6 member 2), and DAT1 (dopamine active transporter gene). The outcomes include antisocial behavior, anger, depression, ADHD (attention deficit hyperactivity disorder), educational attainment, etc. Generally, the psychopathological effects can be qualified as internalizing and externalizing. The environments involved include child abuse, early adversity, and multiple aspects of parenting. The findings are complex, including differential effects according to age, gene, environment, and outcome. Moreover, the qualifications of G × G × E, G × E × E, and G × E × D interactions reveal the complexities in behavioral genetics research. The chapter examines other genetic processes, such as epigenetics, differential susceptibility, and NLDST. Some of the most striking findings in the chapter relate to the longitudinal associations found. Clearly, just as the environment early in life is now considered as having an enduring impact so, too, should the effects of genes; they are not overwhelmed in their causal impact on behavior by environmental impacts. Once more, the interaction of genes and environment in behavioral causality stands out according to the empirical research.