The Genetics Revolution

Abstract

The study of causality of behavior is marked by fields undergoing rapid expansion, including the field of genetics. The genetic revolution has witnessed the classic model of genotype → transcription → protein → phenotype evolve to become a supercomplex one of multiple “-omics” (genomics, epigenomics, etc.). The research on candidate genes that aims to find simple gene–behavior associations has been supplemented by genome-wide association studies and genome-wide complex trait analysis (GWAS, GCTA, respectively). The classic search for the heritability in behavioral variation explanation has been supplemented for a search of “missing” heritability. Instead of straightforward genetic main effects, researchers also look for Gene × Environment interaction. These include MAOA × Maltreatment interaction in antisocial behavior outcome. Aside from considering G × E influences on behavior, one needs to consider multiple genes interacting with E and also multiple environmental factors in interaction beyond their interaction with G (G × G × E and G × E × E, respectively), as well as all these types of interactions with D (development). Also, there are correlated G × E findings (rGE), which lie more on the genetic than the environmental side of behavioral causal influence (e.g., phenotypes underlain by certain genotypes lead to behaviors that influence the environment, rather than vice versa). In addition, research is demonstrating epigenetic effects (gene silencing) on genes, which lies more on the environmental side relative to the genetic side of behavioral causal influence. These examples illustrate that even in the area of genetics of behavior the dividing line between genes and environment is fuzzy and interactive. There are numerous key genetic terms in the chapter, given its genetic focus. They include CNVs (copy number variations), VNTRs (variable number of random repeats), and LPR (repeat length polymorphisms). Among the genetic polymorphisms in the chapter, one will find 5-HTTLPR (serotonin transporter polymorphism), COMT (catechol-O-methyltransferase), DRD4 (dopamine receptor D4), and MAOA (monoamine oxidase A). The chapter considers broader phenomena related to genes, such as biointelligence, evolvability, versatility, and polygenetic scores. As for my contributions to the field, I suggest investigation of the “phenome” to better understand the disparate and sometimes conflicting or nonreplicated results on the genome (not to mention my concept of the “loveome”).