The field of psychology has been greatly influenced by the study of genetics. Decades of research have demonstrated that both genetic and environmental factors play a role in a variety of behaviors in humans and animals (e.g. Grigorenko & Sternberg, 2003). Aggression has been one of the main behaviors studied to understand how genes and the environment interact. In social psychology, aggression is usually defined as behavior intended to harm another person who wants to avoid that harm (Allen & Anderson, 2017). The genetic basis of aggression, however, remains poorly understood. Aggression is a multi-dimensional concept, but it can be generally defined as behavior that inflicts pain or harm on another.
The genetic-developmental theory states that individual differences in a continuous phenotype result from the action of a large number of genes, each exerting an effect that works with environmental factors to produce the trait. This type of trait is influenced by multiple factors making it more complex and difficult to study than a simple Mendelian trait (one gene for one phenotype).
History Past thoughts on genetic factors influencing aggression, specifically in regard to sex chromosomes, tended to seek answers from chromosomal abnormalities. Four decades ago, the XYY genotype was (erroneously) believed by many to be correlated with aggression. This idea began after early chromosome studies suggested that men with an extra Y chromosome might be more prone to violent behavior. In 1965 and 1966, researchers at the MRC Clinical & Population Cytogenetics Research Unit led by Dr. Court Brown at Western General Hospital in Edinburgh reported finding a much higher than expected nine XYY men (2.9%) averaging almost 6ft. tall in a survey of 314 patients at the State Hospital for Scotland; seven of the nine XYY patients were intellectually disabled. In their initial reports published before examining the XYY patients, the researchers suggested they might have been hospitalized because of aggressive behavior. When the XYY patients were examined, the researchers found their assumptions of aggressive behavior were incorrect. Unfortunately, many science and medicine textbooks quickly and uncritically incorporated the initial, incorrect assumptions about XYY and aggression—including psychology textbooks on aggression.
The XYY genotype first gained wide notoriety in 1968 when it was raised as a part of a defense in two murder trials in Australia and France. In the United States, five attempts to use the XYY genotype as a defense were unsuccessful—in only one case in 1969 was it allowed to go to a jury—which rejected it. These court cases helped spread the false ideas that having an extra Y chromosome made some people more violent, but later studies found no evidence for it.
Results from several decades of long-term follow-up of scores of unselected XYY males identified in eight international newborn chromosome screening studies in the 1960s and 1970s have replaced pioneering but biased studies from the 1960s (that used only institutionalized XYY men), as the basis for current understanding of the XYY genotype and established that XYY males are characterized by increased height but are not characterized by aggressive behavior. Though the link currently between genetics and aggression has turned to an aspect of genetics different from chromosomal abnormalities, it is important to understand where the research started and the direction it is moving in today.
Heritability As with other topics in behavioral genetics, aggression is studied in three main experimental ways to help identify what role genetics plays in the behavior: Heritability studies – studies focused to determine whether a trait, such as aggression, is heritable and how it is inherited from parent to offspring. These studies make use of genetic linkage maps to identify genes associated with certain behaviors such as aggression. Mechanism experiments – studies to determine the biological mechanisms that lead certain genes to influence types of behavior like aggression. Genetic behavior correlation studies – studies that use scientific data and attempt to correlate it with actual human behavior. Examples include twin studies and adoption studies.
These three main experimental types are used in animal studies, studies testing heritability and molecular genetics, and gene/environment interaction studies. For example, researchers may use mice and rats to better understand how certain genes are linked to aggressive behavior and how these traits show up in people in different situations. Recently, important links between aggression and genetics have been studied and the results are allowing scientists to better understand the connections. Even though things like how someone is raised and their environment matter a lot, more research shows that genetics play an important role in behavior.
Selective breeding The heritability of aggression has been observed in many animal strains after noting that some strains of birds, dogs, fish, and mice seem to be more aggressive than other strains. Selective breeding has demonstrated that it is possible to select for genes that lead to more aggressive behavior in animals. Selective breeding examples also allow researchers to understand the importance of developmental timing for genetic influences on aggressive behavior. A study done in 1983 (Cairns) produced both highly aggressive male and female strains of mice dependent on certain developmental periods to have this more aggressive behavior expressed. These mice were not observed to be more aggressive during the early and later stages of their lives, but during certain periods of time (in their middle-age period) were more violent and aggressive in their attacks on other mice. In another study, mice selectively bred for aggressive behavior showed differences in attack behavior and neurochemical levels in the brain compared to non-aggressive strain. This demonstrates how aggression related traits can be genetically inherited and expressed under specific experimental conditions. Selective breeding is a quick way to select for specific traits and see those selected traits within a few generations of breeding. These characteristics make selective breeding an important tool in the study of genetics and aggressive behavior.
Mouse studies Mice are often used as a model for human genetic behavior since mice and humans have homologous genes coding for homologous proteins that are used for similar functions at some biological levels. Mice aggression studies have led to some interesting insight in human aggression. Using reverse genetics, the DNA of genes for the receptors of many neurotransmitters have been cloned and sequenced, and the role of neurotransmitters in rodent aggression has been investigated using pharmacological manipulations. Serotonin has been identified in the offensive attack by male mice against intruder male mice. Mutants were made by manipulating a receptor for serotonin by deleting a gene for the serotonin receptor. These mutant male mice with the knockout alleles exhibited normal behavior in everyday activities such as eating and exploration, but when prompted, attacked intruders with twice the intensity of normal male mice. In offense aggression in mice, males with the same or similar genotypes were more likely to fight than males that encountered males of other genotypes. Another interesting finding in mice dealt with mice reared alone. These mice showed a strong tendency to attack other male mice upon their first exposure to the other animals. The mice reared alone were not taught to be more aggressive; they simply exhibited the behavior. This implicates the natural tendency related to biological aggression in mice since the mice reared alone lacked a parent to model aggressive behavior.
Oxidative stress arises as a result of excess production of reactive oxygen species in relation to defense mechanisms, including the action of antioxidants such as superoxide dismutase 1 (SOD1). Knockout of the Sod1 gene was experimentally introduced in male mice leading to impaired antioxidant defense. These mice were designated (Sod1-/-). The Sod1-/- male mice proved to be more aggressive than both heterozygous knockout males (Sod1+/-) that were 50% deficient in SOD1, and wild-type males (Sod1+/+). The basis for the association of oxidative stress with increased aggression has not yet been determined.
Further evidence supporting the genetic basis of aggression in mice comes from knockout studies targeting serotonin pathways. In particular, mice lacking the Tph2 gene, which is critical for brain specific serotonin synthesis, exhibited significantly elevated aggression in resident intruder tests, with up to seven times more attacks compared to wild type mice. These mice also showed reduced anxiety like behaviors in standard behavioral assays such as the elevated plus maze and novelty suppressed feeding test. This results provides strong evidence that central serotonin deficiency directly contributes to aggressive behavior.
Drosophila studies As with most insects, aggressive behaviors between male flies commonly occur in the presence of courting a female and when competing for resources. Such behaviors often involve raising wings and legs towards the opponent and attacking with the whole body. Thus, it often causes wing damage, which reduces their fitness by removing their ability to fly and mate.
In order for aggression to occur, male flies produce sounds to communicate their intent. A 2017 study found that songs promoting aggression contain pulses occurring at longer intervals. RNA sequencing from fly mutants displaying over-aggressive behaviors found more than 50 auditory-related genes (important for transient receptor potentials, Ca2+ signaling, and mechanoreceptor potentials) to be upregulated in the AB neurons located in Johnston's organ. In addition, aggression levels were reduced when these genes were knocked out via RNA interference. This signifies the major role of hearing as a sensory modality in communicating aggression.
Other than hearing, another sensory modality that regulates aggression is pheromone signaling, which operates through either the olfactory system or the gustatory system depending on the pheromone. An example is cVA, an anti-aphrodisiac pheromone used by males to mark females after copulation and to deter other males from mating. This male-specific pheromone causes an increase in male-male aggression when detected by another male's gustatory system. However, upon inserting a mutation that makes the flies irresponsive to cVA, no aggressive behaviors were seen. This shows how there are multiple modalities for promoting aggression in flies.
Specifically, when competing for food, aggression occurs based on amount of food available and is independent of any social interactions between males. Specifically, sucrose was found to stimulate gustatory receptor neurons, which was necessary to stimulate aggression. However, once the amount of food becomes greater than a certain amount, the competition between males lowers. This is possibly due to an over-abundance of food resources. On a larger scale, food was found to determine the boundaries of a territory since flies were observed to be more aggressive at the food's physical perimeter.