Genetics of aggression

Source: Wikipedia, the free encyclopedia.

The field of psychology has been greatly influenced by the study of genetics.[1] 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). 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.[2]

The genetic-developmental theory states that individual differences in a continuous

Mendelian trait (one gene for one phenotype).[3]

History

Past thoughts on genetic factors influencing aggression, specifically in regard to sex chromosomes, tended to seek answers from

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 6 ft. tall in a survey of 314 patients at the State Hospital for Scotland; seven of the nine XYY patients were mentally retarded.[5] 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.[6]

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.[7]

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.[8][9]
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
:

These three main experimental types are used in animal studies, studies testing heritability and molecular genetics, and gene/environment interaction studies. Recently, important links between aggression and genetics have been studied and the results are allowing scientists to better understand the connections.[10]

Selective breeding

The

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.[11] 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

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.[13]

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.[14] 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+/+).[14] The basis for the association of oxidative stress with increased aggression has not yet been determined.

Biological mechanisms

Experiments designed to study biological mechanisms are utilized when exploring how

genes and studying the effect(s) of the manipulation.[15]

Molecular genetics

A number of

pharmaceuticals to fix the pathway problems and hopefully show an observed change in aggressive behavior.[16]

Human behavior genetics

In determining if a

DRD2 genes are heavily related to the genetics of aggression.[17][18] The DAT1 gene plays a role for its heavy relation to regulation of neurotransmission. The DRD2 Gene results in humans finding seemingly rewarding paths such as drug abuse. Through studies, DRD2 seems to be a risk factor in delinquency when children have related family trauma events.[19]

DAT1 is a gene that regulates dopamine levels in the brain. This study revealed that variations in the DAT1 gene were correlated with higher levels of aggression. Some people that have variations of the DAT1 gene exhibit more aggressive behaviors. DAT2 controls how the brain responds to dopamine. Certain combinations of DAT1 and DAT2 genes were linked to an increase or decrease in aggressive behaviors. While the relationship remains unclear, there is certainly a correlation between certain forms of DAT1 and DAT2 and varying combinations of each. [20] Changes in these genes can cause changes in neurotransmitter levels. When typical neurotransmitter levels change, other bodily behaviors are also affected. Examples of other functions that are impacted are intelligence, mood, and memory. [21]

Twin studies

Twin studies are studies typically conducted comparing

fraternal twins. They aim to reveal the importance of environmental and genetic influences for traits, phenotypes, and disorders. Before the advancement of molecular genetics, twin studies were almost the only mode of investigation of genetic influences on personality. Heritability was estimated as twice the difference between the correlation for identical, or monozygotic, twins and that for fraternal, or dizygotic, twins. Early studies indicated that personality was fifty percent genetic. Current thinking holds that each individual picks and chooses from a range of stimuli and events largely on the basis of their genotype creating a unique set of experiences; basically meaning that people create their own environments.[13] It has been determined that there is a window in childhood that certain trauma events can trigger a lifetime of aggressive behavior.[citation needed
]

Adoption studies

Adoption studies are a specific research designs that involve comparing traits between an adopted child and their biological and adoptive parents. These experiments aim to assess both biological and environmental factors that may be attributed to aggression. Adoption studies have shown stronger similarities between adopted children and their biological parents, indicating that there is a genetic component at play. However, children have also shown similarities with their adoptive parents, indicating that there are environmental factors as well. These studies further support the complex nature of aggression by proving that there are both biological and environmental factors involved. More research needs to be conducted to truly prove the causes of aggression. [22]

Genetics of aggression over time

Over time, studies pertaining to the genetics of aggression have improved, and become an interesting research topic for those looking for research opportunities. Experiments started in 1963 with the

Milgram's experiment. The results of this experiment proved that in certain situations, people can be coaxed into aggression and violence. The next big experiment pertaining to the genetics of aggression took place in 1973 as part of the Stanford prison experiment. The conclusion drawn from this experiment was that in many cases, aggression is very unexpected at certain points. It was considered to be "elicited." This also revealed that aggression is often triggered in situations where someone feels an ideology that they hold a very powerful authority over someone else. It was concluded from both experiments that social aspects prove to be a big factor in the way people act aggressively. It was also concluded that every person has a potential to output aggressive behavior, but what is different between people is the extent of the point it takes to reach that output.[citation needed
]

Male vs female aggression

Aggression can manifest in different ways between biological males and females. A study evaluated these differences by using EEG and ECG to monitor neurobiological responses to aggravating stimuli. It was shown that anger and physical aggression was much greater in men than women. Men also scored higher on a scale regarding reactive aggression. The EEG test also supported the idea that women show weaker responses regarding aggression. It was also shown that men and women follow different pathways in the brain when aggression is invoked, although further studies are needed in order to solidify these findings. [23]

Environmental factors

Aggression can have many causes, including environmental factors. Environmental factors include any physical, chemical, and biological environmental factors that can influence aggression. Studies have shown that neighborhood greenspace can vastly reduce aggressive behaviors in children and adolescents. One proposed explanation for this finding is that greenspace has been proven to reduce stress and depression. HIgher stress and depression levels in parents have been shown to increase aggressive behaviors in children. By lowering stress and depression in parents, children are more likely to show a decrease in aggressive behaviors. In addition, greenspace promotes participation in physical activity and social involvement. Another study revealed that low-frequency, high-intensity, and continuous noises were associated with more aggressive behaviors. [24]

See also

Notes

  1. S2CID 17398272
    .
  2. PMID 27061441
    .
  3. ^
    ISBN 1-59385-110-3
    .
  4. PMID 4727279
    .
  5. ^ Court Brown, W.M. (1967). Human Population Cytogenetics. Amsterdam: North-Holland Publishing Company.
  6. ISBN 0-7216-5160-7
    .
  7. ISBN 0-471-95719-4
    .
  8. ISBN 0-443-06434-2
    .
  9. ISBN 0-8018-7928-0
    .
  10. ^
    ISBN 0-19-516876-3
    .
  11. ISBN 90-286-2851-7
    .
  12. ^ Southwick, Charles H. (1970). Animal Aggression: Selected Readings. London: Litton Educational Publishing Inc.
  13. ^
    ISBN 0-471-95719-4
    .
  14. ^
    PMID 25524980
    .
  15. ^ Stangor, Charles; Walinga, Jennifer (2019-06-28). "4.4 Is Personality More Nature or More Nurture? Behavioural and Molecular Genetics". Introduction to Psychology.
  16. ^
    S2CID 14070721
    .
  17. PMID 24193094
    .
  18. PMID 15964153
    .
  19. PMID 25419014
    .
  20. PMID 24193094
    .
  21. ^ "The genetics of violent behavior". The Jackson Laboratory. Retrieved 2024-12-02.
  22. ^ "Genetic Factors - Psychology: AQA A Level". senecalearning.com. Retrieved 2024-12-02.
  23. PMID 30636903
    .
  24. PMID 27343886
    .

References
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