Genetic Origins of Aggression

12 Key excerpts on "Genetic Origins of Aggression"

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  Biological Psychiatry

  • Edward Bittar(Author)
  • 1999(Publication Date)
  • Elsevier Science

    (Publisher)

  It should be admitted at the outset that even focusing on particular expressions of aggression, such as assault, homicide, or rape, does not lead to simple associations with biological factors. This review broadly looks at some of the more recent writings on the role(s) of biological factors in aggression with the intention of illustrating the modem approaches and concerns. AGGRESSION AND GENES Behavior genetics (e.g., Royce and Mos, 1979) is currently a growth area of research. In spite of the public misconception that scientists are looking for the gene involved in aggression, it is obvious that genes interact, influence developing ana-tomical and physiological systems, and are involved in interplay with the environ-ment. For many years, people have been intrigued about suggestions of links between genetic endowment and human hostility (e.g., Christiansen, 1968; Owen, 1972; Cadaret, 1978; Gottesman et al., 1983; Mednick et a1.,1987). This area has been recently substantially reviewed and re-evaluated by Carey (1994) and a Sym-posium on Genetics of Criminal and Antisocial Behaviour (edited by Bock and Goode, 1996). Carey (1994) concludes that there is a trend in most studies (of vio-lence and human genetics), albeit not always a statistically significant one, consis-tent with the hypothesis of a genetic effect on adult and perhaps adolescent anti-social behaviour. (p. 42). He points out, however, that it is not easy to integrate this literature into contemporary criminological research on violence in the U.S. In addition, the genetics of antisocial behavior do not fit any simple additive model. Carey (1994) points out that the joint effects of marital assortment, temporal trends over time, nonadditive genetic variance, special twin effects, etc., must be considered in studying the genetics of antisocial behaviour (p. 42). The evidence for a genetic effect primarily on offenses involving physical aggression is not impressive.

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  Aggression and Violence

  Genetic, Neurobiological, and Biosocial Perspectives

  • David M. Stoff, Robert B. Cairns(Authors)
  • 2014(Publication Date)
  • Psychology Press

    (Publisher)

  aggression is therefore not a phenotype for genetic analysis. Narrower or better-defined categories of aggression can be utilized; much of the relevant work on aggression is on neuropsychological phenotypes and psychiatric diagnoses, which are associated with forms of aggression but which represent goals in their own right. A full appreciation of the genetic antecedents of aggression would require a better understanding of what aggression is, as well as the identification of genetic and nongenetic origins of interindividual differences in a wide variety of behaviors. Changing the definition of aggressive behavior will obviously change the genes involved.

  Both within and outside the laboratory, pharmacological manipulations of neurochemical systems moderate and augment impulsive and aggressive behaviors. By manipulating serotonin, particular murine-aggressive behaviors can be augmented or reduced. Androgen levels also play a role in determining aggressiveness, for example, rough-and-tumble play (Levine, 1966 ; see also Gariépy, Lewis, and Cairns, chap. 3 , this volume). In humans, aggressive behavior is frequently released only when the individual is intoxicated. These interactions between aggression and drugs resemble gene–environment interactions in behavior. More importantly, for the purpose of discovering the determinants of aggression, results from behavioral pharmacology may also serve to identify the neurochemical pathways where genetic variants alter individual variation in the predisposition to such behaviors.

  Functionally variant alleles cause heritable behavioral variation in impulsiveness and aggressivity. In animals, the behavioral variation resulting from the differential action of these alleles is exemplified by behavioral differences between species and between strains of animals (Plomin, 1990

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  The Social Psychology of Aggression

  3rd Edition

  • Barbara Krahé(Author)
  • 2020(Publication Date)
  • Routledge

    (Publisher)

  With regard to the question of whether or not aggression is an inevitable part of human nature and individual character, research showing the impact of genetic factors has sometimes been construed as suggesting a deterministic, and thus pessimistic, view – if individuals carry the aggressive genes, they will grow up to be aggressive. However, such a view is rejected by behaviour geneticists. They stress that individuals’ genetic make-up may predispose them towards becoming an aggressive person, but environmental factors play a crucial role in determining whether or not that predisposition will actually be expressed in aggressive behaviour. As noted by Van Goozen, Fairchild, Snoek, and Harold (2007), a genetic disposition towards aggressive behaviour may become manifested in behaviour in a negative family environment, or it may be suppressed in a positive environment. As children inherit the genetic disposition towards aggression from their parents, they are likely to grow up in a more aggression-prone family environment (Moffitt, 1993). To complicate matters further, children with a genetic disposition towards aggression may elicit negative responses from their social environment through their aggressive behaviour, also pointing to the interactive influences of nature and nurture.

  The critical role of environmental factors is also demonstrated by evidence from the field of epigenetics . This research has shown that adverse experiences affecting individuals at sensitive periods of life, especially in prenatal development and early infancy, may trigger changes in the function of genes that lead to cognitive and emotional deficits involved in aggressive behaviour (Palumbo, Mariotti, Iofrida, & Pellegrini, 2018; Waltes et al., 2016). These findings show that genetic (inherited) and environmental (acquired) factors mutually influence each other, which may explain why individual differences in aggressive behaviour are highly stable over time. We will return to the issue of stability in more detail in Chapter 4 .

  epigenetics: field of study showing that adverse experiences may change a person’s genes related to aggressive behaviour.

  H ormones and aggression

  hormones: higher levels of testosterone and lower levels of cortisol have been linked to aggression, but they need to be considered in combination with environmental influences.

  Another line of biological research on aggression is concerned with the role of hormonal and other physiological processes in explaining variations in aggressive behaviour (Archer & Carré, 2017; Van Goozen, 2005). An obvious candidate for examination is the male sex hormone testosterone, both to account for individual differences among men in their aggressive tendencies, and to explain the widely demonstrated gender differences in physical aggression (see Chapter 4

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  The Radical Right

  Biopsychosocial Roots and International Variations

  • Klaus Wahl(Author)
  • 2019(Publication Date)
  • Palgrave Macmillan

    (Publisher)

  2012 ).

  Violence is often seen as an element of right-wing extremism. Aggressiveness is strongly dependent on genetic and epigenetic factors. Several twin studies found aggression and other forms of externalizing and antisocial behavior to not only be strongly influenced by genetic factors but also by environmental factors like stress in childhood (Baker, Jacobson, Raine, Lozano, & Bezdjian, 2007 ; Eley, Lichtenstein, & Moffitt, 2003 ; Pérusse & Gendreau, 2005 ; Rhee & Waldman, 2002 ; Rowe, Almeida, & Jacobson, 1999 ; Wichers et al., 2013 ).

  Genetic, epigenetic , and environmental factors are interacting : biological variables influence social behavior and, vice versa, ecological risk factors and social behavior (e.g., poverty or exposure to violence at home) influence biological variables. Particularly, two genes regulating impulse control, the monoamine oxidase A (MAO A) low-activity genotype (contributing to low dopamine turnover rate) and the cadherin 13 (CDH13) gene (associated with attention-deficit/hyperactivity disorder, ADHD) were connected with extremely violent behavior (Tiihonen et al., 2014 ). In addition, a polymorphism of the MAO A gene conditioned the influence of child abuse on antisocial outcomes over the course of one’s life. This was revealed by observations of parents who spanked their children . Such physical punishment itself was correlated with aggressiveness of children, but the majority of spanked children did not develop behavioral problems. To understand this fact, several studies suggested that genes might play a key role in moderating some environmental risk factors (gene-environment interaction ) (Boutwell, Franklin, Barnes, & Beaver, 2011 ; Buckholtz & Meyer-Lindenberg, 2008 ; Caspi et al., 2002 ). Another example of gene-environment interactions is that prenatal smoke and drug exposure conditioned the influence of genetic risk factors in the prediction of aggressive behavior (Bendersky, Bennett, & Lewis, 2006 ; Huijbregts, Séguin, Zoccolillo, Boivin, & Tremblay, 2007 ; Petkovsek, Boutwell, Beaver, & Barnes, 2014 ; Sood et al., 2001 ; Yochum et al., 2014

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  Intermittent Explosive Disorder

  Etiology, Assessment, and Treatment

  • Emil F. Coccaro, Michael S. McCloskey(Authors)
  • 2019(Publication Date)
  • Academic Press

    (Publisher)

  epi genetic markers. Notably, while most clinical studies focus on antisocial personality disorder, (epi)genetic research in psychiatric disorders that have aggression as a core symptom (such as IED) is scarce. Multidisciplinary collaborative research of genetic and epigenetic factors at various ages throughout the lifespan in well-characterized clinical and nonclinical study samples is needed to further shed light on the specific genetic and epigenetic contributions to (different types of) aggression including IED.

  Keywords

  Behavioral genetic research design; Neurobiology of Aggression; population; Tryptophan hydroxylases; Oxytocin

  Contents

  • Aggressive Behavior
  • Behavioral Genetic Research Design
  • Behavioral Genetic Research Design: Generalizability and Assumptions
    • Generalizability From Twin Studies to the General Population
    • The Equal Environment Assumption (EEA)
    • Random Mating
    • Gene–Environment Interaction and Correlation
    • Generalizability From Adoption Studies to the General Population
  • Metaanalyses and Systematic Reviews Summarizing Studies Examining the Influence of Genetic and Environmental Factors on Aggressive Behavior
  • Recent Studies Using a Behavioral Genetic Research Design
  • Neurobiology of Aggression—Where to Look for the Relevant Genes?
  • Candidate Gene Studies
    • Regulation of Monoamine Level: MAOA and MAOB
    • Serotonin Transporter 5-HTT (SLC6A4)
    • 5-HT Receptors and Tryptophan Hydroxylases
    • Components of the Dopaminergic System
    • Oxytocin and Arginine Vasopressin Systems
    • Other Candidate Genes of Interest
  • Genome-Wide Association Studies (GWASs)
    • GWASs of Aggression
  • Epigenetics of Aggression
  • Conclusion
  • References

  Aggressive Behavior

  Aggressive behavior is commonly defined as a behavior that is intended to cause pain or harm to another person who is motivated to avoid that harm (Bushman & Huesmann, 2010 ). This harm can take many forms and aggressive behavior is divided into various subtypes, based on in what way and situation this behavior is carried out. Subtypes include (but are not limited to) reactive, hostile, or affective aggressive behavior; proactive or instrumental aggressive behavior; indirect or relational aggressive behavior and verbal aggression (Allen & Anderson, 2017 ). Violence is considered a more extreme form of aggressive behavior that has severe physical harm as its goal. Aggressive behavior and violence are considered to be on the same continuum, where aggressive behavior is at the less severe and violence at the more severe end (Allen & Anderson, 2017

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  Social Psychology

  • Saba Safdar, Catherine A. Sanderson(Authors)
  • 2021(Publication Date)
  • Wiley

    (Publisher)

  Other evidence that suggests the role of genetics in predicting aggressive behaviour comes from longitudinal research indicating that children who are highly aggressive early in life are more likely to be aggressive later. For example, men and women with high-level childhood adversity were asso- ciated with increased risk of perpetrating compared to increased risk among men and women with low-level adversity (Roberts, McLaughlin, Conron, & Koenen, 2011). In one study of twins, over 750 participants at two age points, age 9 to 10 and 14 to 15 years, were examined (Niv, Tuvblad, Raine, & Baker, 2013). Participants were gathered from Los Angeles where their accompanying parent participated in daylong clinical interviewing and answering questionnaires that were aimed at assessing home and school environment, behaviour, personality, and psychopathol- ogy of both twins as well as of the parent. This study examined the structure of genetic and environ- mental influences on aggression and rule-breaking in order to examine change and stability across the span of childhood to mid-adolescence. Aggression and rule-breaking were found to be influenced by a latent common factor of antisocial behavior (ASB) within each wave of data collection. The variance in the childhood-age common factor of ASB was influenced by 41 percent genetics, 40 percent shared environment, and 19 percent non-shared environment. In adolescence, 41 percent of variance in the common factor were genetic, while both shared and non-shared environments remained stable over time. Additionally, both aggression and rule-breaking within each wave were found to have unique influences not common across subscales or across waves, highlighting specificity of genetic and envi- ronmental effects on different problem behaviours at both ages (Niv et al., 2013).

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  Violence Rewired

  Evidence and Strategies for Public Health Action

  • Richard Whittington, James McGuire(Authors)
  • 2020(Publication Date)
  • Cambridge University Press

    (Publisher)

  The most common finding of reviews in this area is that very little is discovered that is of any real substance. If genetic influences were a main driver of human aggressiveness, it would be reasonable to expect there to be more persuasive results from the sequence of studies just reviewed. The discrepancy between the conclusions of heritability stud- ies and the outcomes of both candidate gene and genome-wide studies gives rise to some uncertainty over existing models of how genes work in influencing features of the human phenotype. 90 Origins Parallels in Research on Mental Disorders When considering the roles of genetic influences on aggression, there are illuminating parallels we can draw with research on the genetics of schizophrenia and other major psychiatric diagnoses. As with aggression and violence, the definition of many of these involves a mixture of sometimes quite dissimilar phenomena. There are high levels of hetero- geneity within disorder categories and of comorbidity between them. There are consequent disagreements as to the scientific validity of some of the constructs employed (Hyman, 2010). Nevertheless, evidence from the type of twin and allied studies outlined above has indicated a high level of heritability for schizophrenia, and many psychiatric texts and research papers refer to it as a heritable brain disease. At an individual case level, clinical reports almost routinely include information on a patient’s first- and second-degree relatives who have been diagnosed with mental disorders. Given those presuppositions, there has been extensive research into the genes that might be responsible for schizophrenia. In recent years that work has extended to encompass several other diagnostic categories in addition to schizophrenia itself, coordinated by a worldwide research group, the Psychiatric Genomics Consortium (PGC), which as of 2018 included more than 800 researchers from over forty countries (Plomin, 2018).

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  Origins of Aggression

  • Willard W. Hartup, Jan de Wit, Willard W. Hartup, Jan de Wit(Authors)
  • 2019(Publication Date)
  • De Gruyter Mouton

    (Publisher)

  Then the means by which aggression is affected must be determined. Considering first genetic differences, these may influence aggression by diverse routes such as the production of changes in effectors or in the stimuli presented to another individual, or changes in the ability to profit by experience, or in diverse other mechanisms as well as in those specifically associated with aggression. But there is also a special difficulty in studying genetic influences on aggression in mammals which arises from the facts that (a) aggressiveness is also affected by the early social environment, and especially by the type of maternal care received; (b) the early social environment provided by the social companions is influenced by their genetic constitution, and this (especially in the case of the mother) is likely to be closely linked to that of the subject; and (c) the early social experience depends on interactive relationships, so that, for instance, the maternal care received depends on the behavior of the subject as well as on that of the mother. The possible complexities are considerable (Figure 5). Turning now to studies of the influence of experiential factors on aggression, it seems important that the factors manipulated in ex-perimental studies should be relatively small. For example, the usefulness of assessing the effects of rearing animals in isolation Figure 5. Diagrammatic representation of the complexities arising in studies of the genetic bases of aggression in mammals. The discontinuous lines indicate the effects of unspecified causal factors Genetic constitution of social companions > I Social behavior of companions Interactional T relationship N Genetic constitution of subject Social behavior of subject Aggressive behavior of subject The study of aggression 13 seems rather doubtful. Rearing in isolation is such an extreme con-dition and could affect aggression in diverse ways.

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  Drug Abuse and Antisocial Behavior

  A Biosocial Life Course Approach

  • Christopher P. Salas-Wright, Michael G. Vaughn, Jennifer M. Reingle González(Authors)
  • 2017(Publication Date)
  • Palgrave Macmillan

    (Publisher)

  In the case of substance use disorders, the powerful modulatory role played by complex environmental factors on brain processes which further muddle the picture, is particularly relevant. This is because, in the absence of drug exposure, itself an environmental factor, the specific addiction phenotype would remain hidden, even in the presence of an overwhelming genetic load. On the other hand, brain development and architecture, which are partly determined by genetic factors, can be affected by exposure to drugs. These two way interactions highlight the importance of genes involved in human brain development and function in the subsequent emergence of personality styles and emotional behavior reactivities. (p. 773)

  And yet, despite the enormous complexity, critical advances have been made in uncovering clues about the genetics of these multifactorial phenotypes.

  Genetics, Addiction, and Antisocial Behavior

  The Genetic Framework for Studying Addiction

  Studying the genetic architecture of addiction requires a unique and powerful set of interrelated techniques and methods. These techniques include heritability estimates, molecular genetics, and gene–environment interplay (which include studies of gene–environment interaction as well correlation studies). Each offers a unique contribution to our understanding of the inter-relationships between genetics and addiction, as well as antisocial behavior. As expected of almost any technique, each method faces a number of important limitations. It is worthwhile here to take a look the fundamental method and contribution of each of the major approaches used in studying the influence of genetic factors in addiction, antisocial behavior, and human behavior in general.

  Heritability Estimates

  Behavioral geneticists usually organize the variance in addiction (and other behaviors as well) along three quantitative dimensions. One of these three dimensions is heritability (h2 ) which, of course, reflects the contribution of genetics to addiction. The remaining two dimensions are environmental in nature. One is known as the shared environment (c2 ) and the other the nonshared environment (e2 ). These are often difficult to explain, but—if you think of a study of adoptive and nonadoptive siblings—one can think of the shared influence of family, household, and community factors (e.g., family stress, the number of books in the home, or exposure to community violence) to be the shared environment. The nonshared

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  Aggression and Violence

  A Social Psychological Perspective

  • Brad J. Bushman(Author)
  • 2016(Publication Date)
  • Routledge

    (Publisher)

  Personal predispositions are influenced over time by a variety of biological and environmental influences that lead to the development of characteristic emotional reactions, cognitions, and cognitive processing. Consequently, some people grow up to be more predisposed to behave more aggressively in almost any situation. Situational determinants then prime the cognitions and emotional reactions linked to the situation in associative memory (Bargh & Pietromonaco, 1982; Fiske & Taylor, 1984). Extreme situations can instigate almost anyone to behave aggressively. Second, habitual aggressive behavior usually emerges early in life, and early aggressive behavior is very predictive of later aggressive behavior and even of aggressive behavior of offspring (Farrington, 1985; Huesmann et al., 1984; Olweus, 1979). Process models for aggressive behavior explain this continuity over time and across generations by the development of cognitive and emotional predispositions to aggression that last over time. Third, predispositions to severe aggression are most often a product of multiple interacting social and biological factors (Huesmann, 1997), including genetic predispositions (Cloninger & Gottesman, 1987; Mednick et al., 1984), environment/ genetic interactions (Caspi et al., 2002; Lagerspetz & Lagerspetz, 1971), central nervous system (CNS) trauma and neurophysiological abnormalities (Moyer, 1976), early temperament or attention difficulties (Kagan, 1988), arousal levels (Raine et al., 1990), hormonal levels (Olweus et al., 1988), family violence (Widom, 1989), cultural perspectives (Staub, 1996), poor parenting (Patterson, 1995), inappropriate punishment (Eron et al., 1971), environmental poverty and stress (Guerra et al., 1995), peer-group identification (Patterson et al., 1991), and other factors

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  The SAGE Handbook of Evolutionary Psychology

  Integration of Evolutionary Psychology with Other Disciplines

  • Todd K. Shackelford, Todd K. Shackelford, Editor(Authors)
  • 2020(Publication Date)
  • SAGE Publications Ltd

    (Publisher)

  Note that while these three genes would have some influence over the propensity for aggression, none would determine the use (or non-use) of aggression in any particular situation; rather, all that these allelic combinations would produce are different propensities that may or may not surface in different situations. Individuals with a high genetic propensity for aggression are not destined to aggress; likewise, even those with the lowest risk for aggression may become violent if embedded in a certain environment. Therefore, behavioral responses result from a combination of genetic influences and environmental stimuli. For example, in a landmark study by Caspi et al. (2002), they investigated whether the effect of a genetic polymorphism – MAOA – was partially responsible for producing variation in antisocial phenotypes. The researchers reported that MAOA in and of itself had no influence on antisocial outcomes; however, MAOA was associated with antisocial phenotypes for males who had been maltreated in childhood, but not for males who were not maltreated. Taken together, these findings highlight the role that environments play when it comes to genetic effects.

  The second way genes are connected to phenotypes is via what is known as a monogenic effect, where one gene is the cause of one particular phenotype. Sickle-cell disorder, as an example, is an inherited disorder that affects red blood cells. Individuals with sickle-cell disease were born with two sickle-cell genes, one from each parent, and thus the disorder is due to a monogenic effect. Lastly, pleiotropy captures the effects that a single gene has on various phenotypes. The allele that causes the disorder phenylketonuria, for example, leads to an absence or deficiency of the enzyme (phenylalanine hydroxylase) responsible for processing the essential amino acid phenylalanine. These amino acids are important for proper growth and development, and, without treatment, affected individuals may experience neurological symptoms in addition to other psychiatric disturbances.

  The genetic origins of complex human traits, such as personality and social behaviors, are largely polygenic, and, as a result, the influence of any particular gene on any particular trait tends to be very small and may be statistically undetectable. Even so, genetic polymorphisms are of particular interest to scientists because they have the potential to explain phenotypic variance. Genes that do not vary – that is, they are not polymorphic – could explain human universals, but they are typically assumed to be unable to explain phenotypic differences (though, theoretically, they could explain phenotypic differences via epigenetic effects, a topic that is beyond the scope of this chapter (but see Bateson, 2014)). As a result, most of the research that has attempted to examine genes associated with phenotypes has focused on examining whether different alleles of a polymorphism are correlated with phenotypic differences. For example, in an early candidate gene association study, researchers looked to see whether a specific genetic polymorphism – specifically, the D4 dopamine receptor gene (D4DR) – was associated with the human personality trait of novelty seeking (Ebstein et al., 1996). Individuals who score higher than average on the TPQ Novelty Seeking scale are characterized as impulsive, exploratory, excitable, quick-tempered, and extravagant, whereas those who score lower than average tend to be reflective, rigid, loyal, slow-tempered, and frugal. Researchers found that higher scores on the Novelty Seeking test were significantly associated with the long allele for the D4DR gene. Thus, they found evidence of an association between a specific allele and a behavioral outcome.

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  Social Psychology: A Complete Introduction: Teach Yourself

  • Paul Seager(Author)
  • 2014(Publication Date)
  • Teach Yourself

    (Publisher)

  Having looked at some of the issues to be resolved when studying aggression systematically, it is now possible to look at two general approaches – biological explanations (nature) vs. learning explanations (nurture) – which have attempted to account for why people behave aggressively.

  Biological explanations for aggression

  This approach takes the form of ‘instinct theories’ of aggression which explain why humans have an innate need to aggress. According to Freud, aggression is inevitable, and his early psychodynamic theory suggested that it was a reaction to frustration experienced in pursuit of pleasure and the satisfaction of the libido. He later modified his idea to allege that, alongside the desire for self-preservation, referred to as Eros (the life instinct), there was a second instinct more focused on destruction, referred to as Thanatos (the death instinct). He claimed that this destructive aggressive energy needed to be continually turned away from the individual towards the outside, in order to prevent self-destruction: aggressive behaviour thus serves as an outlet when Eros and Thanatos are in conflict. This is sometimes referred to as a hydraulic model – aggression is a way of dissipating the build-up of pressure. From Freud’s model we get the idea of catharsis, whereby hostility and aggression are diffused in a non-destructive way.

  Key idea: Eros and Thanatos

  According to psychodynamic theory, to protect Eros (the life instinct) within an individual, the destructive energies of Thanatos (the death instinct) must be continually deflected away, and this manifests outwardly as aggression.

  Another biological theory of aggression, similar to Freud’s theory in as much that it is a hydraulic model, comes from Lorenz, who believed that aggression has a species serving function. Lorenz claimed that aggression is an innate behavioural disposition which derives from the idea of natural selection, and increases the species’ chance of survival. The potential for conflict leads to geographical dispersion which has the effect of ensuring that members of the same species have sufficient resources to survive and flourish. Applying an animal model to humans, he claimed that hierarchies developed and fights between rivals ensured selection of the strongest and healthiest to lead. Ultimately, aggression builds up and needs to be released in a socially acceptable way (hence it is referred to as a hydraulic model). In animals this is done through threat displays and the ritualization of aggression; very rarely do fights lead to permanent injury or death due to their use of appeasement gestures. It is questionable whether this model can really be applied to humans, who have developed weapons that can kill from a distance.

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