Aggression

Cross references:   Agonistic Behavior    Impulsivity     Sadism  
Stress
   Fear   Male Dominance Hierarchy    Learned Helplessness   



Searching PubMed for "testosterone aggression" located 1,618 references: 
https://www.ncbi.nlm.nih.gov/pubmed/?term=testosterone+aggression   
   

Searching Google for "aggression" located 59,700,000 references: 
https://www.google.com/search?q=aggression&ie=utf-8&oe=utf-8   


Aggression (Wiki)  
    "In psychology, as well as other social and behavioral sciences, aggression refers to behavior between members of the same species that is intended to cause pain or harm. Predatory or defensive behavior between members of different species is not normally considered "aggression.""  
    "
There are two broad categories of aggression. These include hostile, affective, or retaliatory aggression and instrumental, predatory, or goal-oriented aggression  Empirical research indicates that there is a critical difference between the two, both psychologically and physiologically.
"       
    "Aggression is overt, often harmful, social interaction with the intention of inflicting damage or other unpleasantness upon another individual. It may occur either in retaliation or without provocation. In humans, frustration due to blocked goals can cause aggression. Human aggression can be classified into direct and indirect aggression, whilst the first is characterized by physical or verbal behavior intended to cause harm to someone, the second one is characterized by a behavior intended to harm social relations of an individual or a group.    

    In definitions commonly used in the social sciences and behavioral sciences, aggression is a response by an individual that delivers something unpleasant to another person.[2] Some definitions include that the individual must intend to harm another person.[3] Predatory or defensive behavior between members of different species may not be considered aggression in the same sense.

    Aggression can take a variety of forms, which may be expressed physically, or communicated verbally or non-verbally: including anti-predator aggression, defensive aggression (fear-induced), predatory aggression, dominance aggression, inter-male aggression, resident-intruder aggression, maternal aggression, species-specific aggression, sex-related aggression, territorial aggression, isolation-induced aggression, irritable aggression, and brain-stimulation-induced aggression (hypothalamus).  

    There are two subtypes of human aggression:  

(1) controlled-instrumental subtype (purposeful or goal-oriented); and 

(2) reactive-impulsive subtype (often elicits uncontrollable actions that are inappropriate or undesirable). Aggression differs from what is commonly called assertiveness, although the terms are often used interchangeably among laypeople (as in phrases such as "an aggressive salesperson").[4]

Contents

  • 1 Overview
  • 2 Etymology
  • 3 Ethology
  • 4 Evolutionary explanations
  • 5 Physiology

    • 5.1 Brain pathways
    •     "Many researchers focus on the brain to explain aggression. Numerous circuits within both neocortical and subcortical structures play a central role in controlling aggressive behavior, depending on the species, and the exact role of pathways may vary depending on the type of trigger or intention.[1]
          In mammals, the hypothalamus and periaqueductal gray of the midbrain are critical areas, as shown in studies on cats, rats, and monkeys. These brain areas control the expression of both behavioral and autonomic components of aggression in these species, including vocalization. Electrical stimulation of the hypothalamus causes aggressive behavior[61] and the hypothalamus has receptors that help determine aggression levels based on their interactions with serotonin and vasopressin.[62] These midbrain areas have direct connections with both the brainstem nuclei controlling these functions, and with structures such as the amygdala and prefrontal cortex.
          Stimulation of the amygdala results in augmented aggressive behavior in hamsters,[63][64] while lesions of an evolutionarily homologous area in the lizard greatly reduce competitive drive and aggression (Bauman et al. 2006).[65] In rhesus monkeys, neonatal lesions in the amygdala or hippocampus results in reduced expression of social dominance, related to the regulation of aggression and fear.[66] Several experiments in attack-primed Syrian golden hamsters, for example, support the claim of circuity within the amygdala being involved in control of aggression.[64] The role of the amygdala is less clear in primates and appears to depend more on situational context, with lesions leading to increases in either social affiliatory or aggressive responses.
          The broad area of the cortex known as the prefrontal cortex (PFC) is crucial for self-control and inhibition of impulses, including inhibition of aggression and emotions. Reduced activity of the prefrontal cortex, in particular its medial and orbitofrontal portions, has been associated with violent/antisocial aggression.[1][67] In addition, reduced response inhibition has been found in violent offenders, compared to non-violent offenders.[68]
          The role of the chemicals in the brain, particularly neurotransmitters, in aggression has also been examined. This varies depending on the pathway, the context and other factors such as gender. A deficit in serotonin has been theorized to have a primary role in causing impulsivity and aggression. At least one epigenetic study supports this supposition.[69] Nevertheless, low levels of serotonin transmission may explain a vulnerability to impulsiveness, potential aggression, and may have an effect through interactions with other neurochemical systems. These include dopamine systems which are generally associated with attention and motivation toward rewards, and operate at various levels. Norepinephrine, also known as noradrenaline, may influence aggression responses both directly and indirectly through the hormonal system, the sympathetic nervous system or the central nervous system (including the brain). It appears to have different effects depending on the type of triggering stimulus, for example social isolation/rank versus shock/chemical agitation which appears not to have a linear relationship with aggression. Similarly, GABA, although associated with inhibitory functions at many CNS synapses, sometimes shows a positive correlation with aggression, including when potentiated by alcohol.[70][71]
          The hormonal neuropeptides vasopressin and oxytocin play a key role in complex social behaviours in many mammals such as regulating attachment, social recognition, and aggression. Vasopressin has been implicated in male-typical social behaviors which includes aggression. Oxytocin may have a particular role in regulating female bonds with offspring and mates, including the use of protective aggression. Initial studies in humans suggest some similar effects.[72][73]
          In human, aggressive behavior has been associated with abnormalities in three principal regulatory systems in the body serotonin systems, catecholamine systems, and the hypothalamic-pituitary-adrenocortical axis. Abnormalities in these systems also are known to be induced by stress, either severe, acute stress or chronic low-grade stress[74]"       

    • 5.2 Testosterone
    •     "See also: Testosterone § Aggression
          Hormones are chemicals that circulate in the body to affect cells and the nervous system, including the brain. Testosterone is a steroid hormone from the androgen group, which is most linked to the prenatal and postnatal development of the male gender and physique, which in turn has been linked on average to more physical aggression in many species. Early androgenization as an organizational effect on the developing brains of both males and females, making more neural circuits that control sexual behavior as well as intermale and interfemale aggression become more sensitive to testosterone.[75]  
    •      Thus, aggressive behavior tends to increase with testosterone. There are noticeable sex differences in aggression. Testosterone is present to a lesser extent in females, who may be more sensitive to its effects. Animal studies have also indicated a link between incidents of aggression and the individual level of circulating testosterone. However, results in relation to primates, particularly humans, are less clear cut and are at best only suggestive of a positive association in some contexts.[76]
          In humans, there is a seasonal variation in aggression associated with changes in testosterone.[77] For example, in some primate species, such as rhesus monkeys and baboons, females are more likely to engage in fights around the time of ovulation as well as right before menstruation.[75] If the results were the same in humans as they are in rhesus monkeys and baboons, then the increase in aggressive behaviors during ovulation is explained by the decline in estrogen levels. This makes normal testosterone levels more effective.[78] Castrated mice and rats exhibit lower levels of aggression. Males castrated as neonates exhibit low levels of aggression even when given testosterone throughout their development.  

    •     Challenge hypothesis

          The challenge hypothesis outlines the dynamic relationship between plasma testosterone levels and aggression in mating contexts in many species. It proposes that testosterone is linked to aggression when it is beneficial for reproduction, such as in mate guarding and preventing the encroachment of intrasexual rivals. The challenge hypothesis predicts that seasonal patterns in testosterone levels in a species are a function of mating system (monogamy versus polygyny), paternal care, and male-male aggression in seasonal breeders. This pattern between testosterone and aggression was first observed in seasonally breeding birds, such as the song sparrow, where testosterone levels rise modestly with the onset of the breeding season to support basic reproductive functions.[79] The hypothesis has been subsequently expanded and modified to predict relationships between testosterone and aggression in other species. For example, chimpanzees, which are continuous breeders, show significantly raised testosterone levels and aggressive male-male interactions when receptive and fertile females are present.[80] Currently, no research has specified a relationship between the modified challenge hypothesis and human behavior, or the human nature of concealed ovulation, although some suggest it may apply.[77] 

    •     Effects on the nervous system
          Testosterone to Estradiol conversion

          Another line of research has focused on the proximate effects of circulating testosterone on the nervous system, as mediated by local metabolism within the brain. Testosterone can be metabolized to 17b-estradiol by the enzyme aromatase, or to 5-alpha-dihydrotestosterone (DHT) by 5a-reductase.[1]
          Aromatase is highly expressed in regions involved in the regulation of aggressive behavior, such as the amygdala and hypothalamus. In studies using genetic knock-out techniques in inbred mice, male mice that lacked a functional aromatase enzyme displayed a marked reduction in aggression. Long-term treatment with estradiol partially restored aggressive behavior, suggesting that the neural conversion of circulating testosterone to estradiol and its effect on estrogen receptors influences inter-male aggression. In addition, two different estrogen receptors, ERa and ERb, have been identified as having the ability to exert different effects on aggression in mice. However, the effect of estradiol appears to vary depending on the strain of mouse, and in some strains it reduces aggression during long days (16 h of light), while during short days (8 h of light) estradiol rapidly increases aggression.[81]
          Another hypothesis is that testosterone influences brain areas that control behavioral reactions. Studies in animal models indicate that aggression is affected by several interconnected cortical and subcortical structures within the so-called social behavior network. A study involving lesions and electrical-chemical stimulation in rodents and cats revealed that such a neural network consists of the medial amygdala, medial hypothalamus and periaqueductal grey (PAG), and it positively modulates reactive aggression.[82] Moreover, a study done in human subjects showed that prefrontal-amygdala connectivity is modulated by endogenous testosterone during social emotional behavior.[83]
          In human studies, testosterone-aggression research has also focused on the role of the orbitofrontal cortex (OFC). This brain area is strongly associated with impulse control and self-regulation systems that integrate emotion, motivation, and cognition to guide context-appropriate behavior.[84] Patients with localized lesions to the OFC engage in heightened reactive aggression.[85] Aggressive behavior may be regulated by testosterone via reduced medial OFC engagement following social provocation.[84] When measuring participants' salivary testosterone, higher levels can predict subsequent aggressive behavioral reactions to unfairness faced during a task. Moreover, brain scanning with fMRI shows reduced activity in the medial OFC during such reactions. Such findings may suggest that a specific brain region, the OFC, is a key factor in understanding reactive aggression. 

    •     General associations with behavior

      Scientists have for a long time been interested in the relationship between testosterone and aggressive behavior. In most species, males are more aggressive than females. Castration of males usually has a pacifying effect on aggressive behavior in males. In humans, males engage in crime and especially violent crime more than females. The involvement in crime usually rises in the early teens to mid teens which happen at the same time as testosterone levels rise. Research on the relationship between testosterone and aggression is difficult since the only reliable measurement of brain testosterone is by a lumbar puncture which is not done for research purposes. Studies therefore have often instead used more unreliable measurements from blood or saliva.[86]
          The Handbook of Crime Correlates, a review of crime studies, states most studies support a link between adult criminality and testosterone although the relationship is modest if examined separately for each sex. However, nearly all studies of juvenile delinquency and testosterone are not significant. Most studies have also found testosterone to be associated with behaviors or personality traits linked with criminality such as antisocial behavior and alcoholism. Many studies have also been done on the relationship between more general aggressive behavior/feelings and testosterone. About half the studies have found a relationship and about half no relationship.[86]
          Studies of testosterone levels of male athletes before and after a competition revealed that testosterone levels rise shortly before their matches, as if in anticipation of the competition, and are dependent on the outcome of the event: testosterone levels of winners are high relative to those of losers. No specific response of testosterone levels to competition was observed in female athletes, although a mood difference was noted.[87] In addition, some experiments have failed to find a relationship between testosterone levels and aggression in humans.[88][89][90]
          The possible correlation between testosterone and aggression could explain the "roid rage" that can result from anabolic steroid use,[91][92] although an effect of abnormally high levels of steroids does not prove an effect at physiological levels."    

    •     5.3 Dehydroepiandrosterone
    •     "Dehydroepiandrosterone (DHEA) is the most abundant circulating androgen hormone and can be rapidly metabolized within target tissues into potent androgens and estrogens. Gonadal steroids generally regulate aggression during the breeding season, but non-gonadal steroids may regulate aggression during the non-breeding season. Castration of various species in the non-breeding season has no effect on territorial aggression. In several avian studies, circulating DHEA has been found to be elevated in birds during the non-breeding season. These data support the idea that non-breeding birds combine adrenal and/or gonadal DHEA synthesis with neural DHEA metabolism to maintain territorial behavior when gonadal testosterone secretion is low. Similar results have been found in studies involving different strains of rats, mice, and hamsters. DHEA levels also have been studied in humans and may play a role in human aggression. Circulating DHEAS (its sulfated ester) levels rise during adrenarche (~7 years of age) while plasma testosterone levels are relatively low. This implies that aggression in pre-pubertal children with aggressive conduct disorder might be correlated with plasma DHEAS rather than plasma testosterone, suggesting an important link between DHEAS and human aggressive behavior.[81]" 

           5.4 Glucocorticoids
         
      "Glucocorticoid hormones have an important role in regulating aggressive behavior. In adult rats, acute injections of corticosterone promote aggressive behavior and acute reduction of corticosterone decreases aggression; however, a chronic reduction of corticosterone levels can produce abnormally aggressive behavior. In addition, glucocorticoids affect development of aggression and establishment of social hierarchies. Adult mice with low baseline levels of corticosterone are more likely to become dominant than are mice with high baseline corticosterone levels.   
    •     Glucocorticoids are released by the hypothalamic pituitary adrenal (HPA) axis in response to stress, of which cortisol is the most prominent in humans. Results in adults suggest that reduced levels of cortisol, linked to lower fear or a reduced stress response, can be associated with more aggression. However, it may be that proactive aggression is associated with low cortisol levels while reactive aggression may be accompanied by elevated levels. Differences in assessments of cortisol may also explain a diversity of results, particularly in children.[76]
          The HPA axis is related to the general fight-or-flight response or acute stress reaction, and the role of catecholamines such as epinephrine, popularly known as adrenaline.
      "   

    • 5.5 Pheromones 

    •     "In many animals, aggression can be linked to pheromones released between conspecifics. In mice, major urinary proteins (Mups) have been demonstrated to promote innate aggressive behavior in males,[93][94] and can be mediated by neuromodulatory systems.[95] Mups activate olfactory sensory neurons in the vomeronasal organ (VNO), a subsystem of the nose known to detect pheromones via specific sensory receptors, of mice[94] and rats.[96] Pheremones have also been identified in fruit flies, detected by neurons in the antenna, that send a message to the brain eliciting aggression; it has been noted that aggression pheremones have not been identified in humans.[97]"

    • 6 Genetics
    • 7 Society and culture
    • 8 See also
    • 9 References
    • 10 External links  " 



1998
Aggression and violence: examining the theories.
    https://www.ncbi.nlm.nih.gov/pubmed/9732597
"Theories of aggressive and violent behaviour fall into a confusing range of categories. In this review, the author attempts to make sense of the different concepts and describes the theory that underpins each of them."
     109 Similar articles:
https://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed&from_uid=9732597



  • Anterior hypothalamic neural activation and ... aggression ... voles (PubMed)- 2007   
    Only abstract available online. 
        "
    Male prairie voles (Microtus ochrogaster) display mating-induced pair bonding indicated by social affiliation with their female partners and aggression toward unfamiliar conspecifics. ... Males that were pair-bonded for 2 weeks displayed intense levels of aggression toward a female or male conspecific stranger but maintained a high level of social affiliation with their familiar female partners. These social interactions induced increases in neural activation, indicated by increased density of
    Fos-immunoreactive staining (Fos-ir) in several brain regions including the bed nucleus of the stria terminalis (BNST), medial preoptic area (MPOA), paraventricular nucleus (PVN), anterior cortical (AcA), and medial nuclei (MeA) of the amygdala. In the anterior hypothalamus (AH), increased density of Fos-ir staining was found specifically to be associated with aggression toward unfamiliar female or male strangers. In addition, higher densities of AH cells that were stained for tyrosine hydroxylase (TH) or vasopressin (AVP) were also labeled with Fos-ir in these males displaying aggression toward a conspecific stranger compared with males displaying social affiliation toward their female partner. Together, our results indicate that dopamine and vasopressin in the AH may be involved in the regulation of enduring aggression associated with pair bonding in male prairie voles."  


















Comments