Editing Aggression (section)

==Physiology==

===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.<ref name=":6" /><ref name=":4" />

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 nervous system|autonomic]] components of aggression in these species, including vocalization. Electrical stimulation of the hypothalamus causes aggressive behavior<ref>{{cite journal |doi=10.1016/0006-8993(83)90764-3 |pmid=6681724 |title=Discriminant analysis of the localization of aggression-inducing electrode placements in the hypothalamus of male rats |journal=Brain Research |volume=260 |issue=1 |pages=61–79 |year=1983 |last1=Kruk |first1=Menno R. |last2=Van Der Poel |first2=A.M. |last3=Meelis |first3=W. |last4=Hermans |first4=J. |last5=Mostert |first5=P.G. |last6=Mos |first6=J. |last7=Lohman |first7=A.H.M. |s2cid=3231548 }}</ref> and the hypothalamus has receptors that help determine aggression levels based on their interactions with serotonin and vasopressin.<ref>{{cite journal |pmid=9151749 |pmc=6573530 |year=1997 |last1=Ferris |first1=C. F. |title=Vasopressin/serotonin interactions in the anterior hypothalamus control aggressive behavior in golden hamsters |journal=The Journal of Neuroscience |volume=17 |issue=11 |pages=4331–40 |last2=Melloni |first2=R. H. Jr. |last3=Koppel |first3=G |last4=Perry |first4=K. W. |last5=Fuller |first5=R. W. |last6=Delville |first6=Y |doi=10.1523/JNEUROSCI.17-11-04331.1997 }}</ref> In rodents, activation of [[estrogen receptor]]-expressing neurons in the ventrolateral portion of the [[ventromedial hypothalamus]] (VMHvl) was found to be sufficient to initiate aggression in both males and females.<ref>{{cite journal |last1=Lee |first1=H |title=Scalable control of mounting and attack by Esr1+ neurons in the ventromedial hypothalamus |journal=Nature |date=2014 |volume=509 |issue=7502 |pages=627–32 |doi=10.1038/nature13169 |pmid=24739975 |pmc=4098836 |bibcode=2014Natur.509..627L }}</ref><ref>{{cite journal |last1=Hashikawa |first1=K |title=Esr1+ cells in the ventromedial hypothalamus control female aggression |journal=Nat. Neurosci. |date=2017 |volume=11 |issue=20 |pages=1580–1590 |doi=10.1038/nn.4644 |pmid=28920934 |pmc=5953764 }}</ref> Midbrain areas involved in aggression 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,<ref>{{cite journal |doi=10.1037/0735-7044.110.2.401 |pmid=8731066 |title=Brief, high-frequency stimulation of the corticomedial amygdala induces a delayed and prolonged increase of aggressiveness in male Syrian golden hamsters |journal=Behavioral Neuroscience |volume=110 |issue=2 |pages=401–12 |year=1996 |last1=Potegal |first1=M. |last2=Hebert |first2=M. |last3=Decoster |first3=M. |last4=Meyerhoff |first4=J. L. }}</ref><ref name="Potegal, M 1996. pp. 869-880"/> while [[lesions]] of an [[homology (biology)|evolutionarily homologous]] area in the lizard greatly reduce competitive drive and aggression (Bauman et al. 2006).<ref>{{cite journal |doi=10.1016/0031-9384(84)90088-X |pmid=6538977 |title=Role of the amygdala in the reproductive and aggressive behavior of the lizard, Anolis carolinensis |journal=Physiology & Behavior |volume=32 |issue=1 |pages=147–51 |year=1984 |last1=Greenberg |first1=Neil |last2=Scott |first2=Michelle |last3=Crews |first3=David |s2cid=9987359 }}</ref> 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.<ref>{{cite journal |doi=10.1037/0735-7044.120.4.749 |pmid=16893283 |title=The expression of social dominance following neonatal lesions of the amygdala or hippocampus in rhesus monkeys (Macaca mulatta) |journal=Behavioral Neuroscience |volume=120 |issue=4 |pages=749–60 |year=2006 |last1=Bauman |first1=M. D. |last2=Toscano |first2=J. E. |last3=Mason |first3=W. A. |last4=Lavenex |first4=P. |last5=Amaral |first5=D. G. |url=http://doc.rero.ch/record/6372/files/lavenex_esd.pdf }}</ref> Several experiments in attack-primed Syrian golden hamsters, for example, support the claim of circuitry within the amygdala being involved in control of aggression.<ref name="Potegal, M 1996. pp. 869-880">{{cite journal |doi=10.1016/0306-4522(96)00236-9 |pmid=8951880 |title=Attack priming in female Syrian golden hamsters is associated with a c-fos-coupled process within the corticomedial amygdala |journal=Neuroscience |volume=75 |issue=3 |pages=869–80 |year=1996 |last1=Potegal |first1=M. |last2=Ferris |first2=C.F. |last3=Hebert |first3=M. |last4=Meyerhoff |first4=J. |last5=Skaredoff |first5=L. |s2cid=24136851 |url=https://zenodo.org/record/1258481 }}</ref> 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. [[Amygdalotomy]], which involves removing or destroying parts of the amygdala, has been performed on people to reduce their violent behaviour.

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 cortex|orbitofrontal]] portions, has been associated with violent/antisocial aggression.<ref>Paus, T. 'Mapping Brain Development' in [https://books.google.com/books/about/Developmental_origins_of_aggression.html?id=XmSfJEl2v4sC Developmental Origins of Aggression], 2005, The Guilford Press.</ref> In addition, reduced [[response inhibition]] has been found in violent offenders, compared to non-violent offenders.<ref name=":6">{{Cite journal|last1=Meijers|first1=J.|last2=Harte|first2=J. M.|last3=Meynen|first3=G.|last4=Cuijpers|first4=P.|date=1 February 2017|title=Differences in executive functioning between violent and non-violent offenders|url=https://www.cambridge.org/core/journals/psychological-medicine/article/div-classtitledifferences-in-executive-functioning-between-violent-and-non-violent-offendersdiv/51D2EDD628447218922BA833A6F59D85|journal=Psychological Medicine|volume=47|issue=10|pages=1784–1793|doi=10.1017/S0033291717000241|pmid=28173890|s2cid=4481557|issn=0033-2917|hdl=1871.1/371bdff2-a6df-45ee-a1fd-90995ea811d7|hdl-access=free}}</ref>

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.<ref name=pmid27720744>{{cite journal |doi=10.1016/j.bbr.2016.10.009 |pmid=27720744 |title=The association of serotonin receptor 3A methylation with maternal violence exposure, neural activity, and child aggression |journal=Behavioural Brain Research |volume=325 |issue=Pt B |pages=268–277 |year=2016 |last1=Schechter |first1=Daniel S. |last2=Moser |first2=Dominik A. |last3=Pointet |first3=Virginie C. |last4=Aue |first4=Tatjana |last5=Stenz |first5=Ludwig |last6=Paoloni-Giacobino |first6=Ariane |last7=Adouan |first7=Wafae |last8=Manini |first8=Aurélia |last9=Suardi |first9=Francesca |last10=Vital |first10=Marylene |last11=Sancho Rossignol |first11=Ana |last12=Cordero |first12=Maria I. |last13=Rothenberg |first13=Molly |last14=Ansermet |first14=François |last15=Rusconi Serpa |first15=Sandra |last16=Dayer |first16=Alexandre G. |doi-access=free }}</ref> 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.<ref>{{cite journal |doi=10.1016/j.bbr.2008.01.003 |pmid=18281105 |title=Development of violence in mice through repeated victory along with changes in prefrontal cortex neurochemistry |journal=Behavioural Brain Research |volume=189 |issue=2 |pages=263–72 |year=2008 |last1=Caramaschi |first1=Doretta |last2=De Boer |first2=Sietse F. |last3=De Vries |first3=Han |last4=Koolhaas |first4=Jaap M. |hdl=11370/f683911d-3c8b-4ba6-a6bb-12cbaf11dead |s2cid=14888253 |url=https://pure.rug.nl/ws/files/6717763/2008BehavBrainResCaramaschi.pdf |hdl-access=free }}</ref><ref>Pihl, RO & Benkelfat, C. 'Neuromodulators in the Development and Expression of Inhibition and Aggression' in [https://books.google.com/books/about Developmental_origins_of_aggression.html?id=XmSfJEl2v4sC Developmental Origins of Aggression], 2005, The Guilford Press.</ref>

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.<ref>{{cite book |doi=10.1016/S0079-6123(08)00428-7 |pmid=18655894 |chapter=Neuropeptides and social behaviour: Effects of oxytocin and vasopressin in humans |title=Advances in Vasopressin and Oxytocin – from Genes to Behaviour to Disease |volume=170 |pages=337–50 |series=Progress in Brain Research |year=2008 |last1=Heinrichs |first1=M |last2=Domes |first2=G |isbn=978-0-444-53201-5 }}</ref><ref>{{cite journal |doi=10.1016/j.biopsycho.2007.09.001 |pmid=17931766 |title=Attachment, aggression and affiliation: The role of oxytocin in female social behavior |journal=Biological Psychology |volume=77 |issue=1 |pages=1–10 |year=2008 |last1=Campbell |first1=Anne |s2cid=33228118 |url=http://dro.dur.ac.uk/10217/1/10217.pdf?DDD27+dul4eg }}</ref>

In human, [[aggressive behavior]] has been associated with abnormalities in three principal regulatory systems in the body [[serotonin|serotonin systems]], [[catecholamine|catecholamine systems]], and the [[hypothalamic–pituitary–adrenal axis]]. Abnormalities in these systems also are known to be induced by [[Stress (biology)|stress]], either severe, acute stress or chronic low-grade stress<ref>{{cite journal |doi=10.1300/J076v36n01_04 |title=Effects of the ''Transcendental Meditation'' Program on Neuroendocrine Abnormalities Associated with Aggression and Crime |journal=Journal of Offender Rehabilitation |volume=36 |issue=1–4 |pages=67–87 |year=2003 |last1=Walton |first1=Kenneth G. |last2=Levitsky |first2=Debra K. |s2cid=144374302 }}</ref>

===Testosterone===
{{See also|Testosterone#Aggression}}
Early androgenization has 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.<ref name="Carlson, N. 2013">Carlson, N. 'Hormonal Control of Aggressive Behavior' Chapter 11 in [Physiology of Behavior],2013, Pearson Education Inc.</ref> 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.<ref name="van goozen">Van Goozen, S. 'Hormones and the Developmental Origins of Aggression' Chapter 14 in [https://books.google.com/books/about/Developmental_origins_of_aggression.html?id=XmSfJEl2v4sC Developmental Origins of Aggression], 2005, The Guilford Press.</ref>

In humans, there is a seasonal variation in aggression associated with changes in testosterone.<ref name="Archer 319–345" /> 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.<ref name="Carlson, N. 2013"/> 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.<ref>"[http://www.babymed.com/ovulation/3-important-physical-ovulation-symptoms,2001-2015 Three Important Physical Ovulation Symptoms]" from BabyMed.com</ref> 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 breeder]]s.

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.<ref name="Wingfield, John C., Ball, Gregory F., Dufty Jr, Alfred M., Hegner, Robert E., Ramenofsky, Marilyn 1987 602–608">{{cite journal |bibcode=1987AmSci..75..602W |title=Testosterone and Aggression in Birds |journal=[[American Scientist]] |volume=75 |issue=6 |pages=602–8 |last1=Wingfield |first1=John C. |last2=Ball |first2=Gregory F. |last3=Dufty |first3=Alfred M. |last4=Hegner |first4=Robert E. |last5=Ramenofsky |first5=Marilyn |year=1987 }}</ref> 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.<ref>{{cite journal |doi=10.1016/j.anbehav.2003.03.013 |title=Dominance, aggression and testosterone in wild chimpanzees: A test of the 'challenge hypothesis' |journal=[[Animal Behaviour (journal)|Animal Behaviour]] |volume=67 |pages=113–23 |year=2004 |last1=Muller |first1=Martin N |last2=Wrangham |first2=Richard W |s2cid=8041587 }}</ref> 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.<ref name="Archer 319–345">{{cite journal |doi=10.1016/j.neubiorev.2004.12.007 |title=Testosterone and human aggression: An evaluation of the challenge hypothesis |journal=[[Neuroscience & Biobehavioral Reviews]] |volume=30 |issue=3 |pages=319–45 |year=2006 |last1=Archer |first1=John |pmid=16483890|s2cid=26405251 }}</ref>

====Effects on the nervous system====
[[File:Testosterone estradiol conversion.png|thumb|left|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 [[estradiol]] by the enzyme [[aromatase]], or to [[dihydrotestosterone]] (DHT) by [[5α-reductase]].<ref name="Soma2008" />

Aromatase is highly expressed in regions involved in the regulation of aggressive behavior, such as the amygdala and hypothalamus. In studies using genetic knockout 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 receptor]]s influences inter-male aggression. In addition, two different estrogen receptors, [[ERα]] and [[ERβ]], 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.<ref name="Soma2008">{{cite journal |doi=10.1016/j.yfrne.2007.12.003 |pmid=18280561 |title=Novel mechanisms for neuroendocrine regulation of aggression |journal=[[Frontiers in Neuroendocrinology]] |volume=29 |issue=4 |pages=476–89 |year=2008 |last1=Soma |first1=Kiran K. |last2=Scotti |first2=Melissa-Ann L. |last3=Newman |first3=Amy E.M. |last4=Charlier |first4=Thierry D. |last5=Demas |first5=Gregory E. |s2cid=32650274 }}</ref>

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.<ref>{{cite journal |doi=10.2174/157015907780866929 |pmid=18615178 |pmc=2435345 |title=The Neurobiological Bases for Development of Pharmacological Treatments of Aggressive Disorders |journal=[[Current Neuropharmacology]] |volume=5 |issue=2 |pages=135–47 |year=2007 |last1=Siegel |first1=Allan |last2=Bhatt |first2=Suresh |last3=Bhatt |first3=Rekha |last4=Zalcman |first4=Steven }}</ref> Moreover, a study done in human subjects showed that prefrontal-amygdala connectivity is modulated by endogenous testosterone during social emotional behavior.<ref>{{cite journal |doi=10.1093/cercor/bhr001 |pmid=21339377 |pmc=3169658 |title=Endogenous Testosterone Modulates Prefrontal-Amygdala Connectivity during Social Emotional Behavior |journal=[[Cerebral Cortex (journal)|Cerebral Cortex]] |volume=21 |issue=10 |pages=2282–90 |year=2011 |last1=Volman |first1=I. |last2=Toni |first2=I. |last3=Verhagen |first3=L. |last4=Roelofs |first4=K. }}</ref>

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.<ref name="Mehta, P. H., Beer, J. 2009 2357–2368">{{cite journal |doi=10.1162/jocn.2009.21389 |pmid=19925198 |title=Neural Mechanisms of the Testosterone–Aggression Relation: The Role of Orbitofrontal Cortex |journal=[[Journal of Cognitive Neuroscience]] |volume=22 |issue=10 |pages=2357–68 |year=2010 |last1=Mehta |first1=Pranjal H. |last2=Beer |first2=Jennifer |citeseerx=10.1.1.518.2751 |s2cid=710598 }}</ref> Patients with localized lesions to the OFC engage in heightened reactive aggression.<ref>{{cite journal |doi=10.1176/appi.ajp.2008.07111774 |pmid=18346997 |pmc=4176893 |title=Neurobiology of Aggression and Violence |journal=[[American Journal of Psychiatry]] |volume=165 |issue=4 |pages=429–42 |year=2008 |last1=Siever |first1=Larry J. }}</ref> Aggressive behavior may be regulated by testosterone via reduced medial OFC engagement following social provocation.<ref name="Mehta, P. H., Beer, J. 2009 2357–2368"/> 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.<ref name=Ellis2009>''Handbook of Crime Correlates''; Lee Ellis, [[Kevin M. Beaver]], [[John Paul Wright|John Wright]]; 2009; Academic Press</ref>

''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 personality disorder|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.<ref name=Ellis2009/>

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.<ref name="PMID 10097017">{{cite journal |doi=10.1017/s0140525x98001228 |title=Testosterone and dominance in men |journal=[[Behavioral and Brain Sciences]] |volume=21 |issue=3 |year=1998 |last1=Mazur |first1=Allan |last2=Booth |first2=Alan |pmid=10097017 |pages=353–63; discussion 363–97|citeseerx=10.1.1.421.3005 |s2cid=9462611 }}</ref> In addition, some experiments have failed to find a relationship between testosterone levels and aggression in humans.<ref>{{cite journal |doi=10.1016/S0149-7634(05)80117-4 |pmid=8309650 |title=Aggression in humans: What is its biological foundation? |journal=Neuroscience & Biobehavioral Reviews |volume=17 |issue=4 |pages=405–25 |year=1993 |last1=Albert |first1=D.J. |last2=Walsh |first2=M.L. |last3=Jonik |first3=R.H. |s2cid=28557481 }}</ref><ref name=":5">{{cite journal |doi=10.1016/j.jpsychires.2006.04.009 |pmid=16765987 |title=CSF testosterone: Relationship to aggression, impulsivity, and venturesomeness in adult males with personality disorder |journal=[[Journal of Psychiatric Research]] |volume=41 |issue=6 |pages=488–92 |year=2007 |last1=Coccaro |first1=Emil F. |last2=Beresford |first2=Brendan |last3=Minar |first3=Philip |last4=Kaskow |first4=Jon |last5=Geracioti |first5=Thomas }}</ref><ref>{{cite journal |doi=10.1097/00004583-199311000-00015 |pmid=8282667 |title=Testosterone and Aggression in Children |journal=Journal of the American Academy of Child & Adolescent Psychiatry |volume=32 |issue=6  |pages=1217–22 |year=1993 |last1=Constantino |first1=John N. |last2=Grosz |first2=Daniel |last3=Saenger |first3=Paul |last4=Chandler |first4=Donald W. |last5=Nandi |first5=Reena |last6=Earls |first6=Felton J. }}</ref>

The possible correlation between testosterone and aggression could explain the "roid rage" that can result from [[anabolic steroid]] use,<ref>{{cite journal |doi=10.1097/01.wnr.0000234752.03808.b2 |pmid=16957604 |title=Neurosteroids regulate mouse aggression induced by anabolic androgenic steroids |journal=[[NeuroReport]] |volume=17 |issue=14 |pages=1537–41 |year=2006 |last1=Pibiri |first1=Fabio |last2=Nelson |first2=Marianela |last3=Carboni |first3=Giovanni |last4=Pinna |first4=Graziano |s2cid=42991833 }}</ref><ref>{{cite journal |doi=10.1002/hup.470050407 |title=High-dose anabolic steroids in strength athletes: Effects upon hostility and aggression |journal=Human Psychopharmacology: Clinical and Experimental |volume=5 |issue=4 |pages=349–56 |year=1990 |last1=Choi |first1=P. Y. L. |last2=Parrott |first2=A. C. |last3=Cowan |first3=D. |s2cid=37157824 }}</ref> although an effect of abnormally high levels of steroids does not prove an effect at physiological levels.

===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.<ref name="Soma2008"/>

===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.<ref name="Soma2008"/>

Glucocorticoids are released by the [[Hypothalamic–pituitary–adrenal axis|hypothalamic pituitary adrenal]] (HPA) axis in response to [[stress (biological)|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.<ref name="van goozen"/>

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.

===Pheromones===
In many animals, aggression can be linked to [[pheromone]]s released between [[conspecifics]]. In mice, [[major urinary proteins]] (Mups) have been demonstrated to promote innate aggressive behavior in males,<ref name="BBCreport">{{cite news |title=Aggression protein found in mice |work=[[BBC News]] |date=5 December 2007 |url=http://news.bbc.co.uk/2/hi/science/nature/7129176.stm |access-date=26 September 2009}}</ref><ref name=Chamero1>{{cite journal |author=Chamero P |title=Identification of protein pheromones that promote aggressive behaviour |journal=Nature |volume=450 |issue=7171 |pages=899–902 |date=December 2007 |pmid=18064011 |doi=10.1038/nature05997 |author2=Marton TF |author3=Logan DW |display-authors=3 |last4=Flanagan |first4=Kelly |last5=Cruz |first5=Jason R. |last6=Saghatelian |first6=Alan |last7=Cravatt |first7=Benjamin F. |last8=Stowers |first8=Lisa|bibcode=2007Natur.450..899C |s2cid=4398766 }}</ref> and can be mediated by neuromodulatory systems.<ref>{{cite journal |doi=10.1523/JNEUROSCI.0099-15.2015 |pmid=26224860 |pmc=4518052 |title=Differential Muscarinic Modulation in the Olfactory Bulb |journal=Journal of Neuroscience |volume=35 |issue=30 |pages=10773–85 |year=2015 |last1=Smith |first1=R. S. |last2=Hu |first2=R. |last3=Desouza |first3=A. |last4=Eberly |first4=C. L. |last5=Krahe |first5=K. |last6=Chan |first6=W. |last7=Araneda |first7=R. C. }}</ref> Mups activate [[olfactory sensory neuron]]s in the [[vomeronasal organ]] (VNO), a subsystem of the nose known to detect pheromones via specific [[sensory receptor]]s, of mice<ref name=Chamero1/> and rats.<ref name=Krieger1>{{cite journal |doi=10.1074/jbc.274.8.4655 |pmid=9988702 |title=Selective Activation of G Protein Subtypes in the Vomeronasal Organ upon Stimulation with Urine-derived Compounds |journal=Journal of Biological Chemistry |volume=274 |issue=8 |pages=4655–62 |year=1999 |last1=Krieger |first1=J. |last2=Schmitt |first2=A. |last3=Lobel |first3=D. |last4=Gudermann |first4=T. |last5=Schultz |first5=G. |last6=Breer |first6=H. |last7=Boekhoff |first7=I. |doi-access=free }}</ref> Pheremones have also been identified in [[Drosophila melanogaster|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.<ref>[https://web.archive.org/web/20091209075216/http://media.caltech.edu/press_releases/13308 Caltech Scientists Discover Aggression-Promoting Pheromone in Flies] Caltech press release, 2009</ref>