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Biological Evolution of Violence and Aggression. II: Brains, Neurotransmitters, and Hormones

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This chapter continues the exploration of biological causes of aggression and violence. It addresses the effects of different regions of the brain, including limbic and cortical structures; neurotransmitters; and, hormones, on aggression and violence. For all of these putative biological causes of aggression, caution is warranted due to the mixed evidence and the tendency to adopt overly simplistic models of biological causation. The implications for prevention and treatment are briefly discussed, but are dealt with in much more detail in Chap. 11, Individual Biological Interventions for Violence and Aggression. Psychopharmacology and Hormonal Treatments and Chap. 12, Individual Biological Interventions for Violence and Aggression. II. Other Biological Treatments.

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... Признается актуальность изучения биологической основы агрессии [8,9]. Механизмы агрессивного поведения ряд авторов связывают с нарушением нейротрансмиссии биогенных аминов и гормональной дисрегуляцией [10][11][12]. ...
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Chapter
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Aggression is a crucial survival behavior: it is employed to defend territory, compete for food and mating opportunities, protect kin, and resolve disputes. Although widely differing in its behavioral expression, aggression is observed across many species. The neural substrates of aggression have been investigated for nearly a century and two highly conserved circuitries emerge as critical substrates for generating and modulating aggression. One circuitry centers on the medial hypothalamus. Activity of the medial hypothalamic cells closely correlates with attacks and can bi-directionally modulate aggressive behaviors. The other aggression-related circuit involves the mesolimbic dopamine cells. Dopaminergic antagonists are the most commonly used treatment for suppressing human aggression in psychotic patients. Animal studies support essential roles of dopaminergic signaling in the nucleus accumbens in assessing the reward value of aggression and reinforcing the aggressive behaviors. In this review, we will provide an overview regarding the functions of medial hypothalamus and dopaminergic system in mediating aggressive behaviors and the potential interactions between these two circuitries.
Chapter
The neuropeptide oxytocin (OT) has a solid reputation as a facilitator of social interactions such as parental and pair bonding, trust, and empathy. The many results supporting a pro-social role of OT have generated the hypothesis that impairments in the endogenous OT system may lead to antisocial behavior, most notably social withdrawal or pathological aggression. If this is indeed the case, administration of exogenous OT could be the “serenic” treatment that psychiatrists have for decades been searching for.
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Importance: Graves disease is the most common cause of persistent hyperthyroidism in adults. Approximately 3% of women and 0.5% of men will develop Graves disease during their lifetime. Observations: We searched PubMed and the Cochrane database for English-language studies published from June 2000 through October 5, 2015. Thirteen randomized clinical trials, 5 systematic reviews and meta-analyses, and 52 observational studies were included in this review. Patients with Graves disease may be treated with antithyroid drugs, radioactive iodine (RAI), or surgery (near-total thyroidectomy). The optimal approach depends on patient preference, geography, and clinical factors. A 12- to 18-month course of antithyroid drugs may lead to a remission in approximately 50% of patients but can cause potentially significant (albeit rare) adverse reactions, including agranulocytosis and hepatotoxicity. Adverse reactions typically occur within the first 90 days of therapy. Treating Graves disease with RAI and surgery result in gland destruction or removal, necessitating life-long levothyroxine replacement. Use of RAI has also been associated with the development or worsening of thyroid eye disease in approximately 15% to 20% of patients. Surgery is favored in patients with concomitant suspicious or malignant thyroid nodules, coexisting hyperparathyroidism, and in patients with large goiters or moderate to severe thyroid eye disease who cannot be treated using antithyroid drugs. However, surgery is associated with potential complications such as hypoparathyroidism and vocal cord paralysis in a small proportion of patients. In pregnancy, antithyroid drugs are the primary therapy, but some women with Graves disease opt to receive definitive therapy with RAI or surgery prior to becoming pregnant to avoid potential teratogenic effects of antithyroid drugs during pregnancy. Conclusions and relevance: Management of Graves disease includes treatment with antithyroid drugs, RAI, or thyroidectomy. The optimal approach depends on patient preference and specific patient clinical features such as age, history of arrhythmia or ischemic heart disease, size of goiter, and severity of thyrotoxicosis. Physicians should be familiar with the advantages and disadvantages of each therapy to best counsel their patients.
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This chapter summarizes the evidence describing the roles that monoamines -5-hydroxytryptamine (5-HT), norepinephrine (NE), and dopamine (DA)-exert in the mediation of aggressive behavior. Aggression is diverse in its behavioral patterns and functions, and endogenous amines, acids, steroids, and peptides may have different effects on each kind of aggression. The importance of escalated forms of aggression is highlighted in an effort to model the harmful acts of aggression and violence in humans. Monoamines have powerful modulatory effects on aggression, and reciprocally, aggression alters monoamines. It is important to delineate the specific conditions and behaviors-when 5-HT appears to be inhibitory, and when NE and DA are aggression stimulating. The effects of monoamines are likely to be due to their interactions with other neurotransmitters, such as gamma-aminobutyric acid (GABA) and glutamate, and neuropeptides, such as vasopressin and opioids.
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Methamphetamine (MA), a psychostimulant drug, was first produced in Germany and Japan in the late 1800s. MA use and trafficking have been a problem since the 1970s in the United States (U.S.) [National Drug Intelligence Center (NDIC). (2006). National Drug Threat Assessment 2006. Retrieved March 18, 2006 from http://www.usdoj.gov.ndic/pubs11/18862/MA.htm] and have increased in recent years [Office of Applied Studies (OAS). (September 16, 2005). The National Survey on Drug Use and Health report: Methamphetamine use, abuse, and dependence: 2002, 2003, and 2004. Rockville, MD: Substance Abuse and Mental Health Services Administration]. MA is associated with violent behavior yet the nature of this relation remains poorly understood, largely due to methodological shortcomings. The present paper critically examines the empirical literature on MA use and its relation to violence. Methodological issues and challenges are discussed and suggestions for future research are provided.
Article
Squirrel monkeys were provided with a chain-pulling response which produced an inanimate object that could be attacked. In the absence of pain-shock, little or no chain-pulling occurred. When pain-shocks were delivered, chain-pulling responses increased. The chain-pulling response was successively reinforced, extinguished, reinforced, and again extinguished by presenting or withdrawing the opportunity to attack as the reinforcing event. Aggression appears to be a distinctive motivational state which is produced by aversive stimulation and which can be used to condition and maintain new behavior.
Article
Objective: the purpose of the study is to give an account of psychiatric symptoms, aggressiveness and violent behaviour among users of anabolic androgenic steroids (AAS). The method used is retrospective evaluation based on information from forensic psychiatric evaluations (FPE), police reports and court records. Fourteen violent offenders were evaluated for current or previous use of AAS. The results suggest that AAS may produce violent behaviour and other mental disturbances, including psychosis. Besides previously described AAS-related violence, termed ‘roid rage’, two new patterns are described: (1) the cold-blooded executioner (‘Terminator’), and (2) the temporary AAS-user who takes the drug for the purpose of encouragement shortly before a criminal act (‘Stürmscknapps behaviour’). The effects of AAS on the central nervous system seem to be particularly detrimental to individuals with an inherent psychiatric disorder. It appears that use of AAS may lead to violent acts in vulnerable persons not only during current use but also after withdrawal.
Article
Objective: To describe our institutional experience with deep-brain stimulation (DBS) used in the treatment of aggressive and disruptive behavior refractory to conservative treatment. Methods: With stereotactic methodology and under general anesthesia, seven patients (from 2002 to 2010) were given DBS in the posterior hypothalamic region, bilaterally, and with the aid of intraoperative microrecording. Results: Six of seven patients presented a clear reduction in the aggression and disruptive bouts, with subsequent simplification of familiar management. Conclusions: DBS of the posterior hypothalamic region could be an effective treatment for patients affected by mental retardation in whom disruptive and drug-refractory aggressive behavior coexists. Although several experimental data are available on this target, further studies are necessary to confirm the long-term efficacy and safety of this procedure.
Chapter
Dopamine (DA) and glutamate are part of intricate neurobiological mechanisms mediating different kinds of aggressive behavior, involving the canonical amines and acids, neuropeptides, and neurosteroids in corticomesolimbic circuits (1). Beginning with invertebrates, the critical role of serotonin (5-HT) for aggression-inhibiting mechanisms has emerged, and it is important to understand how other transmitters, such as DA and glutamate, interact with serotonergic mechanisms. The two major sources of information for delineating the role of glutamate and DA in aggressive behavior are (1) neurobiological studies of preclinical model systems, mostly in rodents and cats, and (2) investigations into the mechanisms for pharmacotherapeutic interventions in clinical settings. The epidemiological statistics on criminal violence, emergency room visits, and public health records of treating violent individuals and victims of violence document the magnitude and urgency of the problem and the need for increasing the understanding the neurobiological basis of these adaptive and pathological behaviors. Although most acts of violence are committed by individuals who are not in mental health settings, and although most mentally ill patients are not violent, the rate of injury resulting from violent acts is higher for mental health staff than injurious accidents for heavy construction and mining professions (2,3). Up to 22% of psychiatric inpatients committed aggressive acts within the last 2 wk (4).
Article
Neuropeptides in the arginine vasotocin/arginine vasopressin (AVT/AVP) family play a major role in the regulation of social behavior by their actions in the brain. In mammals, AVP is found within a circuit of recriprocally connected limbic structures that form the social behavior neural network. This review examines the role played by AVP within this network in controlling social processes that are critical for the formation and maintenance of social relationships: social recognition, social communication and aggression. Studies in a number of mammalian species indicate that AVP and AVP V1a receptors are ideally suited to regulate the expression of social processes because of their plasticity in response to factors that influence social behavior. The pattern of AVP innervation and V1a receptors across the social behavior neural network may determine the potential range and intensity of social responses that individuals display in different social situations. Although fundamental information on how social behavior is wired in the brain is still lacking, it is clear that different social behaviors can be influenced by the actions of AVP in the same region of the network and that AVP can act within multiple regions of this network to regulate the expression of individual social behaviors. The existing data suggest that AVP can influence social behavior by modulating the interpretation of sensory information, by influencing decision making and by triggering complex motor outputs. This article is part of a Special Issue entitled Oxytocin, Vasopressin, and Social Behavior.
Article
Callous-unemotional violence associated with antisocial personality disorder is often called 'predatory' because it involves restricted intention signaling and low emotional/physiological arousal, including decreased glucocorticoid production. This epithet may be a mere metaphor, but may also cover a structural similarity at the level of the hypothalamus where the control of affective and predatory aggression diverges. We investigated this hypothesis in a laboratory model where glucocorticoid production is chronically limited by adrenalectomy with glucocorticoid replacement (ADXr). This procedure was proposed to model important aspects of antisocial violence. Sham and ADXr rats were submitted to resident/intruder conflicts, and the resulting neuronal activation patterns were investigated by c-Fos immunocytochemistry. In line with earlier findings, the share of attacks aimed at vulnerable targets (head, throat and belly) was dramatically increased by ADXr, while intention signaling by offensive threats was restricted. Aggressive encounters activated the mediobasal hypothalamus, a region involved in intra-specific aggression, but sham and ADXr rats did not differ in this respect. In contrast, the activation of the lateral hypothalamus that is tightly involved in predatory aggression was markedly larger in ADXr rats; moreover, c-Fos counts correlated positively with the share of vulnerable attacks and negatively with social signaling. Glucocorticoid deficiency increased c-Fos activation in the central amygdala, a region also involved in predatory aggression. In addition, activation patterns in the periaqueductal gray - involved in autonomic control - also resembled those seen in predatory aggression. These findings suggest that antisocial and predatory aggression are not only similar but are controlled by overlapping neural mechanisms.
Article
Traditional theories propose that testosterone should increase dominance and other status-seeking behaviors, but empirical support has been inconsistent. The present research tested the hypothesis that testosterone's effect on dominance depends on cortisol, a glucocorticoid hormone implicated in psychological stress and social avoidance. In the domains of leadership (Study 1, mixed-sex sample) and competition (Study 2, male-only sample), testosterone was positively related to dominance, but only in individuals with low cortisol. In individuals with high cortisol, the relation between testosterone and dominance was blocked (Study 1) or reversed (Study 2). Study 2 further showed that these hormonal effects on dominance were especially likely to occur after social threat (social defeat). The present studies provide the first empirical support for the claim that the neuroendocrine reproductive (HPG) and stress (HPA) axes interact to regulate dominance. Because dominance is related to gaining and maintaining high status positions in social hierarchies, the findings suggest that only when cortisol is low should higher testosterone encourage higher status. When cortisol is high, higher testosterone may actually decrease dominance and in turn motivate lower status.
Article
Although the anterior hypothalamus has been implicated in the control of aggression in various rodent species, little is known about the neurochemical mechanisms mediating this control. It has been established that flank marking, which occurs with high frequency during agonistic encounters in hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. The present study was undertaken to determine whether intraspecific aggression in this species is similarly influenced by vasopressin in this area of the hypothalamus. Adult male hamsters, surgically implanted with guide cannulae aimed at the anterior hypothalamus, were microinjected with three different concentrations of the V1-receptor antagonist d(CH2)5Tyr(Me)AVP or a vehicle control of 0.9% NaCl. Sixty minutes after each microinjection a smaller male hamster was introduced into the home cage of the treated hamster. The resident hamsters showed a significant dose-dependent reduction in the number of biting attacks on the intruders over the 10 minute test period. The V1-receptor antagonist also caused a significant increase in the resident hamster's latencies to attack the intruder. However, the resident hamsters' total contact time with the intruder was unaffected by drug treatment suggesting that the reduction of aggression was not due to a generalized effect upon social behavior. The specificity of the drug treatment was further supported by the observation that it did not affect resident hamsters' sexual motivation or ability to mount a receptive female. These data suggest that vasopressin-sensitive neurons in the anterior hypothalamus are involved in the control of intraspecific aggression in male hamsters.
Article
Aggressive behavior is controlled at multiple anatomical levels within the human brain. To illustrate hierarchical neural controls over aggression, we compare and contrast the roles of the hypothalamus, amygdaloid complex, and orbital prefrontal cortex in terms of their distinctive sensory inputs, effector channels, and principles of integration as deduced from observations in animals and man. We illustrate characteristic syndromes of human aggression resulting from hypothalamic, temporolimbic, or frontal cortical lesions. The application of this perspective to research on criminal violence is discussed.
Article
Male and female rats housed together in small groups both became aggressive toward strange rats placed into their cages. However, male rats mainly attack male intruders and female rats mainly attack female intruders. The hormonal requirements for this aggression are also sexually dimorphic. Castration of the male residents causes a decrease in aggressive behavior, but ovariectomy of the female residents has little effect on their aggression. Replacement therapy to castrated males with 500 microgram/day of testosterone propionate (TP) restores all components of aggressive behavior within 2-3 weeks. Replacement therapy with 5 microgram/day of estradiol benzoate for 3 weeks had no effect on castrated males' aggressive behavior, nor did it cause the males to start attacking female intruders. Replacement therapy to ovariectomized females had a quite different effect. Treatment with EB or EB and progesterone reduced or blocked attack toward intruder females but did not alter the low level of attack toward males. Treatment with TP for 3 weeks also slightly reduced attack toward female intruders but increased the probability of attack toward male intruders. The sex-specificity of aggression and the differential influence of hormones suggests that different mechanisms may be responsible for aggression in males and in females.
Article
Although human aggression is frequently inferred to parallel aggression based on testosterone in nonprimate mammals, there is little concrete support for this position. High- and low-aggression individuals do not consistently differ in serum testosterone. Aggression does not change at puberty when testosterone levels increase. Aggression does not increase in hypogonadal males (or females) when exogenous testosterone is administered to support sexual activity. Similarly, there are no reports that aggression increases in hirsute females even though testosterone levels may rise to 200% above normal. Conversely, castration or antiandrogen administration to human males is not associated with a consistent decrease in aggression. Finally, changes in human aggression associated with neuropathology are not consistent with current knowledge of the neural basis of testosterone-dependent aggression. In contrast, human aggression does have a substantial number of features in common with defensive aggression seen in nonprimate mammals. It is present at all age levels, is displayed by both males and females, is directed at both males and females, and is not dependent on seasonal changes in hormone levels or experiential events such as sexual activity. As would be expected from current knowledge of the neural system controlling defensive aggression, aggression in humans increases with tumors in the medial hypothalamus and septal region, and with seizure activity in the amygdala. It decreases with lesions in the amygdala. The inference that human aggression has its roots in the defensive aggression of nonprimate mammals is in general agreement with evidence on the consistency of human aggressiveness over age, with similarities in male and female aggressiveness in laboratory studies, and with observations that some neurological disturbances contribute to criminal violence. This evidence suggests that human aggression has its biological roots in the defensive aggression of nonprimate mammals and not in hormone-dependent aggression based on testosterone.
Article
The drug-violence relationship exists for several reasons, some direct (drugs pharmacologically inducing violence) and some indirect (violence occurring in order to attain drugs). Moreover, the nature of that relationship is often complex, with intoxication, neurotoxic, and withdrawal effects often being confused and/or confounded. This paper reviews the existing literature regarding the extent to which various drugs of abuse may be directly associated with heightened interpersonal violence. Alcohol is clearly the drug with the most evidence to support a direct intoxication-violence relationship. The literatures concerning benzodiazepines, opiates, psychostimulants, and phencyclidine (PCP) are idiosyncratic but suggest that personality factors may be as (or more) important than pharmacological ones. Cannabis reduces likelihood of violence during intoxication, but mounting evidence associates withdrawal with aggressivity. The literature on the relationship between steroids and aggression is largely confounded, and between 3,4-methylenedioxymethamphetamine (MDMA) and aggression insufficient to draw any reasonable conclusions. Conclusions and policy implications are briefly discussed.
Article
This study is a follow-up investigation of a forensic psychiatric sub-population 6-8 years after forensic psychiatric evaluation. The aim was to examine the long-term validity of biological markers of psychopathy and antisocial behavior over time. Data on criminal records were obtained at follow-up from the National Council for Crime Prevention. Basic data included findings of psychiatric and psychological assessments, as well as values for serum triiodothyronine (T3) and free thyroxin (FT4), and platelet monoamine oxidase (MAO) activity, all obtained during the forensic psychiatric examination. Criminal recidivists at follow-up had higher serum T3 levels than non-recidivists, and much higher values than normal controls, while their levels of free T4 were lower. The T3 levels in criminal recidivists correlated to psychopathy- and aggression-related personality traits as measured by the Karolinska Scale of Personality. In violent recidivists, a remarkably high correlation was noted between T3 levels and Irritability and Detachment, traits that have previously been linked to the dopaminergic system. Stepwise multiple regression analyses confirmed the relationships of T3 levels and platelet MAO activity with personality traits in criminal recidivists. The predictive validity of biological markers of psychopathy, T3 and platelet MAO, measured during forensic psychiatric investigation, is stable over time. The results indicate chronic alterations of the hypothalamic-pituitary-thyroid axis in this group of subjects.
Article
Anabolic steroid abuse in athletes has been associated with a wide range of adverse conditions, including hypogonadism, testicular atrophy, impaired spermatogenesis, gynaecomastia, and psychiatric disturbance. But what effect does steroid abuse have on the cardiovascular system?
Article
Aberrant social behavior is a hallmark of many cognitive, mood, and neurological disorders, although the specific molecular mechanisms underlying the behavioral deficits are not well understood. The neurotransmitter noradrenaline (NA) has been implicated in some of these disorders, as well as in several aspects of social behavior in humans and animals. We tested dopamine beta-hydroxylase knockout (Dbh -/-) mice that lack NA in various social behavior paradigms. Dbh -/- mice have relatively normal performance in the elevated plus maze, light/dark box, and open field test - three measures of anxiety - and a social recognition test. In contrast, Dbh -/- mice displayed a specific deficit in a social discrimination task and had a nearly complete absence of resident-intruder aggression. These results indicate that intact NA signaling is required for some types of social memory and aggression, but that a lack of NA does not greatly affect anxiety in mice. Further exploration of NA deficits in neurological disease may reveal mechanisms of aberrant social behavior.
Article
We review here aggression-related human psychopathologies and propose that human aggressiveness is mainly due to three major factors: (i) brain dysfunction affecting aggression-controlling brain centers (e.g. in certain types of brain lesions, epilepsy, Alzheimer disease, etc.); (ii) hypoarousal associated with chronically low plasma glucocorticoids, which foster violence by diminishing emotional barriers that limit such behaviors (e.g. in conduct disorder and antisocial personality disorder); (iii) hyperarousal which leads to irritability and outbursts (e.g. in depression, intermittent explosive disorder, chronic fatigue, etc.). Different disorders are associated with different types of aggressiveness; e.g. hypoarousal is often associated with instrumental aggression, whereas hyperarousal is associated with uncontrollable outbursts. Many psychological disorders have been simulated in laboratory models, which were used to assess aggressiveness. Little effort was invested, however, in assessing the abnormal dimension of such aggressiveness. We present here three models that appear especially suitable to assess abnormal aspects of rodent aggression: (i) abnormal attack targeting (head, throat, and belly) that is induced by hypoarousal in rats and models violence in hypoarousal-driven human aggression (ii) 'escalated' aggression (increased aggressive response due to frustration or instigation), which models irritability and hyperarousal-driven aggressiveness; and (iii) context-independent attacks induced by hypothalamic stimulation or genetic manipulations. These three models address different aspects of abnormal aggressiveness, and can become extremely useful in three areas: in evaluating and assessing models of human psychopathologies, in studying transgenic animals, and in developing new treatment strategies. Research based on these or similar models do not address aggressiveness in quantitative terms, but follows the development of abnormal aspects, and the possibilities of their specific treatment.
Article
Radioiodine is considered the treatment of choice for hyperthyroidism, but in some situations, methimazole therapy is preferred, such as in cats with pre-existing renal insufficiency. Methimazole blocks thyroid hormone synthesis, and controls hyperthyroidism in more than 90% of cats that tolerate the drug. Unfavorable outcomes are usually due to side effects such as gastrointestinal (GI) upset, facial excoriation, thrombocytopenia, neutropenia, or liver enzyme elevations; warfarin-like coagulopathy or myasthenia gravis have been reported but are rare. Because restoration of euthyroidism can lead to a drop in glomerular filtration rate, all cats treated with methimazole should be monitored with BUN and creatinine, in addition to serum T4, complete blood count, and liver enzymes. Transdermal methimazole is associated with fewer GI side effects, and can be used in cats with simple vomiting or inappetance from oral methimazole. Hypertension may not resolve immediately when serum T4 is normalized, and moderate to severe hypertension should be treated concurrently with-atenolol, amlodipine, or an ACE inhibitor. Alternatives to methimazole include carbimazole, propylthiouracil, or iodinated contrast agents.
Hormones and aggression
  • P F Brain
  • PF Brain
National Research Council, Division of Behavioral and Social Sciences and Education, Commission on Behavioral and Social Sciences and Education, & Panel on the Understanding and Control of Violent Behaviors
  • P F Brain
  • PF Brain
The Wiley handbook of violence and aggression
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Exploring the experiences of people with hypo-and hyperthyroidism
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  • MA Nexø
Aggressive behavior in psychiatric patients in relation to hormonal imbalance
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Testosterone and depression: Systematic review and meta-analysis
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Hormonal aspects of aggression and violence
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  • AJ Reiss
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  • JA Roth