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This chapter provides a brief background on the nature of personality traits and what is required to establish their validity. The popular Aggression Questionnaire is singled out and described in some detail in regard to its relationships with a number of other personality variables. Also highlighted are a number of personality theories including the macho and Machiavellian personality each having special relevance for sports aggression. The strength of one's identification with an athlete or sports team is similarly shown to be predictive of aggression. The question of the value of training in the martial arts as a means of reducing the student's aggression is addressed against the background of existing research. Biological influences including sex differences, chromosomes, and testosterone are examined with respect to aggression. The question of parallels between fighting fish and a schoolyard fight is raised in a concluding section.

In this chapter we provide an overview of recent research on the biopsychological correlates of implicit motives. We review evidence for a role of gonadal steroids (testosterone and estradiol) as well as stress axis activation in power motivation arousal and satisfaction/frustration, summarize recent research on the role of progesterone and affiliation motivation, and discuss a possible role for arginine–vasopressin in achievement motivation. We also present findings from brain imaging work that indicate that the needs for power, affiliation, and achievement modulate activity in a core motivational circuit consisting of striatum, amygdala, orbitofrontal cortex, and insula when nonverbal social incentives are processed.

This chapter focuses on two neurochemical signals that control aggression—serotonin (5-hydroxytryptamine, or 5-HT) and vasopressin (VP). 5-HT and VP appear to play significant roles in the regulation of impulsivity and aggression. 5-HT reduces aggressive responding, while VP enhances arousal and aggression in a context-dependent manner. The interaction between the brain and the environment is regulated, in part, by changes in gonadal and adrenal steroids. The stress of social subjugation alters the levels of testosterone and stress hormones, affecting gene transcription and translation. The VP/5-HT systems are sensitive to changes in these steroid hormones linking the neurochemical regulation of aggression to environmental events.

This chapter utilizes conspecific, offensive aggression in males and females as model systems to exemplify androgenic influences on aggressive behavior. This form of aggression is a productive behavior exhibited between same-sex conspecifics; its effects are reflected in dominance status and access to resources.

Aggression is a form of behavior with the goal of causing damage to another individual. Evolutionarily it developed in response to competition for mates or vital resources. In humans aggressive behavior has become more nuanced, but its goals and causes are essentially the same. A genetic basis for aggression is shown in animals by the ability to selectively breed aggressive behavior to produce extremely aggressive strains in individuals. In humans, twin studies have also made clear that aggression has a strong genetic component. The role of the hormone testosterone is certainly involved, although the exact pathways are unclear. Brain levels of the neurotoxin serotonin correlate with aggression, and genetic manipulation of these levels can enhance or reduce aggressive behavior. A role for the neurotransmitter nitrous oxide has been demonstrated to influence aggression in both animals and humans.

Homo oeconomicus is the agent at the heart of neoliberalism, whose capacity to make autonomous, rational choices animates the system as a whole. This chapter calls the bluff on his claim to stand in for an unmarked humanity, identifying the ways he operates as a masculine figure. The chapter tracks him through three sites: Foucault’s lectures on neoliberalism; an ethnographic account of a trading desk set at a hub of the global money supply; and the scientific investigation and public discussion of the disruptive role of testosterone in financial markets during the 2008 crisis. In each arena, a distinctive iteration of masculinity emerges as crucial to its functioning. Viewed together these three snapshots illuminate neoliberalism’s fundamentally gendered nature and suggest masculinity’s role in keeping its social structuring out of view.

This chapter provides current and updated information on the care of the ageing hypogonadal man from diagnosis to treatment options and monitoring. In most cases, these aspects of care are straightforward. The informed clinician has the responsibility to either refer appropriately or to manage effectively and safely the patient with late onset hypogonadism (LOH), also known as androgen decline in the ageing male (ADAM). It is important to emphasize that only symptomatic late-onset hypogonadism (SLOH) needs to be treated. The man without sequelae from low levels of serum testosterone requires follow-up but not necessarily androgen replacement or supplementation.

Trade-offs between reproduction and maintenance can compromise health. Male hormones such as testosterone regulate energy allocation between reproductive effort and survival; this is made evident when immunological challenges cause changes in reproductive hormones. Female hormones adjust energy allocation between investment in ovarian function, somatic investment, and present offspring (lactation), implementing trade-offs between present and future reproduction. Metabolic hormones respond to environmental cues to sequester or liberate energetic resources such as glucose and fat. Mismatch between environmental conditions and the expression of metabolic hormones are likely to underlie variation in obesity and diabetes. Lifetime variation in endogenous reproductive hormones suggests a trade-off between early benefits for reproduction and later costs against survivorship expressed in population differences in the incidence of reproductive tumors, such as breast and prostate cancer.

This chapter explores the relationship between male plumage color and social status. Experiments show that red feather coloration does not function as a signal of status in either the breeding or non-breeding season. Drabber males are actually socially dominant to brighter red males. Testosterone implants increase male dominance but reduce male feather coloration, perhaps explaining why drabber males are socially dominant.

Klinefelter syndrome (KS) was first identified by Dr. Harry Klinefelter in 1942 (Klinefelter, Reifenstein, and Albright 1942) in a report of nine tall men with hypogonadism, sparse body hair, gynecomastia, and infertility. The associated chromosome disorder 47XXY was identified several years later (Jacobs and Strong 1959). The full phenotype consists of hypogonadism, low testosterone levels, infertility, gynecomastia, sparse body hair, eunuchoid body habitus, long legs and arm span, and above-average height. However, except for hypogonadism (small testes), which is present in nearly all individuals with XXY, the physical phenotype may be quite variable. In live-born males, KS has an incidence of 1:500 to 1:1,000 (Bojesen, Juul, and Gravholt 2003; Hamerton, Canning, Ray, and Smith 1975; Ratcliffe, Bancroft, Axworthy, and McLaren 1982; Rovet, Netley, Keenan, Bailey, and Stewart 1996), with a further incidence of 1:300 in spontaneous abortions (Hassold and Jacobs 1984). Klinefelter syndrome is the most common of the sex chromosome abnormalities and the second most common chromosomal disorder after Down syndrome. The possibility that incidence is increasing has also been raised (Morris, Alberman, Scott, and Jacobs 2008). Despite this, possibly as a consequence of poor identification, the syndrome has been studied less extensively than, for example, Turner syndrome (45XO) and many other developmental disorders. Boys with KS are generally tall and long-limbed but with increasing height in the population, these characteristics alone are not necessarily distinguishing. Individuals with KS are generally not immediately identifiable, and many cases of KS remain unidentified throughout life. Up to two-thirds of cases may never be identified clinically (Lanfranco, Kamischke, Zitzmann, and Nieschlag 2004). There is no clearly identifiable facial appearance, although mandibular prognathism (a prominent lower jaw and extended chin) is reported on group analysis using radiographic cephalometry (Brown, Alvesalo, and Townsend 1993). Increased genetic screening now means that 10% of cases in the United Kingdom are diagnosed prenatally on the basis of karyotype, with a further 25% of cases diagnosed during childhood (Abramsky and Chapple 1997). However, this means that 65% of cases reach puberty undiagnosed. In Belgium, fewer than 10% of expected cases are diagnosed before puberty (Bojesen et al. 2003).

This chapter examines the theoretical and empirical research into evolutionary aspects of four complex issues of human behaviour in sports. We highlight how evolutionary approaches have promoted our understanding of human sports and competition. To begin with, we describe the relationship between sports competitions and testosterone levels and elucidate how winning and losing leads to different, sometimes status-changing, endocrine responses. Secondly, we look at ‘home advantage’ and examine how hormonal and psychological research has aided our understanding of this well-known phenomenon. The next section focuses on possible evolutionary explanations as to why left-handers may have an advantage in physical combat in both traditional and westernized societies. The final section examines colour influences on human behaviour in general and on sports competition in particular, focusing specifically on the significance of the colour red in human competitive interactions. These four themes serve to highlight the value of evolutionary approaches in enhancing and enriching our understanding of human sports competitions.

This chapter examines the role of the hormone testosterone in the development of social cognition. Research findings from human studies designed to elucidate the behavioral effects of both prenatal and postnatal testosterone exposure in children and young adults are summarized. Effects are found to be both time and dose dependent, with exposure to abnormal hormone levels having a limited impact outside the 'critical window' in development. Particular attention is given to the role of prenatal hormone exposure, which appears to be vital for early organization of the brain. In later life, measurements of circulating hormone levels and the administration of testosterone are found to predict behavior, but the effect is thought to be one of 'activation' or 'fine-tuning' of the early organization of the brain. Possible directions for valuable future research are discussed.

This chapter reviews some studies that have examined the influence of gonadal steroids on the learning of the passive avoidance task, and also examines the relationship between the effects of testosterone on passive avoidance tasks and on other tasks and situations. Furthermore, it explores issues that have not, as yet, received much experimental attention. Many effects of the gonadal steroids are sex dependent. Thus testosterone strongly facilitates attack pecking in male chicks but has little effect on attack pecking in females. The rapidity with which testosterone affects performance in the passive avoidance task clearly distinguishes it from actions of steroids that involve genomic interactions. However, a number of gonadal steroids exert rapid effects on neural activity. The underlying neurochemical basis of these effects is not clear.

Research on free-living songbirds has revealed novel and important insights into the various contexts in which 17β-estradiol (E₂) activates aggressive behavior. In the Pacific Northwest, male song sparrows defend territories during the breeding season (when circulating testosterone levels are elevated) and during the nonbreeding season (when circulating testosterone levels are nondetectable). The ecological context of territorial aggression differs greatly across seasons, but several lines of evidence indicate that both breeding and nonbreeding aggression depend on the conversion of testosterone into E₂ by aromatase. Remarkably, there appears to be a seasonal shift in the source of androgen substrate for brain aromatase: from a systemic source (the testes) in the breeding season to a local source (the brain itself) in the nonbreeding season. This seasonal shift may have evolved to reduce the exposure of peripheral tissues and other brain areas to the deleterious effects of testosterone and E₂.

The central role of neuronal aromatase activity in masculinization of the rodent brain has been firmly established for almost 40 years, yet the myriad of mechanisms by which the principal product of aromatization, estradiol, organizes the neural substrate to predispose adult behavior continue to be elucidated. Unexpected roles for inflammatory mediators and components of the immune system in sexual differentiation elucidate novel principles of brain development. Long-standing puzzles associated with female brain development, both feminization and defeminization, are being solved by unexpectedly rapid and developmentally delayed actions of estradiol, respectively. Neurosteroidogenesis in discrete brain regions, culminating with estradiol but possibly beginning with cholesterol, hints at additional roles for aromatization in brain development outside the confounds of the classical organizational/activational hypothesis and affecting cognitive regions such as the cortex, hippocampus, and cerebellum. Collectively, it is clear that we are far from the final chapter in determining how aromatization influences brain and behavior.

In the avian brain, aromatase is constitutive and inducible in neurons and glia respectively. Glial aromatase is rapidly and dramatically upregulated in astroglia (astrocytes and radial glia) independent of brain region, in response to perturbation of the neuropil. Estrogens, synthesized by induced aromatization in glial cells, are potent mitigators of apoptotic degeneration and may accelerate neuronal replacement following brain damage. Specifically, aromatase inhibition increases, and estradiol replacement decreases secondary degeneration at the site of primary damage in the passerine brain. Indeed, the characteristic wave of secondary degeneration observed in mammals following compromise of the brain, is severely dampened in the passerine brain and is only revealed following inhibition of inducible glial aromatization. Further, the rate of injury-induced neurogenesis is increased in birds receiving estradiol replacement relative to those treated with an aromatase inhibitor alone. This chapter reviews data on the structural and functional consequences of glial aromatization. It highlights emerging data on the signals that invariably accompany brain damage and their potential role as inductive signals for the transcription and translation of the aromatase gene specifically in glial cells. The robust and cell-specific expression of aromatase in the passerine brain continues to provide an excellent model for the study of the provision of estrogens to neural targets with temporal and spatial specificity. In addition to basic scientific questions, passerine songbirds may serve as superb animal models toward understanding clinical syndromes involving brain damage, ischemia/anoxia, and neurodegeneration.