30 Chapter 2 diurnal pattern are associated with psychopathology (Adam et al., 2017); however, most research has focused on stress-induced cortisol surges. Like testosterone, this hormone follows a pulsatile and diurnal pattern, in which levels are high in the morning, surging within 30–40 minutes after waking, followed by a steep drop for a few hours and a steady decline until the lowest point at bedtime. Cortisol is the end product of the hypothalamus–pituitary–adrenal (HPA) axis. The hypothalamus secretes corticotropin-releasing hormone (CRH), which stimulates the anterior pituitary to release adrenocorticotropic hormone (ACH); this travels via the bloodstream to the adrenal cortex where it stimulates the production of cortisol. Cortisol in turn inhibits the pituitary and the hypothalamus, forming a negative feedback loop, and is able to exert both rapid non-genomic and slow genomic effects in the brain (Joëls, Pu, Wiegert, Oitzl, & Krugers, 2006). Cortisol binds to glucocorticoid and mineralocorticoid receptors in brain areas important in regulating the fight–flight response, such as frontal areas, amygdala, and hippocampus (Lupien, Maheu, Tu, Fiocco, & Schramek, 2007). It has an important role in regulating homeostatic systems, affecting arousal, metabolic processes, and the immune system (Sapolsky, Romero, & Munck, 2000). During the initial phase of the stress response, epinephrine from the adrenal medulla triggers norepinephrine release in the basolateral amygdala, among other regions, which induces an increase in vigilance by prioritizing sensory processing and activation of the amygdala (Osborne, Pearson-Leary, & McNay, 2015). Subsequent cortisol release regulates the stress response by downregulating amygdala responsivity and decreasing anxiety-driven selective attention to threat (Henckens, van Wingen, Joëls, & Fernández, 2010, n = 72; Putman & Roelofs, 2011; van Peer et al., 2009, n = 21, small effect sizes), besides affecting activity in areas involved in the planning and execution of motor responses (Montoya, Bos, Terburg, Rosenberger, & van Honk, 2014, n = 20). Animal research has shown that higher cortisol levels are associated with social avoidance behavior (Sapolsky, 1990). Studies featuring stress-induced cortisol surges and cortisol administration in healthy humans extend these findings by showing that elevated levels of cortisol are associated with increased avoidance of social threat on the AAT (Roelofs et al., 2005, n = 22, small to medium effect sizes; van Peer et al., 2007, n = 40, lare effect sizes). The HPG axis works in antagonism with the hypothalamus–pituitary–adrenal (HPA) axis, in such a way that the end product of the latter (i.e., cortisol, released in response to stress) disrupts production and inhibits actions of testosterone, which in turn inhibits the stress-induced activation of the HPA axis at the hypothalamus (Viau, 2002). Both neuroendocrine axes are important in the regulation of social–motivational behavior and show a complex interaction: basically, higher basal cortisol levels, and low testosterone, are associated with social subordination stress and avoidance behavior, whereas higher basal testosterone and low cortisol facilitate social dominance and approach behavior
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