Stress hormones in psychophysiological research: Emotional, behavioral, and cognitive implications.

SCOPE AND PURPOSE This chapter describes regulation of the stress hormones and their measurement and interpretation in psychophysiological research. A hormone is a signaling molecule, secreted by a gland that travels via the bloodstream to a distant target tissue and exerts an action on that target. A stressor, by its very nature, is an event that poses a real or potential threat to well-being. The resulting stress response engages numerous protective systems, including communication by hormonal messengers, to reduce the threat (Lovallo, 2016). Choosing a list of stress hormones is necessarily arbitrary since no hormone is active only during times of stress. For example, the primary stress hormone cortisol (CORT), serves normal homeostatic functions and it regulates the stress response (Munck, Guyre, & Holbrook, 1984). Similarly, the catecholamines, epinephrine (EPI) and norepinephrine (NE), are elevated during states of stress, but NE in particular is employed in normal physiological regulation. Other hormones, such as the sex steroids, may be affected by stress, but are not typically classified as stress hormones(Kudielka, BuskeKirschbaum, Hellhammer, & Kirschbaum, 2004). Since physiology does not show us a clear boundary, we will confine this discussion to the core stress hormones, CORT, and the catecholamines. A good example of this boundary problem is the case of the hormone oxytocin. Oxytocin was first identified as a posterior pituitary hormone that caused uterine contractions during the birth process and stimulatedmilk production afterward (Dale, 1909). Interestingly for stress and behavior, it was later found to act as a neuropeptide in the brain, where its actions reinforce parenting and socialaffiliative behaviors in most species (Insel, 1992). In turn, parenting and social behaviors are responsive to stress (Weaver et al., 2004) and so are the actions of oxytocin (Grimm et al., 2014; Starr-Phillips & Beery, 2014). Oxytocin may buffer some acute and chronic effects of stress due to actions in the brain (Montag & Reuter, 2014; Smith & Wang, 2014; Tops, Koole, IJzerman, & Buisman-Pijlman, 2014; Uvnas-Moberg, Handlin, & Petersson, 2014), and peripheral oxytocin may be responsive to stress in girls exposed to early life adversity (Seltzer, Ziegler, Connolly, Prososki, & Pollak, 2014). This illustrates how oxytocin affects nurturing behaviors in the short term, with consequences for stress reactivity, and also affects subsequent parenting behaviors in offspring exposed to stress during development (Preston, 2013). However, for present purposes, changes in oxytocin actions during and after stress, and their programming of the stress axis, are properly seen as secondary to the core of the acute stress response. Moreover, the social effects of oxytocin are due to its peptide actions and not to its classic hormonal functions. We will discuss CORT as central to the stress response and the catecholamines as secondary. CORT acts on all peripheral tissues, but it also crosses the blood–brain barrier, allowing it to regulate brain function during acute stress episodes and to influence behavior during future episodes. The CORT literature has grown rapidly over the past 35 years because of its impact on behavior and health. In contrast, the catecholamines do not cross the blood–brain barrier, although EPI influences the central nervous system indirectly by way of the vagus nerve (McGaugh & Roozendaal, 2002). Although we refer to the catecholamines as hormones, this designation is correct only for EPI, as discussed below. In leaving some topics out, we note that the stress literature is too large to allow a full review of endocrine effects during stress, even when confined to CORT and the catecholamines. Some topics will not be discussed in detail, such as stress response differences due to: sex (Kirschbaum, Wust, & Hellhammer, 1992; Turner & Weaver, 1985), age (Ehlert, 2013; Kudielka, Hellhammer, & Wust, 2009; Kudielka et al., 1998), obesity (Epel et al., 2000; Jessop, Dallman, Fleming, & Lightman, 2001; Nieuwenhuizen & Rutters, 2008; Steptoe, Kunz-Ebrecht, Brydon, & Wardle, 2004), diurnal cycles (Kudielka, Federenko, Hellhammer, & Wust, 2006), immune system function (Bauer, 2008; Cacioppo et al., 1995; McEwen et al., 1997), posttraumatic stress disorder (Schelling et al., 2006; Yehuda et al., 2010; Zoladz & Diamond, 2013), or depression (Herbert, 2013; Pariante & Miller, 2001). Similarly,