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  • However an accumulation of evidence later indicated that

    2018-11-13

    However, an accumulation of evidence later indicated that vulnerable individuals identified in diathesis–stress models might instead be viewed as sensitive, developmentally plastic, and malleable vis-à-vis environmental influences, regardless of their valence. This alternate perspective led to the biological sensitivity to context model (Boyce and Ellis, 2005) and the differential-susceptibility hypothesis (Belsky and Pluess, 2009), both of which share features with the concept of sensory processing sensitivity (Aron and Aron, 1997) from the personality literature. These independently developed but complementary and influential models have been joined under the umbrella term neurobiological susceptibility (Ellis et al., 2011; see also Moore and Depue, in press, Pluess (in press), and Stamps (2015) for highly relevant reviews of this general concept). The central tenet of these models is that individuals vary in their sensitivity to psychosocial contexts as a function of biological factors that are innate and/or conferred by early experience. Individuals low in sensitivity to the environment will fare similarly across all environments, whereas highly sensitive individuals will be both more vulnerable to adverse contexts and more responsive to salubrious contexts. For example, for individuals with the low- as opposed to high-activity MAOA genotype, not only have high levels of childhood adversity been associated with extreme antisocial behavior (Caspi et al., 2002) but low levels of adversity have been associated with low or even absent antisocial behavior (Foley et al., 2004). Based on this and similar findings, a variety of biologically-rooted sensitivity or susceptibility factors have been identified that include candidate genes (e.g., MAOA; serotonin-transporter-linked polymorphic region, 5-HTTLPR; dopamine D4 receptor gene, DRD4; dopamine D2 receptor gene, DRD2); high stress reactivity in the form of adrenocortical, immune, or physiological response (e.g., higher domoic acid reactivity; higher vagal withdrawal or respiratory sinus arrhythmia reactivity; low vagal tone); and biologically-based behavioral phenotypes such as temperament (e.g., behavioral inhibition; difficult temperament) and personality (e.g., neuroticism; sensory-processing sensitivity). These factors are thought to shape the way that individuals perceive, attend and react to, and behave within their environments, and to ultimately moderate environmental effects on emerging competencies and psychopathologies (Boyce and Ellis, 2005). Moderation is expected because individuals’ underlying biological systems are thought to differentially monitor the environment to match its demands. For example, the biologically-based tendency toward hyperreactivity to novelty in infancy, known as behavioral inhibition, may manifest as social reticence and anxiety in childhood despite a strong motivation to interact with peers (Coplan et al., 1994; Rubin et al., 2009). Conflict between high-avoidance and high-approach motivations may lead individuals to be particularly sensitive to the social milieu as they alternately check cues tapping either motivation, thus reinforcing either through experience (Caouette and Guyer, 2014). Over time, highly susceptible individuals who encountered supportive environments may learn to take advantage of the positive, supportive features of their surroundings, while those exposed to risk and adversity may be more vigilant for and reactive to environmental threats and hazards. Similar accounts could be generated for other susceptibility factors, which tend to be associated with negative emotionality and converge on learning through careful observation – pausing before acting rather than acting first. The ensuing, potent registration of experience upon the nervous system may more greatly enable neural processes to track survival-related subtleties (Belsky, 2005; Suomi, 1997; Wolf et al., 2008). The degree to which individuals “tune” to the environment may be calibrated through genetic expressions, stress reactivity, and, as we propose, structural and functional neural characteristics that are context-sensitive and reactive to environmental cues, particularly within the social domain during adolescence (Meaney, 2001; Nelson and Guyer, 2011; Nelson et al., 2005). This heightened social sensitivity makes adolescence an important and model developmental period for investigating susceptibility at the neurobiological level. However, despite the proposal that biological susceptibility comprises a “complex, integrated, and highly conserved repertoire of central neural and peripheral neuroendocrine responses” (Boyce and Ellis, 2005, p. 271; emphasis added), direct measures of brain structure and function have been largely unexamined as sensitivity factors (but see Yap et al., 2008 and Whittle et al., 2011, for exceptions). As interactions between biology and environment sometimes explain more variance in outcomes than do main effects (Beauchaine et al., 2008), accounting for these neural factors can clarify why some adolescents may be more primed for good or bad outcomes given their combination of neural susceptibility and social-contextual exposures.