American Psychologist

Beyond Storm and Stress: Typicality, Transactions, Timing, and Temperament to Account for Adolescent Change
Tom Hollenstein and Jessica P. Lougheed Online First Publication, August 5, 2013. doi: 10.1037/a0033586

CITATION Hollenstein, T., & Lougheed, J. P. (2013, August 5). Beyond Storm and Stress: Typicality, Transactions, Timing, and Temperament to Account for Adolescent Change. American Psychologist. Advance online publication. doi: 10.1037/a0033586

Beyond Storm and Stress

Typicality, Transactions, Timing, and Temperament to Account for Adolescent Change
Tom Hollenstein and Jessica P. Lougheed Queens University, Kingston

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Adolescent storm and stress has been a focal yet controversial developmental framework for over a century. In the present article, we challenge the current perspective that storm and stress is neither ubiquitous nor inevitable but probable. Instead, we argue, storm and stress is a vestigial developmental framework, and we propose a more comprehensive approach to understanding adolescent-typical changes based on six premises: (1) The biological changes of adolescence are inevitable and ubiquitous; (2) adolescent biological changes drive various mechanisms of adolescent behavior; (3) adolescent biological changes are shaped by environmental inuences; (4) individual differences in adolescent emotional-behavior changes are domain specic and vary in intensity; (5) there are individual differences in the age of onset and duration of periods of adolescent change; and (6) individual differences in the duration and intensity of transitions in emotional arousal are functionally modulated by burgeoning emotion regulation skills. We conclude with the more comprehensive 4T (typicality, transactions, temperament, and timing) approach and suggestions to guide adolescent research in the 21st century. Keywords: adolescence, development, storm and stress, individual differences, variability

t is quite difcult to nd a review of adolescence that does not refer to the storm and stress hypothesis. The term was rst used by G. Stanley Hall in his 1904 tome to refer to the decrease in self-control (storm) and the corresponding increase in sensitivity to arousing stimuli (stress) that typically characterize adolescent behavior. Across the ensuing decades of the 20th century, the prevailing perspectives on this developmental phenomenon have oscillated between deterministic explanations (e.g., To be normal during the adolescent period is by itself abnormal, Anna Freud, 1958, p. 267; cf. Arnett, 1999) and purely environmental accounts (e.g., Benedict, 1934; Mead, 1928). As the polarity of the age-old naturenurture debate gave way to the current acceptance of a dynamic interaction between biology and environment (Oyama, Grifths, & Gray, 2003), so too did the question of storm and stress became more nuanced. The contemporary perspective is that although adolescence may be stormy and/or stressful for some, it is not typically a developmental problem, nor is it inevitable or ubiquitous (Arnett, 1999;

Larson & Ham, 1993; Laursen, Coy, & Collins, 1998; Steinberg, 2001). In the present article, we challenge this dominant conclusion to suggest that storm and stress may no longer be a useful framework for understanding adolescent-typical behavior and changes. It has inspired a century of debate on whether storm and stress is ubiquitous or inevitable. However, the fundamental question may not be whether storm and stress occurs in every adolescent; rather, the fundamental questions may be when do changes occur and how do they manifest? Specically, the all-or-nothing approach of the storm and stress hypothesis, much like the nature nurture debate, is rooted in a false dichotomy and does little to facilitate our understanding of how adolescents develop and change. In the rst section, we begin by showing that the operationalization of storm and stress has been isolated to a narrow set of behaviors and that this approach has neglected other domains of emotion-related changes in adolescence. Next, we review the adolescent changes that are undeniably ubiquitous and inevitable in typically developing populations biological and cognitive maturity. We argue that the range of individual differences in the timing of adolescent changes renders most of the empirical data uninterpretable with respect to the ubiquity and intensity of storm and stress. To replace storm and stress, we offer the 4T (typicality, transactions, temperament, and timing) approach and conclude with suggestions for guiding future research with this framework.

Storm and Stress Reconsidered

What does storm and stress really mean?1 Arnett (1999) provided an eloquent summary of storm and stress, both in historical terms and in reference to current understanding.

Tom Hollenstein and Jessica P. Lougheed, Department of Psychology, Queens University, Kingston, Ontario, Canada. We wish to thank Nicholas B. Allen and Michael C. Seto for helpful comments on drafts of this manuscript. Correspondence concerning this article should be addressed to Tom Hollenstein, Department of Psychology, Queens University, Kingston, Ontario K7L 3N6, Canada. E-mail: tom.hollenstein@queensu.ca
1 Hall (1904) adopted the term storm and stress from the Sturm und Drang literary movement of the late 18th century. Translations of the phrase also include storm and pressure, and it has connotations of excessive emotionality or strong inspiration (Walz, 1927).

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2013 American Psychological Association 0003-066X/13/$12.00 Vol. 68, No. 6, 000 000 DOI: 10.1037/a0033586

Tom Hollenstein

His review focused on an admittedly nonexhaustive set of behaviors that have been discussed and/or measured throughout the past century by anthropologists, psychoanalysts, and contemporary scholars: (a) conict with parents, (b) mood disruptions, and (c) risk behavior. Indeed, these are primary domains of difculty for adolescents and those around them. Changes in each of these domains are thought to be more probable during adolescence but not inevitable. Several crucial details of this view should be noted, as these reect the dominant scientic opinion today. First, the developmental sequence of peak occurrences in each of the three domains follows the order presented above. The peak in the frequency of parentadolescent conict (or number of different conict types) occurs in early adolescence, whereas the intensity of these conicts peaks later, in mid-adolescence (Laursen et al., 1998; Paikoff & Brooks-Gunn, 1991). Mood disruptionsmost notably, depressive episodes and symptomstend to peak in mid-adolescence (Graber, 2004). The tendency to engage in risky behaviors is the last of this triumvirate to peak, in late adolescence (Steinberg, 2008). Second, Arnett (1999) made the unequivocal assertion that [t]he claim that adolescent storm and stress is characteristic of all adolescents and that the source of it is purely biological is clearly false (p. 317). Thus, the extreme hypothesis credited to Hall, Freud, and others has apparently failed to be supported by the data. For the sake of clarity, consider the two components of this refuted claim, inevitability and biological determinism, separately. On the one hand, there is the inevitability hypothesis that no adolescent can avoid at least some degree of storm and stress. The more nuanced (i.e., cautious) contemporary view is that storm and stress is a tendencya statistical 2

average that incorporates individual differences, including those who never experience any typical adolescent difculties. Thus, storm and stress is not inevitable according to this view. On the other hand, the old-school biological determinism hypothesis has not been borne out either; rather it has given way to a more balanced, interactionist view. Biological mechanisms such as genes, hormones, and neural structures are typically seen as factors that create vulnerabilities to environmental inuences, and some attempt has been made to acknowledge bidirectional inuences between biology and environment (e.g., Susman & Rogol, 2004). Thus, although biological changes are in some sense synonymous with adolescence (i.e., puberty) and certainly inevitable for a typically developing population, the effect of these changes on adolescent behavior is not thought to be direct. A third aspect of Arnetts (1999) trio of storm and stress domains (conict, mood, and risk taking) is that they are each manifestations of more primary emotional processes. Indeed, adolescent-onset behavioral changes involve two interrelated processes: emotional arousal and emotion regulation (Steinberg, 2008, 2010). Changes in arousal or arousability can manifest in many ways, including increased sensitivity to social stressors; responses to rewards, as well as the type and number of objects that elicit those responses; and passions, broadly construed (e.g., sexual, moralistic, recreational). This is what Hall (1904) meant by stress. On the other hand, there are decits or at least inadequacies of self-regulation (Halls storm). Changes in the regulation of arousal relate to the development of cognitive abilities enabled by neural maturation and to the habits that emerge in response to increased arousal, such as coping mechanisms, rumination, and inhibitory control (Allen & Sheeber, 2008; Dahl, 2001). Thus, conict, mood, and risk-taking problems may be more generally subsumed as arousal and regulation problems with specic manifestations (internal vs. external) or occurring in specic contexts (intra- versus interpersonal). Despite the clarity of this revised storm and stress account, there are still several problems with the model. First, it is not really a developmental explanation. For example, the descriptive accounts of the average age of onset in each domain do not begin to explain this sequence. Why doesnt risk taking precede family conict? These orderly temporal patterns beg for a coherent developmental explanation. Second, the scientic consideration of inevitability is further compromised by focusing on extreme occurrences of adolescent behavior to the neglect of more mundane manifestations. Finally, the dominant, almost exclusive, methods used to support or refute any claims of adolescent storm and stress have been analyses at the aggregate level of one, or perhaps two, domains. This approach is inadequate for several reasons: (a) The manifestation of biologically driven, environmentally mediated change varies greatly across individuals. One adolescent may struggle with a negative self-image that perpetuates social isolation, while another may aggressively battle parents over autonomy issues. A study examining risk-taking Month 2013 American Psychologist

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ity and regulation are indeed important processes for adolescents, framing our theoretical understanding of adolescent development around this 109-year-old description may no longer deserve the prominence it has been afforded.

Storm and Stress Redefined

Since Halls (1904) time, we have signicantly expanded and deepened our understanding of development, emotions, biology, and adolescence. Recent progress in developmental neuroscience, for example, has accelerated this understanding and inspired a few more inclusive models of adolescent development (Casey, Jones, & Somerville, 2011; Steinberg, 2008). Based on these and other advances, we introduce the 4T approach, which is supported by the following six premises about adolescent emotional development. The rst three build progressively through (1) the inevitability of biological changes to (2) biological inuences on behavior to (3) environmental inuences on biological changes. The latter three relate to aspects of individual differences that build off the rst three premises. 1. The biological changes of adolescence are inevitable and ubiquitous. Except in rare medical conditions, all adolescents experience species-typical structural and functional changes in physiology. On the structural side are changes in body height, fat distribution, secondary sex characteristics, and other organizational effects of hormones (Brooks-Gunn, Graber, & Paikoff, 1994; Susman, Houts, et al., 2010). Adolescent neuronal structure also undergoes signicant transformations (Blakemore, Burnett, & Dahl, 2010; Casey, Jones, & Hare, 2008; Paus, 2010; Spear, 2000, 2003). The number and pattern of synaptic connections, especially in the prefrontal cortex, are shaped by synaptic pruning (Giedd, 2004). These structural changes occur across species from rats to primates and confer the requisite manifestations of adulthood (Brenhouse, Dumais, & Andersen, 2010). Functionally, there are a host of neurochemical changes in adolescence. Diurnal rhythms of neurohormones in both the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-gonadal axes begin to uctuate at different rates, amplitudes, and periods (McCartney et al., 2009). Levels of gonadal hormones, testosterone and estradiol, rise to adult levels by late adolescence (Susman & Rogol, 2004). Neurotransmitters, most notably dopamine, also increase in volume and location, shifting from limbic to cortical innervations (Spear, 2000, 2003). There are other functional changes that are not unique to adolescence but that continue from childhood through adulthood in a relatively linear fashion, such as myelination (Giedd, 2004). In sum, the overwhelming conclusion based on the data is that there are inevitable and ubiquitous biological changes that are endemic to adolescence. 2. Adolescent biological changes drive various mechanisms of adolescent behavior. That biological changes play a role in adolescent behavior is not a claim of biological determinism, and thus is a departure from Hall (1904). However, it is undeniable that across the age span, strong biological mechanisms of behavior both direct 3

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Jessica P. Lougheed

behavior would miss both of these manifestations. (b) The timing and duration of these adolescent emotional changes can vary between individuals across a rather wide age range (see Figure 1). For example, menarche can occur any time between the ages of 10 and 16 and still be considered in the physiologically normal range (Paikoff & BrooksGunn, 1991). Furthermore, the timing (onset and completion) and tempo (rate) of pubertal maturation vary widely across individuals and are starting to be seen as a potential source of adolescent-typical problems (Marceau, Ram, Houts, Grimm, & Susman, 2011; Susman, Dockray, et al., 2010). In this way, relatively early or late pubertal maturation may be within the range of what is considered medically normative yet may not be normative in terms of psychological well-being (Marceau et al., 2011; Susman, Dockray, et al., 2010). Peak age periods of family conict, mood disruptions, and risk taking also vary between individuals (Darling, 2008; Holsen, Kraft, & Vitters, 2000; ONeal, 2001). These issues expose a critical gap between the theoretical model and data. With such a wide age window in which adolescent change can manifest, and with a wide range of possible manifestations and intensities, it is difcult to falsify the claim that adolescent storm and stress is ubiquitous and inevitable. Even the most carefully conducted longitudinal studies have failed to test this claim directly because of variable-centered (i.e., aggregate) analytical methods, a narrow set of behaviors of interest, infrequent measurement occasions, and/or a developmental age period that is too brief. Thus, rejection of the extreme storm and stress hypothesis a ` la Hall (1904) may have been premature. However, the proposition that a more nuanced modern version of storm and stress is more parsimonious may be suspect as well. We argue that although arousabilMonth 2013 American Psychologist

Figure 1 Typical Starts, Ends, and Average Ages (in Years) of Adolescent Developmental Markers

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Note. Large circles indicate means. 1 Adrenarche begins between ages 6 and 9 for females and a year later in males, thus around age 8 for females and age 9 for males (Blakemore et al., 2010; Dorn & Biro, 2011). 2 Menarche typically happens between ages 10 and 16.5 (Strasburger & Brown, 1991), with the average age being 12 years (McClintock & Herdt, 1996). Approximately 50% of girls start to ovulate between between 2 and 2.9 years after menarche (Apter, 1980). 3 The median age for spermarche is approximately 13 years, with spermarche occurring between ages 11 and 15 (Nielsen et al., 1986). 4 Breast budding (Tanner Stages 2 to 4) typically occurs between ages 8 and 13 (Dyk, 1993; Strasburger & Brown, 1991). The average age of attaining Tanner Stage 2 is approximately 11 years (Marshall & Tanner, 1969; Roche, Wellens, Attie, & Siervogel, 1995). 5 Breasts typically reach maturity (Tanner Stage 5) between ages 13 and 18, with the average age being 15 years (Dyk, 1993; Marshall & Tanner, 1969; Strasburger & Brown, 1991). 6 Testes begin development between ages 9.5 and 13.5, with the average age of reaching Tanner Stage 2 being 11 years (Marshall & Tanner, 1970; Strasburger & Brown, 1991). 7 Testes reach maturity between ages 13.5 and 17, with 15 years being the average at which Tanner Stage 5 is attained (Marshall & Tanner, 1970; Strasburger & Brown, 1991). 8 The penile growth spurt typically starts between ages 10.5 and 14.5, with age 13 being the average at which Tanner Stage 3 is attained (Dyk, 1993; Marshall & Tanner, 1970). 9 The penis typically reaches adult size between the ages of 12.5 and 16.5, with the average age being 15 years (Dyk, 1993; Marshall & Tanner, 1970; Strasburger & Brown, 1991). 10 The female height spurt typically occurs between ages 9.5 and 14.5, with the average age for peak height velocity being 12 years; the average age for the occurrence of peak weight velocity is 12.5 years (Dyk, 1993; Susman & Rogol, 2004). The male height spurt typically occurs between ages 10.5 and 16, with the average age for male peak height velocity being 14 and the peak weight velocity being reached slightly after peak height velocity (Dyk, 1993; Susman & Rogol, 2004). 11 Frontal lobe gray matter peaks at age 12 for males and age 11 for females, and parietal lobe gray matter peaks at age 12 for males and age 10 for females (Poletti, 2009). Temporal lobe gray matter peaks at age 17 for males and females (Shaw et al., 2008). 12 Female depressive affect increases between ages 13 and 15, shows no change between ages 15 and 18, and decreases between ages 18 and 19 (Holsen, Kraft, & Vitters, 2000). Male depressive affect decreases between ages 18 and 19, with no difference being shown between ages 13 and 18. The smallest sex differences in depressive affect are at ages 13 and 19; the largest differences are at ages 15 and 18 (Holsen et al., 2000). 13 The frequency of family conflict declines from early to mid-adolescence and again from mid- to late adolescence (Collins & Laursen, 2004), with the rate of conflict declining further in late adolescence (Laursen et al., 1998). The intensity of family conflicts increases from early to mid-adolescence, with conflicts being less frequent but more heated in mid-adolescence than in early adolescence (Laursen et al., 1998). 14 Substance use increases from age 11 (Brown et al., 2004), with the average age of first use being 14 years (Gruber & Pope, 2002). 15 Drinking behaviors have been reported in children as young as 10 years old, with the average age of onset being 15.5 years (Pitknen, Lyyra, & Pulkkinen, 2005). 16 The average age for first intercourse is 15 years (Wells & Twenge, 2005). The greatest risk of HIV, STDs, and unwanted pregnancy occurs between ages 15 and 19 (Kotchick, Shaffer, Forehand, & Miller, 2001).

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and mediated effectsare among the most parsimonious with the data. Rapid hormonal changes due to medical intervention, stress, menstruation, menopause, or other inuences have demonstrable and consistent effects on behavior (e.g., Pope, Kouri, & Hudson, 2000). The list of examples could continue for many pages. For the current purposes, it is enough to note that key features of socioemotional behavior, such as sensitivity thresholds, soothability, reward experience, and the evaluation of emotional signicance, are all mediated by basic biological mechanisms (Casey et al., 2011; Steinberg, 2010). The open question is which of these processes are unique to adolescence and which are developmentally independent individual differences (i.e., temperament). Despite a concentrated effort to nd direct effects of pubertal hormones on adolescent behavior, the general conclusion in the eld is that these effects are consistent but small (Buchanan, Eccles, & Becker, 1992), explaining about 6% of the variance (Susman, 1997). Why would this be? Any one of us would become more aggressive if given high doses of testosterone (e.g., Pope et al., 2000), more frightened with doses of norepinephrine (e.g., Schachter & Singer, 1962), and more socially oriented with nasally administered oxytocin (e.g., MacDonald et al., 2011). With increases in adrenal hormones beginning around age 6 (e.g., Blakemore et al., 2010) and gonadal hormones continuing to increase after pubertal maturity is reached (Schulz, Molenda-Figueira, & Sisk, 2009), why wouldnt there be a direct correlation between hormone levels and aggression, anxiety, and so forth? The accepted explanation is a hormone environment interaction accounting for individual differences in behavior (Buchanan et al., 1992) in which features of the adolescent environment enhance the effect of hormones on behavior (Powers, 2011). One example is the relationship between testosterone and adolescent aggression (Rowe, Maughan, Worthman, Costello, & Angold, 2004). The effects of testosterone on aggressive behavior are strongest under conditions of perceived social threat (Rowe et al., 2004), and peer groups become more salient and hierarchical in adolescence than in childhood (Brown & Klute, 2003). The adolescent peer-group context may provide a functional motivation for socially dominant behaviors that is unique to this part of the life span (Rowe et al., 2004). As such, the effects of testosterone on adolescent behavior are likely in part due to unique aspects of the adolescent social environment. Beyond hormonal effects, with the advent of noninvasive neuroimaging we have begun to make important inroads into understanding how adolescent biological development may explain behavior during this age period. Several prominent models point to changes in the socioemotional (e.g., limbic) subsystems of the brain that mediate arousability and emerge nonlinearly in early adolescence, as the cognitive control subsystems that mediate regulation (e.g., prefrontal cortex) mature in a relatively linear fashion from childhood to adulthood (Casey et al., 2008, 2011; Steinberg, 2008, 2010). Synthesizing the evidence from adolescent brain research, Dahl (2001) thought the gap in the maturation of these two subsystems might Month 2013 American Psychologist

explain adolescents struggles with conict, mood, and risk. Bottom-up emotional processes in early adolescence go relatively unchecked by top-down regulatory processes, and the result is greater instances of impulsivity and sensitivity that underlie conict, mood, and risk taking. In addition to endocrine and central nervous system development, changes in the autonomic nervous system (e.g., Hollenstein, McNeely, Eastabrook, Mackey, & Flynn, 2012) and the hypothalamic-pituitary-adrenal (HPA) axis (e.g., McCormick & Mathews, 2007) across adolescence also relate to adolescent-typical behavior. Thus, the ubiquitous and inevitable biological changes of adolescence highlighted in Premise 1 also have some impact on adolescent behavior, though we are only beginning to understand how these systems work individually and in relation to one another. 3. Adolescent biological changes are shaped by environmental inuences. If biological mechanisms are non-deterministically responsible for behavior, then the nature of this inuence can only be understood within an integrated biosocial perspective (e.g., Gottlieb & Willoughby, 2006; Magnusson, 1999). Indeed, the fatal blow to the naturenurture debate comes from the continual discoveries of gene environment interactions that deny preeminence to either nature or nurture (Oyama et al., 2003; Pinker, 2004). This symbiosis is at the heart of the integration of the adolescent into the social and cultural environment in which he or she will mate and reproduce (Steinberg & Belsky, 1996). Several examples illustrate this point. Recently, polymorphisms of several genes (e.g., the 5HT transporter gene, which regulates serotonin levels) have helped to explain individual differences in psychosocial outcomes but only for those who have specic environmental experiences, such as exposure to intoxicants, stress, or abuse (Caspi et al., 2003, 2005). Adolescent depression (e.g., Eley et al., 2004), cannabis-induced psychosis (Caspi et al., 2005), and alcohol use (Nilsson et al., 2005) are a few of the outcomes that can be explained not by the polymorphisms alone but by gene environment interactions. Another example of environmental inuences on biological processes of adolescent maturation is the effect of family conditions on the timing of pubertal development (Steinberg, 1988). Accelerated pubertal maturation and lower age of menarche have been associated with the absence of a biological father during a girls childhood and with less supportive and more harsh family interactions (e.g., Belsky et al., 2007; Steinberg, 1988), even after controlling for potential genetic mechanisms. Thus, the dynamic interplay between psychosocial and biological factors has effects on the relative timing of pubertal maturation. Reproductive maturation is only part of adolescent biological changes. As previously mentioned, structural and functional neuronal transformations also transpire due to exogenous input; that is, environmental factors affect biological processes, which then direct behavior. The clearest examples of this translation of experience into behavior via biological mechanisms are understood in terms of syn5

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aptic pruning. Experience shapes synaptic pathways, forging and embellishing some connections while neglecting and reducing others. It is not controversial to apply this mechanism to the understanding of piano playing skills in the motor cortex, but it is important to think of adolescenttypical behavior in this way as well. With the rates of synaptic pruning in the frontal cortex during early adolescence estimated at 30,000 synapses per second (Rakic, Bourgeois, & Goldman-Rakic, 1994) and 40% of synapses in layer 3 (Brenhouse & Andersen, 2011), adolescents are clearly poised to adapt to the special circumstances of their environment by forgoing some specialized abilities while becoming more efcient with others. This developmentally determined pruning can be categorized into experienceexpectant versus experience-dependent neuroplasticity (Greenough & Black, 1992). First, the overproduction of synapses in childhood is met by the evolutionary-based expectation that appropriate experience will provide the information that the nervous system needs in order to select the appropriate subset of synaptic connections (Greenough & Black, 1992, p. 163). Stereoscopic vision was the rst and most obvious example of experience-expectant pruning to be documented (Wiesel & Hubel, 1965), but the principle applies to any normative, species-typical input. In contrast, experience-dependent pruning is necessarily idiosyncratic, reecting the unique experiences of the individual. Whether perfecting a Chopin nocturne or watching 10 hours of TV per day, the adolescent is crystallizing into the adult they are to become through experiences that sculpt their brains. Thus, the adolescent environment triggers normative behavior changes such as interest in peers, sex, and risk taking through experience-expectant processes, while at the same time it specializes and individuates adolescent characteristics through experience-dependent processes. These rst three premises implicate the ubiquity of biological changes and relations between biology and behavior in adolescence. However, these endemic transitions also vary in content, intensity, and timing between individuals. That is, though every adolescent will experience endocrine, neuronal, and autonomic changes, how these changes manifest are idiosyncratic. Thus, the next three premises cover the individual differences of adolescent development. 4. Individual differences in adolescent emotional behavior changes are domain specic and vary in intensity. The most salient, well-researched, and problematic behaviors of adolescence are all related to emotions. Depression, anxiety, aggression, risk taking, sexual behavior, suicide, interpersonal conict, self-injury, and passionate interests in the arts, athletics, and peer relations all stem from emotional processes. As detailed later in Premise 6, the upwelling of arousal in early adolescence is met with regulatory and coping behaviors carved from experience to produce unique manifestations in each adolescent. For example, any given adolescent faced with some form of peer rejection may respond by withdrawing, aggressing, or investing more energy in family or peers who do not reject them. The point is that each emotionally challenging event 6

in adolescenceand adolescence is rife with stressful interpersonal and emotionally challenging events (Larson & Ham, 1993)is met with some regulatory compensation. Importantly, this regulatory compensation is more mature than in preadolescence but also manifests in relatively unique ways across individuals. From this information, two important observations can be made. First, each individual has a domain or range of domains of adolescent change that is most prominent. Typically, bungee jumpers are not holed up in their rooms for 16 hours a day, and socially anxious adolescents are not sexually promiscuous. However, the reality is that the high school team captain can be suicidal and the most anxious student can engage in delinquent behavior. Adolescent-typical behaviors occur in every possible combination. Unfortunately, mostly for pragmatic reasons, researchers tend to take a compartmentalized, variable-centered approach to adolescent development. A study focusing exclusively on delinquency necessarily neglects social anxiety and vice versa. Furthermore, due to a combination of societal urgency and funding priorities, adolescent research has predominantly been focused on problems and pathology at the expense of the understanding of normative development (Steinberg & Morris, 2001). As such, the evidence for or against the storm and stress hypothesis in the general population is lacking. The second, related, observation is that the intensity of an adolescents aggression, depressive symptoms, and so forth is a within-individual experience, a relative change. In this case, between-subjects comparisons are biased toward interpreting the most extreme cases in any particular domain. We care less about the occasionally aggressive than the frequently aggressive and focus more on the physical or sexual risk takers than on the academic or social risk takers. As a result, Arnett (1999) and others concluded that storm and stress is probable but not inevitable. From the theoretical perspective of modeling adolescent change, however, comparisons cannot be interindividual but rather should be intraindividual (Magnusson, 1999; Molenaar & Campbell, 2009). The comparison case for any individual adolescent is not the aggregate, but his or her former and future selves. Thus, the relative intraindividual changes across all possible domains are the criteria for assessing patterns of adolescent development. 5. There are individual differences in the age of onset and duration of periods of adolescent change. Biologically, there is great variability in developmental timing across individuals. For example, 90%95% of girls have their rst menses within a four-year age window, roughly between the ages of 11 and 15 (Anderson, Dallal, & Must, 2003; Strasburger & Brown, 1991). That is, a girl with her rst menses in Grade 6 and another with hers in Grade 11 are both considered as developing typically, at least physically. In fact, all markers of typical physical development have a wide age range of onset (see Figure 1). Across typically developing individuals, each maturational event can vary by as much as ve years. Moreover, the timing of developmental onset can be distinguished from the tempo or rate of maturation from start to nish (Mendle, Harden, Brooks-Gunn, & Graber, 2010). For exMonth 2013 American Psychologist

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ample, Marceau and colleagues (2011) t logistic curves to longitudinal measures of pubertal maturation to nd that internalizing problems were associated with both earlier timing and faster tempo for girls. What is not yet known is how the timing and tempo of adolescent physical maturation domains relate to one another and, more pertinent to the present model, to other aspects of socioemotional behavior. Figure 1 depicts the range and timing of normative developmental domains. Consider a hypothetical individual adolescent progressing through these maturational milestones. The age at which this individual reaches each of these milestones is different from that of all of his or her peers. That is, the relative timing of these maturation events with respect to one other (e.g., age of growth spurt relative to age of peak frontal lobe pruning relative to age of everything else) is unique to each individual. Thus, not only are tempo and timing important, but the rhythm of these changes may be important as well. Moreover, as we come to understand the neural changes driven by hormones, genetics, and environment, the developmental shifts in synaptic pruning and the proliferation of neurotransmitters and their receptors will necessarily be added to this repertoire of salient maturational milestones with timing differences. Considering the emotion-related changes in adolescence in light of timing, tempo, and rhythm reveals a more complete picture of adolescent development. Prominent theory and research suggest that maturational disparities underlie more extreme manifestations of emotion-related behavior change such as anxiety, depression, and delinquency (Ge & Natsuaki, 2009). If one takes a more normative developmental approach, these maturational disparities must also be seen to underlie any individual differences in these domains as well. This timing approach could also help to explain aggregate tendencies for interpersonal conict in early adolescence, mood disruptions in mid-adolescence, and more extreme risk-taking in late adolescence (Graber, 2004; Laursen et al., 1998; Steinberg, 2008). The addition of timing factors to the biological and environmental processes described in the previous premises provides a more thorough developmental context for the direct examination of the storm and stress hypothesis. 6. Individual differences in the duration and intensity of transitions in emotional arousal are functionally modulated by emotion regulation skills. We are born with biological mechanisms of emotional arousal but must learn through experience how to regulate our emotions. To borrow from Greenough and Black (1992), arousal is experience expectant, but regulation is experience dependent. This is perhaps exemplied most clearly in two current models of normative adolescent emotional development (Casey et al., 2011; Steinberg, 2008). In these models, the onset of adolescence is characterized by rapid changes in mechanisms of arousal, notably in the subcortical limbic system and ventral regions of the cortex. In contrast, the more cognitive mechanisms of executive control and selfregulation develop gradually and linearly across adolescence. This contrast of arousal and regulation is an overMonth 2013 American Psychologist

simplied but useful heuristic for adolescent emotional development. The core assertion of these models is that there is a period of time during which adolescents faculties for arousal exceed their capacities for regulating that arousal. The typical time span and degree of this discrepancy is not yet known, but certainly there is interindividual variability in the duration and intensity of this discrepancy.

Moving Beyond Storm and Stress: The 4T Approach

We have provided six premises relevant to the storm and stress hypothesis. We have reviewed biological, psychological, and environmental determinants of adolescent behavior and considered issues of relative timing and the array of emotion-related domains. With all of these in mind, we assert that even the more nuanced modern version of storm and stress is facile and outmoded. As we have shown in the six premises, the general conclusion that storm and stress is neither ubiquitous nor inevitable may be suspect for several reasons. First, it neglects relevant processes that are ubiquitous and inevitable. Second, storm and stress has never been formally and comprehensively stated as a hypothesis; hence it is not clear exactly what it is that is not ubiquitous or inevitable. Thus, storm and stress has not been adequately tested directly (Arnett, 1999). Finally, and most important, storm and stress is a limited view of the multifaceted, organic processes at play during adolescent development. The fact that the concept holds sway with parents and the general public may reect more of a complaint from an adult perspective: wanting teens to behave in accordance with adult norms regardless of the developmental function of adolescent-typical behavior. Despite the rejection of Anna Freuds extreme perspective, the retention of the concept of storm and stress, however cautiously, still pathologizes adolescence to some degree. This is not a reasonable basis for scientic understanding. Instead, we propose that it is time to move on from the dichotomy of storm and stress, to integrate the deeper and more complex understanding we have of adolescent biology and behavior, and to turn our attention to more comprehensive models of adolescent normative development. To this end, we offer the 4T approach, which requires the integration of the following: typicality, temperament, transactions, and timing. We discuss each of these in turn. Typicality By typical, we mean the normative processes of transitioning out of childhood and through adolescence. One of the problems with adolescent research, especially of late, is that it relies too heavily on the problem behaviors and pathologies that emerge during this period (Steinberg & Morris, 2001). Indeed, this is important work, and it is at least somewhat directed by shifts in funding priorities. However, the premise of this developmental psychopathology approach is that these problems are deviations from what is typical (Cicchetti & Rogosch, 2002), and yet we dont really understand what is typical very well at all. 7

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Moreover, studying the individuation of adolescents as they experiment and specialize is difcult (though not impossible) for controlled research; all but the most extreme behaviors can easily be recorded and compared. Nevertheless, equipped with the sophisticated tools and multidisciplinary approaches of the 21st century, the eld is up for the challenge. Temperament Temperament no longer exclusively refers to a developmentally xed, trait-like package of emotional responses (Laceulle, Nederhof, Karreman, Ormel, & van Aken, 2012). Instead, it is a way to summarize intraindividual emotional response tendencies (e.g., sensitivity, regulation) at a given moment in ones life, which can change due to developmental maturation and environmental inuences (e.g., stress). In this respect, temperamental change in adolescence is the rough equivalent of storm and stress. We argue that most of adolescent-typical changes are emotionrelated in that they are affected by or affect temperamental responses. Any coherent model of adolescent development, therefore, must account for the sensitivity thresholds, intensity, domain, duration, and regulatory control of emotions. Thus, a temperamental focus allows theory and research to go beyond simply testing whether an adolescent stormed or stressed to provide a more integrated understanding of how adolescent emotional landscapes change and stabilize in transactions with both biology and environment. Transactions Transactions between within-person physiology and the environmental milieu in which the person is situated are the bedrock of understanding the causes of behavior (Gottlieb & Willoughby, 2006; Magnusson & Cairns, 1996). The central and autonomic nervous systems, the HPA axis, and the endocrine systems are in constant, dynamic interaction with each other and with environmental forces to produce behavior moment by moment. These transactions are the processes of complex, adaptive dynamic systems. That we can understand the development of the individual as a dynamic system is not a new idea (Hollenstein, 2011). What we are calling for is a more specic application of a dynamic systems approach to the understanding of adolescent-typical phenomena (Granic, Dishion, & Hollenstein, 2003; Kunnen, 2012). As the core of the 4T approach, transactions between biology and environment force us to go beyond simple dichotomies (Hall, 1904) or broad descriptive accounts (e.g., Lerner & Castellino, 2002) to provide explanatory mechanisms of adolescent change. For example, advances in epigenetics are now providing a window into individual differences in responses to stress actions and interactions with signicant others alter the way that genes are expressed (Meaney, 2010). We assert that, because development is best viewed as a dynamic system (Smith & Thelen, 2003), biology environment transactions must be a central focus of adolescent theory and research. 8

Timing Finally, as we have argued in several ways, timing is an important and often overlooked aspect of adolescent development (Granic, 2005). The challenges in understanding adolescence stem from the diverse timing of changes at this age. In infancy, we can chart progress on the order of weeks and months. In adolescence, a similar mapping must reect individual differences of years. Timing can refer to the age of onset or completion of various adolescent-typical changes (see Figure 1) as well as the tempo or rate of these changes (Marceau et al., 2011; Mendle et al., 2010) and the relative timing of two or more changes (e.g., spermarche and family conict). Moreover, timing and dynamics are integral to any systemic approach such as 4T (Granic, 2005). Temporal dynamics, whether at the scale of seconds or years, will confound any cross-sectional or variable-centered research design, thus limiting what can be gained from such designs. Moreover, chronological age can be a poor proxy for equating adolescents in terms of their functional maturity. Pubertal status is one alternative, but there may be other maturational markers that can be used more effectively in determining the functional mechanisms of adolescent behavior (Galambos, Kolaric, Sears, & Maggs, 1999). Degree of myelination in the prefrontal cortex, peak growth spurt, and diurnal variability in hormone concentrations (Bond, Vella, Kiparissis, & WynneEdwards, 2006) are just a few of the possibilities. We suggest that, taken together, these four Ts may be a useful framework to guide future theory and research. The integration of typicality, temperament, transactions, and timing leads to some fundamental research questions and recommendations. First, what exactly are the changes typical of all adolescents (i.e., what is inevitable)? It is essential to press on with basic research by deemphasizing a problem-focused or pathological approach in lieu of discovering what is truly adolescent typical. Second, how does adolescent development transpire? The criterion for detecting change is intra- rather than interindividual. These changes do not need to be problematic or pathological, just different from before or after this critical period. Hence, there is limited utility in cross-sectional and variable-centered designs. Instead, longitudinal, person-centered designs and methodology provide the necessary insight (Bergman, Magnusson, & El-Khouri, 2003; Magnusson & Cairns, 1996; Molenaar & Campbell, 2009). Third, how does timing relate to adolescent-typical behavior? It is necessary to build on recent creative examinations of the effects of timing (Marceau et al., 2011; Mendle et al., 2010; Susman, Dockray, et al., 2010) to begin to understand how diverse timing-related factors relate to adolescent behavior. Fourth, how domain specic are individual differences in adolescent-typical changes? For any given individual, the overt manifestations of adolescent change may occur in only one or a few of the possible domains (e.g., affective, internalizing, externalizing, risk taking, interpersonal conict). Despite those individual differences, there may be common underlying mechanisms that could explain these manifestations. Research intended to document adolescentMonth 2013 American Psychologist

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typical change would need to be as domain inclusive as possible to answer this question. By extension, the fth question is: What are the underlying transactional mechanisms of adolescent-typical change? Research that accounts for reciprocal transactions between biology and environment is the primary mechanism that can move the eld away from the dominance of unidirectional explanations toward more parsimonious models.

Conclusion
Development is systemicsimultaneously atomistic and interpersonal (Smith & Thelen, 2003; Witherington, 2007). Because of the complexities and temporal variability endemic to adolescence, perhaps there is no other age period that so greatly requires a systemic approach. There are ubiquitous and inevitable aspects of adolescence that definitely inuence individual differences in adolescent thoughts, feelings, and behavior through transactions with the environmental context. It is time we moved on from ideas based in 19th-century thinking; storm and stress is a vestigial developmental framework. The 4T approach provides a systems-based framework that will facilitate the greater understanding of adolescence needed for the 21st century.
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