12
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

Hollenstein & Lougheed 2013 Online

Embed Size (px)

Citation preview

Page 1: Hollenstein & Lougheed 2013 Online

American Psychologist

Beyond Storm and Stress: Typicality, Transactions,Timing, and Temperament to Account for AdolescentChangeTom Hollenstein and Jessica P. LougheedOnline First Publication, August 5, 2013. doi: 10.1037/a0033586

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

Page 2: Hollenstein & Lougheed 2013 Online

Beyond Storm and StressTypicality, Transactions, Timing, and Temperament to Account for

Adolescent Change

Tom Hollenstein and Jessica P. LougheedQueen’s University, Kingston

Adolescent “storm and stress” has been a focal yet con-troversial developmental framework for over a century. Inthe present article, we challenge the current perspectivethat storm and stress is neither ubiquitous nor inevitablebut probable. Instead, we argue, storm and stress is avestigial developmental framework, and we propose amore comprehensive approach to understanding adoles-cent-typical changes based on six premises: (1) The bio-logical changes of adolescence are inevitable and ubiqui-tous; (2) adolescent biological changes drive variousmechanisms of adolescent behavior; (3) adolescent biolog-ical changes are shaped by environmental influences; (4)individual differences in adolescent emotional-behaviorchanges are domain specific and vary in intensity; (5) thereare individual differences in the age of onset and durationof periods of adolescent change; and (6) individual differ-ences in the duration and intensity of transitions in emo-tional arousal are functionally modulated by burgeoningemotion regulation skills. We conclude with the more com-prehensive 4T (typicality, transactions, temperament, andtiming) approach and suggestions to guide adolescent re-search in the 21st century.

Keywords: adolescence, development, storm and stress,individual differences, variability

I t is quite difficult to find a review of adolescence thatdoes not refer to the “storm and stress” hypothesis. Theterm was first used by G. Stanley Hall in his 1904 tome

to refer to the decrease in self-control (storm) and thecorresponding increase in sensitivity to arousing stimuli(stress) that typically characterize adolescent behavior.Across the ensuing decades of the 20th century, the pre-vailing perspectives on this developmental phenomenonhave oscillated between deterministic explanations (e.g.,“To be normal during the adolescent period is by itselfabnormal,” Anna Freud, 1958, p. 267; cf. Arnett, 1999) andpurely environmental accounts (e.g., Benedict, 1934;Mead, 1928). As the polarity of the age-old nature–nurturedebate gave way to the current acceptance of a dynamicinteraction between biology and environment (Oyama,Griffiths, & Gray, 2003), so too did the question of stormand stress became more nuanced. The contemporary per-spective is that although adolescence may be stormy and/orstressful for some, it is not typically a developmentalproblem, nor is it inevitable or ubiquitous (Arnett, 1999;

Larson & Ham, 1993; Laursen, Coy, & Collins, 1998;Steinberg, 2001).

In the present article, we challenge this dominantconclusion to suggest that storm and stress may no longerbe a useful framework for understanding adolescent-typicalbehavior and changes. It has inspired a century of debate onwhether storm and stress is ubiquitous or inevitable. How-ever, the fundamental question may not be whether stormand stress occurs in every adolescent; rather, the funda-mental questions may be when do changes occur and howdo they manifest? Specifically, the all-or-nothing approachof the storm and stress hypothesis, much like the nature–nurture debate, is rooted in a false dichotomy and does littleto facilitate our understanding of how adolescents developand change. In the first section, we begin by showing thatthe operationalization of storm and stress has been isolatedto a narrow set of behaviors and that this approach hasneglected other domains of emotion-related changes inadolescence. Next, we review the adolescent changes thatare undeniably ubiquitous and inevitable in typically de-veloping populations—biological and cognitive maturity.We argue that the range of individual differences in thetiming of adolescent changes renders most of the empiricaldata uninterpretable with respect to the ubiquity and inten-sity of storm and stress. To replace storm and stress, weoffer the 4T (typicality, transactions, temperament, andtiming) approach and conclude with suggestions for guid-ing future research with this framework.

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

Tom Hollenstein and Jessica P. Lougheed, Department of Psychology,Queen’s University, Kingston, Ontario, Canada.

We wish to thank Nicholas B. Allen and Michael C. Seto for helpfulcomments on drafts of this manuscript.

Correspondence concerning this article should be addressed to TomHollenstein, Department of Psychology, Queen’s University, Kingston,Ontario K7L 3N6, Canada. E-mail: [email protected]

1 Hall (1904) adopted the term “storm and stress” from the Sturm undDrang literary movement of the late 18th century. Translations of thephrase also include storm and pressure, and it has connotations of exces-sive emotionality or strong inspiration (Walz, 1927).

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

1Month 2013 ● American Psychologist© 2013 American Psychological Association 0003-066X/13/$12.00Vol. 68, No. 6, 000–000 DOI: 10.1037/a0033586

Page 3: Hollenstein & Lougheed 2013 Online

His review focused on an admittedly nonexhaustive set ofbehaviors that have been discussed and/or measuredthroughout the past century by anthropologists, psychoan-alysts, and contemporary scholars: (a) conflict with parents,(b) mood disruptions, and (c) risk behavior. Indeed, theseare primary domains of “difficulty” for adolescents andthose around them. Changes in each of these domains arethought to be more probable during adolescence but notinevitable. Several crucial details of this view should benoted, as these reflect the dominant scientific opinion to-day.

First, the developmental sequence of peak occurrencesin each of the three domains follows the order presentedabove. The peak in the frequency of parent–adolescentconflict (or number of different conflict types) occurs inearly adolescence, whereas the intensity of these conflictspeaks later, in mid-adolescence (Laursen et al., 1998; Pai-koff & Brooks-Gunn, 1991). Mood disruptions—most no-tably, depressive episodes and symptoms—tend to peak inmid-adolescence (Graber, 2004). The tendency to engagein risky behaviors is the last of this triumvirate to peak, inlate adolescence (Steinberg, 2008).

Second, Arnett (1999) made the unequivocal assertionthat “[t]he claim that adolescent storm and stress is char-acteristic of all adolescents and that the source of it ispurely biological is clearly false” (p. 317). Thus, the ex-treme hypothesis credited to Hall, Freud, and others hasapparently failed to be supported by the data. For the sakeof clarity, consider the two components of this refutedclaim, inevitability and biological determinism, separately.On the one hand, there is the inevitability hypothesis thatno adolescent can avoid at least some degree of storm andstress. The more nuanced (i.e., cautious) contemporaryview is that storm and stress is a tendency—a statistical

average that incorporates individual differences, includingthose who never experience any “typical” adolescent dif-ficulties. Thus, storm and stress is not inevitable accordingto this view. On the other hand, the old-school biologicaldeterminism hypothesis has not been borne out either;rather it has given way to a more balanced, interactionistview. Biological mechanisms such as genes, hormones, andneural structures are typically seen as factors that createvulnerabilities to environmental influences, and some at-tempt has been made to acknowledge bidirectional influ-ences between biology and environment (e.g., Susman &Rogol, 2004). Thus, although biological changes are insome sense synonymous with adolescence (i.e., puberty)and certainly inevitable for a typically developing popula-tion, the effect of these changes on adolescent behavior isnot thought to be direct.

A third aspect of Arnett’s (1999) trio of storm andstress domains (conflict, mood, and risk taking) is that theyare each manifestations of more primary emotional pro-cesses. Indeed, adolescent-onset behavioral changes in-volve two interrelated processes: emotional arousal andemotion regulation (Steinberg, 2008, 2010). Changes inarousal or arousability can manifest in many ways, includ-ing increased sensitivity to social stressors; responses torewards, as well as the type and number of objects thatelicit those responses; and passions, broadly construed(e.g., sexual, moralistic, recreational). This is what Hall(1904) meant by “stress.” On the other hand, there aredeficits or at least inadequacies of self-regulation (Hall’s“storm”). Changes in the regulation of arousal relate to thedevelopment of cognitive abilities enabled by neural mat-uration and to the habits that emerge in response to in-creased arousal, such as coping mechanisms, rumination,and inhibitory control (Allen & Sheeber, 2008; Dahl,2001). Thus, conflict, mood, and risk-taking problems maybe more generally subsumed as arousal and regulationproblems with specific manifestations (internal vs. exter-nal) or occurring in specific contexts (intra- versus inter-personal).

Despite the clarity of this revised storm and stressaccount, there are still several problems with the model.First, it is not really a developmental explanation. Forexample, the descriptive accounts of the average age ofonset in each domain do not begin to explain this sequence.Why doesn’t risk taking precede family conflict? Theseorderly temporal patterns beg for a coherent developmentalexplanation. Second, the scientific consideration of inevi-tability is further compromised by focusing on extremeoccurrences of adolescent behavior to the neglect of moremundane manifestations. Finally, the dominant, almost ex-clusive, methods used to support or refute any claims ofadolescent storm and stress have been analyses at theaggregate level of one, or perhaps two, domains. Thisapproach is inadequate for several reasons: (a) The mani-festation of biologically driven, environmentally mediatedchange varies greatly across individuals. One adolescentmay struggle with a negative self-image that perpetuatessocial isolation, while another may aggressively battle par-ents over autonomy issues. A study examining risk-taking

TomHollenstein

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

2 Month 2013 ● American Psychologist

Page 4: Hollenstein & Lougheed 2013 Online

behavior would miss both of these manifestations. (b) Thetiming and duration of these adolescent emotional changescan vary between individuals across a rather wide agerange (see Figure 1). For example, menarche can occur anytime between the ages of 10 and 16 and still be consideredin the physiologically normal range (Paikoff & Brooks-Gunn, 1991). Furthermore, the timing (onset and comple-tion) and tempo (rate) of pubertal maturation vary widelyacross individuals and are starting to be seen as a potentialsource of adolescent-typical problems (Marceau, Ram,Houts, Grimm, & Susman, 2011; Susman, Dockray, et al.,2010). In this way, relatively early or late pubertal matu-ration may be within the range of what is consideredmedically normative yet may not be normative in terms ofpsychological well-being (Marceau et al., 2011; Susman,Dockray, et al., 2010). Peak age periods of family conflict,mood disruptions, and risk taking also vary between indi-viduals (Darling, 2008; Holsen, Kraft, & Vittersø, 2000;O’Neal, 2001).

These issues expose a critical gap between the theo-retical model and data. With such a wide age window inwhich adolescent change can manifest, and with a widerange of possible manifestations and intensities, it is diffi-cult to falsify the claim that adolescent storm and stress isubiquitous and inevitable. Even the most carefully con-ducted longitudinal studies have failed to test this claimdirectly because of variable-centered (i.e., aggregate) ana-lytical methods, a narrow set of behaviors of interest,infrequent measurement occasions, and/or a developmentalage period that is too brief. Thus, rejection of the “extreme”storm and stress hypothesis a la Hall (1904) may have beenpremature. However, the proposition that a more nuancedmodern version of storm and stress is more parsimoniousmay be suspect as well. We argue that although arousabil-

ity and regulation are indeed important processes for ado-lescents, framing our theoretical understanding of adoles-cent development around this 109-year-old descriptionmay no longer deserve the prominence it has been afforded.

Storm and Stress RedefinedSince Hall’s (1904) time, we have significantly expandedand deepened our understanding of development, emo-tions, biology, and adolescence. Recent progress in devel-opmental neuroscience, for example, has accelerated thisunderstanding and inspired a few more inclusive models ofadolescent development (Casey, Jones, & Somerville,2011; Steinberg, 2008). Based on these and other advances,we introduce the 4T approach, which is supported by thefollowing six premises about adolescent emotional devel-opment. The first three build progressively through (1) theinevitability of biological changes to (2) biological influ-ences on behavior to (3) environmental influences on bio-logical changes. The latter three relate to aspects of indi-vidual differences that build off the first three premises.

1. The biological changes of adolescence are inev-itable and ubiquitous. Except in rare medical conditions,all adolescents experience species-typical structural andfunctional changes in physiology. On the structural side arechanges in body height, fat distribution, secondary sexcharacteristics, and other organizational effects of hor-mones (Brooks-Gunn, Graber, & Paikoff, 1994; Susman,Houts, et al., 2010). Adolescent neuronal structure alsoundergoes significant transformations (Blakemore, Burnett,& Dahl, 2010; Casey, Jones, & Hare, 2008; Paus, 2010;Spear, 2000, 2003). The number and pattern of synapticconnections, especially in the prefrontal cortex, are shapedby synaptic pruning (Giedd, 2004). These structuralchanges occur across species from rats to primates andconfer the requisite manifestations of adulthood (Bren-house, Dumais, & Andersen, 2010).

Functionally, there are a host of neurochemicalchanges in adolescence. Diurnal rhythms of neurohor-mones in both the hypothalamic-pituitary-adrenal and hy-pothalamic-pituitary-gonadal axes begin to fluctuate at dif-ferent rates, amplitudes, and periods (McCartney et al.,2009). Levels of gonadal hormones, testosterone and es-tradiol, rise to adult levels by late adolescence (Susman &Rogol, 2004). Neurotransmitters, most notably dopamine,also increase in volume and location, shifting from limbicto cortical innervations (Spear, 2000, 2003). There areother functional changes that are not unique to adolescencebut that continue from childhood through adulthood in arelatively linear fashion, such as myelination (Giedd,2004). In sum, the overwhelming conclusion based on thedata is that there are inevitable and ubiquitous biologicalchanges that are endemic to adolescence.

2. Adolescent biological changes drive variousmechanisms of adolescent behavior. That biologicalchanges play a role in adolescent behavior is not a claim ofbiological 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

Jessica P.Lougheed

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

3Month 2013 ● American Psychologist

Page 5: Hollenstein & Lougheed 2013 Online

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

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 9for males (Blakemore et al., 2010; Dorn & Biro, 2011). 2 Menarche typically happens between ages 10 and 16.5 (Strasburger & Brown, 1991), with the averageage 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 Themedian age for spermarche is approximately 13 years, with spermarche occurring between ages 11 and 15 (Nielsen et al., 1986). 4 Breast budding (Tanner Stages2 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 averageage being 15 years (Dyk, 1993; Marshall & Tanner, 1969; Strasburger & Brown, 1991). 6 Testes begin development between ages 9.5 and 13.5, with the averageage of reaching Tanner Stage 2 being 11 years (Marshall & Tanner, 1970; Strasburger & Brown, 1991). 7 Testes reach maturity between ages 13.5 and 17, with15 years being the average at which Tanner Stage 5 is attained (Marshall & Tanner, 1970; Strasburger & Brown, 1991). 8 The penile growth spurt typically startsbetween 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 typicallyreaches 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 occurrenceof 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 formale 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 graymatter 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 lobegray 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 ages15 and 18, and decreases between ages 18 and 19 (Holsen, Kraft, & Vittersø, 2000). Male depressive affect decreases between ages 18 and 19, with no difference beingshown 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 conflictdeclining 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 moreheated 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 usebeing 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(Pitkänen, Lyyra, & Pulkkinen, 2005). 16 The average age for first intercourse is 15 years (Wells & Twenge, 2005). The greatest risk of HIV, STDs, and unwanted pregnancyoccurs between ages 15 and 19 (Kotchick, Shaffer, Forehand, & Miller, 2001).

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

4 Month 2013 ● American Psychologist

Page 6: Hollenstein & Lougheed 2013 Online

and mediated effects—are among the most parsimoniouswith the data. Rapid hormonal changes due to medicalintervention, stress, menstruation, menopause, or other in-fluences have demonstrable and consistent effects on be-havior (e.g., Pope, Kouri, & Hudson, 2000). The list ofexamples could continue for many pages. For the currentpurposes, it is enough to note that key features ofsocioemotional behavior, such as sensitivity thresholds,soothability, reward experience, and the evaluation of emo-tional significance, are all mediated by basic biologicalmechanisms (Casey et al., 2011; Steinberg, 2010). Theopen question is which of these processes are unique toadolescence and which are developmentally independentindividual differences (i.e., temperament).

Despite a concentrated effort to find direct effects ofpubertal hormones on adolescent behavior, the generalconclusion in the field is that these effects are consistent butsmall (Buchanan, Eccles, & Becker, 1992), explainingabout 6% of the variance (Susman, 1997). Why would thisbe? Any one of us would become more aggressive if givenhigh doses of testosterone (e.g., Pope et al., 2000), morefrightened with doses of norepinephrine (e.g., Schachter &Singer, 1962), and more socially oriented with nasallyadministered oxytocin (e.g., MacDonald et al., 2011). Withincreases in adrenal hormones beginning around age 6(e.g., Blakemore et al., 2010) and gonadal hormones con-tinuing to increase after pubertal maturity is reached(Schulz, Molenda-Figueira, & Sisk, 2009), why wouldn’tthere be a direct correlation between hormone levels andaggression, anxiety, and so forth? The accepted explanationis a hormone–environment interaction accounting for indi-vidual differences in behavior (Buchanan et al., 1992) inwhich features of the adolescent environment enhance theeffect of hormones on behavior (Powers, 2011). One ex-ample is the relationship between testosterone and adoles-cent aggression (Rowe, Maughan, Worthman, Costello, &Angold, 2004). The effects of testosterone on aggressivebehavior are strongest under conditions of perceived socialthreat (Rowe et al., 2004), and peer groups become moresalient and hierarchical in adolescence than in childhood(Brown & Klute, 2003). The adolescent peer-group contextmay provide a functional motivation for socially dominantbehaviors that is unique to this part of the life span (Roweet al., 2004). As such, the effects of testosterone on ado-lescent behavior are likely in part due to unique aspects ofthe adolescent social environment.

Beyond hormonal effects, with the advent of nonin-vasive neuroimaging we have begun to make importantinroads into understanding how adolescent biological de-velopment may explain behavior during this age period.Several prominent models point to changes in the socio-emotional (e.g., limbic) subsystems of the brain that medi-ate arousability and emerge nonlinearly in early adoles-cence, as the cognitive control subsystems that mediateregulation (e.g., prefrontal cortex) mature in a relativelylinear fashion from childhood to adulthood (Casey et al.,2008, 2011; Steinberg, 2008, 2010). Synthesizing the evi-dence from adolescent brain research, Dahl (2001) thoughtthe gap in the maturation of these two subsystems might

explain adolescents’ struggles with conflict, mood, andrisk. Bottom-up emotional processes in early adolescencego relatively unchecked by top-down regulatory processes,and the result is greater instances of impulsivity and sen-sitivity that underlie conflict, mood, and risk taking.

In addition to endocrine and central nervous systemdevelopment, 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 alsorelate to adolescent-typical behavior. Thus, the ubiquitousand inevitable biological changes of adolescence high-lighted in Premise 1 also have some impact on adolescentbehavior, though we are only beginning to understand howthese systems work individually and in relation to oneanother.

3. Adolescent biological changes are shaped byenvironmental influences. If biological mechanisms arenon-deterministically responsible for behavior, then thenature of this influence can only be understood within anintegrated biosocial perspective (e.g., Gottlieb & Wil-loughby, 2006; Magnusson, 1999). Indeed, the fatal blowto the nature–nurture debate comes from the continualdiscoveries of gene–environment interactions that denypreeminence to either nature or nurture (Oyama et al.,2003; Pinker, 2004). This symbiosis is at the heart of theintegration of the adolescent into the social and culturalenvironment in which he or she will mate and reproduce(Steinberg & Belsky, 1996). Several examples illustratethis point. Recently, polymorphisms of several genes (e.g.,the 5HT transporter gene, which regulates serotonin levels)have helped to explain individual differences in psychoso-cial outcomes—but only for those who have specific en-vironmental experiences, such as exposure to intoxicants,stress, or abuse (Caspi et al., 2003, 2005). Adolescentdepression (e.g., Eley et al., 2004), cannabis-induced psy-chosis (Caspi et al., 2005), and alcohol use (Nilsson et al.,2005) are a few of the outcomes that can be explained notby the polymorphisms alone but by gene–environmentinteractions.

Another example of environmental influences on bio-logical processes of adolescent maturation is the effect offamily conditions on the timing of pubertal development(Steinberg, 1988). Accelerated pubertal maturation andlower age of menarche have been associated with theabsence of a biological father during a girl’s childhood andwith less supportive and more harsh family interactions(e.g., Belsky et al., 2007; Steinberg, 1988), even aftercontrolling for potential genetic mechanisms. Thus, thedynamic interplay between psychosocial and biologicalfactors has effects on the relative timing of pubertal mat-uration.

Reproductive maturation is only part of adolescentbiological changes. As previously mentioned, structuraland functional neuronal transformations also transpire dueto exogenous input; that is, environmental factors affectbiological processes, which then direct behavior. The clear-est examples of this translation of experience into behaviorvia biological mechanisms are understood in terms of syn-

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

5Month 2013 ● American Psychologist

Page 7: Hollenstein & Lougheed 2013 Online

aptic pruning. Experience shapes synaptic pathways, forg-ing and embellishing some connections while neglectingand reducing others. It is not controversial to apply thismechanism to the understanding of piano playing skills inthe motor cortex, but it is important to think of adolescent-typical behavior in this way as well. With the rates ofsynaptic pruning in the frontal cortex during early adoles-cence estimated at 30,000 synapses per second (Rakic,Bourgeois, & Goldman-Rakic, 1994) and 40% of synapsesin layer 3 (Brenhouse & Andersen, 2011), adolescents areclearly poised to adapt to the special circumstances of theirenvironment by forgoing some specialized abilities whilebecoming more efficient with others. This developmentallydetermined pruning can be categorized into experience-expectant versus experience-dependent neuroplasticity(Greenough & Black, 1992). First, the overproduction ofsynapses in childhood is met by the “evolutionary-basedexpectation that appropriate experience will provide theinformation that the nervous system needs in order to selectthe appropriate subset of synaptic connections” (Gree-nough & Black, 1992, p. 163). Stereoscopic vision was thefirst and most obvious example of experience-expectantpruning to be documented (Wiesel & Hubel, 1965), but theprinciple applies to any normative, species-typical input. Incontrast, experience-dependent pruning is necessarily idio-syncratic, reflecting the unique experiences of the individ-ual. Whether perfecting a Chopin nocturne or watching 10hours of TV per day, the adolescent is crystallizing into theadult they are to become through experiences that sculpttheir brains. Thus, the adolescent environment triggersnormative behavior changes such as interest in peers, sex,and risk taking through experience-expectant processes,while at the same time it specializes and individuatesadolescent characteristics through experience-dependentprocesses.

These first three premises implicate the ubiquity ofbiological changes and relations between biology and be-havior in adolescence. However, these endemic transitionsalso vary in content, intensity, and timing between individ-uals. That is, though every adolescent will experience en-docrine, neuronal, and autonomic changes, how thesechanges manifest are idiosyncratic. Thus, the next threepremises cover the individual differences of adolescentdevelopment.

4. Individual differences in adolescent emotionalbehavior changes are domain specific and vary in in-tensity. The most salient, well-researched, and problematicbehaviors of adolescence are all related to emotions. De-pression, anxiety, aggression, risk taking, sexual behavior,suicide, interpersonal conflict, self-injury, and passionateinterests in the arts, athletics, and peer relations all stemfrom emotional processes. As detailed later in Premise 6,the upwelling of arousal in early adolescence is met withregulatory and coping behaviors carved from experience toproduce unique manifestations in each adolescent. For ex-ample, any given adolescent faced with some form of peerrejection may respond by withdrawing, aggressing, or in-vesting more energy in family or peers who do not rejectthem. The point is that each emotionally challenging event

in adolescence—and adolescence is rife with stressful in-terpersonal and emotionally challenging events (Larson &Ham, 1993)—is met with some regulatory compensation.Importantly, this regulatory compensation is more maturethan in preadolescence but also manifests in relativelyunique ways across individuals. From this information, twoimportant observations can be made. First, each individualhas a domain or range of domains of adolescent change thatis most prominent. Typically, bungee jumpers are not holedup in their rooms for 16 hours a day, and socially anxiousadolescents are not sexually promiscuous. However, thereality is that the high school team captain can be suicidaland the most anxious student can engage in delinquentbehavior. Adolescent-typical behaviors occur in every pos-sible combination. Unfortunately, mostly for pragmaticreasons, researchers tend to take a compartmentalized, vari-able-centered approach to adolescent development. A studyfocusing exclusively on delinquency necessarily neglectssocial anxiety and vice versa. Furthermore, due to a com-bination of societal urgency and funding priorities, adoles-cent research has predominantly been focused on problemsand pathology at the expense of the understanding of nor-mative development (Steinberg & Morris, 2001). As such,the evidence for or against the storm and stress hypothesisin the general population is lacking.

The second, related, observation is that the intensity ofan adolescent’s aggression, depressive symptoms, and soforth is a within-individual experience, a relative change. Inthis case, between-subjects comparisons are biased towardinterpreting the most extreme cases in any particular do-main. We care less about the occasionally aggressive thanthe frequently aggressive and focus more on the physical orsexual risk takers than on the academic or social risk takers.As a result, Arnett (1999) and others concluded that stormand stress is probable but not inevitable. From the theoret-ical perspective of modeling adolescent change, however,comparisons cannot be interindividual but rather should beintraindividual (Magnusson, 1999; Molenaar & Campbell,2009). The comparison case for any individual adolescentis not the aggregate, but his or her former and future selves.Thus, the relative intraindividual changes across all possi-ble domains are the criteria for assessing patterns of ado-lescent development.

5. There are individual differences in the age ofonset and duration of periods of adolescent change.Biologically, there is great variability in developmentaltiming across individuals. For example, 90%–95% of girlshave their first 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 girlwith her first menses in Grade 6 and another with hers inGrade 11 are both considered as developing typically, atleast physically. In fact, all markers of typical physicaldevelopment have a wide age range of onset (see Figure 1).Across typically developing individuals, each maturationalevent can vary by as much as five years. Moreover, thetiming of developmental onset can be distinguished fromthe tempo or rate of maturation from start to finish(Mendle, Harden, Brooks-Gunn, & Graber, 2010). For ex-

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

6 Month 2013 ● American Psychologist

Page 8: Hollenstein & Lougheed 2013 Online

ample, Marceau and colleagues (2011) fit logistic curves tolongitudinal measures of pubertal maturation to find thatinternalizing problems were associated with both earliertiming and faster tempo for girls. What is not yet known ishow the timing and tempo of adolescent physical matura-tion domains relate to one another and, more pertinent tothe present model, to other aspects of socioemotional be-havior.

Figure 1 depicts the range and timing of normativedevelopmental domains. Consider a hypothetical individualadolescent progressing through these maturational mile-stones. The age at which this individual reaches each ofthese milestones is different from that of all of his or herpeers. That is, the relative timing of these maturation eventswith respect to one other (e.g., age of growth spurt relativeto age of peak frontal lobe pruning relative to age ofeverything else) is unique to each individual. Thus, notonly are tempo and timing important, but the rhythm ofthese changes may be important as well. Moreover, as wecome to understand the neural changes driven by hor-mones, genetics, and environment, the developmentalshifts in synaptic pruning and the proliferation of neu-rotransmitters and their receptors will necessarily be addedto this repertoire of salient maturational milestones withtiming differences.

Considering the emotion-related changes in adoles-cence in light of timing, tempo, and rhythm reveals a morecomplete picture of adolescent development. Prominenttheory and research suggest that maturational disparitiesunderlie more extreme manifestations of emotion-relatedbehavior change such as anxiety, depression, and delin-quency (Ge & Natsuaki, 2009). If one takes a more nor-mative developmental approach, these maturational dispar-ities must also be seen to underlie any individualdifferences in these domains as well. This timing approachcould also help to explain aggregate tendencies for inter-personal conflict in early adolescence, mood disruptions inmid-adolescence, and more extreme risk-taking in late ad-olescence (Graber, 2004; Laursen et al., 1998; Steinberg,2008). The addition of timing factors to the biological andenvironmental processes described in the previous prem-ises provides a more thorough developmental context forthe direct examination of the storm and stress hypothesis.

6. Individual differences in the duration and inten-sity of transitions in emotional arousal are functionallymodulated by emotion regulation skills. We are bornwith biological mechanisms of emotional arousal but mustlearn through experience how to regulate our emotions. Toborrow from Greenough and Black (1992), arousal is ex-perience expectant, but regulation is experience dependent.This is perhaps exemplified most clearly in two currentmodels of normative adolescent emotional development(Casey et al., 2011; Steinberg, 2008). In these models, theonset of adolescence is characterized by rapid changes inmechanisms of arousal, notably in the subcortical limbicsystem and ventral regions of the cortex. In contrast, themore cognitive mechanisms of executive control and self-regulation develop gradually and linearly across adoles-cence. This contrast of arousal and regulation is an over-

simplified but useful heuristic for adolescent emotionaldevelopment. The core assertion of these models is thatthere is a period of time during which adolescents’ facultiesfor arousal exceed their capacities for regulating thatarousal. The typical time span and degree of this discrep-ancy is not yet known, but certainly there is interindividualvariability in the duration and intensity of this discrepancy.

Moving Beyond Storm and Stress:The 4T ApproachWe have provided six premises relevant to the storm andstress hypothesis. We have reviewed biological, psycho-logical, and environmental determinants of adolescent be-havior and considered issues of relative timing and thearray of emotion-related domains. With all of these inmind, we assert that even the more nuanced modern ver-sion of storm and stress is facile and outmoded. As we haveshown in the six premises, the general conclusion thatstorm and stress is neither ubiquitous nor inevitable maybe suspect for several reasons. First, it neglects relevantprocesses that are ubiquitous and inevitable. Second, stormand stress has never been formally and comprehensivelystated as a hypothesis; hence it is not clear exactly what itis that is not ubiquitous or inevitable. Thus, storm andstress has not been adequately tested directly (Arnett,1999). Finally, and most important, storm and stress is alimited view of the multifaceted, organic processes at playduring adolescent development. The fact that the conceptholds sway with parents and the general public may reflectmore of a complaint from an adult perspective: wantingteens to behave in accordance with adult norms regardlessof the developmental function of adolescent-typical behav-ior. Despite the rejection of Anna Freud’s extreme perspec-tive, the retention of the concept of storm and stress,however cautiously, still pathologizes adolescence to somedegree. This is not a reasonable basis for scientific under-standing. Instead, we propose that it is time to move onfrom the dichotomy of storm and stress, to integrate thedeeper and more complex understanding we have of ado-lescent biology and behavior, and to turn our attention tomore comprehensive models of adolescent normative de-velopment. To this end, we offer the 4T approach, whichrequires the integration of the following: typicality, tem-perament, transactions, and timing. We discuss each ofthese in turn.

TypicalityBy typical, we mean the normative processes of transition-ing out of childhood and through adolescence. One of theproblems with adolescent research, especially of late, isthat it relies too heavily on the problem behaviors andpathologies that emerge during this period (Steinberg &Morris, 2001). Indeed, this is important work, and it is atleast somewhat directed by shifts in funding priorities.However, the premise of this developmental psychopathol-ogy approach is that these problems are deviations fromwhat is typical (Cicchetti & Rogosch, 2002), and yet wedon’t really understand what is typical very well at all.

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

7Month 2013 ● American Psychologist

Page 9: Hollenstein & Lougheed 2013 Online

Moreover, studying the individuation of adolescents asthey experiment and specialize is difficult (though notimpossible) for controlled research; all but the most ex-treme behaviors can easily be recorded and compared.Nevertheless, equipped with the sophisticated tools andmultidisciplinary approaches of the 21st century, the fieldis up for the challenge.

TemperamentTemperament no longer exclusively refers to a develop-mentally fixed, trait-like package of emotional responses(Laceulle, Nederhof, Karreman, Ormel, & van Aken,2012). Instead, it is a way to summarize intraindividualemotional response tendencies (e.g., sensitivity, regulation)at a given moment in one’s life, which can change due todevelopmental maturation and environmental influences(e.g., stress). In this respect, temperamental change inadolescence is the rough equivalent of storm and stress. Weargue that most of adolescent-typical changes are emotion-related in that they are affected by or affect temperamentalresponses. Any coherent model of adolescent development,therefore, must account for the sensitivity thresholds, in-tensity, domain, duration, and regulatory control of emo-tions. Thus, a temperamental focus allows theory and re-search to go beyond simply testing whether an adolescent“stormed” or “stressed” to provide a more integrated un-derstanding of how adolescent emotional landscapeschange and stabilize in transactions with both biology andenvironment.

TransactionsTransactions between within-person physiology and theenvironmental milieu in which the person is situated are thebedrock of understanding the causes of behavior (Gottlieb& Willoughby, 2006; Magnusson & Cairns, 1996). Thecentral and autonomic nervous systems, the HPA axis, andthe endocrine systems are in constant, dynamic interactionwith each other and with environmental forces to producebehavior moment by moment. These transactions are theprocesses of complex, adaptive dynamic systems. That wecan understand the development of the individual as adynamic system is not a new idea (Hollenstein, 2011).What we are calling for is a more specific application of adynamic systems approach to the understanding of adoles-cent-typical phenomena (Granic, Dishion, & Hollenstein,2003; Kunnen, 2012). As the core of the 4T approach,transactions between biology and environment force us togo beyond simple dichotomies (Hall, 1904) or broad de-scriptive accounts (e.g., Lerner & Castellino, 2002) toprovide explanatory mechanisms of adolescent change. Forexample, advances in epigenetics are now providing awindow into individual differences in responses to stress—actions and interactions with significant others alter theway that genes are expressed (Meaney, 2010). We assertthat, because development is best viewed as a dynamicsystem (Smith & Thelen, 2003), biology–environmenttransactions must be a central focus of adolescent theoryand research.

TimingFinally, as we have argued in several ways, timing is animportant and often overlooked aspect of adolescent devel-opment (Granic, 2005). The challenges in understandingadolescence stem from the diverse timing of changes at thisage. In infancy, we can chart progress on the order ofweeks and months. In adolescence, a similar mapping mustreflect individual differences of years. Timing can refer tothe age of onset or completion of various adolescent-typicalchanges (see Figure 1) as well as the tempo or rate of thesechanges (Marceau et al., 2011; Mendle et al., 2010) andthe relative timing of two or more changes (e.g., sper-marche and family conflict). Moreover, timing and dynam-ics are integral to any systemic approach such as 4T(Granic, 2005). Temporal dynamics, whether at the scale ofseconds or years, will confound any cross-sectional orvariable-centered research design, thus limiting what canbe gained from such designs. Moreover, chronological agecan be a poor proxy for equating adolescents in terms oftheir functional maturity. Pubertal status is one alternative,but there may be other maturational markers that can beused more effectively in determining the functional mech-anisms of adolescent behavior (Galambos, Kolaric, Sears,& Maggs, 1999). Degree of myelination in the prefrontalcortex, peak growth spurt, and diurnal variability in hor-mone concentrations (Bond, Vella, Kiparissis, & Wynne-Edwards, 2006) are just a few of the possibilities.

We suggest that, taken together, these four “Ts” maybe a useful framework to guide future theory and research.The integration of typicality, temperament, transactions,and timing leads to some fundamental research questionsand recommendations. First, what exactly are the changestypical of all adolescents (i.e., what is inevitable)? It isessential to press on with basic research by deemphasizinga problem-focused or pathological approach in lieu ofdiscovering what is truly adolescent typical. Second, howdoes adolescent development transpire? The criterion fordetecting change is intra- rather than interindividual. Thesechanges do not need to be problematic or pathological, justdifferent from before or after this critical period. Hence,there is limited utility in cross-sectional and variable-cen-tered designs. Instead, longitudinal, person-centered de-signs and methodology provide the necessary insight(Bergman, Magnusson, & El-Khouri, 2003; Magnusson &Cairns, 1996; Molenaar & Campbell, 2009). Third, howdoes timing relate to adolescent-typical behavior? It isnecessary to build on recent creative examinations of theeffects of timing (Marceau et al., 2011; Mendle et al., 2010;Susman, Dockray, et al., 2010) to begin to understand howdiverse timing-related factors relate to adolescent behavior.Fourth, how domain specific are individual differences inadolescent-typical changes? For any given individual, theovert manifestations of adolescent change may occur inonly one or a few of the possible domains (e.g., affective,internalizing, externalizing, risk taking, interpersonal con-flict). Despite those individual differences, there may becommon underlying mechanisms that could explain thesemanifestations. Research intended to document adolescent-

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

8 Month 2013 ● American Psychologist

Page 10: Hollenstein & Lougheed 2013 Online

typical change would need to be as domain inclusive aspossible to answer this question. By extension, the fifthquestion is: What are the underlying transactional mecha-nisms of adolescent-typical change? Research that accountsfor reciprocal transactions between biology and environ-ment is the primary mechanism that can move the fieldaway from the dominance of unidirectional explanationstoward more parsimonious models.

ConclusionDevelopment is systemic—simultaneously atomistic andinterpersonal (Smith & Thelen, 2003; Witherington, 2007).Because of the complexities and temporal variability en-demic to adolescence, perhaps there is no other age periodthat so greatly requires a systemic approach. There areubiquitous and inevitable aspects of adolescence that def-initely influence individual differences in adolescentthoughts, feelings, and behavior through transactions withthe environmental context. It is time we moved on fromideas based in 19th-century thinking; storm and stress is avestigial developmental framework. The 4T approach pro-vides a systems-based framework that will facilitate thegreater understanding of adolescence needed for the 21stcentury.

REFERENCES

Allen, N. B., & Sheeber, L. B. (2008). The importance of affectivedevelopment for the emergence of depressive disorder during adoles-cence. In N. B. Allen & L. B. Sheeber (Eds.), Adolescent emotionaldevelopment and the emergence of depressive disorders (pp. 1–10).Cambridge, England: Cambridge University Press. doi:10.1017/CBO9780511551963.001

Anderson, S. E., Dallal, G. E., & Must, A. (2003). Relative weight andrace influence average age at menarche: Results from two nationallyrepresentative surveys of US girls studied 25 years apart. Pediatrics,111, 844–850. doi:10.1542/peds.111.4.844

Apter, D. (1980). Serum steroids and pituitary hormones in female pu-berty: A partly longitudinal study. Clinical Endocrinology, 12, 107–120. doi:10.1111/j.1365-2265.1980.tb02125.x

Arnett, J. J. (1999). Adolescent storm and stress, reconsidered. AmericanPsychologist, 54, 317–326. doi:10.1037/0003-066X.54.5.317

Belsky, J., Steinberg, L. D., Houts, R. M., Friedman, S. L., DeHart, G.,Cauffman, E., . . . NICHD Early Child Care Research Network. (2007).Family rearing antecedents of pubertal timing. Child Development,78(4), 1302–1321. doi:10.1111/j.1467-8624.2007.01067.x

Benedict, R. (1934). Anthropology and the abnormal. Journal of GeneralPsychology, 10, 59–82. doi:10.1080/00221309.1934.9917714

Bergman, L. R., Magnusson, D., & El-Khouri, B. M. (2003). Studyingindividual development in an interindividual context: A person-orientedapproach. Mahwah, NJ: Erlbaum.

Blakemore, S. J., Burnett, S., & Dahl, R. E. (2010). The role of puberty inthe developing adolescent brain. Human Brain Mapping, 31, 926–933.doi:10.1002/hbm.21052

Bond, L. J., Vella, E. T., Kiparissis, Y., & Wynne-Edwards, K. E. (2006).Anthropometry and body composition do not predict bioavailable an-drogen or progesterone concentration in adolescent girls. AmericanJournal of Human Biology, 18, 639–653. doi:10.1002/ajhb.20534

Brenhouse, H. C., & Andersen, S. L. (2011). Developmental trajectoriesduring adolescence in males and females: A cross-species understand-ing of underlying brain changes. Neuroscience and Biobehavioral Re-views, 35, 1687–1703. doi:10.1016/j.neubiorev.2011.04.013

Brenhouse, H. C., Dumais, K., & Andersen, S. L. (2010). Enhancing thesalience of dullness: Behavioral and pharmacological strategies to fa-cilitate extinction of drug-cue associations in adolescent rats. Neuro-science, 169, 628–636. doi:10.1016/j.neuroscience.2010.05.063

Brooks-Gunn, J., Graber, J. A., & Paikoff, R. L. (1994). Studying linksbetween hormones and negative affect: Models and measures. Journalof Research on Adolescence, 4, 469 – 486. doi:10.1207/s15327795jra0404_2

Brown, T. L., Flory, K., Lynam, D. R., Leukefeld, C., & Clayton, R. R.(2004). Comparing the developmental trajectories of marijuana use ofAfrican American and Caucasian adolescents: Patterns, antecedents,and consequences. Experimental and Clinical Psychopharmacology,12(1), 47–56. doi:10.1037/1064-1297.12.1.47

Brown, B. B., & Klute, C. (2003). Friendships, cliques, and crowds. InG. R. Adams & M. D. Berzonsky (Eds.), Blackwell handbook ofadolescence (pp. 330–348). Malden, MA: Blackwell.

Buchanan, C. M., Eccles, J. S., & Becker, J. B. (1992). Are adolescents thevictims of raging hormones? Evidence for activational effects of hor-mones on moods and behavior at adolescence. Psychological Bulletin,111, 62–107. doi:10.1037/0033-2909.111.1.62

Casey, B. J., Jones, R. M., & Hare, T. A. (2008). The adolescent brain.Malden, MA: Blackwell.

Casey, B. J., Jones, R. M., & Somerville, L. H. (2011). Braking andaccelerating of the adolescent brain. Journal of Research on Adoles-cence, 21, 21–33. doi:10.1111/j.1532-7795.2010.00712.x

Caspi, A., Moffitt, T. E., Cannon, M., McClay, J., Murray, R., Harrington,H., . . . Craig, I. W. (2005). Moderation of the effect of adolescent-onsetcannabis use on adult psychosis by a functional polymorphism in thecatechol-o-methyltransferase gene: Longitudinal evidence of a gene xenvironment interaction. Biological Psychiatry, 57, 1117–1127. doi:10.1016/j.biopsych.2005.01.026

Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W., Harrington,H., . . . Poulton, R. (2003). Influence of life stress on depression:Moderation by a polymorphism in the 5-HTT gene. Science, 301,386–389. doi:10.1126/science.1083968

Cicchetti, D., & Rogosch, F. A. (2002). A developmental psychopathol-ogy perspective on adolescence. Journal of Consulting and ClinicalPsychology, 70, 6–20. doi:10.1037/0022-006X.70.1.6

Collins, W., & Laursen, B. (2004). Changing relationships, changingyouth. Journal of Early Adolescence, 24, 55– 62. doi:10.1177/0272431603260882

Dahl, R. E. (2001). Affect regulation, brain development, and behavioral/emotional health in adolescence. CNS Spectrums, 6, 60–72.

Darling, N. (2008). Putting conflict in context. Monographs of the Societyfor Research in Child Development, 73, 169–175. doi:10.1111/j.1540-5834.2008.00478.x

Dorn, L. D., & Biro, F. M. (2011). Puberty and its measurement: A decadein review. Journal of Research on Adolescence, 21, 180–195. doi:10.1111/j.1532-7795.2010.00722.x

Dyk, P. H. (1993). Anatomy, physiology, and gender issues in adoles-cence. In T. P. Gullotta, G. R. Adams & R. Montemayor (Eds.),Adolescent sexuality (pp. 35–56). Thousand Oaks, CA: Sage.

Eley, T. C., Sugden, K., Corsico, A., Gregory, A. M., Sham, P., McGuffin,P., . . . Craig, I. W. (2004). Gene–environment interaction analysis ofserotonin system markers with adolescent depression. Molecular Psy-chiatry, 9, 908–915. doi:10.1038/sj.mp.4001546

Freud, A. (1958). Adolescence. In A. Freud, H. Hartmann, & E. Kris(Eds.), Psychoanalytic study of the child (pp. 255–278). New York,NY: International Universities Press.

Galambos, N., Kolaric, G., Sears, H., & Maggs, J. (1999). Adolescents’subjective age: An indicator of perceived maturity. Journal of Researchon Adolescence, 9, 309–337. doi:10.1207/s15327795jra0903_4

Ge, X., & Natsuaki, M. N. (2009). In search of explanations for earlypubertal timing effects on developmental psychopathology. CurrentDirections in Psychological Science, 18, 327–331. doi:10.1111/j.1467-8721.2009.01661.x

Giedd, J. N. (2004). Structural magnetic resonance imaging of the ado-lescent brain. Annals of the New York Academy of Sciences, 1021,77–85. doi:10.1196/annals.1308.009

Gottlieb, G., & Willoughby, M. T. (2006). Probabilistic epigenesis ofpsychopathology. Hoboken, NJ: Wiley.

Graber, J. A. (2004). Internalizing problems during adolescence. Hobo-ken, NJ: Wiley.

Granic, I. (2005). Timing is everything: Developmental psychopathologyfrom a dynamic systems perspective. Developmental Review, 25, 386–407. doi:10.1016/j.dr.2005.10.005

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

9Month 2013 ● American Psychologist

Page 11: Hollenstein & Lougheed 2013 Online

Granic, I., Dishion, T. J., & Hollenstein, T. (2003). The family ecology ofadolescence: A dynamic systems perspective on normative develop-ment. In G. Adams & M. Berzonsky (Eds.), Blackwell handbook ofadolescence (pp. 60–91). New York, NY: Blackwell.

Greenough, W. T., & Black, J. E. (1992). Induction of brain structure byexperience: Substrates for cognitive development. Hillsdale, NJ: Erl-baum.

Gruber, A. J., & Pope, H. G. (2002). Marijuana use among adolescents.Pediatric Clinics of North America, 49, 389–413. doi:10.1016/S0031-3955(01)00011-6

Hall, G. S. (1904). Adolescence: Its psychology and its relation to phys-iology, anthropology, sociology, sex, crime, religion, and education.Englewood Cliffs, NJ: Prentice-Hall.

Hollenstein, T. (2011). Twenty years of dynamic systems approaches todevelopment: Significant contributions, challenges, and future direc-tions. Child Development Perspectives, 5, 256–259. doi:10.1111/j.1750-8606.2011.00210.x

Hollenstein, T., McNeely, A., Eastabrook, J., Mackey, A., & Flynn, J.(2012). Sympathetic and parasympathetic responses to social stressacross adolescence. Developmental Psychobiology, 54, 207–214. doi:10.1002/dev. 20582

Holsen, I., Kraft, P., & Vittersø, J. (2000). Stability in depressed mood inadolescence: Results from a 6-year longitudinal panel study. Journal ofYouth and Adolescence, 29, 61–78. doi:10.1023/A:1005121121721

Kotchick, B. A., Shaffer, A., Forehand, R., & Miller, K. S. (2001).Adolescent sexual risk behavior: A multi-system perspective. ClinicalPsychology Review, 21, 493–519. doi:10.1016/S0272-7358(99)00070-7

Kunnen, E. S. (2012). A dynamic systems approach to adolescent devel-opment. London, England: Psychology Press.

Laceulle, O. M., Nederhof, E., Karreman, A., Ormel, J., & van Aken,M. A. G. (2012). Stressful events and temperament change during earlyand middle adolescence: The TRAILS study. European Journal ofPersonality, 26, 276–284. doi:10.1002/per.832

Larson, R., & Ham, M. (1993). Stress and “storm and stress” in earlyadolescence: The relationship of negative events with dysphoric affect.Developmental Psychology, 29, 130–140. doi:10.1037/0012-1649.29.1.130

Laursen, B., Coy, K. C., & Collins, W. A. (1998). Reconsidering changesin parent-child conflict across adolescence: A meta-analysis. ChildDevelopment, 69, 817–832. doi:10.2307/1132206

Lerner, R. M., & Castellino, D. R. (2002). Contemporary developmentaltheory and adolescence: Developmental systems and applied develop-mental science. Journal of Adolescent Health, 31, 122–135. doi:10.1016/S1054-139X(02)00495-0

MacDonald, E., Dadds, M. R., Brennan, J. L., Williams, K., Levy, F., &Cauchi, A. J. (2011). A review of safety, side-effects and subjectivereactions to intranasal oxytocin in human research. Psychoneuroendo-crinology, 36, 1114–1126. doi:10.1016/j.psyneuen.2011.02.015

Magnusson, D. (1999). On the individual: A person-oriented approach todevelopmental research. European Psychologist, 4, 205–218. doi:10.1027//1016-9040.4.4.205

Magnusson, D., & Cairns, R. (1996). Developmental science: Toward aunified framework. In R. B. Cairns, G. H. Elder, & E. J. Costello (Eds.),Developmental science (pp. 7–30). Cambridge, England: CambridgeUniversity Press.

Marceau, K., Ram, N., Houts, R. M., Grimm, K. J., & Susman, E. J.(2011). Individual differences in boys’ and girls’ timing and tempo ofpuberty: Modeling development with nonlinear growth models. Devel-opmental Psychology, 47, 1389–1409. doi:10.1037/a0023838

Marshall, W. A., & Tanner, J. M. (1969). Variations in pattern of pubertalchanges in girls. Archives of Disease in Childhood, 44, 291–303.doi:10.1136/adc.44.235.291

Marshall, W. A., & Tanner, J. M. (1970). Variations in the pattern ofpubertal changes in boys. Archives of Diseases in Childhood, 45,13–23. doi:10.1136/adc.45.239.13

McCartney, C. R., Prendergast, K. A., Blank, S. K., Helm, K. D., Chhabra,S., & Marshall, J. C. (2009). Maturation of luteinizing hormone (go-nadotropin-releasing hormone) secretion across puberty: Evidence foraltered regulation in obese peripubertal girls. Journal of Clinical En-docrinology and Metabolism, 94, 56–66. doi:10.1210/jc.2008-1252

McClintock, M. K., & Herdt, G. (1996). Rethinking puberty: The devel-opment of sexual attraction. Current Directions in Psychological Sci-ence, 5, 178–183. doi:10.1111/1467-8721.ep11512422

McCormick, C. M., & Mathews, I. Z. (2007). HPA function in adoles-cence: Role of sex hormones in its regulation and the enduring conse-quences of exposure to stressors. Pharmacology, Biochemistry andBehavior, 86, 220–233. doi:10.1016/j.pbb.2006.07.012

Mead, M. (1928). Coming of age in Samoa. New York, NY: Morrow.Meaney, M. J. (2010). Epigenetics and the biological definition of gene �

environment interactions. Child Development, 81, 41–79. doi:10.1111/j.1467-8624.2009.01381.x

Mendle, J., Harden, K. P., Brooks-Gunn, J., & Graber, J. A. (2010).Development’s tortoise and hare: Pubertal timing, pubertal tempo, anddepressive symptoms in boys and girls. Developmental Psychology, 46,1341–1353. doi:10.1037/a0020205

Molenaar, P. C. M., & Campbell, C. G. (2009). The new person-specificparadigm in psychology. Current Directions in Psychological Science,18, 112–117. doi:10.1111/j.1467-8721.2009.01619.x

Nielsen, C. T., Skakkebaek, N. E., Richardson, D. W., Darling, J. A.,Hunter, W. M., Jørgensen, M., . . . Müller, J. (1986). Onset of therelease of spermatozoa (spermarche) in boys in relation to age, testic-ular growth, pubic hair, and height. Journal of Clinical Endocrinologyand Metabolism, 62, 532–535. doi:10.1210/jcem-62-3-532

Nilsson, K. W., Sjöberg, R. L., Damberg, M., Alm, P. O., Öhrvik, J.,Leppert, J., . . . Oreland, L. (2005). Role of the serotonin transportergene and family function in adolescent alcohol consumption. Alcohol-ism: Clinical and Experimental Research, 29, 564–570. doi:10.1097/01.ALC.0000159112.98941.B0

O’Neal, K. K. (2001). Adolescent risk behaviors and developmentalcontextualism: A person-oriented approach. Dissertation Abstracts In-ternational: Section A. Humanities and Social Sciences, 62, 1956-a.

Oyama, S., Griffiths, P. E., & Gray, R. D. (2003). Cycles of contingency:Developmental systems and evolution. Cambridge, MA: MIT Press.

Paikoff, R. L., & Brooks-Gunn, J. (1991). Do parent–child relationshipschange during puberty? Psychological Bulletin, 110, 47– 66. doi:10.1037/0033-2909.110.1.47

Paus, T. (2010). Growth of white matter in the adolescent brain: Myelinor axon? Brain and Cognition, 72, 26–35. doi:10.1016/j.bandc.2009.06.002

Pinker, S. (2004). Why nature & nurture won’t go away. Daedalus, 133,5–17. doi:10.1162/0011526042365591

Pitkänen, T., Lyyra, A., & Pulkkinen, L. (2005). Age of onset of drinkingand the use of alcohol in adulthood: A follow-up study from age 8–42for females and males. Addiction, 100, 652–661.

Poletti, M. (2009). Adolescent brain development and executive func-tions: A prefrontal framework for developmental psychopathologies.Clinical Neuropsychiatry: Journal of Treatment Evaluation, 6, 155–165.

Pope, H. G., Kouri, E. M., & Hudson, J. I. (2000). Effects of supraphysi-ologic doses of testosterone on mood and aggression in normal men: Arandomized controlled trial. Archives of General Psychiatry, 57, 133–140. doi:10.1001/archpsyc.57.2.133

Powers, S. I. (2011). Genes, hormones, and family behavior: What makesadolescence unique? New York, NY: Springer Science � BusinessMedia.

Rakic, P., Bourgeois, J. P., & Goldman-Rakic, P. S. (1994). Synapticdevelopment of the cerebral cortex: Implications for learning, memoryand mental illness. Progress in Brain Research, 102, 227–243. doi:10.1016/S0079-6123(08)60543-9

Roche, A. F., Wellens, R., Attie, K., & Siervogel, R. (1995). The timingof sexual maturation in a group of US white youth. Journal of PediatricEndocrinology and Metabolism, 8, 11–18. doi:10.1515/JPEM.1995.8.1.11

Rowe, R., Maughan, B., Worthman, C. M., Costello, E. J., & Angold, A.(2004). Testosterone, antisocial behavior, and social dominance inboys: Pubertal development and biosocial interaction. Biological Psy-chiatry, 55, 546–552. doi:10.1016/j.biopsych.2003.10.010

Schachter, S., & Singer, J. E. (1962). Cognitive, social, and physiologicaldeterminants of emotional state. Psychological Review, 69, 379–399.doi:10.1037/h0046234

Schulz, K. M., Molenda-Figueira, H. A., & Sisk, C. L. (2009). Back to thefuture: The organizational–activational hypothesis adapted to puberty

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

10 Month 2013 ● American Psychologist

Page 12: Hollenstein & Lougheed 2013 Online

and adolescence. Hormones and Behavior, 55, 597–604. doi:10.1016/j.yhbeh.2009.03.010

Shaw, P., Kabani, N. J., Lerch, J. P., Eckstrand, K., Lenroot, R., Gogtay,N., . . . Wise, S. P. (2008). Neurodevelopmental trajectories of thehuman cerebral cortex. Journal of Neuroscience, 28, 3586–3594. doi:10.1523/JNEUROSCI.5309-07.2008

Smith, L. B., & Thelen, E. (2003). Development as a dynamic system.Trends in Cognitive Sciences, 7, 343–348. doi:10.1016/S1364-6613(03)00156-6

Spear, L. P. (2000). The adolescent brain and age-related behavioralmanifestations. Neuroscience and Biobehavioral Reviews, 24, 417–463. doi:10.1016/S0149-7634(00)00014-2

Spear, L. P. (2003). Neurodevelopment during adolescence. New York,NY: Cambridge University Press.

Steinberg, L. (1988). Reciprocal relation between parent–child distanceand pubertal maturation. Developmental Psychology, 24, 122–128. doi:10.1037/0012-1649.24.1.122

Steinberg, L. (2001). We know some things: Parent–adolescent relation-ships in retrospect and prospect. Journal of Research on Adolescence,11, 1–19. doi:10.1111/1532-7795.00001

Steinberg, L. (2008). A social neuroscience perspective on adolescentrisk-taking. Developmental Review, 28, 78–106. doi:10.1016/j.dr.2007.08.002

Steinberg, L. (2010). A behavioral scientist looks at the science of ado-lescent brain development. Brain and Cognition, 72, 160–164. doi:10.1016/j.bandc.2009.11.003

Steinberg, L., & Belsky, J. (1996). An evolutionary perspective on psycho-pathology in adolescence. Rochester, NY: University of Rochester Press.

Steinberg, L., & Morris, A. S. (2001). Adolescent development. Journalof Cognitive Education and Psychology, 2, 55– 87. doi:10.1891/194589501787383444

Strasburger, V. C., & Brown, R. T. (1991). Adolescent medicine: Apractical guide. Boston, MA: Little, Brown.

Susman, E. J. (1997). Modeling developmental complexity in adoles-cence: Hormones and behavior in context. Journal of Research onAdolescence, 7(3), 283–306. doi:10.1207/s15327795jra0703_3

Susman, E. J., Dockray, S., Granger, D. A., Blades, K. T., Randazzo, W.,Heaton, J. A., & Dorn, L. D. (2010). Cortisol and alpha amylasereactivity and timing of puberty: Vulnerabilities for antisocial behav-iour in young adolescents. Psychoneuroendocrinology, 35, 557–569.doi:10.1016/j.psyneuen.2009.09.004

Susman, E. J., Houts, R., Steinberg, L., Belsky, J., Cauffman, E., DeHart,G. (2010). Longitudinal development of secondary sexual characteris-tics in girls and boys between ages 9 1/2 and 15 1/2 years. Archives ofPediatrics & Adolescent Medicine, 164, 166 –173. doi:10.1001/archpediatrics.2009.261

Susman, E. J., & Rogol, A. (2004). Puberty and psychological develop-ment. In R. M. Lerner, & L. Steinberg (Eds.), Handbook of adolescentpsychology (2nd ed., pp. 15–44). Hoboken, NJ: Wiley.

Walz, J. A. (1927). Early references to storm and stress in Germanliterature. Modern Language Notes, 42(8), 531–538. doi:10.2307/2914032

Wells, B. E., & Twenge, J. M. (2005). Changes in young people’s sexualbehavior and attitudes, 1943–1999: A cross-temporal meta-analysis.Review of General Psychology, 9, 249–261. doi:10.1037/1089-2680.9.3.249

Wiesel, T. N., & Hubel, D. H. (1965). Extent of recovery from the effectsof visual deprivation in kittens. Journal of Neurophysiology, 28, 1060–1072.

Witherington, D. (2007). The dynamic systems approach as metatheoryfor developmental psychology. Human Development, 50, 127–153.doi:10.1159/000100943

Thi

sdo

cum

ent

isco

pyri

ghte

dby

the

Am

eric

anPs

ycho

logi

cal

Ass

ocia

tion

oron

eof

itsal

lied

publ

ishe

rs.

Thi

sar

ticle

isin

tend

edso

lely

for

the

pers

onal

use

ofth

ein

divi

dual

user

and

isno

tto

bedi

ssem

inat

edbr

oadl

y.

11Month 2013 ● American Psychologist