Summary of the following articles:
- GE & NATSUAKI (2009): IN SEARCH OF EXPLANATIONS FOR EARLY PUBERTAL TIMING EFFECTS ON DEVELOPMENTAL PSYCHOLOGY
- STEINBERG & SCOTT (2003): LESS GUILTY BY REASON OF ADOLESCENCE: DEVELOPMENTAL IMMATURITY, DIMINISHED RESPONSIBILITY AND THE JUVENILE DEATH PENALTY
GE & NATSUAKI (2009): IN SEARCH OF EXPLANATIONS FOR EARLY
PUBERTAL TIMING EFFECTS ON DEVELOPMENTAL PSYCHOLOGY
We describe four emerging lines of thinking for explaining why early puberty exerts its
influences on externalizing and internalizing psychopathologies. The focus of this report is
the effect of pubertal timing (i.e., timing at which an individual undergoes puberty), rather
than pubertal transition (i.e., physical maturation during puberty) per se.
The hormonal influence hypothesis
Two components of puberty, adrenarche and gonadarche, are important in the study of
hormonal influence on risk for psychopathology.
● Adrenarche, which typically occurs between ages 6 and 9 refers to the maturation of
the hypothalamic-pituitary adrenal (HPA) axis; in this period, adrenal androgens
begin to rise. Adrenal androgens are related to dominance, depression, and
antisocial conduct.
● Gonadarche, which begins at approximately ages 9 to 11, involves the maturation of
the hypothalamic-pituitary-gonadal (HPG) acis. Hormones of the HPG axis,
gonadotropins, increase rapidly during the pubertal transition.
Although the results are somewhat mixed, individual differences in concentration in
testosterone, and estradiol are related to negative affect, behavior problems, and aggressive
tendencies.
What happens to behaviors if timing of hormonal increases is accelerated and secretions are
initiated earlier?
● One theoretical possibility is that the developing brain’s sensitivity to pubertal
hormones decreases with time, marking early maturation as a potential correlate of
behavior.
● Another possibility is that earlier maturers not only begin secreting puberty-related
hormones earlier but also secrete more of the hormones even after completing
pubertal transition.
Although it is intuitively appealing to directly ascribe the rise of psychopathology at puberty
to a surge of hormonal activities, the empirical findings for such a link in humans are
fragmented and equivocal. No existing data we are aware of have systematically
documented an “interlocking” dynamic between changes in hormonal activity and increases
in psychopathology over time.
It is also important for researchers to attend to the confounding nature of hormonal changes,
puberty, and age in examining their relations to psychopathology. As “being older” connotes
myriad other risk factors in addition to rising hormones, isolating the real effect of hormones
requires testing the effects of individual variations in hormonal levels on psychopathology
controlling for age.
The maturation disparity hypothesis
According to this hypothesis, it is the gap between physical and psychosocial maturity that
place early (physical) maturers at risk for developing psychopathology. Because early
matures experience a briefer prelude to pubertal change than do their peers, they might be
less well prepared socially and cognitively for the biological and psychosocial challenges at
puberty.
Despite its plausibility, this hypothesis has more often been implied rather than directly
tested. Fortunately, recent development in social and cognitive neuroscience provides a
, fresh look at this hypothesis. Research has demonstrated that portions of the prefrontal
cortex that subserve executive functions or self-regulatory control continue to develop well
beyond puberty. From this view, the higher rates of psychopathology among early maturers
are expected because their slow-developing neurocognitive systems are mismatched with
the fast-approaching social and effective challenges at the onset of puberty; early maturers’
consolidation of self-regulatory skills in both cognitive and emotional domains lags behind
the social and emotional demands they face at the onset of puberty.
The contextual amplification hypothesis
Researchers subscribing to this hypothesis maintain that the rapodi biological changes at
puberty, coupled with adverse contexts (e.g. stressful environment, interpersonal challenges,
family conflict, neighborhood disorder), further exacerbate these problems. Adaptation is
particularly difficult for children who negotiate an early pubertal transition in a stressful social
environment because new challenges at the entry to puberty and a widening array of social
stressors may overtax their relatively undeveloped coping resources.
A few studies of peer-group experiences at puberty provide the clearest case for the
contextual amplification effect. Several researchers inferred that risks of girls’ early
maturation could arise particularly in mixed-sex contexts because their sensitivity to peer
norms and pressures from boys is heightened at puberty. Residing in a disadvantaged
neighborhood also places early maturers at risk for deviant peer association and
externalizing behavior.
Although the essence of the contextual amplification hypothesis lies in the moderating role of
context, the picture becomes murkier when considering multiple pathways and influences
together. Stressful life experiences, family adversities, deviant peers, lack of parental
supervision and harsh parenting, and schools and neighborhood conditions are all
intertwined, and each confounds the interpretation of the effects of the other.
The accentuation hypothesis
Finally, the accentuation hypothesis proposes that demanding life transitions characterized
by high novelty, ambiguity, and uncertainty - early physical maturation being an example -
tend to accentuate, rather than diminish, previous emotional and behavioral difficulties
during those periods. Here, puberty is viewed as a precipitator that magnifies pre existing
individual differences (e.g., the irritable becomes aggressive and the capable take charge).
Empirical testing of this theoretically elegant hypothesis is not an easy task. Because its
essence is the temporal order and timing of events, a rigorous examination of this
hypothesis requires a longitudinal design based on a large representative sample, with
detailed assessment of dispositional vulnerabilities before the onset of puberty and
assessment of psychopathological outcomes after puberty onset. These challenges may
explain why there have been so few empirical tests of this hypothesis.
Additional issues: sex and racial/ethnic differences
Although not a focus of this paper, sex and ethnic differences add considerable complexities
when testing these hypotheses because:
a. Early maturiaotn effects have been consistently observed for girls but the results are
mixed for boys.
b. In adolescence, girls are more likely than boy to manifest internalizing
psychopathology, while boys show more externalizing problems.
c. Girls and boys undergo different hormonal changes at puberty.
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