Summary of the articles for exam 1
The teenage brain: Surging hormones-brain-behavior interactions
during puberty
The surge of hormones that starts the cascade of physical changes known as puberty, typically begins
before the teenage years. It occurs before the menarche (12.5 years). For understanding the proximal
effects of this surge of pubertal hormones on neurobehavioral systems, we should not focus on the
teenage years but, rather, on the more earlier window of development when there is a dramatic
change in hormonal levels.
Why study the effects of surging pubertal hormones? (1) Puberty is the fundamental basis of the
transition from childhood to adolescence; (2) the biological components of pubertal maturation
provide targets for the development and testing of mechanistic hypotheses; (3) the focus on puberty
creates unique opportunities for translational research with animal studies; and (4) there is growing
evidence for shifts in social and affective processing during puberty that may play a crucial role in
biasing developmental pathways which can have long-term effects on health, education, well-being.
Why focus on social and affective influences of pubertal hormones?
Growing evidence from studies in both humans and animals has suggested that pubertal hormones
may influence (bias) some neural and neurobehavioral tendencies of social and affective processing.
Neuroendocrine and hormonal aspects of puberty
Puberty is an endocrinological event leading to sexual maturation. The start of puberty is
characterized by the reactivation of the hypothalamus-pituitary-gonadal (HPG) axis, which starts to
produce GnRH, which produce other hormones. Those hormones play a role in the development of
secondary sexual characteristics and neurobehavioral changes during puberty. The development of
reproductive capabilities involve changes in the body, but also changes in neural systems. The brain is
a major target for sex-steroid hormones. Sex steroids act on the brain in two different ways:
- Through organizational effects that permanently change the structure of the brain.
- Through activational effects that temporarily change the activity of neural systems.
Pubertal hormones and (neuro) behavioral changes during adolescence
Testosterone: Increased levels of testosterone during adolescence have been associated with
increased approach-related behaviors, such as proactive aggression, risk taking, sensation seeking
and sensitivity to rewards. In this the social environment plays an important role. Findings
demonstrate that the social environment not only mediates the effects of testosterone on behavior
but also influences actual levels of testosterone itself.
Estradiol: Data suggest that increased pubertal estradiol in females is related to lessened behavioral
inhibition and increased risk taking, and predict stronger activity within the ventral striatum after
high-risk gambles.
Interactions between social-affective processing systems in the brain and cognitive control systems
can lead to healthy adaptation to the complex and rapidly changing social contexts of adolescence.
However, these interactions can also lead to negative trajectories. And those can spiral into large-
scale complex behavioral consequences.
Example: There is evidence for a circadian shift in sleep preferences at puberty (tendency to prefer
staying up later at night). This effect may be small, but in combination with social and behavioral
factors, it contributed to a situation where a lot of students are chronically sleep deprived.
Insufficient sleep has a cascade of negative effects on other aspects of emotion, behavior, cognition,
, and learning, which can, in turn, further interfere with the regulation of sleep and arousal: a spiral of
negative effects.
In search of explanations for early pubertal timing effects on
developmental psychopathology
Early pubertal maturation has been identified as a potential risk factor for internalizing and
externalizing problems during adolescence. However, questions about the mechanism that link early
pubertal timing and psychopathology remain. Here are four emerging lines of thinking for explaining
why early puberty exerts its influences on externalizing and internalizing psychopathologies:
- The hormonal influence hypothesis: Predicts that an increase in hormones at puberty leads
to increased psychopathology.
o There is no existing empirical data that have systematically documented an
‘interlocking’ dynamic between changes in hormonal activity and increases in
psychopathology over time. More research is needed.
- The maturation disparity hypothesis: Focuses on the gap between physical, social and
psychological maturation in early maturers that exacts the toll on individuals’ adjustment.
o This hypothesis has not been tested often. But there is evidence that that the higher
rates of psychopathology among early maturers are expected because their slow-
developing neurocognitive systems are mismatched with the fast-approaching social
and affective challenges at the onset of puberty.
- The contextual amplification hypothesis: Proposes that that experiencing early pubertal
transition in a disadvantaged context increase the risk for psychopathology.
o There is evidence for this hypothesis, but better methodological designs and statistics
are required to tease apart their complex web of effects.
- The accentuation hypotheses: Maintains that preadolescent vulnerabilities and challenges
during early pubertal transition together increase problems. Early puberty is viewed as a
precipitator that magnifies preexisting individual differences.
o This hypothesis has rarely been tested, mostly because it isn’t an easy task. There are
a lot of challenges, like you need a longitudinal design based on a large
representative sample.
Sex and ethnic differences add considerable complexities when testing these hypotheses because:
1. Early maturation effects have been consistently observed for girls but the results are mixed
for boys
2. In adolescence, girls are more likely than boys to manifest internalizing psychopathology,
while boys show more externalizing problems
3. Girls and boys undergo different hormonal changes at puberty
4. The two sexes differ in the sequence, timing, and manifestation of growth in primary and
secondary sex characteristics, weight, and height, as well as in body composition
5. There are racial/ethnic differences in rates of physical maturation
Those hypotheses each emphasize a single dimension, but they are by no means independent of each
other, and they can help piece together the web of pathways from pubertal timing to developmental
psychopathology.
The teenage brain: Surging hormones-brain-behavior interactions
during puberty
The surge of hormones that starts the cascade of physical changes known as puberty, typically begins
before the teenage years. It occurs before the menarche (12.5 years). For understanding the proximal
effects of this surge of pubertal hormones on neurobehavioral systems, we should not focus on the
teenage years but, rather, on the more earlier window of development when there is a dramatic
change in hormonal levels.
Why study the effects of surging pubertal hormones? (1) Puberty is the fundamental basis of the
transition from childhood to adolescence; (2) the biological components of pubertal maturation
provide targets for the development and testing of mechanistic hypotheses; (3) the focus on puberty
creates unique opportunities for translational research with animal studies; and (4) there is growing
evidence for shifts in social and affective processing during puberty that may play a crucial role in
biasing developmental pathways which can have long-term effects on health, education, well-being.
Why focus on social and affective influences of pubertal hormones?
Growing evidence from studies in both humans and animals has suggested that pubertal hormones
may influence (bias) some neural and neurobehavioral tendencies of social and affective processing.
Neuroendocrine and hormonal aspects of puberty
Puberty is an endocrinological event leading to sexual maturation. The start of puberty is
characterized by the reactivation of the hypothalamus-pituitary-gonadal (HPG) axis, which starts to
produce GnRH, which produce other hormones. Those hormones play a role in the development of
secondary sexual characteristics and neurobehavioral changes during puberty. The development of
reproductive capabilities involve changes in the body, but also changes in neural systems. The brain is
a major target for sex-steroid hormones. Sex steroids act on the brain in two different ways:
- Through organizational effects that permanently change the structure of the brain.
- Through activational effects that temporarily change the activity of neural systems.
Pubertal hormones and (neuro) behavioral changes during adolescence
Testosterone: Increased levels of testosterone during adolescence have been associated with
increased approach-related behaviors, such as proactive aggression, risk taking, sensation seeking
and sensitivity to rewards. In this the social environment plays an important role. Findings
demonstrate that the social environment not only mediates the effects of testosterone on behavior
but also influences actual levels of testosterone itself.
Estradiol: Data suggest that increased pubertal estradiol in females is related to lessened behavioral
inhibition and increased risk taking, and predict stronger activity within the ventral striatum after
high-risk gambles.
Interactions between social-affective processing systems in the brain and cognitive control systems
can lead to healthy adaptation to the complex and rapidly changing social contexts of adolescence.
However, these interactions can also lead to negative trajectories. And those can spiral into large-
scale complex behavioral consequences.
Example: There is evidence for a circadian shift in sleep preferences at puberty (tendency to prefer
staying up later at night). This effect may be small, but in combination with social and behavioral
factors, it contributed to a situation where a lot of students are chronically sleep deprived.
Insufficient sleep has a cascade of negative effects on other aspects of emotion, behavior, cognition,
, and learning, which can, in turn, further interfere with the regulation of sleep and arousal: a spiral of
negative effects.
In search of explanations for early pubertal timing effects on
developmental psychopathology
Early pubertal maturation has been identified as a potential risk factor for internalizing and
externalizing problems during adolescence. However, questions about the mechanism that link early
pubertal timing and psychopathology remain. Here are four emerging lines of thinking for explaining
why early puberty exerts its influences on externalizing and internalizing psychopathologies:
- The hormonal influence hypothesis: Predicts that an increase in hormones at puberty leads
to increased psychopathology.
o There is no existing empirical data that have systematically documented an
‘interlocking’ dynamic between changes in hormonal activity and increases in
psychopathology over time. More research is needed.
- The maturation disparity hypothesis: Focuses on the gap between physical, social and
psychological maturation in early maturers that exacts the toll on individuals’ adjustment.
o This hypothesis has not been tested often. But there is evidence that that the higher
rates of psychopathology among early maturers are expected because their slow-
developing neurocognitive systems are mismatched with the fast-approaching social
and affective challenges at the onset of puberty.
- The contextual amplification hypothesis: Proposes that that experiencing early pubertal
transition in a disadvantaged context increase the risk for psychopathology.
o There is evidence for this hypothesis, but better methodological designs and statistics
are required to tease apart their complex web of effects.
- The accentuation hypotheses: Maintains that preadolescent vulnerabilities and challenges
during early pubertal transition together increase problems. Early puberty is viewed as a
precipitator that magnifies preexisting individual differences.
o This hypothesis has rarely been tested, mostly because it isn’t an easy task. There are
a lot of challenges, like you need a longitudinal design based on a large
representative sample.
Sex and ethnic differences add considerable complexities when testing these hypotheses because:
1. Early maturation effects have been consistently observed for girls but the results are mixed
for boys
2. In adolescence, girls are more likely than boys to manifest internalizing psychopathology,
while boys show more externalizing problems
3. Girls and boys undergo different hormonal changes at puberty
4. The two sexes differ in the sequence, timing, and manifestation of growth in primary and
secondary sex characteristics, weight, and height, as well as in body composition
5. There are racial/ethnic differences in rates of physical maturation
Those hypotheses each emphasize a single dimension, but they are by no means independent of each
other, and they can help piece together the web of pathways from pubertal timing to developmental
psychopathology.
