Many of us remember
adolescence as an emotionally-trying time. Although modern psychology largely
discredits the storm-and-stress hypothesis of adolescence (developmentally
defined as the time between the onset of puberty and the time when people take
on adult roles and responsibilities), it remains true that adolescents
experience emotional changes both in terms of what they respond to and in terms
of how they respond to their stressors. [Entering adolescence allows for more
abstract reasoning that tends to lead to psychological phenomena such as the
imaginary audience (adolescents feel that they are always being watched—it matters
what they wear and who they hang out with, and if they trip on the stairs or
stumble over their words it’s the end of the world because everyone will notice
and remember) and the personal fable (related to the imaginary audience and risk
behavior, linked to the idea that “bad things happen to other people”); Arnett, 2013].
Recent research on the developing adolescent brain
reveals that these changes are related to changes in the HPA axis. As a recap,
both the sympathetic nervous system (SNS; leading to release of epinephrine and
norepinephrine that allow you to fight or fly) and HPA axis contribute to the
stress response. With respect to the HPA axis, neurons in the hypothalamic
paraventricular nucleus (PVN) release corticotropin-releasing hormone (CRH),
which triggers release of adrenocorticotropic hormone (ACTH) from the anterior
pituitary. ACTH then stimulates the adrenal glands to secrete glucocorticoids (GC’s)
such as cortisol in humans (and cortisterone in rodents). When the stressor
ends, the GC’s negatively feedback on the hypothalamus to shut the system off
and thereby prevent further release of CRH and ACTH. While in the short run
this response is adaptive (allowing for mobilization of energy stores,
enhancement of immune reactions, and increased learning and memory abilities)
with chronic stressors—such as constant social pressures in the adolescent
years—it becomes maladaptive, eventually leading to metabolic disorders,
impaired immune function, and impaired cognitive functions (Romeo, 2013).
Although the HPA axis exists and works throughout life,
it undergoes several changes during adolescence. Firstly, researchers found
that preadolescent rodents had hormonal stress responses lasting 45 to 60
minutes longer when compared to pre-weanling and adult rats. This change was
abrupt, and the ACTH responses matured later than corticosterone responses
(Romeo, 2013). Romeo (2013) argues that these data reveal that each node along
the HPA axis develops differently (at different rates and intensities) during
adolescence. Further, research found that human boys and girls in late
adolescence (15-17 years old) had higher stress-induced cortisol levels than
early adolescents or children ages 9-13. All of these data show that
adolescents undergo changes in their HPA axes that confer with heightened
stress responses.
To explain these heightened responses of the HPA axis,
Romeo comes up with several hypotheses. For me, the most convincing hypothesis is
that these changes in the HPA axis during adolescence involve both activation
and feedback. When exposed to a stressor, neural activity in the CRH-containing
cells of the PVN is greater in adolescent than in adult animals. This finding
seems to indicate that the activity of the HPA axis is initially greater in adolescence.
However, the story does not end here. Subsequent studies found that treating
adolescent animals with a synthetic glucocorticoid combated the stress-induced
corticosterone response in prepubertal rats less affectively than in adult
rats. This finding then suggests that—on top of the increased activity
indicated above—periadolescent animals also have less GC-dependent negative
feedback on the HPA axis.
This heightened sensitivity can lead to chronic stress
that is particularly maladaptive in adolescence. In adolescence, the brain
regions that are most vulnerable to the effects of stress—namely, the
hippocampus, prefrontal cortex (PFC), and amygdala—are all still developing. These
stress-sensitive regions are also exposed to greater and more prolonged levels
of GC’s due to increases in hormonal stress reactivity. These effects can be
devastating when combined with environmental factors such as prolonged stress. Research
has shown that previous exposure to chronic stress in adolescence reduces
structural plasticity in the hippocampus and the PFC while increasing
plasticity in the amygdala [in other words, adolescents exposed to previous
chronic stress become less able to cognitively adapt to stressful situations (due
to decreased plasticity in the hippocampus and PFC) that they become more
emotionally sensitive to (due to increased plasticity in the amygdala)]. Moreover,
the social stress that comes with the imaginary audience in adolescence further
decreases neural plasticity by inhibiting neurogenesis and synaptic
connectivity. These changes then lead to compromised emotional function and
cognitive skills. Even after recovering from chronic stress, some of the
adolescent animals’ structural and functional changes never recovered—showing that
chronic stress for the adolescent can be particularly devastating because it at
least has the potential lead to permanent, detrimental effects on both emotion
and cognition.
Overall, although this research is still in its
preliminary stages and scientists are still testing hypotheses relating to
what, exactly, causes the increased HPA functioning, it does suggest a possible
developmental model of stress-related psychological disorders. Romeo suggests
that these changes in the adolescent brain—changes interfering with the
functioning of the HPA axis—make the adolescent particularly vulnerable to
psychological disorders. This vulnerability is perhaps why psychological
disorders occur at such high rates in adolescence (1 in 5 Americans between the
ages of 13 and 18, according to the NIMH). This possible pathology of anxiety
disorders—relating specifically to the development and sensitivity of the HPA
axis during adolescence—indicates the need to teach and make available proper
stress-management techniques (e.g. progressive relaxation, massage therapy,
animal-assisted therapy, exercise) to adolescents, as they are particularly
prone to experiencing and suffering the long-term, negative effects of chronic
stress which, in turn, means that they particularly need to have
stress-management outlets to prevent them from experiencing these long-term,
negative effects.
Arnett, J. J. (2013). Adolescence and Emerging Adulthood (5th
ed.). Indianapolis, IN: Pearson.
National Institute of
Mental Health (NIMH). Any disorder among children. Retrieved from http://www.nimh.nih.gov/statistics/1ANYDIS_CHILD.shtml
I find that numerous assumptions are constantly made about why teenagers act the way they do, probably in some desperate attempt to understand the adolescent mind. One, now proven, misnomer I often hear is it’s due to all the “raging hormones” they have. After reviewing the literature you cited, I found it interesting how it was specifically noted that gonadal hormone levels during the pubescent stages are not responsible for the HPA stress changes seen in adolescents (Romeo, 2013). I agree with the argument made in the study, which you mentioned as well, that these changes can be largely due to the plasticity differences in stress-sensitive regions of the brain including the PFC, amygdala and hippocampus. We know that the PFC is not completely developed until early, to mid-twenties, so it is necessary to examine what that lack in development could mean for the impaired cognitive abilities one would need to properly handle certain psychological stressors.
ReplyDeleteI was curious if there was a biological reasoning for these physiological differences in the adolescent HPA axis, and if there was a positive reason for this seemingly negative increase in stress response. I began looking into the evolutionary model of adolescence and found some literature discussing risk-taking behavior and how this used to be, and sometimes still is, is necessary for adolescents (pertaining to multiple species) to partake in in order to survive (Ellis et al., 2012). It’s interesting to think about the underlying reasons for why it might be necessary for adolescents to have this increased stress response. For example, situations of fight or flight may be encountered more frequently for adolescent animals in the wild as they struggle to survive on their own or assert their dominance in a new pack. Animals either below or above this stage in development may not undergo these stressors to the same degree or frequency, therefore, the adolescent has developed a more heightened sensitivity to the stressor like we see in the HPA axis. However, we also have become increasingly aware that a chronic and increased stress response, especially in human adolescents in today’s western societies where the dangers they face are more psychological than physical, can do more harm than good.
I wonder if there is some merit to how these physiological changes in adolescents came to be about and if they are still necessary for humans in particular.
References:
Ellis B, Del Giudice M, Wilson D, et al. The evolutionary basis of risky adolescent behavior: implications for science, policy, and practice. Developmental Psychology [serial online]. May 2012:48(3):598-623. Available from: MEDLINE, Ipswich, MA. Accessed November 30, 2013.
Romeo, R. D. (2013). The teenage brain: The stress response and the adolescent brain. Current Directions in Psychological Science, 22, 140-145. doi: 10.1177/0963721413475445
I definitely agree that there's a highly adaptive reason for these changes. We read 12 articles about the teenage brain for adolescent psychology, and a lot of them focused on how adolescence is a time of heightened social interaction--it's the time when they have to go out into the world and learn how to assume adult responsibilities. Another article we read talked about how adolescents tend to be sensitive to these social situations and to new cues to be stressed, but to be less sensitive to other stress cues (e.g. environmental stress cues), which the article interpreted as allowing adolescents to have the courage to go into new environments more often but be able to respond appropriately with stress when confronted with something like a predator (e.g. a mouse's mother will no longer provide for her adolescent mouse, who has to learn to leave its mother. The mouse leaves and has to be unstressed enough to be able to leave and go into new environments, but it also has to respond to different sounds--like flapping wings because a hawk has spotted it and is swooshing in).
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