The recent APA Stress in America Survey (2013) revealed that U.S. adolescents perceive higher levels of stress than adults, with many reporting that they feel overwhelmed (31 percent), depressed (30 percent) or tired due to stress (36 percent) during the school year. Of importance, these experiences are associated with unhealthy eating, sleeping and exercise patterns that take a toll on the teens’ physical and mental health, not only in the short term but also well into adulthood. It is thus not surprising that the incidence of many forms of psychopathology spikes during adolescence, with 22.2 percent experiencing mental disorders with severe impairment and distress (Merikangas et al., 2010). Overlooked at a broad scale but suggested as playing a critical role in the significant changes in adolescents’ stress and risk is the onset of puberty. With this onset come dramatic increases in the activity of stress-response systems and in emotional reactivity, which, when combined with other profound social, cognitive and physical changes that accompany the transition to adolescence, creates the perfect storm for potential problems, but, as described here, also for potential interventions.
Social Support as a Stress Buffer
In contrast to a strong focus on adolescence as a risk period of development, much less attention has been paid to identifying protective factors that reduce this risk. Perhaps one of the most important — and easily implemented — protective factors is that of social support from close relationships. Certainly the benefits of social support are not unique to adolescence: Support facilitates coping with stress and is associated with widespread benefits for physical and mental health across life, in humans and non-human animals. Mechanistically, social support seems to provide a buffer that reduces or blocks physiological stress responses to stressful situations. This social buffering occurs throughout life (Hostinar, Sullivan, & Gunnar, 2014). For instance, parental presence can completely block increases in the production of the stress hormone cortisol in 12 to 18-month-olds receiving an inoculation, so long as those infants are securely attached to their parents (Gunnar et al., 1996). In adults, preparing for a laboratory public-speaking task with a romantic partner present can similarly dampen or block cortisol production during the speech itself (Kirschbaum, Klauer, Filipp, & Hellhammer, 1995).
There is surprisingly little experimental research, though, on stress-buffering effects of social support during late childhood and adolescence. Across several studies with collaborators at the University of Minnesota (Megan Gunnar, Anna Johnson), we have been exploring whether parent support retains the ability to block stress responses for participants developmentally spanning the pubertal transition. We have included participants with a range of childhood experiences, including those living in an international orphanage early in life and those living their entire lives in middle-class U.S. families. Some of the key questions that have been emerging have important implications for adolescent development and intervention.
Can Parents Help Lower Stress During Adolescence?
To study the potency of parent support during later development, we invited 81 pre-teenagers (ages 9-10) and teenagers (ages 15-16) who were situation before and after the onset of puberty, respectively, to perform a public speaking task in the laboratory, a very common experimental paradigm that induces mild to moderate behavioral and biological stress responses. Some participants in each age group were randomly assigned to receive help and support from their parent when preparing their speech; others received support from a friendly stranger. Pre-teens with parent support had their cortisol stress response completely blocked, even though they gave the speech alone in another room. Pre-teens with support from the stranger, however, showed the commonly observed stress response. The teenagers, in contrast, showed a strong stress response regardless of whether they prepared with their parent or the stranger (Hostinar, Johnson, & Gunnar, 2014). We are now exploring whether changes in the benefits of parental support result from puberty-related maturational changes or perhaps as a result of shifts in adolescents’ social networks and orientation to peers, who may become the primary support providers.
Do Early Social Experiences Shape Later Responsiveness to Parent Support?
As mentioned, the early-life experiences of the children we have been studying have varied substantially. In a new investigation, we compared the pre-teens and teens raised in their birth families to 80 age-matched participants who spent the first few years of life in orphanages overseas before being adopted into U.S. homes (adoptions took place by the time children were age 5). In contrast to the biological-family raised pre-teens described above, adopted pre-teens did not show a reduction in their cortisol response to the speech when their parent had been present during preparation. They, like the biological-family raised teens described above and the adopted teens, showed no benefit of parental presence. Thus, pre-teens who suffered early-life deprivation did not seem to experience the full benefits of parent support. Perhaps the first years of life are a sensitive period for establishing the capacity to experience stress relief in close relationships, and as such early social neglect has harmful and long-lasting stress-regulatory consequences. The next steps will be to determine why the pre-teens (and possibly adolescents) failed to benefit from parental support and to test ways of buffering stress responses when parents do not seem to serve in this capacity.
Conclusions and Next Steps: Is the Transition to Puberty an Opportune Period for Interventions?
The rapid changes that occur during the transition to adolescence, especially in neurobehavioral reorganization, present both challenges and opportunities for altering developmental trajectories. According to the pubertal recalibration hypothesis, the brain and the hypothalamic-pituitary-adrenocortical (HPA) stress system undergo a period of heightened plasticity during puberty (Romeo, Karatsoreos, & McEwen, 2006). Adolescent rodents, for instance, show increased growth of new neurons in the hippocampus after chronic stress, in contrast to the declining number of neurons observed in adult animals (Toth et al., 2008). Indirect evidence in humans points to similar patterns: The effects of early-life adversity are less notable after puberty if current circumstances are low-stress, while exposure to major stressors during adolescence increases risk for lingering adverse effects on later stress reactivity. Neural plasticity in early adolescence, therefore, may be a double-edged sword, such that both positive and negative experiences seem to be amplified. As such, intervening to alter stress reactivity precisely during this period may be particularly effective in shifting trajectories toward more positive long-term outcomes.
Our findings are also suggestive of the need for greater variations in the types of interventions that one might consider. For instance, parent support was beneficial in blocking stress responses for pre-teens, but not teenagers. Parental support, therefore, should be harnessed to its maximum potential in clinical interventions for pre-teenagers, but more diverse strategies may need to be implemented for older youth. Moreover, when intervening with populations who experience early-life adversity, caution needs to be taken in assuming that social support is comparably beneficial. The full manifestation of social stress-buffering effects during childhood and adolescence may not be evident, a possibility in need of more comprehensive investigation. Other strategies that serve as a buffer to stress reactivity and its negative consequences need to be created and systematically tested, especially ones that are tailored for adolescents. The results will lay a foundation for better interventions that target the developmental period when children and teens are most receptive to the potential benefits.
References
American Psychological Association (2013). Stress in America Survey.
Gunnar, M. R., Brodersen, L., Nachmias, M., Buss, K., & Rigatuso, R. (1996). Stress reactivity and attachment security. Developmental Psychobiology, 29, 191-204.
Hostinar, C. E., Johnson, A. E., & Gunnar, M. R. (2014). Parent support is less effective in buffering cortisol stress responses for adolescents compared to children. Developmental Science. [Epub ahead of print] doi: 10.1111/desc.12195.
Hostinar, C. E., Sullivan, R. M., & Gunnar, M. R. (2014). Psychobiological mechanisms underlying the social buffering of the HPA axis: A review of animal models and human studies across development. Psychological Bulletin®, 140(1), 256-82. doi: 10.1037/a0032671.
Kirschbaum, C., Klauer, T., Filipp, S. H., & Hellhammer, D. H. (1995). Sex-specific effects of social support on cortisol and subjective responses to acute psychological stress. Psychosomatic Medicine, 57, 23-31.
Merikangas, K. R., He, J. P., Burstein, M., Swanson, S. A., Avenevoli, S., Cui, L., … Swendsen, J. (2010). Lifetime prevalence of mental disorders in U.S. adolescents: Results from the National Comorbidity Survey Replication –Adolescent Supplement (NCS-A). Journal of the American Academy of Child and Adolescent Psychiatry, 49(10), 980-9. doi:10.1016/j.jaac.2010.05.017.
Romeo, R. D. (2010). Pubertal maturation and programming of hypothalamic-pituitary-adrenal reactivity. Frontiers in Neuroendocrinology, 31(2), 232–40. doi:10.1016/j.yfrne.2010.02.004
Toth, E., Gersner, R., Wilf-Yarkoni, A., Raizel, H., Dar, D. E., Richter-Levin, G., … Zangen, A. (2008). Age-dependent effects of chronic stress on brain plasticity and depressive behavior. Journal of Neurochemistry, 107(2), 522–32. doi:10.1111/j.1471-4159.2008.05642.x