Chronic stress in childhood, adolescence and adulthood has been associated with increased rates of physical health problems and psychological disorders (Repetti, Taylor, & Seeman, 2002). As adolescence has been characterized by increased rates of mental health problems, increased attention has focused on mechanisms by which adolescents can be buffered from stressors. I am interested in the extent to which parents and friends can reduce responses to stress, which is termed social buffering.
My work focuses on the hypothalamic-pituitary-adrenal (HPA) axis because it is central to the stress response system. Social buffering of the HPA axis by parents has been demonstrated as early as infancy (Gunnar & Donzella, 2002). My work with my colleagues has shown that parental buffering is observed in later childhood among pre-pubertal children, but not among those in mid-late puberty (Doom et al., in press). What is not known is whether friends can elicit the stress buffering effect for children, and, if so, whether that effect becomes more potent during adolescence. If social buffering by friends is not effective in adolescence and parents also fail to be able to provide an HPA axis buffer, this may increase the risk of psychopathology.
The precise neurobiological mechanisms behind the social buffering effect are not fully understood. One potential mechanism is oxytocin, a hormone that is known to be stimulated in close social relationships (Carter, 2014). Just like the HPA system, the oxytocin system undergoes significant changes during puberty that might drive alterations in social buffering. My dissertation study will examine associations between parent versus friend support, cortisol reactivity, and oxytocin at two points in development, 9-10 years and 15-16 years, to elucidate whether the oxytocin system should be examined as a contributor to the shift in social buffering. I will test whether social buffering shifts from parents to peers during adolescence or if there is a time during which adolescents are unable to derive benefits from either type of social partner.
Methods
My dissertation study, which is currently underway, builds directly on my previous work. Children will be 9- and 10-years old and the adolescents will be 15- and 16-years old. I will use the Trier Social Stress Test for Children (TSST-C) as the stress task, which involves the participant giving a speech about him or herself and then performing a challenging math task in front of a two-way mirror. They are told that two teachers and the experimenter are watching from behind the mirror to judge their speech and that the speech will be filmed. Half of each age will prepare for the speech with their primary caregiver and half with a friend. A total of 120 participants will be assigned equally for age, sex, and condition (parent/friend). Saliva samples will be collected eight times throughout the session—both before and after the stressor—to measure the stress hormone cortisol. Urine will be collected at the beginning and the end of the session to assess how much oxytocin was produced.
Significance and Future Directions
This study will be the first to examine the effectiveness of parent and best friend support across both childhood and adolescence to understand whether the role of social buffering may switch from parents to best friends across this period. This study will deepen our understanding of peer relationships by gaining insight into whether friends may act as buffers against life stress. If there is a gap between adolescents being buffered by their parents and friends, this could be a period during which stressors are especially potent, having the most detrimental effects on health. As adolescence is a period associated with increased incidence of mental illness, particularly depression, the loss of parental stress buffering during adolescence may play a role as the HPA axis is involved in the onset and maintenance of depression. My future work will build on my dissertation study by focusing on the role of peers as stress buffers in the onset of emotional disorders and substance abuse in adolescence. Investigating whether internalizing and externalizing symptoms are associated with failure of parents and peers to buffer the individual from stress will provide insight into the etiology of psychiatric disorders. The current study will be the first step in this line of research by examining the effectiveness of friends versus parents in buffering physiological responses to stress.
In addition, I am interested in the neurobiological mechanisms by which adolescents transition away from using parents as social buffers. This will be the first study to examine oxytocin across childhood and adolescence in response to different types of support. If oxytocin shows a similar pattern to cortisol in this study, my future work will focus on oxytocin as a potential protective mechanism between social buffering and positive health outcomes. As oxytocin confers protective psychological and physical effects on individuals, administering oxytocin or increasing oxytocin levels naturally through social interaction with others who are effective social buffers may be methods of preventing or alleviating psychopathology.
I would like to thank APA Div. 7 for their generous support in helping me to complete my dissertation study and disseminate my results to the scientific community.
References
Carter C.S. (2014). Oxytocin pathways and the evolution of human behavior. Annual Review of Psychology , 65, 17–39.
Doom, J.R., Hostinar, C.E., VanZomeren-Dohm, A., & Gunnar, M.R. (in press). The roles of puberty and age in explaining the diminished effectiveness of parental buffering of HPA reactivity and recovery in adolescence. Psychoneuroendocrinology.
Gunnar, M.R., & Donzella, B. (2002). Social regulation of the cortisol levels in early human development. Psychoneuroendocrinology, 27 , 199–220.
Repetti, R.L., Taylor, S.E., & Seeman, T.E. (2002). Risky families: family social environments and the mental and physical health of offspring. Psychological Bulletin, 128, 330–366.