Developmental Programming of Shyness: A Longitudinal, Prospective Study Across Four Decades

• In Event: 3-160 - Developmental Models of Shyness: Origins, Maintenance, and Outcomes

Integrative Statement

Developmental programming hypotheses posit that individuals who are exposed to prenatal and early postnatal stressors may have altered maturation of central and peripheral physiological systems responsible for temperament and personality (Gartstein & Skinner, 2017). One ubiquitous temperamental characteristic that may be particularly relevant to study in the context of developmental programming is shyness. Shyness is a trait characterized by fear and inhibition in response to social novelty and/or situations of perceived social-evaluation (Melchior & Cheek, 1990).

Previous work has shown that exposure to prenatal adversity can increase the sensitivity of the hypothalamic–pituitary–adrenal (HPA) axis and amygdala, which are responsible for stress-reactivity and detection of fearful or threatening stimuli, respectively (Gluckman, Hanson, & Buklijas, 2010). Likewise, shyness is characterized by physiological and behavioral stress-reactivity, as well as increased detection of threat-related stimuli. Thus, it is possible that the experience of early adversity may result in alterations in stress response systems that underlie the development of shyness. However, to date, not work has examined the influence of prenatal exposures on the etiology and trajectory of shyness within a longitudinal, developmental framework.

In the present longitudinal, prospective study, we examined trajectories of shyness from childhood to adulthood in three groups of individuals (N=254) with varying degrees of prenatal adversity as indicated by the number of stressful exposures: extremely low birth weight (ELBW; <1000 grams) survivors prenatally exposed to exogenous corticosteroids (ELBW+S; n=56); ELBW survivors not prenatally exposed to exogenous corticosteroids (ELBW+NS; n=56); and normal birth weight (NBW; n=142) controls. Shyness was assessed using questionnaires administered across four assessments corresponding to childhood, adolescence, young adulthood, and adulthood (age 8, age 14, age 23, age 32). We used multilevel modeling to examine if birth weight status and corticosteroid exposure influenced the mean-level trajectory of shyness from age 8 to 32 years, adjusting for intellectual quotient, socioeconomic status, and sex.
Results indicated that ELBW+S participants had significantly higher levels of shyness in childhood relative to the ELBW+NS participants (β = 0.42; p < .05), with a stable trajectory into adulthood (as indicated by a non-significant slope: β = -0.01; p = ns). The NBW and ELBW+NS participants did not significantly differ on childhood shyness (β = 0.45; p = ns), but there was divergence in shyness levels from childhood to adulthood in the ELBW+NS and NBW participants. As illustrated in Figure 1, the NBW participants demonstrated decreases in shyness into adulthood relative to the ELBW+NS participants (β = -0.01; p < .05) who displayed relative increases, with levels comparable to the ELBW+S participants by adulthood.

We speculate that individuals exposed to multiple prenatal stressors (i.e., ELBW+S) may be developmentally programmed to be more sensitive to detecting social threat, with one manifestation of this being an early-developing childhood shyness that remains stable into adulthood, while increasing levels of shyness among ELBW+NS individuals may reflect a later-developing shyness influenced more by postnatal social context. We discuss the implications of these findings for understanding the developmental origins and developmental course of human shyness from childhood through adulthood.

Authors

• Kristie L. Poole, McMaster University
  Presenting Author

• Saroj Saigal, McMaster University
  Non-Presenting Author

• Ryan J. Van Lieshout, McMaster University
  Non-Presenting Author

• Louis Schmidt, McMaster University
  Non-Presenting Author