Early Life Adversity Accelerates Child-Adolescent Development - Papers & Essays



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Early Life Adversity Accelerates Child-Adolescent Development

Most developmental thinking regards adverse developmental experiences (e.g., harsh parenting) and environmental exposures (e.g., poverty) as factors and forces that undermine developmental well-being. And this is so whether thinking in terms of attachment theory, social-learning theory, life-course sociological theory and other developmental perspectives as well. Here I consider an alternative—or complement—to this prevailing viewpoint, contending that adversity—or at least certain kinds—can accelerate development, while viewing relevant evidence through an evolutionary-developmental (evo-devo) lens. "Accelerated" here does not mean precocious in any positive—or negative—sense of the term; it simply refers to developmental phenomena occurring earlier than otherwise would be the case.

Evolutionary life-history theory calls attention to the regulatory effects of both early-life experiences and concurrent life conditions. Where it differs from traditional developmental models—and informs us—is in how it regards the nature of environmental effects. Rather than guided by an implicit, if not explicit, health model emphasizing "optimal" or healthy development versus dysfunction/dysregulation/disorder, it casts environmental effects in adaptive terms. Effects of varying early-life conditions, then, are not considered inherently better or worse so much as facilitating the dispersion of genes in future generations.

Belsky and associates (1991) drew on this evolutionary perspective when positing that early-life adversity (e.g., marital conflict, hostile parenting) would not only foster an opportunistic, advantage-taking social orientation, consistent with traditional theories, but that it would also accelerate pubertal—and thus reproductive—development. Why? Because in a high-risk world this should increase the chance of the individual reproducing, the ultimate goal of all living things, before dying or becoming seriously compromised. Ever since the early 1990s, evidence has emerged consistent with theorizing that early-life adversity would predict accelerated pubertal development, especially in females (Belsky, 2012). Herein I summarize mostly very recent evidence of adversity-induced accelerations in other domains of biological development (Belsky, 2019).


Pubertal development is a highly complex physiological process, indeed, one still not fully understood. Suggestive evidence indicates that the "coupling" of two hormones—cortisol, a product of the hypothalamic-pituitary-adrenal axis, and testosterone, a product of the hypothalamic-pituitary-gonadal axis—not only changes with development, but can be affected by early-life conditions. Although it is well established that cortisol and testosterone are inversely or negatively correlated in adulthood (i.e., one high, the other low) due to the reciprocal gonodal hormone suppression of the HPA and HPG axes, two new findings are especially noteworthy. First, such hormonal "coupling" changes from childhood to adolescence, going from positively to negatively correlated, especially in girls (Matchock et al., 2007). Second, this change to the adult coupling pattern occurs earlier—and is more pronounced—for girls exposed to early-life adversity (i.e., parental depression, family anger) than non-exposed age-mates (Ruttle et al., 2015).

Cellular Aging

Two different genetic indicators of cellular aging provide evidence of accelerating effects of adversity.


Telomeres play a critical role in the maintenance of chromosomal integrity. They consist of repeated DNA sequences that cap and protect eukaryotic chromosomes. With increasing age telomeres shorten substantially, thus making telomere length a biomarker of biological aging. Especially notable, then, are repeated findings that prenatal stress predicts shorter telomeres at birth, as does growing up in an extremely deprived Romanian orphanage *1 (Humphreys et al., 2016). Perhaps even more compelling is longitudinal evidence that exposure to family or neighborhood violence in middle childhood forecasts accelerated erosion or shortening of telomeres from age 5 to 10 years.

Epigenetic Aging

In order for a person's genes to affect development, they must be expressed; this means, that whether or not our particular genes come to influence us, will depend on whether or not they are expressed. Epigenetics is the study of genetic expression. As, it turns out, early-life experiences can affect the expression of genes. But it is also the case that as we age, gene expression can change. Indeed, a subset of genes are "turned off" by a chemical process of methylation so reliably as we age, that their condition can be used to create an index of biological aging. Thus, two individuals could be of the exact same chronological age, say 45 years old, but of different biological ages, with one being 43 and the other 47. Notably, early-life adversity appears to speed up the methylation of the subset of genes that index biological age. Such accelerated biological development has been observed in response to exposure to violence and sexual abuse.

Brain Development

Neuroscience also provides evidence of accelerated development following early-life adversity, this time involving connections between the amygdala and prefrontal cortex, particularly medial regions. Whereas the amygadala is involved in emotional responsiveness, the prefrontal cortex is involved in regulating, controlling and planning behavior. Notably, exposure to institutional care, traumatic experiences, and harsh parenting have each been found to foster more adult-like connections between these two brain regions.


As summarized herein, there is repeated indication across a number of biological systems that being maltreated, exposed to poverty, growing up in a conflicted family or violent neighborhood or, perhaps worse, in an understaffed orphanage, can accelerate certain aspects of development. Such discoveries take on additional importance when it is appreciated that both early-life adversity and accelerated biological development are themselves associated with increased morbidity and mortality risk later in life.

These observations raise the question of why development would operate this way—being accelerated in childhood in the face of adverse conditions and associated with increased risk of poor health or even an early death later in life. Because of the central importance of reproduction, evolutionary-minded theorists interpret these apparent consequences of growing up under conditions of adversity as evidence of a "trade-off", not simply as adversity-induced wear and tear on the developing individual that undermines well-being. Compromised health and longevity, evo-devo thinkers contend, are a "cost" natural selection has imposed—or at least accepted—in exchange for the benefit of increasing the chances of reproducing.

This evo-devo understanding of accelerated developments considered should reinforce efforts to reduce children's exposure to adversity, while also encouraging us to think differently about human development. For too long we have viewed children through the lens of romantic idealism rather than of evolution. Darwinian natural selection has not crafted children to be secure, curious, caring and achievement striving—unless contextual conditions and/or genetic make-up incline them to be so. Under other developmental and genetic conditions, children should—and do—develop differently. Often these alternative ways of functioning are evolutionarily, biologically, and even psychologically strategic, not disturbed or disordered, even if this is not widely appreciated or in line with more traditional ways of thinking. Thus, treating accelerations as "natural" and evolved responses to certain adverse developmental experiences and exposures, just like many delays and other developmental difficulties, brings us closer to an understanding of the nature of development. So if we don't want this evolved developmental wisdom to manifest itself—in accelerated development and poor physical and mental health as a result of particular early-life adversities—then we need to change the contextual conditions that give rise to it.

  • *1 During and even after communist times in Romania, many children were put in orphanages, referred to here as "institutions", which were poorly staffed by untrained caregivers who had far too many very young children, from birth upwards, to care for. Indeed, the quality of care was quite terrible. Much post-communism research revealed children in these institutions were very much developmentally delayed as a result of the poor care they received.


    • Belsky, J. (2012). The development of human reproductive strategies progress and prospects. Current Directions in Psychological Science, 21(5), 310-316.
    • Belsky, J. (2019). Early Life Adversity Accelerates Child-Adolescent Development. Current Directions in Psychological Science, 28, 241-246. Belsky, J., & Pluess, M. (2013). Beyond risk, resilience, and dysregulation: Phenotypic plasticity and human development. Development and Psychopathology, 25, 1243-1261.
    • Belsky, J., Steinberg, L., & Draper, P. (1991). Childhood experience, interpersonal development, and reproductive strategy: An evolutionary theory of socialization. Child Development, 62(4), 647-670.
    • Humphreys, K. L., Esteves, K., Zeanah, C. H., Fox, N. A.,Nelson, C. A., & Drury, S. S. (2016). Accelerated telomere shortening: Tracking the lasting impact of early institutional care at the cellular level. Psychiatry Research, 346, 95-100. doi:10.1016/j.psychres.2016.09.023

    Recommended Readings

    • Belsky, J., & Shalev, I. (2016). See reference list. Reviews theory of and evidence for an evolutionary trade-off between adversity-induced accelerated development and increased morbidity and mortality.
    • Janovic et al. (2017). See reference list. Provides evidence that exposure to violence accelerates epigenetic aging.
    • Thijssen, S., et al. (2017). See reference list. Provides evidence that insensitive parenting accelerates the development of the amygdala-medial prefrontal cortex circuit.
Jay_Belsky.jpg Jay Belsky

Jay Belsky is Robert M. and Natalie Reid Dorn Professor of Human Development at the University of California, Davis. Dr. Belsky is a nationally and internationally recognized expert in the field of child development and family studies. His areas of special expertise are the effects of day care, parent-­child relations during the infancy and early childhood years, the transition to parenthood, the etiology of child maltreatment and the evolutionary basis of parent and child functioning. He is the author of more than 400 scientific articles and chapters and of several books. Jay received his B.A. from Vassar College (1974) where he majored in Psychology and his M.S. in Child Development (1976) and Ph.D. in Human Development and Family Studies (1978) from Cornell University. He spent the first 21 years of his career at Penn State University, rising to the rank of Distinguished Professor before moving to London where he worked for 12 years as Professor of Psychology and founding Director of the Institute for the Study of Children, Families and Social Issues at Birkbeck University of London. He moved to California to assume his current position in 2011.