Stressful early life experiences and immune dysregulation across the lifespan

doi:10.1016/j.bbi.2012.06.014

Brain, Behavior, and Immunity

Volume 27, January 2013, Pages 8-12

https://doi.org/10.1016/j.bbi.2012.06.014 Get rights and content

Abstract

There is considerable evidence that stressful early life events influence a variety of physical health problems later in life. Childhood adversity has been linked to elevated rates of morbidity and mortality from a number of chronic diseases. Immune dysregulation may be one potential pathway that explains this link. In this mini-review, we summarize human studies demonstrating that severe early life stressors have lasting immune consequences. We propose a model outlining potential biobehavioral pathways that explain how early life stressors leave people vulnerable to these maladaptive outcomes. Finally, we suggest ideas for future work to test different aspects of this model.

Highlight

► Stressful early life experiences make people more vulnerable to immune dysregulation in adulthood.

Introduction

There is mounting evidence that stressful early life events influence a variety of physical health problems later in life. Indeed, childhood adversity has been linked to elevated rates of morbidity and mortality from a number of chronic diseases (Miller et al., 2011). For example, people who experienced severe life stressors as children (e.g., abuse, neglect, family conflict, low socioeconomic conditions) are at greater risk factor for cardiovascular disease, type II diabetes, cancer, and a variety of somatic difficulties than those who did not have these early life experiences (Miller et al., 2011). Although adults who experienced early life adversity often have poor health practices, the connection between severe psychological stress early in life and adult health exists even after accounting for these factors (Miller et al., 2011).

The pathways linking early adversity to adult health are clearly multifaceted. They include both behavioral and physiological components. Emerging evidence suggests that immune dysregulation may be one potential pathway linking stressful early life events to physical health problems.

In this mini-review, we summarize work demonstrating that severe early life stressors explain some of the variation in immune responses seen in adults. Specifically, we review work showing that early adversity is associated with elevated inflammation, telomere shortening, latent herpes virus reactivation, and a poorer response to an immunogenic tumor. We focus our review on these four markers because of their links to early adversity. We then propose a model outlining potential biobehavioral pathways that explains how early life stressors leave people vulnerable to these maladaptive outcomes. Finally, we suggest ideas for future work to test different aspects of this model. Because of space constraints, the focus of our review is entirely on human studies.

Section snippets

Inflammation

Inflammation has well-documented associations with early life stress. Inflammation is a risk factor for cardiovascular disease, type II diabetes, osteoporosis, periodontal disease, and rheumatoid arthritis (Ershler and Keller, 2000, Libby, 2007). Children who were maltreated have elevated inflammation compared with those who were not maltreated (Danese et al., 2010). This association persists in adulthood. For example, in a large-scale longitudinal prospective study, those who were neglected

Mechanisms

In sum, severe early life stress may have lasting long-term consequences for immune dysregulation. There are likely many different mechanisms that underlie these associations. Adults who experienced severe stressors as children are more likely to develop poorer health habits, including poorer sleep patterns and nutrition, less exercise, and greater alcohol and cigarette use (Miller et al., 2011). The effects appear to remain significant even after controlling for health behaviors (Miller et

Future directions

In sum, our model suggests that those who experienced severe early life events are at greater risk for immune dysregulation compared with those who did not experience such adversities because they (a) are more psychologically and physiological sensitive to stress, and (b) have fewer social and psychological resources available to help them cope with stress. Accordingly, they exhibit greater immune dysregulation. Although evidence supports different aspects of this model, more research is

Acknowledgments

Work on this paper was supported in part by NIH Grants CA131029, CA126857, the Kathryn & Gilbert Mitchell endowment, the S. Robert Davis endowment, and an American Cancer Society Postdoctoral Fellowship Grant PF-11-007-01-CPPB.

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Invited ReviewStressful early life experiences and immune dysregulation across the lifespan

Abstract

Highlight

Introduction

Section snippets

Inflammation

Mechanisms

Future directions

Acknowledgments

Brain, Behavior, and Immunity

Brain, Behavior, and Immunity

Biological Psychiatry

Biological Psychiatry

Biological Psychology

Telomeres and human aging: facts and fibs

Science of Aging, Knowledge, and Environment

A mechanism converting psychosocial stress into mononuclear cell activation

Proceedings of the National Academy of Sciences of the United States of America

Association between plasma IL-6 response to acute stress and early-life adversity in healthy adults

Neuropsychopharmacology

Maternal warmth buffers the effects of low early-life socioeconomic status on pro-inflammatory signaling in adulthood

Molecular Psychiatry

Epigenetics, brain, behavior, and the environment

Hormones

Biological embedding of stress through inflammation processes in childhood

Molecular Psychiatry

Childhood maltreatment predicts adult inflammation in a life-course study

Proceedings of the National Academy of Sciences

A growth curve analysis of the course of dysthymic disorder: the effects of chronic stress and moderation by adverse parent-child relationships and family history

Journal of Consulting and Clinical Psychology

Family poverty is associated with cytomegalovirus antibody titers in US children

Health Psychology

Accelerated telomere shortening in response to life stress

Proceedings of the National Academy of Sciences of the United States of America

Age-associated increased interleukin-6 gene expression, late-life diseases, and frailty

Annual Review of Medicine

Relationships and inflammation across the lifespan: Social developmental pathways to disease

Social and Personality Psychology Compass

Basal cell carcinoma: stressful life events and the tumor environment

Archives of General Psychiatry

Stress-induced immune dysfunction: Implications for health

Nature Reviews Immunology

Invited Review
Stressful early life experiences and immune dysregulation across the lifespan