Stressful early life experiences and immune dysregulation across the lifespan
Open accessAbstract
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.
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ELA has been linked in human studies and animal experimentation to chronic inflammation and low-level immunosuppression, including impairment of mucosal immunity in children and cellular immunity in adolescents and adults.
“ELA has been linked in human studies and animal experimentation to chronic inflammation [59] and low-level immunosuppression, including impairment of mucosal immunity in children [60] and cellular immunity (e.g., poorer control of latent viral infection) in adolescents [61] and adults [62].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [59]
Section 2.1 (Inflammation; page unavailable) reports elevated inflammation after early-life adversity in human studies, including an association persisting into adulthood. But the Introduction says the review focuses entirely on human studies, so it does not substantiate the sentence’s reference to animal experimentation. The immunosuppression examples carry separate citations and are not assessed as claims attributed to this source. (LLM, conf=0.86)
Experimental — accuracy not yet measuredEarly-life stress is a critical factor in lifelong immune dysregulation.
“early-life stress has been identified as a critical factor in lifelong immune dysregulation.”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [48]
The elevated inflammatory markers in individuals with adverse childhood experiences suggest a sustained pro-inflammatory state.
“Individuals with adverse childhood experiences often exhibit elevated inflammatory markers even decades later, suggesting a sustained pro-inflammatory state [48].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [48]
Individuals with adverse childhood experiences often exhibit elevated inflammatory markers even decades later.
“Individuals with adverse childhood experiences often exhibit elevated inflammatory markers even decades later, suggesting a sustained pro-inflammatory state [48].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [48]
Early-life psychological stress-from abuse, neglect, maltreatment, bullying or low socioeconomic conditions-can intensify neural threat responses, increase inflammatory activity, change immune competence, and produce SCI across the lifespan.
“exposure to psychological stress early in life—for example, in the form of abuse, neglect, maltreatment, bullying or living in a low socioeconomic environment—can heighten neural responses to threat that can upregulate inflammatory activity170, alter immuno-competence and lead to SCI throughout the lifecycle27,169”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [169]
Childhood conditions have a major influence on later metabolic and immune responses, which then drive SCI in adulthood.
“childhood circumstances significantly impact metabolic and immune responses later in life, which in turn promote SCI in adulthood8,26,27,168,169”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [169]
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- Authors
- Fagundes, C. P., Glaser, R., & Kiecolt-Glaser, J. K.
- Affiliations
- The Ohio State University (US)
- Institute for Behavioral Medicine (US)
- Corresponding author
- Fagundes, Christopher P.
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2013-01
- Volume
- 27
- Issue
- 1
- Pages
- 8-12
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC3518756
- OpenAlex
- W2096023481
- Cited by
- 371
- References
- 43
- Citations by year
- 2026: 9 · 2025: 21 · 2024: 33 · 2023: 29 · 2022: 36 · 2021: 39 · 2020: 25 · 2019: 38 · 2018: 31 · 2017: 30 · 2016: 21 · 2015: 30 · 2014: 18 · 2013: 10
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (CA126857, R01CA126857, CA131029, R01CA131029)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Social Sciences › Psychology › Clinical Psychology › Resilience and Mental Health
- Keywords
- early life stress, childhood adversity, immune dysregulation, chronic disease, allostatic load
- MeSH terms
- Adaptation, Psychological, Child, Child Abuse, Humans, Inflammation, Neoplasms, Risk Factors, Stress, Physiological, Stress, Psychological, Epigenesis, Genetic, Telomere Shortening
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