Cumulative Childhood Stress and Autoimmune Diseases in Adults

Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Division of Adult and Community Health, 4770 Buford Highway, N.E., MS K-50, Atlanta, GA 30341-3717, USA.
Psychosomatic Medicine (Impact Factor: 3.47). 02/2009; 71(2):243-50. DOI: 10.1097/PSY.0b013e3181907888
Source: PubMed


To examine whether childhood traumatic stress increased the risk of developing autoimmune diseases as an adult.
Retrospective cohort study of 15,357 adult health maintenance organization members enrolled in the Adverse Childhood Experiences (ACEs) Study from 1995 to 1997 in San Diego, California, and eligible for follow-up through 2005. ACEs included childhood physical, emotional, or sexual abuse; witnessing domestic violence; growing up with household substance abuse, mental illness, parental divorce, and/or an incarcerated household member. The total number of ACEs (ACE Score range = 0-8) was used as a measure of cumulative childhood stress. The outcome was hospitalizations for any of 21 selected autoimmune diseases and 4 immunopathology groupings: T- helper 1 (Th1) (e.g., idiopathic myocarditis); T-helper 2 (Th2) (e.g., myasthenia gravis); Th2 rheumatic (e.g., rheumatoid arthritis); and mixed Th1/Th2 (e.g., autoimmune hemolytic anemia).
Sixty-four percent reported at least one ACE. The event rate (per 10,000 person-years) for a first hospitalization with any autoimmune disease was 31.4 in women and 34.4 in men. First hospitalizations for any autoimmune disease increased with increasing number of ACEs (p < .05). Compared with persons with no ACEs, persons with >or=2 ACEs were at a 70% increased risk for hospitalizations with Th1, 80% increased risk for Th2, and 100% increased risk for rheumatic diseases (p < .05).
Childhood traumatic stress increased the likelihood of hospitalization with a diagnosed autoimmune disease decades into adulthood. These findings are consistent with recent biological studies on the impact of early life stress on subsequent inflammatory responses.

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Available from: William S Pearson
    • "Exposure to childhood trauma is associated with a host of negative outcomes, including, but not limited to, post-traumatic stress disorder (PTSD). As demonstrated in investigations such as the Adverse Childhood Experiences (ACE) study (Felitti et al. 1998; Anda et al. 2006; Dube et al. 2009), childhood adversity has been associated with adult outcomes, such as suicide, depression, alcohol use, drug use, and physical consequences, such as autoimmune disorders. The term 'toxic stress' has been used to describe multiple chronic stressors in childhood, including abuse, neglect , parental substance use, or parental depression, which may lead to changes in learning, behavior, and physiology that have an impact throughout adulthood (Garner & Shonkoff, 2012; Shonkoff & Garner, 2012). "
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    ABSTRACT: To develop latent classes of exposure to traumatic experiences before the age of 13 years in an urban community sample and to use these latent classes to predict the development of negative behavioral outcomes in adolescence and young adulthood. A total of 1815 participants in an epidemiologically based, randomized field trial as children completed comprehensive psychiatric assessments as young adults. Reported experiences of nine traumatic experiences before age 13 years were used in a latent class analysis to create latent profiles of traumatic experiences. Latent classes were used to predict psychiatric outcomes at age ⩾13 years, criminal convictions, physical health problems and traumatic experiences reported in young adulthood. Three latent classes of childhood traumatic experiences were supported by the data. One class (8% of sample), primarily female, was characterized by experiences of sexual assault and reported significantly higher rates of a range of psychiatric outcomes by young adulthood. Another class (8%), primarily male, was characterized by experiences of violence exposure and reported higher levels of antisocial personality disorder and post-traumatic stress. The final class (84%) reported low levels of childhood traumatic experiences. Parental psychopathology was related to membership in the sexual assault group. Classes of childhood traumatic experiences predict specific psychiatric and behavioral outcomes in adolescence and young adulthood. The long-term adverse effects of childhood traumas are primarily concentrated in victims of sexual and non-sexual violence. Gender emerged as a key covariate in the classes of trauma exposure and outcomes.
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    • "Furthermore, women abused as children are more likely to produce children with autism [20]. Stressors experienced during childhood have been associated with the subsequent onset of wheezing in children between birth and one year as well as inhibiting specific immune responses toward vaccines [5] [21] [22] [23] [24]. "

    Full-text · Article · Jan 2015
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    • "Rearing environments that are enriched with good parental care, suitable protection, and engaging sensory stimulation offer resilience to insults later in life such as psychological stressors (Francis et al., 2002) or even pathological infection (Johnson et al., 2014). In contrast, early life adversity (ELA) such as parental deprivation, neglect, abuse, or exposure to threats has been repeatedly shown to yield a myriad of deviations in brain circuitry, stress-responsivity, cognitive function, and general health (Anda et al., 2008; Dube et al., 2009; Brown et al., 2010). In this review, we will discuss the current progress in understanding intervening variables that underlie vulnerability, resilience, and behavior after ELA, with a focus on the evolving knowledge of neuroimmune influences. "
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    ABSTRACT: Exposure to adversity and stress early in development yields vulnerability to mental illnesses throughout the lifespan. Growing evidence suggests that this vulnerability has mechanistic origins involving aberrant development of both neurocircuitry and neuro-immune activity. Here we review the current understanding of when and how stress exposure initiates neuroinflammatory events that interact with brain development. We first review how early life adversity has been associated with various psychopathologies, and how neuroinflammation plays a role in these pathologies. We then summarize data and resultant hypotheses describing how early life adversity may particularly alter neuro-immune development with psychiatric consequences. Finally, we review how sex differences contribute to individualistic vulnerabilities across the lifespan. We submit the importance of understanding how stress during early development might cause outright neural or glial damage, as well as experience-dependent plasticity that may insufficiently prepare an individual for sex-specific or life-stage specific challenges.
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