Lifetime Adversity – Inflammation – CRP Levels
A recent study published in Brain, Behavior and Immunity suggests that adversity during childhood and trauma during adulthood are associated with elevated high sensitivity C-reactive protein (hsCRP).
This is perhaps the first large population-based study to assess the connection between adulthood trauma exposure and inflammation.
Strong evidence links childhood stress exposure with adverse health outcomes. Adversity in childhood increases risk for adult-onset mood and anxiety disorders in the general population, and depression and post-traumatic stress disorder (PTSD) in military personnel.
Childhood adversities also increase risk for physical illnesses including cardiovascular disease, diabetes, and metabolic disorders. Among adults, those with combat or non-combat trauma exposure had an increased rate of psychiatric disorders and physical illnesses including heart failure, stroke, and autoimmune disorders.
The biological mechanisms underlying the link between trauma and poor health are not well understood, but there is evidence that inflammation may play a key role. Emerging evidence indicates that elevated inflammation is associated with psychopathology. Large bodies of research now link depressive and anxiety disorders with elevated levels of inflammation.
PTSD has also been linked with elevated levels of inflammatory markers, including C-reactive protein (CRP) and higher levels of CRP predicted risk for PTSD symptoms in a prospective study of 2610 war zone–deployed marines.
Both childhood adversity and specific types of adulthood trauma exposure have been associated with elevated levels of systemic inflammation. Childhood maltreatment has been linked with elevated levels of high sensitivity C-reactive protein (hsCRP) in participants 20 years later.
Similarly, childhood adversity, defined as having experienced one or more unusually stressful events in childhood, has been associated with elevated adulthood levels of systemic inflammation.
Of note, childhood adversity appears to increase vulnerability to the effects of later stressful events. For example, stress sensitization models hypothesize that childhood adversity may sensitize individuals to psychiatric psychopathology by lowering their tolerance to later stressors.
In the Brain, Behavior and Immunity study over 11,000 adults ranging from age 59 to 79 years participated in the Health and Retirement Study. Subjects were screened for childhood adversity by reporting whether they had experienced repeating a year of school, having parents with drug or alcohol problems, or being physically abused before the age of 18 years.
Subjects then reported if, after age 18, they had experienced any of seven traumatic life events: death of a child, natural disaster, combat, having a family member addicted to drugs or alcohol, being assaulted, having a life-threatening illness or accident or having a spouse or child with such. Data were adjusted for age, gender, race, education, year of collection, and other possible confounders.
Joy E. Lin et al. from the School of Medicine, University of California, San Francisco, USA report that childhood adversity and adulthood trauma were independently associated with elevated levels of hsCRP, while subjects who had experienced both had higher hsCRP levels as compared to subjects with a history of adulthood trauma only. Of note, subjects who had experienced childhood adversity also had increased prevalence of adulthood trauma.
It is known that childhood and adulthood stress is associated with higher risk for physical illness such as cardiovascular disease, diabetes, and even autoimmunity.
The mechanisms are not well-understood, however, although chronic low-grade inflammation is thought to play a role based on studies of patients with depression, anxiety and post-traumatic stress disorder. While hsCRP is a nonspecific marker in and of itself, it is an easy way to detect low levels of inflammation.
The association of both childhood adversity and adulthood trauma with elevated inflammation, reported in this study, could be linked to mechanisms underlying the increased morbidity and/or mortality in subgroups of stress-exposed individuals.
Large population-based studies such as the present study help establish associations which in turn can direct further investigation into molecular mechanisms and risk modifiers, eventually contributing to individual patient care.
Source: Brain Behav Immun. 2016 Mar; 53:105-12. doi: 10.1016/j.bbi.2015.11.015. Epub 2015 Nov 23
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