Early Life Stressors Linked to Persistent Inflammation and Endocrine Abnormalities

January 27, 2011 · Posted in Neurobiology, Risk Factors 

Epigenetics is a relatively new area of study that examines changes in DNA regulation and structure that can come about as a result of environmental events, as opposed to the genetic inheritance (DNA sequence) people receive through their parents’ genes.  Epigenetic effects occur when an environmental stressor or chemical causes methyl or acetyl groups to attach to DNA or to histones (around which DNA are wound). These epigenetic changes determine how difficult it is to turn on genes coded in the DNA (see here for more information about the way the environment produces these epigenetic effects).

After the jump: Several studies presented at the 65th Annual Scientific Convention of the Society of Biological Psychiatry earlier this year suggested a link between environmental stress and both inflammation and abnormalities in DNA.
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Researcher Alicia K. Smith of Emory University reported that in a population of African American patients, a history of total life stressors was associated with increases in inflammatory cytokines interleukin 2, interleukin 6, and TNF-alpha. In addition, there was evidence of increased DNA methylation in almost a fifth of 27,578 specific binding sites in the participants with more stress.

A history of trauma in patients experiencing a first episode of psychosis was associated with significant increases in the inflammatory markers c-reactive protein (CRP), interleukin 6, and TNF-alpha, reported Valeria Mondelli of King’s College London.

A history of childhood maltreatment was associated with evidence of inflammation in adults with major depressive disorder, according to a study presented by Sara Zeugmann of the University of Medicine in Berlin.  Neglect was associated with increases in the proteins fibrinogen and resistin, sexual abuse with increases in the protein adiponectin, and physical abuse with increases in TNF-alpha.

A history of childhood physical abuse was associated with decreases in cortisol response to stress in adulthood among healthy women, reported Linda L. Carpenter of Brown University.

A history of neglect was associated with lower levels of CSF ?-endorphin and met-enkephalin in a study presented by Barbara Stanley of Columbia University.  These lower levels were also found among study participants who engaged in repetitive self-injury in adulthood.

Victoria Arango of Columbia University reported that in the brains of suicide victims who had undergone childhood adversity compared with those without such a history, there was evidence of decreased cell replication in the dentate gyrus, a part of the brain that plays a critical role in learning and memory.

Editor’s note:  These data from studies of people converge with data from animal studies that show that early life adversity is associated with reductions in BDNF and neurogenesis and increases in markers of inflammation.  Taken together, these abstracts form an increasingly strong story indicating that a history of early life adversity can have long-lasting neurobiological consequences including inflammation and changes in brain chemistry that can affect the health and behavior of animals and humans throughout their lifetime.

This evidence may shed light on an earlier research question. The data of Banks et al. (published in the Journal of the American Medical Association in 2006) indicated that white males aged 55 to 65 in the British Isles were healthier than their well-matched counterparts in the US. The greater abnormalities in those from the US included a variety of measures, such as increases in blood pressure, hemoglobin A1C (a marker of diabetes and insulin resistance), cholesterol, and triglycerides.  Banks and collaborators did not know the reasons for such findings, but they suggested the possibility of greater exposure to stressful life experiences in the US compared with the British Isles. The new data about the link between early life stressors and later inflammatory processes makes such an explanation at least plausible.

These data also indicate that individuals who never receive a formal diagnosis of post-traumatic stress disorder (PTSD) can still have long-lasting neurobiological consequences from adverse environmental experiences they have experienced.


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