27 05 2015
Childhood trauma contribute enormously to mental health problems in the society. Understanding the brain /psychological mechanisms mediating such effects are crucial to help us develop interventions. Low BDNF levels are associated with childhood trauma among adults with mental disorders. It is also noted that trauma interact with BDNF val66 met polymorphism, where met allele carriers are at higher risk. Another pathway to consider is cytokines, where trauma might be activating and maintaining elevated levels of inflammatory cytokines.
Adults with a history of childhood trauma and psychiatric disorders show decrease in BDNF and increase in cytokines levels. A history of childhood trauma may set in changes in immune system functioning i.e. leading to a permanent chronic inflammatory state . Lower BDNF expression in adulthood is related to poorer cognitive performance smaller hippocampal volumes , and increased psychiatric comorbidity .
Do trauma lead to early detectable changes in BDNF and cytokines? Bucker J et al report the results of a study asking this question.
Children who experienced early trauma ( i.e. trauma before age 4) were recruited from a foster home and child protection programme in South Brazil. They were between the ages of 3 and 12. A matching control group was also recruited. A structured interview identified psychiatric diagnosis ( in accordance with DSM-IV criteria (K-SADS-E)). Socio demographic variables as well as trauma history were collected in detail. BDNF plasma levels were measured by ELISA. Concentration of plasma cytokines were determined by flow cytometry.
There were 36 children with trauma and 26 children without trauma. Both groups were comparable in age gender, IQ and education years. Trauma groups BMI was higher. Half of the children in trauma group had been exposed to more than one type of trauma. 20% reported sexual abuse. 75% of trauma group had subsyndromal psychiatric symptoms.
Trauma group showed significant high levels of BDNF and TNF Alpha, when controlled for previous infection status. This is in contrast to the finding of lower BDNF in adults who experienced child hood trauma. This may be a compensatory mechanism that is activated in response to trauma. It is possible that it may reflect the resilience mechanims, given that the children are away from traumatic environment and that they currently do to have any psychiatric diagnosis. To check whether being in a safer environment was the reason for higher BDNF, authors checked the relationship between the ‘ time since trauma cessation’ and BDNF levels . No relationship was observed between these two.
The small sample size means that study lacks statistical power for subanalyses. Absence of a specific instrument to quantify aspects such as the severity and intensity of trauma is another limitation. The control group can be described as ‘supernormal’ due to the fact that they included only children without psychiatric symptoms.
Trauma during childhood sets in motion biological changes that are detectable early on. Observed changes indicate effect on neural plasticity and inflammation. Changes observed in children ( in case of BDNF) are different from that in adults. Further research is needed to see why some of those exposed to trauma show better outcomes than others, and to determine vulnerability/ safety ‘windows’ in relation to age of trauma.
Summary of the article:
Bücker J, Fries GR, Kapczinski F, Post RM, Yatham LN, Vianna P, Bogo Chies JA, Gama CS, Magalhães PV, Aguiar BW, Pfaffenseller B, Kauer-Sant’Anna M. Acta Psychiatr Scand. 2015 May;131(5):360-8.