The study is an extensive analysis that aims to prove that obesity has a mediating role between pregnancy inflammation and childhood trauma. About 25% of children in the US have experienced some type of abuse and neglect. This exposure leaves these children at risk of adverse health outcomes such as depression, migraines and arthritis.
Inflammation poses a health risk to adults and according to psychobiological models, it is greatly affected by childhood trauma. It causes an increase in inflammatory markers during pregnancy that have been linked to preterm birth. Although limited, studies have shown that people who have experienced early trauma have a higher chance of being obese. Given that adipocytes secrete proinflammatory markers such as IL-6 that modulate hepatic C-reactive protein production, obesity is therefore tied to inflammation and is a way of linking early childhood trauma with pregnancy inflammation. To put this to context, obesity that occurs before one gets pregnant has an association with elevation of serum CRP, IL-6 and TNF-α all being markers of inflammation. This situation therefore justifies the need to do investigation on the relation between childhood trauma and its effects of early life exposures on maternal biology.
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Method
Observations and studies where done on seventy-seven women recruited from the Ohio State University Wexner Medical Center (OSUWMC) Prenatal Clinic and the community of Columbus, Ohio. The duration of the study was from 2011 to 2014. The current analyses included women who participated in at least two study visits without the exception of the third visit at which childhood trauma was accessed. In the first study visit, a documented consent was obtained and the participant were sufficiently compensated financially at the completion of each visit.
There were several measures that were used and they include:
Demographics that sought to determine the race, age, marital status, annual household income, education, and number of prior births were collected at the first study visit.
Health behaviors. Smoking, exercise, and prenatal vitamin use were determined and measured via self-report at the first study visit.
Childhood trauma. Here, a 28-item Childhood Trauma Questionnaire was used and included 5 subscales: emotional abuse, physical abuse, sexual abuse, emotional neglect, and physical neglect. Respondents rated each item on a 5-point scale. In this case, CTQ was administered in third visit to reduce the burden of the participants in the other visits and to allow for rapport to be built.
Depressive symptoms were measured using the Centre for Epidemiologic Studies Depression Scale (CES-D). This scale comprises 20 items assessing cognitive, emotional, interpersonal and somatic depressive symptoms.
Blood was collected into vacutainer tubes and CRP, serum IL-6 and TNF-α were tested and extrapolated from a standard curve calculated using a four-parameter logistic fit with MSD work bench 3.0 software.
Statistical Analyses were conducted using two softwares, SPSS 22.0 and SAS 9.4 and the missing data were addressed using the restricted maximum likelihood estimation method. All appropriate markers were log transformed to fit the normality assumption and adjusted for race, income, education, smoking status, medical conditions, and depressive symptoms. To demonstrate the effect of BMI after these adjustments, the statistics were done with and without the BMI inclusion. Process macros were employed to estimate indirect effects and bias-corrected 95% bootstrap confidence intervals based on 10,000 samples.
Results
Study visits were done during early, mid and late pregnancy. Demographic characteristics, health behaviors, and trauma variables for the total sample were tabulated. The average maternal age was 25.58 years, the range was from 18 to 33 years, standard deviation was 4.14 and, 51% were white women.
In the overall sample, CRP showed a significant quadratic effect. IL-6 and TNF-α also, increased between the early and mid-pregnancy but remained constant between the mid to late pregnancy. Higher levels of CRP were associated with emotional abuse, physical abuse and emotional neglect and these effects remained even after adjusting for income, race, education, smoking status, medical conditions, and depressive symptoms. However, as in the null hypothesis, the addition of BMI in type 3 models made the effects of emotional abuse and physical abuse less significant supporting a mediating role for BMI in the association between childhood trauma and elevated CRP. The most significant effect of emotional neglect reduced with inclusion of BMI but remained significant.
Linear mixed models were conducted to examine whether exposure to abuse or neglect affected the IL-6 levels across pregnancy and no significant effects were observed in relation to the CTQ subscales. Similarly, they were conducted to determine whether exposure to abuse or neglect affected TNF-α and no significant effects were observed in relation to CTQ subscales.
Process models were examined for each model to determine the mediating role of obesity between childhood trauma and inflammation. All the different demographics were included in these analyses as covariates. Significant indirect effect findings remained when the respective inflammatory marker at each timepoint was used as opposed to an average value across pregnancy. BMI did not serve as a mediator in other models.
Discussion
In this study of pregnant women, childhood trauma predicted an elevated CRP. These effects persisted even after inclusion of demographics such as race, income, smoking status and depressive symptoms. These revelations remain even in studies linking childhood trauma with elevated CRP and IL-6 in non-pregnant. In contrast, the association between childhood trauma and TNF-α was not replicated. On the basis of two studies, the first one being on 145 racially diverse women assessed at mid and late pregnancy, greater lifetime exposure to traumatic events resulted in elevated serum TNF-α but not IL-6. For the second one, 133 Latina adolescents assessed at mid and late pregnancy showed interaction between child abuse exposure and depression in predicting serum IL-6.
Prior studies have linked childhood abuse and neglect with prepregnancy overweight and obesity. Moreover, a study on nonpregnant women observed associations between child abuse and neglect exposure with increased levels of serum CRP were mediated by BMI. Linear mixed models concurred with this however, this was not supported in a more robust PROCESS analysis. Therefore, mitigating the effects of trauma could be done by intervening and targeting maternal obesity.
Childhood period is the period where human beings are the most vulnerable during which exposure to stressor can have long-term effects on physiology. This early exposure may contribute to epigenetic changes resulting in altered glucocorticoid receptor functioning which play a vital role in regulating inflammation. This alteration is likely to sustain dysregulated patterns of functioning. As such, HPA dysregulation provides a pathway in which inflammation is linked to childhood trauma. Moreover, it also increases risk to obesity as administration of corticotropin releasing hormone (CRH) increases consumption of calorie intake. Childhood trauma exposure is likely to cause eating disorder and poorer sleep quality, both risk factors of obesity.
In this study, it is noted that relationship between physical abuse and inflammation is best described as indirect through prepregnancy BMI vs direct. Therefore, it suggests that inclusion and evaluation of obesity status is necessary in determining the right clinical interventions to inflammation. Also, in literature, some data show that relationships between emotional and sexual abuse with prepregnancy obesity did not emerge, aligning with findings of this study. These findings are: while emotional abuse and neglect were directly associated with CRP, these effects were not mediated by prepregnancy BMI.
Conclusion
The study shares some eye-opening insights on inflammation that occur during different stages of pregnancy. Inflammation during pregnancy is a common occurrence and this study offers a new perspective to view this issue. I would use this information by changing my approach to negative perinatal effects by first addressing maternal obesity just before pregnancy.
References
Amanda, M., Lisa, M. & Kyle, P., Examination of the Role of Obesity in the Association Between Childhood Trauma and Inflammation During Pregnancy. Health Psychology, 37(2), 114-124.doi: http://dx.doi.org/10.1037/hea0000559
Choi, K. W., & Sikkema, K. J. (2016). Childhood Maltreatment and Perinatal Mood and Anxiety disorders a Systematic Review. Trauma Violence & Abuse, 17, 427-453.
Christian, L. M. (2015). Stress and Immune function during Pregnancy: An emerging focus in mind-body medicine. Current Directions in Psychological Science, 24, 3-9.
