
Assessing for Trauma and ACEs in Behavioral Pediatric Healthcare
The health and well-being of Americans are facing a dangerous decline. This decline includes the emotional, economic and developmental safety of our youth and the future of America. In order to secure health outcomes for the American public, creating well-educated and healthy adult populations who can be active health participants in the global economy, in spite of the viral pandemic, corona-19, COVID-19, is paramount. In 2013 and 2014, policy by the American Pediatric Association, The Center for Child Development at Harvard and Mental Health America published public health policies implicating the future of public education, our nation’s workforce and the state of health care at large. In these reports, advocacy for a new era in public health, which presented information for the system-wide recognition of the new science in neuroscience, molecular biology, genomics, developmental psychology, epidemiology and sociology documenting the insights into human development, adverse childhood experiences, stress and chronic illness be taken to build strong foundational programs in healthcare. Their arguments initiated the conclusive dialogue for all fields in the understanding of the role of toxic stress & trauma in childhood, as antecedents to declining health and chronic illness. The following will represent an investigative response to and in-conjunction with the public health summaries of The American Academy of Pediatrics (2013) & Mental Health America (2016) through a systematic review of the literature on assessing for ACEs in primary and behavioral pediatric care.
Defining Adverse Childhood Experiences
There is well established evidence that childhood adversities such as abuse or neglect can result in lifelong negative health outcomes. This body of evidence has resulted in growing awareness of the concept entitled toxic stress, which is described as the chronic and frequent activation of the stress response from exposure to serious childhood adversity (Dvir, Ford, Hill, & Frazier, 2014). Negative health outcomes for children who experience toxic stress reflect the physiological, epigenetic and cognitive consequences that the brain and body pay for adapting to stressful and traumatic experiences. The Adverse Childhood Experience (ACE) study (Felitti et al, 1988), found a bidirectional relationship between ACEs scores and many leading causes of death in adults including cardiovascular disease. It also found increased on-set for the development of psychiatric disorders like PTSD, depression, psychosis and schizophrenia (Slavich et al.,2019; Felitti et al.,1988). The relationship between ACEs and toxic stress is a major contributor to the foundations of health policy in today’s healthcare initiatives.
The term “ACEs” is an acronym for Adverse Childhood Experiences. It was first developed in
a groundbreaking study conducted in 1995 by the Centers for Disease Control and Kaiser
Permanent. It was also the subject of formal research exploration by Fetilli in 1988. In the
“ACEs” study, three specific kinds of adversity children were exposed to were – abuse, neglect,
physical/ sexual violence and household dysfunction.
The key findings from the study published since are (1) ACEs are quite common, more than two- thirds of the population report experiencing one ACE, and nearly a quarter have experienced three or more. (2) There is a powerful, persistence correlation between the number of ACEs experienced and the chance of poor outcomes later in life, including dramatically increased risk of heart disease, diabetes, obesity, depression, substance abuse, smoking, poor academic achievement, time out of work, and early death (Harvard Center for the Developing Child, 2020).
Population: Where does the Literature Intersect?
All children face and experience moments of diversity and adversity. While trauma may be very significant the impact of a traumatic event can be buffered by pro-social support figures. However, when the trauma is prolonged and severe enough, the impact can be deeply distressing and cause chronic injury. Among these are children faced with contributing social determinants of health including those who are sent to social services, those living in low socioeconomic conditions and those in chronically violent/ hostile environments.
Environment
Environmental factors like violence, low socioeconomic conditions and lack of
nutritional resources impact the development of stress along the spectrum.
Mental Health & Chronic Illness
Chronic Illness is defined as the consequences of low grade inflammation across the life spectrum including physical and psychological ailments. It has been reported that those with higher scores of ACEs, experience low to mild long-term chronic health conditions like depression, suicidality, autoimmune dysregulation, asthma, headaches and neurological deficits like cognitive focus and functioning.
High Levels of Chronic Inflammation
Elevated levels of inflammation are exhibited through biomarkers of proinflammatory cytokines from the myeloid region. These biomarkers can be found in many chronic
illnesses like cancer, autoimmune disorders and neurological disorders are labeled as CRP, TNF-a, IL-10, IL-6, IL-1.
ACEs and Inflammation
Research on the science behind the psychoneuroendocrine system is expansive as it relates to toxic stress aiding in the development of long-term chronic disease, which may be mediated through the secretion of long-lasting inflammation. Understanding inflammation as a major causal factor to the association between ACEs and chronic disease is important when modifying programmatic content, developing novel psychopharmacological therapies (anti-inflammatory), assessing for ACEs and teaching advanced mental health therapies to qualified practitioners.
In studies documenting the understanding of inflammation in relation with ACEs, research found
higher rates of pro-inflammatory biomarkers in individuals who self-reported adverse childhood experiences, including a meta-analysis of women who had undergone childhood sexual abuse (CSA) displaying higher levels of Il-6, CRP and IL-10.Supporting these connections in animal studies, are rats who underwent a postnatal maternal separation protocol during infancy
and showcased increased levels of IL-6 later in the lifespan (Gangley & Brenhouse, 2015; Hennessy et al., 2010). In epidemiological follow-up studies in New Zealand, researchers discovered by following 1,000 participants from birth to 32 years, who showcased episodes of critical maltreatment including abuse, social isolation and economic hardship developing twice as likely consequences to suffer from chronic inflammation in later life (Halaris, 2017). Therefore, the connection between high-inflammation and ACEs is consistent throughout the research literature. Yet, determining the exact biological and physiological role inflammation plays as a specific variable in the association between ACEs and chronic disease is still not quite understood. With scientific literature in neuroscience that can detail the neurological impact of ACEs on the endocrine system, there is little research identifying how activating the long-term stress response can produce negative health risk outcomes and morbidity. However, health risk behaviors are directly mediated by their relationship with childhood abuse (Chartier, Walker, Naimark, 2009). Often, individuals cope with the effects of adult symptoms of childhood trauma by engaging in unhealthy, avoidant behaviors, such as overeating, smoking, and excessive alcohol use (Su et al, 2015). Although, the relationship between health risks and ACEs is highly known, there is little information is given on the development of inflammation & ACEs as pathways to increased risk for negative health outcomes including physical inactivity, poor sleep, poor emotional regulation, dietary decision-making, obesity and race.

Long-term Chronic Inflammation May Have Three Intervention Points
Further research and development into the science of toxic stress is still being administered as it relates to understanding how ACEs and toxic stress create long-term negative outcomes for disease. The immune system is an intricate part of the factors developed in brain behavior and the prevention of infection. The innate immune system serves as an initial defense system to combat an infection (Slavich, 2019) and has traditionally been a source of fighting against foreign bacteria, antibodies and pathogens which protects us from disease. However, due to its complex nature, when the immune system feels threatened, the response to protect against harm is rapid. When the body senses a biological threat, but the innate immune system is insufficient in fighting off the perceived intrusion, the proliferation of pro-inflammatory myeloid cells will be produced and have a wide-ranging effect on mood, cognition, and behavior (Slavich 2019, Irwin 2008). These cells are exceptional for they have the ability to remember the homeostatic event or experience. There in, resulting in the proliferation of low grade cytogenetic attacks across the lifespan. For instance, IL-1 and IL-6 receptors in the brain interrupt the communication between nerve cells and the hippocampus, inhibiting neural pathways to develop in memory and sensitivity to stress (Barrientos et al, 2009). The findings in these studies suggest that stress-induced activation of inflammatory processes can result in increased inflammatory cytokines such as IL-I, which impairs the brain’s ability to invoke neuroplasticity and neurogenesis.When inflammation in the brain is chronic, the impact on neurogenesis and neuronal activity is highly demonstrative. Inflammation does not only have an impact via the effects of proliferation, survival and cell death, but can affect the integration of new neurons into pre-existing neural networks and the cellular properties of the new cells that survive (Slavich, 2019; Haroon,Raison, & Miller, 2011). Therefore with the development of ACEs, neuroplasticity is not a regenerative intervention, causing a cyclical loop between immune activation & behavior. Interventions can be implemented through supporting and co-regulating the child’s immune system with stress reduction techniques and other biotechnological procedures in the field of pediatrics and gut health. However, without social and behavioral implementation, for the meditating variables like behavioral pathways, increased risk for disease will still occur due to confounding factors. With that being said, a biological intervention for a socioecological problem is a binary approach to a multisystems matrix for disease control.
What’s the Best Solution?
If the body is a structured organism working within the context of its environment in relation to susceptibility of disease. Then, stabilizing the child’s environment is a second-test protocol that may serve as a measure to decrease stress activation at the chronic or severe level. With that, integrated behavioral health and pediatric care models must work to help establish basic assessment strategies to increase the stability of the child’s home life. Understanding the specific population barriers for accepting treatment of integrated care models for psychotherapy and stress reduction is a key initiative in disrupting the behavioral pathways prolonging chronically inflamed children and adolescents. Using a change and intervention model, it is important to implement family-based interventions at early stages of child development including the prenatal and perinatal stage. Beyond assessing ACEs in pediatric healthcare, increasing awareness of the science and brian damage of adverse childhood effects for mothers and fathers having children is a best-case intervention for establishing lines of family and marriage counseling and the integration of childhood pediatrics. Utilizing different change models will be essential in helping to combat the effects of ACEs which could include the transtheoretical model of change at the micro-level within the counseling room and then outwards models to help implement education strategies to mothers regarding the devastating impact that ACEs has on the family unit and the long-term health outcomes of the individual. Implementing social norms theory could be another solution to help mitigate and motivate individuals to integrate and screen for ACEs in childhood pediatrics while implementing therapeutic interventions to help stabilize the immune system.
Citation
Adibfar, A., Saleem, M., Lanctot, K., & Herrmann, N. (2016). Potential biomarkers for depression associated with coronary artery disease: A critical review. Current Molecular Medicine, 16(2),137-164. doi:10.2174/1566524016666160126144143
Barrientos, R. M., Frank, M. G., Hein, A. M., Higgins, E. A., Watkins, L. R., Rudy, J. W., & Maier, S. F. (2009). Time course of hippocampal il-1 β and memory consolidation impairments in aging rats following peripheral infection. Brain, Behavior, and Immunity, 23(1), 46-54. doi:10.1016/j.bbi.2008.07.002
Barth, Schumacher, M., & Herrmann-Lingen, C. (2004). Depression as a risk factor for mortality
in patients with coronary heart disease: A meta-analysis. Psychosomatic Medicine, 66(6), 802- 813. doi:10.1097/01.psy.0000146332.53619.b2
Bhutta, Z. A., Guerrant, R. L., & Nelson, C. A. (2017). Neurodevelopment, Nutrition, and
Inflammation: The Evolving Global Child Health Landscape. Pediatrics, 139(Supplement 1). doi:10.1542/peds.2016-2828d
Bogin, B., & Varea, C. (2020). COVID ‐19, crisis, and emotional stress: A biocultural perspective of their impact on growth and development for the next generation. American Journal of Human Biology. doi:10.1002/ajhb.23474
Brody H., Yu, T., Miller, G. E., & Chen, E. (2015). Discrimination, racial identity, and CYTOKINE levels AMONG african-american adolescents. Journal of Adolescent Health, 56(5), 496-501. doi:10.1016/j.jadohealth.2015.01.017
Carney, R. M., & Freedland, K. E. (2010). Psychotherapies for Depression in People with Heart
Disease. Depression and Heart Disease, 145-168. doi:10.1002/9780470972304.ch6
Chapman P., Liu, Y., Presley-Cantrell, L. R., Edwards, V. J., Wheaton, A. G., Perry, G. S., &
Croft, J. B. (2013). Adverse childhood experiences and frequent insufficient sleep in 5 U.S.
STATES, 2009: A retrospective cohort study. BMC Public Health, 13(1). doi:10.1186/1471-2458 13-3
Chartier J., Walker, J. R., & Naimark, B. (2009). Health risk behaviors and mental health
problems as mediators of the relationship between childhood abuse and adult health. American Journal of Public Health, 99(5), 847-854. doi:10.2105/ajph.2007.122408
Cohen, Janicki-Deverts, D., Doyle, W. J., Miller, G. E., Frank, E., Rabin, B. S., & Turner, R. B.
(2012). Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk.
Danese, & Lewis, S. J. (2016). Psychoneuroimmunology of early-life stress: The hidden wounds of childhood trauma? Neuropsychopharmacology, 42(1), 99-114. doi:10.1038/npp.2016.198
Debnath, Berk, M., & Maes, M. (2020). Changing dynamics Of psychoneuroimmunology during the
Duman, R. S., & Monteggia, L. M. (2006). A neurotrophic model for stress-related mood disorders.
Biological Psychiatry, 59(12), 1116-1127. doi:10.1016/j.biopsych.2006.02.013
Dvir, Ford, J. D., Hill, M., & Frazier, J. A. (2014). Childhood maltreatment, Emotional Dysregulation,and Psychiatric comorbidities. Harvard Review of Psychiatry, 22(3), 149-161. doi:10.1097/hrp.0000000000000014
Fan Y., Jamison, D. T., & Summers, L. H. (2018). Pandemic risk: How large are the expected losses?Bulletin of the World Health Organization, 96(2), 129-134. doi:10.2471/blt.17.199588
Furman, Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., . . . Slavich, G. M.
(2019). Chronic inflammation in the etiology of disease across the life span. Nature Medicine, 25(12),1822-1832. doi:10.1038/s41591-019-0675-0
Ganguly, P., & Brenhouse, H. C. (2015). Broken or maladaptive? Altered trajectories in
neuroinflammation and behavior after early life adversity. Developmental Cognitive Neuroscience, 11,18-30. doi:10.1016/j.dcn.2014.07.001
Garner, A. S. (2013). Home Visiting and the Biology of Toxic Stress: Opportunities to Address Early
Childhood Adversity. Pediatrics, 132(Supplement). doi:10.1542/peds.2013-1021d
Gross, D., Beeber, L., Desocio, J., & Brennaman, L. (2016). Toxic stress: Urgent action needed toreduce exposure to toxic stress in pregnant women and young children. Nursing Outlook, 64(5), 513-515. doi:10.1016/j.outlook.2016.07.011
Halaris, A. (2013, October). Inflammation, heart disease, and depression. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23975043/
Halaris, A. (2019). Inflammation and depression but where does the inflammation come from? Current
Opinion in Psychiatry, 32(5), 422-428. doi:10.1097/yco.0000000000000531
Haroon, E., Raison, C. L., & Miller, A. H. (2011). Psychoneuroimmunology Meets
Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior.
Neuropsychopharmacology, 37(1), 137-162. doi:10.1038/npp.2011.205
Head, Murray, J., Sarrassat, S., Snell, W., Meda, N., Ouedraogo, M., . . . Cousens, S. (2015).
Can mass media interventions reduce child mortality? The Lancet, 386(9988), 97-100.
doi:10.1016/s0140-6736(14)61649-4
Irwin R. (2008). Human psychoneuroimmunology: 20 years of discovery. Brain, Behavior, and Immunity, 22(2), 129-139. doi:10.1016/j.bbi.2007.07.013
Kirby, J. N. (2016). The Role of Mindfulness and Compassion in Enhancing Nurturing Family Environments. Clinical Psychology: Science and Practice, 23(2), 142-157. doi:10.1111/cpsp.12149
Kohman A., & Rhodes, J. S. (2013). Neurogenesis, inflammation and behavior. Brain, Behavior,
and Immunity, 27, 22-32. doi:10.1016/j.bbi.2012.09.003
Lo H., Ho, W., Lau, E. N., Lo, C., Mak, W. W., Ng, S., . . . Leung, C. W. (2019). A brief
mindfulness-based family psychoeducation intervention for chinese young adults with first
episode psychosis: A study protocol. Frontiers in Psychology, 10. doi:10.3389/fpsyg.2019.00516
Luppino S., Wit, L. M., Bouvy, P. F., Stijnen, T., Cuijpers, P., Penninx, B. W., & Zitman, F. G.
(2010). Overweight, obesity, and depression. Archives of General Psychiatry, 67(3), 220. doi:10.1001/archgenpsychiatry.2010.2
Maunder G., Tannenbaum, D. W., Permaul, J. A., Nutik, M., Haber, C., Mitri, M., . . . Hunter, J.
J. (2019). The prevalence and clinical correlates of adverse childhood experiences in a cross-
sectional study of primary care patients with cardiometabolic disease or risk factors. BMC Cardiovascular Disorders, 19(1). doi:10.1186/s12872-019-01277-3
Maunder G., Tannenbaum, D. W., Permaul, J. A., Nutik, M., Haber, C., Mitri, M., . . . Hunter, J.J. (2019). The prevalence and clinical correlates of adverse childhood experiences in a cross-
sectional study of primary care patients with cardiometabolic disease or risk factors. BMC Cardiovascular Disorders, 19(1). doi:10.1186/s12872-019-01277-3
Mcmullin D., Shields, G. S., Slavich, G. M., & Buchanan, T. W. (2020). Cumulative lifetime
stress exposure predicts greater impulsivity and addictive behaviors. Journal of Health Psychology, 135910532093705. doi:10.1177/1359105320937055
Meyers, N. (2010). Circulating stress in schizophrenia: Culture, psychoneuroimmunology and
implications for global mental health. PsycEXTRA Dataset. doi:10.1037/e647202011-001
Midei, A. J., & Matthews, K. A. (2011). Interpersonal violence in childhood as a risk factor for
obesity: A systematic review of the literature and proposed pathways. Obesity Reviews, 12(5).
doi:10.1111/j.1467-789x.2010.00823.x
R E F E R E N C E S
Milas, Klarić, I. M., Malnar, A., Šupe‐Domić, D., & Slavich, G. M. (2019). Socioeconomic status,
social‐cultural values, life stress, and health behaviors in a national sample of adolescents. Stress
and Health, 35(2), 217-224. doi:10.1002/smi.2854
Miller H., Maletic, V., & Raison, C. L. (2009). Inflammation and its discontents: The role of
cytokines in the pathophysiology of major depression. Biological Psychiatry, 65(9), 732-741. doi:10.1016/j.biopsych.2008.11.029
Monteleone, P. (2010). The Association Between Depression and Heart Disease: The Role of
Biological Mechanisms. Depression and Heart Disease, 39-56. doi:10.1002/9780470972304.ch2
Mosovich A., Boone, R. T., Reichenberg, A., Bansilal, S., Shaffer, J., Dahlman, K., . . . Farkouh, M.E. (2007). New insights into the link between cardiovascular disease and depression. InternationalJournal of Clinical Practice, 62(3), 423-432. doi:10.1111/j.1742-1241.2007.01640.x
The Oxford Handbook of Stress and Mental Health. (2018).
doi:10.1093/oxfordhb/9780190681777.001.0001
Park R., Traeger, L., Vranceanu, A., Scult, M., Lerner, J. A., Benson, H., . . . Fricchione, G. L.
(2013). The development of A PATIENT-CENTERED program based on the RELAXATION
response: The Relaxation Response Resiliency Program (3RP). Psychosomatics, 54(2), 165-174. doi:10.1016/j.psym.2012.09.001
Pretty, C., O’Leary, D. D., Cairney, J., & Wade, T. J. (2013). Adverse childhood experiences and
the cardiovascular health of children: A cross-sectional study. BMC Pediatrics, 13(1). doi:10.1186/1471-2431-13-208
Range, B., Gutierrez, D., Gamboni, C., Hough, N. A., & Wojciak, A. (2017). Mass Trauma in the
African American Community: Using Multiculturalism to Build Resilient Systems. Contemporary
Family Therapy, 40(3), 284-298. doi:10.1007/s10591-017-9449-3
Segerstrom, S. C. (2012). Looking into the Future: Conclusion to the Oxford Handbook of
Psychoneuroimmunology. Oxford Handbooks Online. doi:10.1093/oxfordhb/9780195394399.013.0023
Shern L., Blanch, A. K., & Steverman, S. M. (2016). Toxic stress, behavioral health, and the next
major era in public health. American Journal of Orthopsychiatry, 86(2), 109-123.
doi:10.1037/ort0000120
Shonkoff P., Garner, A. S., Siegel, B. S., Dobbins, M. I., Earls, M. F., Mcguinn, L., . . . Wood, D. L.(2011). The lifelong effects of early childhood adversity and toxic stress. Pediatrics, 129(1). doi:10.1542/peds.2011-2663
Slavich, G. M. (2019). Psychoneuroimmunology of stress and mental health. The Oxford Handbook of Stress and Mental Health, 518-546. doi:10.1093/oxfordhb/9780190681777.013.24
Su, Jimenez, M. P., Roberts, C. T., & Loucks, E. B. (2015). The role of adverse childhood
experiences in cardiovascular disease risk: A review with emphasis on plausible
mechanisms. Current Cardiology Reports, 17(10). doi:10.1007/s11886-015-0645-1
Videoconferencing to Reduce Stress Among Hospitalized Children. (2014). Pediatrics, 134(1). doi:10.1542/peds.2013-3912d
Yuan, N., Chen, Y., Xia, Y., Dai, J., & Liu, C. (2019). Inflammation-related biomarkers in
major psychiatric DISORDERS: A cross-disorder assessment of reproducibility and specificity
in 43 META-ANALYSES. Translational Psychiatry, 9(1). doi:10.1038/s41398-019-0570-y
The Comments
What is Somatic Therapy? - Sauna Therapy | Dallas
[…] hormones, feel good chemicals, heart rate, digestion, respiratory rate, eyesight and more. In the science of Psychoneuroimmunology, we understand that oxidative stress that is developed through childhood trauma or trauma can […]