By Jen L’Insalata
Stress has been cited for many adverse physical and mental health conditions and is linked to the proliferation of non-communicable disease epidemics in recent years. During the 1800’s most deaths were related to poor sanitary and hygienic conditions. Most deaths were attributed to outbreaks of cholera, Influenza, typhoid, and tuberculosis spread through unsanitary drinking water (Shern, Blanch, & Steverman, 2016).
In the 21st century, public health is still at risk. The US ranked 36th out of 194 for life expectancy in 2012 with the vast majority of deaths related to obesity, coronary heart disease, lung disease, and substance abuse. Most contemporary chronic illness has its roots in stress and it is estimated that nearly half of Americans will develop resulting mental health and addiction issues at some point during their lifetime (Shern, Blanch, & Steverman, 2016).
It is widely understood that a combination of genetic predisposition coupled with environmental influence shape over all human development. Many alterations in genetic material correlate with environmental stressors. In other words, genetic mutation and expression is strongly influenced by the environments which people are exposed to.
While manageable stress is considered important for healthy human development, toxic stress is not. Frequent, intense, and prolonged exposure to adversity including but not limited to physical and emotional abuse or violence, neglect, and economic hardship account for the source of much toxic stress. Acute or chronic exposure to traumatic events including death and sexual abuse also fall into the toxic stress category as does the persistence of less sever stressors including family instability and income insecurity (Shern, Blanch, & Steverman, 2016).
Stress alters development over the course of a lifetime. Prenatal exposure to stress impacts developing structures of the fetus leading to adverse effects on memory and cognition. Early childhood stress often results in diminished behavioral, emotional, and impulse control. Individuals exposed to toxic stress during late adolescence and early adulthood develop a heightened fear response and are hyper responsive to stress stimuli (Shern, Blanch, & Steverman, 2016). Additionally, stress amplifies the aging process on both the brain and the body as a whole.
Stress causes structural remodeling of the brain and weakens neuro-connections within in the brain. Exposure to stress activates stress hormones and raises cortisol levels. Persistent elevation of cortisol levels increases the adverse effects on the connective structures within the amygdala; a structure commonly linked to cognitive and emotional regulation (Shern, Blanch, & Steverman, 2016 & Pagliaccio, Luby, & … Barch, 2015).
Genetic mutations occur throughout the short alleles of the serotonin transport promoter and produced heightened monoamine oxidise A activity. Heightened activity along the Hypothalamic-Pituitary-Adrenal Axis greatly effects the monoamine/serotonin structures and leads to additional cortisol release. It is the relationship between cortisol and amygdala connectivity that is believed to be a foundational component of internalizing pathology (Pagliaccio, Luby, & … Barch, 2015).
Internalizing pathology such and depression and anxiety contribute additional stress to an individual’s life. Symptoms of both disorders have dehabilitating effects on one’s ability to function in a socioeconomic capacity and produce feeling of dependency on unhealthy relationships and substances. Thus the cycle of stress, cell malfunction, and disorder is perpetuated.
Pagliaccio, D., Luby, J. L., Bogdan, R., Agrawal, A., Gaffrey, M. S., Belden, A. C., & … Barch, D. M. (2015). Amygdala functional connectivity, HPA axis genetic variation, and life stress in children and relations to anxiety and emotion regulation. Journal Of Abnormal Psychology, 124(4), 817-833. doi:10.1037/abn0000094
Shern, D. 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