In humans, childhood neglect has been shown to alter and shape the development of the HPA axis, the key controlling system of the stress reaction ( Reilly and Gunnar, 2019). Additionally, those rodent models raised by nurturing mothers, in turn, were great nurturers of their young ( Champagne et al., 2003). It has been shown that serotonin is effective in suppressing the hormones related to panic, which is directly related to the stress response ( Deakin and Graeff, 1991 Hood et al., 2006). (2003) showed that rats raised by nurturing mothers produced higher levels of serotonin, the happy hormone, later in their lives. Therefore, the allostatic load that an individual experiences is highly variable, as the ability or inability to anticipate stressful events also varies based on the individual ( Szalma, 2008 Schulkin and Sterling, 2019).Įvidence exists correlating neonatal experiences to the level of stress hormones released later in life ( Champagne et al., 2003 Schneiderman et al., 2005). According to allostatic principles, anticipation of a possible stressful event followed by appropriate regulation by the brain is the best way to physiologically regulate one’s stress response ( Ramsay and Woods, 2014). Homeostasis, however, is a broad term, so the term allostasis is used to describe the physiological changes the body makes specifically in response to a stressor to maintain physiological balance ( Schulkin and Sterling, 2019). Homeostasis is the body’s innate and dynamic ability to make physiological changes to maintain an adequate environment to perform all necessary physiological functions, and this definition has been the dominant explanation of self-regulation since it was coined by Walter Cannon in 1929 ( Ramsay and Woods, 2014). This imbalance, termed the stress response, varies in severity and duration from person to person ( Oken et al., 2015). In other words, a stressor is anything that causes a homeostatic imbalance and results in a biological or behavioral reaction to correct this imbalance ( Oken et al., 2015 Murison, 2016). Any stimulus that causes a stress response is a stressor ( Schneiderman et al., 2005), which is defined as any environmental change that causes a shift toward a state of lower utility ( Oken et al., 2015). Stress is experienced in a wide range of situations, including familial pressures, personal finances, academics, and more ( Fairbrother and Warn, 2003 Reddy et al., 2018). The objective of this manuscript is to provide a comprehensive review of stress, what causes stress, and what methods and technologies are being used to measure stress. In addition to PTSD and ASD, increased stress levels have been linked to decreased cardiovascular health ( Poirat et al., 2018) and increased risk of anxiety-depressive symptoms ( Marcatto et al., 2016). These axes are also instrumental in the appropriate termination of the release of stress hormones to maintain homeostasis and proper bodily function ( Murison, 2016), and their effects can be visualized in Figure 1 below. The HPA axis works concurrently with the sympathoadrenal-medullary (SAM) axis of the sympathetic nervous system to stimulate the release of several hormones that prepare the body to survive a stressful situation. Biologically, ASD and PTSD are associated with increased levels of cortisol and abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis while being very different in their psychological severity ( Bakhshian et al., 2013 Marin et al., 2019). The industry standard for diagnosis of mental disorders (DSM-V) recognizes two stress-related disorders: Acute Stress Disorder (ASD) and Post Traumatic Stress Disorder (PTSD) ( Fink, 2009 Bakhshian et al., 2013). Stress is biologically associated with several disorders and related health problems. In the context of this manuscript, stress is defined as any event that disrupts homeostasis, resulting in the release of hormones to return the body to homeostasis. This has led to different definitions being used depending on context – behavioral scientists define stress as the perception of threat with resulting anxiety or discomfort ( Fink, 2009), while neuroendocrinologists define it as any stimulus that triggers the secretion of the adrenocorticotropic hormone and glucocorticoids ( Miller and O’Callaghan, 2002). Selye’s definition was quite narrow, placing a clear emphasis on only the biological aspects of stress. Selye’s subsequent stress experiments started the conversation about stress and its effect on the body ( Rochette and Vergely, 2017). Stress was first defined by in 1936 by Hans Selye, a pioneering endocrinologist from Hungary ( Rochette and Vergely, 2017), as: “the non-specific response of the body to any demand.” ( Fink, 2009).