How the immune system may be a potential mediator for toxic stress through the science of psychoneuroimmunology
When a person experiences trauma, their body triggers immune responses that resemble those activated during an infection. However, the body is unable to interpret the patterns of social and environmental assaults. To comprehend the connection between immune responses, stress, mental health, adverse childhood experiences, and psychological stressors, it is crucial to initiate research and promote clinical training in understanding the immune system's reaction to threats encoded in the social environment. This knowledge can help the body allocate appropriate resources to effectively cope with perceived biological threats that are likely to exist in various environments. These efforts form the foundation of the field of psychoneuroimmunology, which investigates the social impacts of trauma on the immune system.
During traumatic experiences, the activation of the innate immune system leads to immunologic responses that can harm our brain and mental health. The innate immune system is responsible for the initial defense against infections, typically targeting foreign bacteria, antibodies, and pathogens to safeguard our well-being (Slavich, 2019). However, the innate immune system's response to threats is swift and complex, potentially causing damage. Its cells possess remarkable abilities to identify patterns and characteristics of microbes or pathogen-related molecular entities, like lipopolysaccharides (LPS) or specific sequences found in bacterial and viral genomes.
The immune system plays a crucial role in promoting human health and defending against serious illnesses. Inflammation, a vital aspect of this system, is mediated by cells such as cytokines that are essential for eliminating foreign bacteria and viruses. However, when the body faces an attack, whether it be from pathogens or social factors, the brain and immune system communicate to detect potential threats in the environment. In such circumstances, the brain triggers a systemic inflammatory response through the nervous and endocrine systems. Unfortunately, due to various environmental, biological, and health-related risk factors, excessive activation of proinflammatory responses can lead to sustained damage to the body’s genetic and biological systems.
C-reactive Protein
c-reactive protein is an inflammatory protein that is found in childhood sexual abuse (CSA), bullying and obesity.
IL-1, IL-6 family receptors
There are 10 members of the IL-1 family receptors. IL-1R1 binds IL-1α, IL-1β, and IL-1Ra and IL-R1 binds either IL-1β or IL-1α. IL-1R2 is a decoy receptor for IL-1β. They have been shown to produce anti-neurogenetic effects including neuronal differentiation & proliferation. They’re also seen in health risk related behaviors and depression.
TNF-α
Tumor necrosis factor (TNF)-α is classified as a homotrimeric transmembrane protein with a prominent role in systemic inflammation. Macrophages/monocytes are capable to produce TNF-α in the acute phase of inflammation, and this cytokine drives a wide range of signaling events within cells, leading to necrosis or apoptosis
Neurogenesis, the process of generating new neurons, has been identified as a significant factor in alleviating symptoms of depression and anxiety, particularly in response to antidepressant medication (Duman and Monteggia, 2006). Multiple studies have explored the connection between neurogenesis and the effectiveness of antidepressants, with stress levels in the body playing a crucial role. Chronic stress, for example, has been found to hinder neurogenesis and contribute to relapses in depressive episodes. The impact of cytokines from the innate immune system on neurogenesis has also been observed. Stress has been shown to impede gene growth production and reduce neurogenic activity, potentially increasing vulnerability to mental health issues like depression and autoimmune disorders. Various studies have demonstrated that stress-induced activation of cytokines can lead to increased inflammatory processes that impair the brain’s ability to engage in neuroplasticity. When inflammation becomes chronic in the brain, it significantly affects neurogenesis and neuronal activity. In addition to influencing proliferation, survival, and cell death, brain inflammation can disrupt the integration of new neurons into existing neural networks and alter the cellular properties of surviving cells (Slavich, 2019; Haroon, Raison, and Miller, 2011).
Adverse Childhood Experiences
The intimate connection between ACEs and inflammation is due to disruption of the developing brain and immune system in conjunction with highly stressful events which changes the brain architecture of the child. Throughout the literature, ACEs represents a potential dependent variable for inflammation, cardiovascular disease and mental illness.
Cardiovascular Disease
ACEs has been shown to be a developmental risk factor for cardiovascular disease. And recent literature has documented the relationship between inflammation and CVD to be substantial, however, the exact mechanisms causing its connection is still not quite understood. Depression has been proven to be a risk-factor in the development of CVD as well as the leading cause of higher mortality rates in individuals diagnosed.
Mental Illness like Depression
The connection between mental stress and mental illness like depression is found frequently throughout the literature. Depression has been known to have high levels of inflammatory cytokines and ACEs has been shown as a developmental risk factor for its emergence. Not to mention, in epidemiological studies, CVD and depression have show to have a bidirectional relationship.
Numerous studies have consistently shown that sleep deprivation is associated with increased levels of depression, stress, and anxiety. Furthermore, insufficient sleep quality has been linked to elevated levels of pro-inflammatory cytokines, which can contribute to the development of depression and cardiovascular disease (CVD).
Unhealthy eating patterns are often influenced by psychological stress, leading individuals to consume more high-fat or high-sugar foods as snacks between meals. Moreover, there is a longitudinal association between depression and obesity, both of which are recognized as risk factors for CVD. Research indicates that the disrupted HPA-axis (hypothalamic-pituitary-adrenal axis) creates a feedback loop that promotes cravings for sugary substances.
Physical inactivity may result from adverse childhood experiences (ACEs) during adolescence and is considered a contributing factor that promotes long-term inflammation, obesity, CVD, and depression.
Substance abuse significantly contributes to mortality and is associated with higher levels of inflammation. It is also linked to increased rates of depression, suicide, poverty, and sleep deprivation, all of which have detrimental effects on overall health.
The immune system is a large player in promoting human health and is critical for aversion to chronic disease. A key component of the system is the inflammatory responses, which can be mediated by cells like cytokines. However, when the body is under attack (i.e., bacterial, viral, social) it relies on communication between the brain & nervous system to identify environmental cues which could be potentially threatening. In these circumstances, the brain initiates a systematic inflammatory response via the nervous system and endocrine system. The activation of high pro-inflammatory responses can cause prolonged damage to body’s biological systems. Thus, increasing susceptibility to co-morbidities in the mental health and neurological conditions.
Sustained inflammation comes from cross-sectional pathways in lack of sleep, poor diet, physical inactivity and substance abuse use.
The term “ACEs” stands for Adverse Childhood Experiences, which was initially developed in a groundbreaking study conducted by the Centers for Disease Control and Kaiser Permanente in 1995. It was also the subject of formal research exploration by Fetilli in 1988. The ACEs study focused on three specific types of adversities children are exposed to: abuse, neglect, and household dysfunction, including physical and sexual violence.
Key findings from subsequent studies include: (1) ACEs are quite prevalent, with over two-thirds of the population reporting at least one ACE, and nearly a quarter experiencing three or more. (2) There is a strong and lasting correlation between the number of ACEs experienced and the likelihood of negative outcomes in adulthood. These outcomes include significantly increased risks of heart disease, diabetes, obesity, depression, substance abuse, smoking, poor academic achievement, unemployment, and premature death (Harvard Center for the Developing Child, 2020).
Childhood toxic stress refers to severe, prolonged, or repetitive adversity without the necessary nurturing or support from caregivers to mitigate abnormal stress responses. This toxic stress triggers the activation of the immune system and disruption of the neuroendocrine system, resulting in persistent activation of pro-inflammatory cytokines and cortisol, leading to chronic inflammatory states. These inflammatory states can cause epigenetic alterations that the body struggles to recover from.
Children who experience early life toxic stress are at risk of long-term adverse health effects that may not manifest until adulthood. These effects include maladaptive coping skills, poor stress management, unhealthy lifestyles, mental illness, and physical diseases (Harvard Center for the Developing Child, 2020).
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