These studies indicate a potential connection between childhood trauma and autoimmune diseases. However, it’s essential to conduct more research to completely grasp the intricacies of this relationship. The precise causes of autoimmune diseases remain partially understood, but they are thought to stem from a blend of genetic and environmental factors.
For the present study, AD included the following 21 illnesses identified by a recent National Institutes of Health report (1): Addison’s disease, autoimmune hemolytic anemia, autoimmune thrombocytopenia purpura, celiac disease, dermatomyositis, Graves’ disease, Hashimoto’s thyroiditis, idiopathic myocarditis, idiopathic pulmonary fibrosis, insulin-dependent diabetes mellitus, irritable bowel disease, multiple sclerosis, myasthenia gravis, pernicious anemia, psoriasis, rheumatoid arthritis, scleroderma, Sjogren disease, systemic lupus erythematosus, vitiligo, and Wegener’s granulomatosis. Persons were considered at risk for hospitalization with ICD-9 coded AD as a discharge diagnosis if they were currently enrolled in the HMO at the time of the hospitalization and the hospitalization with ICD-9 coded AD occurred between the baseline survey date and December 31, 2005.
For years, Nakazawa had been plagued by illnesses: Guillain-Barré syndrome that left her temporarily paralyzed (twice), thyroiditis, nerve damage, severe eczema, dangerously low red and white blood cell counts, and more. Then Nagazawa got lucky. She was referred to Anastasia Rowland-Seymour, a Johns Hopkins internist and assistant professor of internal medicine at the School of Medicine. Rowland-Seymour asked a question no doctor had asked Nakazawa: Had she suffered unusual emotional or physical trauma as a child?
Autoimmune disease is recognized as a major health crisis in the United States. Today, 50 million Americans—80 percent of whom are women—suffer one or more autoimmune conditions. Thirty years ago, only one in 400 people developed an autoimmune disease. Today, one in 12 Americans—one in nine women—have an autoimmune disease. More women are diagnosed each year with an autoimmune disease than breast cancer and cardiovascular disease combined.
The significant interrelationship between stress-related disorders, including posttraumatic stress disorder (PTSD), and autoimmune and inflammatory diseases provides compelling evidence that inflammation represents both a mechanism and a target for the treatment of these psychiatric conditions (1–3). Indeed, data indicate that stress-related neuroendocrine alterations can drive inflammatory responses that overlap with those seen in autoimmune and inflammatory disorders. For example, special attention has been paid to the disruptive effects of chronic or traumatic stress on the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system and their effects on the regulation of the inflammatory response.
Posttraumatic stress disorder (PTSD) develops in a subset of individuals upon exposure to traumatic stress. In addition to well-defined psychological and behavioral symptoms, some individuals with PTSD also exhibit elevated concentrations of inflammatory markers, including C-reactive protein, interleukin-6, and tumor necrosis factor-α. Moreover, PTSD is often co-morbid with immune-related conditions, such as cardiometabolic and autoimmune disorders. Numerous factors, including lifetime trauma burden, biological sex, genetic background, metabolic conditions, and gut microbiota, may contribute to inflammation in PTSD.
Retrospective cohort study of 15,357 adult health maintenance organization members enrolled in the Adverse Childhood Experiences (ACEs) Study from 1995 to 1997 in San Diego, California, and eligible for follow-up through 2005.
Sixty-four percent reported at least one ACE. The event rate (per 10,000 person-years) for a first hospitalization with any autoimmune disease was 31.4 in women and 34.4 in men. First hospitalizations for any autoimmune disease increased with increasing number of ACEs (p < .05). Compared with persons with no ACEs, persons with ≥2 ACEs were at a 70% increased risk for hospitalizations with Th1, 80% increased risk for Th2, and 100% increased risk for rheumatic diseases (p < .05).
These findings are in line with previous studies that show associations between childhood trauma, dissociation, alexithymia, and ADs. They indicate that mental health professionals and medical doctors should assess childhood trauma in autoimmune patients.
Trauma in childhood is a grave psychosocial, medical, and public policy problem that has serious consequences for its victims and for society. Developmental traumatology, the systemic investigation of the psychiatric and psychobiological effects of chronic overwhelming stress on the developing child, provides a framework and principles when empirically examining the neurobiological effects of pediatric trauma.
Stress that occurs continually, or is triggered by multiple sources, can take a toll on a child’s health. Toxic stress that children suffer not only shapes their emotional lives as adults, but also affects their physical health and longevity.
The future of any society depends on its ability to foster the healthy development of the next generation. Extensive research on the biology of stress now shows that healthy development can be derailed by excessive or prolonged activation of stress response systems in the body and brain. Such toxic stress can have damaging effects on learning, behavior, and health across the lifespan.
Children who experience early life toxic stress are at risk of long-term adverse health effects that may not manifest until adulthood. This article briefly summarizes the findings in recent studies on toxic stress and childhood adversity following the publication of the American Academy of Pediatrics (AAP) Policy Report on the effects of toxic stress.
Science tells us that young children who experience significantly limited caregiver responsiveness may sustain a range of adverse physical and mental health consequences that actually produce more widespread developmental impairments than overt physical abuse.
Neurobiological systems may be particularly susceptible to deleterious impact of childhood trauma, and the impact of childhood trauma on development and subsequent functional outcomes across the lifespan has been well-documented.
Exposure to early-life adversity (ELA) increases the risk for psychopathologies associated with amygdala-prefrontal cortex (PFC) circuits. While sex differences in vulnerability have been identified with a clear need for individualized intervention strategies, the neurobiological substrates of ELA-attributable differences remain unknown due to a paucity of translational investigations taking both development and sex into account
Childhood trauma is a key risk factor for psychopathology. However, little is known about how exposure to childhood trauma is translated into biological risk for psychopathology. Observational human studies and experimental animal models suggest that childhood exposure to stress can trigger an enduring systemic inflammatory response not unlike the bodily response to physical injury. In turn, these “hidden wounds” of childhood trauma can affect brain development, key behavioral domains (e.g., cognition, positive valence systems, negative valence systems), reactivity to subsequent stressors, and, ultimately, risk for psychopathology. Further research is needed to better characterize the inflammatory links between childhood trauma and psychopathology. Detecting and healing these hidden wounds may help prevent and treat psychopathology emerging after childhood trauma.
The present paper conducted a meta-analysis to establish whether early-life adversity contributes to potentially pathogenic pro-inflammatory phenotypes in adult individuals. The analysis demonstrates that childhood trauma contributes to a pro-inflammatory state in adulthood, with specific inflammatory profiles depending on the specific type of trauma.
Childhood emotional abuse was associated with higher levels of IL-6 in midlife women. Assessing childhood trauma exposure along with inflammatory markers may be important for the development of prevention strategies at midlife to prevent chronic diseases later in life.
Early experiences have been shown to physiologically affect the development of both the brain and the immune system in order to maximize their adaptation to the individual’s unique environment. On the other hand, ACE have been found to be often linked with long lasting alterations in brain integrity and the immune response.
ACE have also been shown to affect the immune/inflammatory status in adulthood; childhood trauma has been shown to be linked to altered peripheral inflammatory markers later in life both in the general population and in psychiatric samples (Baumeister et al., 2016); furthermore, subjects exposed to ACE appear to be more likely to develop rheumatic and autoimmune disorders (Salihoglu et al., 2019).
Why the symptoms are often confused, and how to avoid a misdiagnosis. When kids have behavior and attention issues in school, the first explanation that comes to mind is often ADHD. But exposure to trauma can also cause symptoms that look like ADHD. And trauma is often overlooked when kids are misdiagnosed with ADHD.
In this Guide, we provide definitions of child traumatic stress and ADHD, explain how symptoms can overlap, and summarize some of the differences between the two.