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The following is a compilation of resources exploring the multifaceted dimensions of trauma. Explore studies on childhood trauma, neuroscience, inflammation, ADHD, and more. This page is updated frequently as we work to uncover groundbreaking studies shedding light on the intricate connections between adverse experiences and the human body.
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.
Child abuse is a challenging issue, often requiring careful diagnosis due to its similarity to other conditions. A case study involving a two-year-old child revealed a history of multiple hospital admissions for alleged accidental traumas. However, a diagnosis of Ehlers-Danlos syndrome was made after the first skin biopsy. Subsequently, during a later admission, a bleeding wound raised suspicions of abuse, leading to a medico-legal evaluation that confirmed physical abuse. This case underscores the importance of healthcare professionals being aware of conditions that can mimic abuse symptoms and the need for thorough assessments in suspected cases.
This study explored the connection between Joint Hypermobility Syndrome/Ehlers–Danlos Syndrome (JHS/EDS) and disorders of the gut–brain interaction (DGBIs), specifically irritable bowel syndrome (IBS) and functional dyspepsia (FD). Surveys were sent to 253 JHS/EDS patients, with 193 participants enrolled over one year. Results showed that 67.9% of JHS/EDS patients met the criteria for IBS, and 35.2% had FD. Those with overlapping IBS or FD reported more traumatic exposures and adverse childhood experiences (ACEs) compared to those without these conditions. This suggests that JHS/EDS patients may be more susceptible to developing DGBIs due to secondary environmental triggers like traumatic experiences and ACEs.
Research indicates a notable prevalence of psychiatric disorders among individuals with hypermobile Ehlers–Danlos syndrome (JHS/hEDS). A literature review reveals a strong link between anxiety disorders and JHS/hEDS, alongside emerging evidence of associations with depression, eating disorders, neurodevelopmental conditions, and substance misuse. The underlying mechanisms include genetic risks, autonomic nervous system dysfunction, altered sensory processing, and heightened emotional reactivity observed in neuroimaging studies. Effective management involves integrating psychiatric and psychological interventions, such as medication, psychotherapy, and psychological rehabilitation, alongside modern physiotherapy. A multidimensional approach is crucial for assessing and treating this “neuroconnective phenotype,” emphasizing the need for further research to fully understand and address the psychopathology associated with JHS/hEDS.
Autoimmune thyroid disorders (AITD) represent the most frequent of all autoimmune disorders. Their aetiopathogenesis is incompletely understood, but most likely multifactorial. Early life stress can have long-lasting effects on the immune system. The aim of the present study was to investigate, for the first time, whether patients with AITD are more frequently affected by early life stress. A total of N = 208 women were recruited into a case-control study. Of these, n = 78 (median age: 53, interquartile range: 15) were patients recruited from a thyroid outpatient clinic with confirmed Hashimoto’s thyroiditis, Graves’ disease, or AITD not otherwise specified.
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).
The study examined how adverse childhood experiences (ACE), such as abuse and neglect, impact brain volume in females who experienced prolonged trauma. Using structural magnetic resonance imaging and a detailed interview method called the Maltreatment and Abuse Chronology of Exposure (MACE), researchers assessed ACE severity and type from ages 3 to 17. They found that the severity of neglect during preadolescence and early adolescence had a significant impact on brain structures like the amygdala and hippocampus. These findings suggest that the timing and type of ACE can influence the development of stress-sensitive brain regions, highlighting the importance of early intervention and support for individuals affected by childhood trauma.
Potential long-lasting adverse effects of child maltreatment have been widely reported, although little is known about the distinctive long-term impact of differing types of maltreatment. Our objective for this special article is to integrate findings from the Mater-University of Queensland Study of Pregnancy, a longitudinal prenatal cohort study spanning 2 decades. We compare and contrast the associations of specific types of maltreatment with long-term cognitive, psychological, addiction, sexual health, and physical health outcomes assessed in up to 5200 offspring at 14 and/or 21 years of age. Overall, psychological maltreatment (emotional abuse and/or neglect) was associated with the greatest number of adverse outcomes in almost all areas of assessment. Sexual abuse was associated with early sexual debut and youth pregnancy, attention problems, posttraumatic stress disorder symptoms, and depression, although associations were not specific for sexual abuse. Physical abuse was associated with externalizing behavior problems, delinquency, and drug abuse. Neglect, but not emotional abuse, was associated with having multiple sexual partners, cannabis abuse and/or dependence, and experiencing visual hallucinations. Emotional abuse, but not neglect, revealed increased odds for psychosis, injecting-drug use, experiencing harassment later in life, pregnancy miscarriage, and reporting asthma symptoms. Significant cognitive delays and educational failure were seen for both abuse and neglect during adolescence and adulthood. In conclusion, child maltreatment, particularly emotional abuse and neglect, is associated with a wide range of long-term adverse health and developmental outcomes. A renewed focus on prevention and early intervention strategies, especially related to psychological maltreatment, will be required to address these challenges in the future.
The “invisible epidemic” of childhood sexual abuse is a major public health problem that is twice as common in women as in men. Women and children are extremely vulnerable to victimization, which makes young girls at especially high risk for victimization by childhood sexual abuse. The sheer magnitude of the problem on a public health scale can be seen by recent nationwide surveys that showed that 16% of women have a history of childhood sexual abuse [ [1] ]. This report means that at least one out of every seven women in our society has been the victim of childhood sexual abuse—defined as rape, threat of rape, or unwanted genital fondling—at least once before her eighteenth birthday. Sexual abuse is the most common cause of posttraumatic stress disorder (PTSD) in women, and it affects 10% (approximately 13 million) of women in the country at some time in their lives based on a recent nationwide survey [ [2] ]. It also is commonly associated with depression. Little is known about the neurobiology of early childhood abuse.
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.
A history of maltreatment in childhood may influence adults’ parenting practices, potentially affecting their children. This systematic review examines 97 studies investigating associations of parental childhood victimization with a range of parenting behaviors that may contribute to the intergenerational effects of abuse: abusive parenting, problematic parenting, positive parenting, and positive parental affect. Key findings include: (1) parents who report experiencing physical abuse or witnessing violence in the home during childhood are at increased risk for reporting that they engage in abusive or neglectful parenting; (2) a cumulative effect of maltreatment experiences, such that adults who report experiencing multiple types or repeated instances of victimization are at greatest risk for perpetrating child abuse; (3) associations between reported childhood maltreatment experiences and parents’ problematic role reversal with, rejection of, and withdrawal from their children; (4) indirect effects between reported childhood maltreatment and abusive parenting via adult intimate partner violence; and (5) indirect effects between reported childhood maltreatment and lower levels of positive parenting behaviors and affect via mothers’ mental health. Thus, childhood experiences of maltreatment may alter parents’ ability to avoid negative and utilize positive parenting practices. Limitations of this body of literature include few prospective studies, an overreliance on adults’ self-report of their childhood victimization and current parenting, and little examination of potentially differential associations for mothers and fathers.
Child maltreatment may affect autonomic nervous system (ANS) responsivity, and ANS responsivity may influence the impact of child maltreatment on later outcomes including long-term mental/physical health. This review systematically evaluated the evidence regarding effects of maltreatment on ANS responsivity in children and examined how ANS responsivity may influence the association between maltreatment and psychopathology, with attention to relevant developmental issues. We searched the literature for relevant studies using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched five electronic databases, performed key word searches in relevant journals, hand searched reference sections of relevant articles, and contacted experts in the field. Articles were extracted according to inclusion criteria and their quality assessed. The search produced 1,388 articles; 22 met inclusion criteria. Most of the studies suggested blunted cardiovascular responsivity generally and sympathetic activation specifically in response to stress in maltreated children compared to nonmaltreated children. Findings around vagal responsivity and skin conductance were mixed. Limited evidence was found for ANS responsivity as a moderator or mediator of psychopathology risk among maltreated children. Maltreatment may be associated with blunted sympathetic activation in stressful situations. Differences in ANS responsivity may influence psychopathology risk among maltreated children. Further research is needed to confirm the nature and magnitude of such effects.
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