About Adoptee Rage

Statistics Identify large populations of Adoptees in prisons, mental hospitals and committed suicide.
Fifty years of scientific studies on child adoption resulting in psychological harm to the child and
poor outcomes for a child's future.
Medical and psychological attempts to heal the broken bonds of adoption, promote reunions of biological parents and adult children. The other half of attempting to repair a severed Identity is counselling therapy to rebuild the self.

Wednesday, August 5, 2015

Scientific Proof in Abused Adopted Children RESULTING IN Adult Adoptee Illness and Disease

ADOPTEE RAGE!

Psychoneuroimmunology...Proving Child Abuse Effects In Adult Adoptee Diseases
__________________________________________

Psychoneuroimmunology (PNI), also referred to aspsychoendoneuroimmunology (PENI), is the study of the interaction between psychological processes and the nervous and immune systems of the human body. PNI takes an interdisciplinary approach, Incorporating psychology, neuroscience, immunology physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious disease, endocrinology and rheumatology. 
The main interests of PNI are the interactions between the nervous and immune systems and the relationships between mental processes and health. PNI studies, among other things, the physiological functioning of the neuroimmune system in health and disease; disorders of the neuroimmune system (autoimmune disease, hypersensitivities, immune deficiency); and the physical, chemical and physiological characteristics of the components of the neuroimmune system in vivo, in situ and in vivo.

The immune-brain loop


PNI research is looking for the exact mechanisms by which specific brain immunity effects are achieved. Evidence for nervous system–immune system interactions exists at several biological levels.
The immune system and the brain talk to each other through signaling pathways. The brain and the immune system are the two major adaptive systems of the body. Two major pathways are involved in this cross-talk: the Hypothalamic-pituatary-adrenal axis (HPA axis) and the sympathetic nervous system (SNS). The activation of SNS during an immune response might be aimed to localize the inflammatory response.
The body's primary stress management system is the HPA axis.     The HPA axis responds to physical and mental challenge to maintain homeostasis in part by controlling the body's cortisol level. Dysregulation of the HPA axis is implicated in numerous stress-related diseases, with evidence from meta-analyses indicating that different types/duration of stressors and unique personal variables can shape the HPA response. HPA axis activity and cytokines are intrinsically intertwined: inflammatory cytokines stimulateadrenocortictropic hormone (ACTH) and cortisol secretion, while, in turn, glucocorticoids suppress the synthesis of proinflammatory cytokines.
Molecules called pro-inflammatory cytokines, which include Interleukin-1 (IL-1), Interleukin-2 (IL-2), Interleukin-6 (IL-6), Interleukin-12 (IL-12), Interferon-Gamma (IFN-Gamma) and Tumor necrosis factor alpha (TNF-alpha) can affect brain growth as well as neuronal function. Circulating immune cells such as macrophages, as well as Glial cells ( Microglia and Astrocytes) secrete these molecules. Cytokine regulation of hypothalamic function is an active area of research for the treatment of anxiety-related disorders.
Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis Like the stress response, the inflammatory reaction is crucial for survival. 
Systemic inflammatory reaction results in stimulation of four major programs:
  • the acute-phase reaction
  • Sickness behavior 
  • the pain program
  • the stress response
These are mediated by the HPA axis and the SNS. Common human diseases such as allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro-inflammatory versus anti-inflammatory and T helper (Th1) versus (Th2) cytokine balance.
Recent studies show pro-inflammatory cytokine processes take place during depression, mania and bipolar disease, in addition to autoimmune hypersensitivity and chronic infections.
Chronic secretion of stress hormones,glucocorticoids (GCs) and catecholamines (CAs), as a result of disease, may reduce the effect of neurotransmitters, includingserotonin, norepinephrine and dopamine, or other receptors in the brain, thereby leading to the dysregulation of neurohormones. Under stimulation, norepinephrine is released from the sympathetic nerve terminals in organs, and the target immune cells express adreno-receptors. Through stimulation of these receptors, locally released norepinephrine, or circulating catecholamines such as epinephrine, affect lymphocite traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells.
Glucocorticoids also inhibit the further secretion of corticotropin-releasing hormone from the hypothalamus and ACTH from the pituatary (negative feedback). Under certain conditions stress hormones may facilitate inflammation through induction of signaling pathways and through activation of the Cotricotrophin releasing hormone.
These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health, developing into a "systemic anti-inflammatory feedback" and/or "hyperactivity" of the local pro-inflammatory factors which contribute to the pathogenesis of disease.
This systemic or neuro-inflammation and neuroimmune activation have been shown to play a role in the etiology of a variety of neurodegenerative disorders such as Parkinson's, Alzheimers's disease, multiple schlerosis, pain and AIDS-associated dementia. However, cytokines and chemokines  also modulate central nervous system (CNS) function in the absence of overt immunological, physiological, or psychological challenges.

Psychoneuroimmunological effects

There is now sufficient data to conclude that immune modulation by psychosocial stressors and/or interventions can lead to actual health changes. 
Although changes related to infectious disease and wound healing have provided the strongest evidence to date, the clinical importance of immunological dysregulation is highlighted by increased risks across diverse conditions and diseases. 
For example, stressors can produce profound health consequences. In one epidemiological study, all-cause mortality increased in the month following a severe stressor – the death of a spouse.        
 Theorists propose that stressful events trigger cognitive and affective responses which, in turn, induce sympathetic nervous system and endocrine changes, and these ultimately impair immune function. 
Potential health consequences are broad, but include rates of infection, HIV progression, cancer incidence and progression, and high rates of infant mortality.

Understanding Stress and Immune Function

Stress is thought to affect immune function through emotional and/or behavioral manifestations such as anxiety, fear, tension, anger and sadness and physiological changes such as heart rate, blood pressure and sweating. Researchers have suggested that these changes are beneficial if they are of limited duration, but when stress is chronic, the system is unable to maintain equilibrium or homeostasis. 
In one of the earlier PNI studies, which was published in 1960, subjects were led to believe that they had accidentally caused serious injury to a companion through misuse of explosives.  Since then decades of research resulted in two large meta-analyses, which showed consistent immune dysregulation in healthy people who are experiencing stress.
In the first meta-analysis by Herbert and Cohen in 1993, they examined 38 studies of stressful events and immune function in healthy adults. They included studies of acute laboratory stressors (e.g. a speech task), short-term naturalistic stressors (e.g. medical examinations), and long-term naturalistic stressors (e.g. divorce, bereavement, caregiving, unemployment). They found consistent stress-related increases in numbers of total white blood cells (WBCs), as well as decreases in the numbers of helper T cells, suppressor T cells and cytotoxic T cells, B cells and Natural Killer cells (NK). They also reported stress-related decreases in NK and T cell function, and T cell proliferative responses to phytohaemagglutinin [PHA] and concanavalin A [Con A]. These effects were consistent for short-term and long-term naturalistic stressors, but not laboratory stressors.
In the second meta-analysis by Zorrilla et al. in 2001, they replicated Herbert and Cohen’s meta-analysis. Using the same study selection procedures, they analyzed 75 studies of stressors and human immunity. Naturalistic stressors were associated with increases in number of circulating neutrophils, decreases in number and percentages of total T cell and helper T cells, and decreases in percentages of Natural Killer (NK) cells and cytotoxic T cell lymphocytes. They also replicated Herbert and Cohen’s finding of stress-related decreases in NKCC and T cell mitogen proliferation to Phytohaemagglututinin (PHA) and Concanavalin A (Con A).
More recently, there has been increasing interest in the links between interpersonal stressors and immune function. For example, marital conflict, loneliness, caring for a person with a chronic medical condition, and other forms on interpersonal stress dysregulate immune function.

Communication between the brain and immune function

  • Stimulation of brain sites alters immunity (stressed animals have altered immune systems).
  • Damage to brain hemispheres alters immunity (hemispheric lateralization effects).
  • Immune cells produce cytokines that act on the CNS.
  • Immune cells respond to signals from the CNS.

Communication between neuroendocrine and immune system

  • Glucocorticoids and catecholamines influence immune cells.
  • Endorphins from pituarary & adreal medulla act on immune system.
  • Activity of the immune system is correlated with neurochemical/neuroendocrine activity of brain cells.

Connections between glucocorticoids and immune system

  • Anti-inflammatory hormones that enhance the organism's response to a stressor.
  • Prevent the overreaction of the body's own defense system.
  • Regulators of the immune system.
  • Affect cell growth, proliferation & differentiation.
  • Cause immunosuppression.
  • Suppress cell adhesion, antigen presentation, chemotaxis & cytotoxicity.
  • Increase apoptosis. 

Corticotropin-releasing hormone (CRH)

Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress.
  • CRH is a major regulator of the HPA axis/stress axis.
  • CRH Regulates secretion of Adrenocorticotropic hormone (ACTH).
  • CRH is widely distributed in the brain and periphery
  • CRH also regulates the actions of the Autonomic nervous system ANS and immune system.
Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity.
  • Central mediated since peripheral administration of CRH antagonist does not affect immunosuppression.