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.

Thursday, January 12, 2017

Adopted Infant's Chronic Distress & The Role of HPA Axis


The Adopted Infant's Chronic Distress & Role of HPA Axis
The newborn infant that is forcefully separated from his biological mother, exists in a state of chronic distress. This distress is a direct consequence that constitutes a traumatic event. The infant's brain and body are dysregulated by the birth and removal in this infant's partially developed state. Evolutionary theory states that   at the time of birth, the infant is nine to twelve months premature,  as the infant exists outside of the womb is dependent on the biological mother's maternal drive for continued homeostasis outside of the womb.
The extracted infant processed for adoption, exists in a state of stress induced despair, that the chronic stress from separation creates a new state of homeostasis based in distress, hypervigilant reaction to experienced birth & separation trauma that causes the HPA-Axis to establish homeostasis in these conditions as the infant's normal functioning. Due to the lack of the infant's pre-traumatic experience, the infant's new normal functioning is established is under the conditions of stress and anxiety. The new distressing environment that causes the release high levels of cortisol and stress hormones that flood the bloodstream and arrest normal infant brain growth and function. The brain grows in a dysfunctional compensationary manner that lacking normal structure, connective neurons and building cellular receptors.
The amigdala and hippocampus growth is irregular, distorted and arrested when subjected to incompassionate caregivers that are indifferent to the nonbiological, adopted infant.      

 The hypothalamic–pituitary–adrenal axis (HPA axis or HTPA axis) is a complex set of direct influences and feedback interactions among three endocrine glands: thehypothalamus, the pituatary gland (a pea-shaped structure located below the thalamus), and the adrenal (also called "suprarenal") glands (small, conical organs on top of the kidneys).


Release of CRH from the hypothalamus is influenced by stress physical activity, illness, by blood levels of cortisol and by the sleep/wake cycle (cardiac rythym). In healthy individuals, cortisol rises rapidly after wakening, reaching a peak within 30–45 minutes. It then gradually falls over the day, rising again in late afternoon. Cortisol levels then fall in late evening, reaching a trough during the middle of the night. This corresponds to the rest-activity cycle of the organism.
The HPA axis has a central role in regulating many homeostatic systems in the body, including the metabolic system, cardiovascular system, immune system, reproductive system and central nervous system. The HPA axis integrates physical and psychosocial influences in order to allow an organism to adapt effectively to its environment, use resources, and optimize survival.
Anatomical connections between brain areas such as the amigdala, hippocampus, prefrontal cortex and hypothalamus facilitate activation of the HPA axis. Sensory information arriving at the lateral aspect of the amygdala is processed and conveyed to the central nucleus, which projects to several parts of the brain involved in responses to fear. At the hypothalamus, fear-signaling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis.
Increased production of cortisol during stress results in an increased availability of glucose in order to facilitate fighting or fleeing. As well as directly increasing glucose availability, cortisol also suppresses the highly demanding metabolic processes of the immune system, resulting in further availability of glucose.
Glucocorticoids have many important functions, including modulation of stress reactions, but in excess they can be damaging. Atrophy of the hippocampus in humans and animals exposed to severe stress is believed to be caused by prolonged exposure to high concentrations of glucocorticoids. Deficiencies of the hippocampus may reduce the memory resources available to help a body formulate appropriate reactions to stress.
Studies on people show that the HPA axis is activated in different ways during chronic stress depending on the type of stressor, the person's response to the stressor and other factors. Stressors that are uncontrollable, threaten physical integrity, or involve trauma tend to have a high, flat diurnal profile of cortisol release (with lower-than-normal levels of cortisol in the morning and higher-than-normal levels in the evening) resulting in a high overall level of daily cortisol release. On the other hand, controllable stressors tend to produce higher-than-normal morning cortisol. Stress hormone release tends to decline gradually after a stressor occurs. In PTSD there appears to be lower-than-normal cortisol release, and it is thought that a blunted hormonal response to stress may predispose a person to develop PTSD.
In humans, prolonged maternal stress during gestation is associated with mild impairment of intellectual activity and language development in their children, and with behaviour disorders, self-reported maternal stress is associated with a higher irritability, emotional and attentional problems.
There is growing evidence that prenatal stress can affect HPA regulation in humans. Children who were stressed prenatally may show altered cortisol rhythms. For example, several studies have found an association between maternal depression during pregnancy and childhood cortisol levels. Prenatal stress has also been implicated in a tendency toward depression and short attention span in childhood.There is no clear indication that HPA dysregulation caused by prenatal stress can alter adult behavior.
The role of early life stress in programming the HPA Axis has been well-studied in animal models. Exposure to mild or moderate stressors early in life has been shown to enhance HPA regulation and promote a lifelong resilience to stress. In contrast, early-life exposure to extreme or prolonged stress can induce a hyper-reactive HPA Axis and may contribute to lifelong vulnerability to stress. In one widely replicated experiment, rats subjected to the moderate stress of frequent human handling during the first two weeks of life had reduced hormonal and behavioral HPA-mediated stress responses as adults, whereas rats subjected to the extreme stress of prolonged periods of maternal separation showed heightened physiological and behavioral stress responses as adults.
Several mechanisms have been proposed to explain these findings in rat models of early-life stress exposure. There may be a critical period during development during which the level of stress hormones in the bloodstream contribute to the permanent calibration of the HPA Axis. One experiment has shown that, even in the absence of any environmental stressors, early-life exposure to moderate levels of corticosterone was associated with stress resilience in adult rats, whereas exposure to high doses was associated with stress vulnerability.
Another possibility is that the effects of early-life stress on HPA functioning are mediated by maternal care. Frequent human handling of the rat pups may cause their mother to exhibit more nurturant behavior, such as licking and grooming. Nurturant maternal care, in turn, may enhance HPA functioning in at least two ways. First, maternal care is crucial in maintaining the normal stress hypo responsive period (SHRP), which in rodents, is the first two weeks of life during which the HPA axis is generally non-reactive to stress. Maintenance of the SHRP period may be critical for HPA development, and the extreme stress of maternal separation, which disrupts the SHRP, may lead to permanent HPA dysregulation. Another way that maternal care might influence HPA regulation is by causing epigentic changes in the offspring. For example, increased maternal licking and grooming has been shown to alter expression of the glutocorticoid receptor gene implicated in adaptive stress response. At least one human study has identified maternal neural activity patterns in response to video stimuli of mother-infant separation as being associated with decreased glucocorticoid receptor gene methylation in the context of post-traumatic stress disorder stemming from early life stress. Yet clearly, more research is needed to determine if the results seen in cross-generational animal models can be extended to humans.
Though animal models allow for more control of experimental manipulation, the effects of early life stress on HPA axis function in humans has also been studied. One population that is often studied in this type of research is adult victims of childhood abuse. Adult victims of childhood abuse have exhibited increased ACTH concentrations in response to a psychosocial stress task compared to healthy controls and subjects with depression but not childhood abuse. In one study, adult victims of childhood abuse that are not depressed show increased ACTH response to both exogenous CRF and normal cortisol release. Adult victims of childhood abuse that are depressed show a blunted ACTH response to exoegenous CRH. A blunted ACTH response is common in depression, so the authors of this work posit that this pattern is likely to be due to the participant's depression and not their exposure to early life stress.
Heim and colleagues have proposed that early life stress, such as childhood abuse, can induce a sensitization of the HPA axis, resulting in particular heightened neuronal activity in response to stress-induced CRF release. With repeated exposure to stress, the sensitized HPA axis may continue to hypersecrete CRF from the hypothalamus. Over time, CRF receptors in the anterior pituitary will become down-regulated, producing depression and anxiety symptoms.This research in human subjects is consistent with the animal literature discussed above.
The HPA Axis was present in the earliest vertebrate species, and has remained highly conserved by strong positive selection due to its critical adaptive roles. The programming of the HPA axis is strongly influenced by the perinatal and early juvenile environment, or “early-life environment.” Maternal stress and differential degrees of caregiving may constitute early life adversity, which has been shown to profoundly influence, if not permanently alter, the offspring's stress and emotional regulating systems. Widely studied in animal models (e.g. licking and grooming/LG in rat pups), the consistency of maternal care has been shown to have a powerful influence on the offspring's neurobiology, physiology, and behavior. Whereas maternal care improves cardiac response, sleep/wake rhythm, and growth hormone secretion in the neonate, it also suppresses HPA axis activity. In this manner, maternal care negatively regulates stress response in the neonate, thereby shaping his/her susceptibility to stress in later life. These programming effects are not deterministic, as the environment in which the individual develops can either match or mismatch with the former's “programmed” and genetically predisposed HPA axis reactivity. Although the primary mediators of the HPA axis are known, the exact mechanism by which its programming can be modulated during early life remains to be elucidated. Furthermore, evolutionary biologists contest the exact adaptive value of such programming, i.e. whether heightened HPA axis reactivity may confer greater evolutionary fitness.
Various hypotheses have been proposed, in attempts to explain why early life adversity can produce outcomes ranging from extreme vulnerability to resilience, in the face of later stress. Glucocorticoids produced by the HPA axis have been proposed to confer either a protective or harmful role, depending on an individual's genetic predispositions, programming effects of early-life environment, and match or mismatch with one's postnatal environment. The predictive adaptation hypothesis (1), the three-hit concept of vulnerability and resilience (2) and the maternal mediation hypothesis (3) attempt to elucidate how early life adversity can differentially predict vulnerability or resilience in the face of significant stress in later life. These hypotheses are not mutually exclusive but rather are highly interrelated and unique to the individual.
(1) The predictive adaptation hypothesis: this hypothesis is in direct contrast with the diathesis stress model, which posits that the accumulation of stressors across a lifespan can enhance the development of psychopathology once a threshold is crossed. Predictive adaptation asserts that early life experience induces epigenetic change; these changes predict or “set the stage” for adaptive responses that will be required in his/her environment. Thus, if a developing child (i.e., fetus to neonate) is exposed to ongoing maternal stress and low levels of maternal care (i.e., early life adversity), this will program his/her HPA axis to be more reactive to stress. This programming will have predicted, and potentially be adaptive in a highly stressful, precarious environment during childhood and later life. The predictability of these epigenetic changes is not definitive, however – depending primarily on the degree to which the individual's genetic and epigenetically modulated phenotype “matches” or “mismatches” with his/her environment (See: Hypothesis (2)).
(2) Three-Hit Concept of vulnerability and resilience: this hypothesis states that within a specific life context, vulnerability may be enhanced with chronic failure to cope with ongoing adversity. It fundamentally seeks to explicate why, under seemingly indistinguishable circumstances, one individual may cope resiliently with stress, whereas another may not only cope poorly, but consequently develop a stress-related mental illness. The three “hits” – chronological and synergistic – are as follows: genetic predisposition (which predispose higher/lower HPA axis reactivity), early-life environment (perinatal – i.e. maternal stress, and postnatal – i.e. maternal care), and later-life environment (which determines match/mismatch, as well as a window for neuroplastic changes in early programming). (Figure 1)6 The concept of match/mismatch is central to this evolutionary hypothesis. In this context, it elucidates why early life programming in the perinatal and postnatal period may have been evolutionarily selected for. Specifically, by instating specific patterns of HPA axis activation, the individual may be more well equipped to cope with adversity in a high-stress environment. Conversely, if an individual is exposed to significant early life adversity, heightened HPA axis reactivity may “mismatch” him/her in an environment characterized by low stress. The latter scenario may represent maladaptation due to early programming, genetic predisposition, and mismatch. This mismatch may then predict negative developmental outcomes such as psychopathologies in later life.
Ultimately, the conservation of the HPA axis has underscored its critical adaptive roles in vertebrates, so, too, various invertebrate species over time. The HPA Axis plays a clear role in the production of corticosteroids, which govern many facets of brain development and responses to ongoing environmental stress. With these findings, animal model research has served to identify what these roles are – with regards to animal development and evolutionary adaptation. In more precarious, primitive times, a heightened HPA axis may have served to protect organisms from predators and extreme environmental conditions, such as weather and natural disasters, by encouraging migration (i.e. fleeing), the mobilization of energy, learning (in the face of novel, dangerous stimuli) as well as increased appetite for biochemical energy storage. In contemporary society, the endurance of the HPA axis and early life programming will have important implications for counseling expecting and new mothers, as well as individuals who may have experienced significant early life adversity