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.

Saturday, July 25, 2015

Physiological Mapping Child Maltreatment in the Destruction of the Childhood Br


Maltreatment of Adopted Children Adult Damage

Maltreatment and Migraine

In the current literature on maltreatment and headache, there is limited data specific to migraine, diagnosed using standardized International Headache Society (IHS) criteria. In adults there are 4 studies that specifically address the lifetime prevalence of self-reported physical or sexual abuse in migraineurs diagnosed using IHS criteria. The first was a retrospective chart analysis of over 160 adult headache clinic patients, in which 40% of chronic daily headache (CDH) and 27.3% of episodic migraine patients reported a lifetime history of physical and/or sexual abuse. The second study, a multicenter headache clinic-based survey study of 949 adult female migraineurs, reported a lifetime prevalence of 24% for self-reported physical abuse and of 25% for sexual abuse. In the third study, also a multicenter headache clinic-based survey, of over 750 adults with migraine, 30.8% with CDH and 26.1% with episodic migraine reported physical abuse, while 27.7% with CDH and 29.4% with episodic migraine reported sexual abuse at some point in their lifetime. In the most recent study, in which 2066 post-partum Peruvian women were interviewed, women with lifetime experiences of sexual or sexual violence had increased odds of having migraine meeting IHS criteria (adjusted odds ratio [aOR] 1.44, 95% confidence interval [CI] 1.19, 1.75) and the odds were increased further in those with symptoms of depression (aOR 2.25, 95% CI 1.75, 2.28).
A number of practice-based and population-based studies have demonstrated at least a modest association between headache and childhood abuse, although many are limited to women or to 1 abuse type (table). In the ACE Study, participants of both sexes were queried regarding 8 types of adversity, including emotional, sexual, and physical abuse. Participants were, however, asked only 1 headache-related question, "Are you troubled by frequent headaches?" Frequent headache was nearly 3-fold more common in women than men and associated with each separate type of adversity. Furthermore, there was a positive correlation between the number of adverse childhood events (ACE score) and the prevalence of frequent headache. Despite the higher ACE scores in women, the dose–response relationship was present in both sexes, suggesting that the link of abuse and headache was not sex-dependent (Figure).
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Prevalence of frequent headaches by Adverse Childhood Experiences (ACE) score and sex. Estimates adjusted for age, race, and educational attainment; trend in increasing prevalence by ACE score is significant for both men and women (P < .001).26
Not only does headache appear to be related to childhood maltreatment, headache in the abused is more disabling and frequent, including being more likely to be continuous and to "transform" from episodic to chronic. At least for emotional abuse, these associations with a more severe headache phenotype appear to be independent of other factors, including depression, anxiety, lower educational attainment, obesity, smoking, that are associated with both chronic headache frequency and childhood maltreatment. In this context, it is interesting to note that although emotional abuse has received less scientific and public attention, it may have more lasting consequences and be particularly deleterious when combined with other abuse types.
There has been a growing interest in the relationship of childhood maltreatment and a variety of pain disorders related to migraine. Overall, studies suggest an association between maltreatment and painful disorders, but many factors play into the strength of the association including abuse type, timing, intensity, duration, and relationship of the victim to the perpetrator. The finding that with a greater number of different types of abuse experienced in childhood, the greater the likelihood of multiple pain disorders in adulthood supports a link between abuse and pain, but controversy still exists.

Limitations of Past Research

The use of self-report of past events introduces the limitation of an individual's memory, and the influence of disease status, such as depression, on the memory process. These factors may introduce what is referred to as recall bias into a study, particularly those with a retrospective case–control design. Reluctance to report embarrassing behaviors may lead to intentionally incorrect responses to a personal history questions, a phenomenon known as response bias. When studying childhood trauma in an adult population, the physical and psychologically traumatizing nature of the event, the time elapsed between the event and the interview, the stigma attached to being a victim, and the current psychological state (eg, depression) could each play a role in memory and perception. In the case of depression which is associated with both abuse and pain, 4 studies from general populations have established that although depression influences (to a degree varying between 0% and 33%) the strength of the abuse–pain association, an independent relationship exists.
Despite these caveats, studies in healthcare-seeking populations, with persons who may be more prone to have a condition but also to give positive responses to questions, have similar results to those from non-clinical students and general populations. Furthermore, results from 3 prospective studies support the abuse–pain relationship. One demonstrated that abused children were at increased risk to develop pain later during childhood. Another found that in adults who were pain-free at study enrollment, those who reported having been sexually abused in childhood were more likely to report back pain, and related physical limitations, on 2-year follow-up. A third study using longitudinal data of over 9000 persons from the National Population Health Survey in Canada identified a moderate relationship between arthritis pain developing in adulthood and psychological trauma in childhood or adolescence. The debate regarding the abuse–pain relationship is mainly fuelled by the negative findings from 2 prospective case–control studies in which adults, interviewed regarding pain complaints years after court-documented evidence of abuse as children, reported no increase in pain prevalence. One possible explanation for the discrepancy between results of prospective and retrospective studies is that identification of abuse during childhood leads to treatment that dampens the future effects on health. It is also possible that the use of court documents to define an individual as abused is inaccurate because of the fact that abuse is an under-reported event. This second explanation is supported by the finding that when childhood abuse was defined by self-report rather than by court document, some in the "non-abused" control group (ie, without court-documented abuse) reported having been abused, thus becoming cases. In the analysis of the redefined groups, a relationship of abuse with pain emerged.

The Neurobiology of Childhood Maltreatment

As we have outlined, epidemiological studies demonstrate that (1) women are more likely than men to experience childhood maltreatment; (2) childhood maltreatment is associated with painful conditions, including migraine. In the following paragraphs, we will explore the evidence that childhood maltreatment leads to neurobiological sequelae, some with sex-specific differences, that support the plausibility of a causal link to headache pain.

Functional Changes

Under normal circumstances, stress precipitates a constellation of adaptive responses in the neuroendocrine and autonomic systems that at a central level enhance arousal and cognition, and at a peripheral level modulate immune and cardiovascular function. The neuroendocrinological response to stress is characterized by hypothalamic release of corticotrophin-releasing hormone (CRH), the key mediator to the anterior pituitary's production and release of adrenocorticotrophin (ACTH), which in turn stimulates production and release of glucocorticoids from the adrenal cortex. Systemically circulating glucocorticoids regulate the (hypothalamic-pituitary-adrenal) HPA stress response via negative feedback to the hypothalamus, anterior pituitary and hippocampus. A decrease in glucocorticoid levels or impaired glucocorticoid receptor function might then lead to increased stress responsiveness.
There is considerable preclinical and clinical evidence that chronic early life stress results in long-term changes in HPA axis function and regulation typified by hypersecretion of CRH and ACTH. The initial hypersecretion of cortisol may over time lead to blunting of the cortisol response to CRH and ACTH and relative glucocorticoid resistance. The longitudinal development of HPA dysregulation is suggested by a study of morning cortisol levels measured over the period from girlhood through young womanhood in persons experiencing childhood sexual abuse. Initially, there was cortisol hypersecretion, but over time cortisol hyposecretion ensued. Progressive or cumulative dysregulation of the HPA axis over time as a consequence of early stress is further suggested by the findings of a cross-sectional study of physically and psychologically healthy adults. In this study the cortisol response to a stress challenge in those who reported childhood emotional abuse was more blunted (compared to controls) in the older than in the younger cohort (ie, 36–61 years vs 18–35 years). Lower cortisol levels in response to stress have also been reported in depression, a common condition in abused populations, but data suggest that childhood maltreatment, a condition commonly associated with depression, determines a distinct HPA stress profile. Dysfunction of the HPA axis has also been implicated in a variety of chronic pain conditions. Of note, lower cortisol levels have been reported in persons with fibromyalgia, chronic pelvic pain, endometriosis, and headache. Data specific to migraine showed normal HPA axis function in episodic migraine, but abnormal HPA axis activity in chronic migraine (CM), including in the setting of medication overuse. The CM studies showed higher, rather than lower, cortisol levels. History of early life stress and depression was not factored into the analysis.
Childhood maltreatment is more common in girls than boys, but when abused, are girls more vulnerable to HPA stress axis dysregulation than boys? A 1987 meta-analysis of 12 psychophysiological studies examining the relationship between sex and stress responsiveness suggested that the sex-related response differences were limited, but more recent studies using tests better able to generate adequate HPA axis responses are intriguing. These studies, summarized in a review by Kajantie, demonstrate that differences between age-matched men and women are minimal in the unstressed state, but between puberty and menopause women generally showed lower HPA axis and autonomic responses following a psychological stressor. When the stress response is dissected, the male hypothalamus shows increase sensitivity and CRH leading to increased ACTH synthesis. The premenopausal female adrenal cortex is, however, more sensitive to ACTH, thus counterbalancing the lower ACTH concentrations, and minimizing differences in the production of cortisol. Cortisol bioavailability, however, is decreased in women because estrogen stimulates the synthesis corticosteroid binding globulin. The complex effects of estrogen on HPA axis responsiveness are also reflected by estrogen receptor-beta inhibition of arginine vasopressin (AVP) gene transcription and synthesis. AVP is produced in the hypothalamus and with potentiates ACTH release in the pituitary in addition to directly stimulating cortisol secretion in the adrenal cortex. In a CRH stimulation test combined with AVP administration, young women show greater plasma ACTH and total cortisol responses compared with men, indicating an increased sensitivity of the female pituitary to AVP. Recently, an estrogen-responsive portion of the promoter region of the CRH gene has been indentified, and the significance of this bears exploring.
Early stress also results in a number of other functional changes that may play a role in migraine. Preclinical studies demonstrate that stress increases dopamine levels and attenuates serotonin levels in the amygdala and nucleus accumbens. It also decreases serotonin 1B (5-HT1B) receptor expression as well as reduces the density of both central benzodiazepine receptors and high-affinity GABA-A receptors. Other functional changes linked to early life stress include enhanced electrical irritability in limbic structures, and reduced activity of the cerebellar vermis, which, with the highest density of glucocorticoid receptors during development, may be particularly vulnerable to the effects of stress hormones.
Studies in migraineurs demonstrate an ictal rise in inflammatory cytokines, as well as evidence of a baseline elevation in pro-inflammatory cytokines. Psychological stress also leads to the release of pro-inflammatory cytokines and this has been postulated as a link to the development of chronic pain. Given the growing epidemiological evidence of an association of early abuse and migraine, it is noteworthy that a recent biomarker study has demonstrated inflammatory changes in adults exposed to maltreatment in childhood. Sex differences in these clinical studies have not been examined, but the preclinical finding that estradiol inhibits pro-inflammatory cytokine gene expression, nuclear factor kappa B (NFkB) activation, and pro-inflammatory cytokine production, suggests they may occur.

Structural Changes

Early stressful experiences have been associated with a number of structural neurobiological consequences including attenuated development of the left prefrontal cortex, amygdala, and hippocampus, all structures which interact with each other and play important roles in the pain matrix, as well as in the stress response. The hippocampus, for instance, down-regulates the HPA stress response, and hippocampal atrophy may therefore result in a prolonged response to psychological stressors. The size of the corpus callosum is also reduced in persons who have early stressful experiences. The corpus callosum of boys appears to be particularly vulnerable to the effects of neglect, while that of girls appears to be more susceptible to the adverse effects of sexual abuse. Animal studies indicate that early experience affects the number of corpus callosum axons in females, but only the diameter of corpus callosum axons in males. Hence, there may be marked gender differences in the nature, and extent of corpus callosum vulnerability.
Age of the persons at the time of abuse may also be an important determinant of structural cerebral changes, with different regions showing unique sensitive periods to the effects of stress. In a recent volumetric analysis of brain magnetic resonance imaging scans from young women who had been victims of repeated childhood sexual abuse and healthy female controls, it was found that hippocampal volume was reduced in association with abuse at ages 3–5 years and ages 11–13 years. Corpus callosum was reduced with childhood sexual abuse at ages 9–10 years, and frontal cortex was attenuated in subjects with childhood sexual abuse at ages 14–16 years.


There has been growing evidence that certain genotypes predict vulnerability to environment stressors, including early adverse experiences. This is referred to as a gene–environment (G × E) interaction. The serotonin transporter (5 serotonin transporter-linked polymorphic region [HTTLPR]) genotype, for instance, appears to moderate the effect of childhood maltreatment on adult psychiatric conditions, such as depression and post-traumatic stress disorder. With regards to sex-related differences in the G × E interaction, one study suggested that of those with the vulnerable short/short (SS) genotype, girls were more depressed, and boys less depressed than their peers with long/long (LL) and short/long (SL) genotypes. In another study of adolescents, evidence for G × E held only for girls. The corticotropin releasing hormone receptor 1 (CRH-R1) gene has also been of considerable interest, because it has been associated with protection against adult depressive symptoms in individuals, particularly men, who were maltreated as children. A recent study showed that a CRH-R1 gene polymorphism interacts with male sex to decrease the cortisol response in the dexamethasone-corticotropin-releasing factor (CRF) test.


Recent studies have highlighted the possibility that childhood abuse and early life stress may become hard-coded into the genome, creating an epigenetic memory of events that leads to impaired health at a later date. In a preclinical study, early life stress in mice caused enduring hypersecretion of corticosterone and alterations in passive stress coping and memory accompanied by a persistent increase in AVP expression in neurons of the hypothalamic paraventricular nucleus, demonstrating that early life stress can lead to epigenetic changes that affect the neuroendocrine system as well as behavior. In a study of suicide victims stratified by childhood abuse history, post-mortum brain examination revealed an altered cytosine-methylation pattern in the promoter region of the hippocampal glucocorticoid receptor gene of the abused.

Implications for Treatment

No studies on the impact of childhood maltreatment on treatment response in migraine have been conducted, but the depression literature suggests the possibility of a lower rate of recovery in the abused and a need for tailoring therapy to address emotional, cognitive, behavioral issues as well as the neurobiological basis of disease. Preclinical studies suggest that treatment with serotonin-specific reuptake inhibitors may actually reverse some of the neurobiological effects of maltreatment, including decreasing the CRH response to stress. The emerging field of epigenetics presents the prospect of new therapies, including such strategies of methyl supplementation. There are also a number of psychotherapeutic approaches to treat adults abuse in childhood, including emotion-focused therapy. Given the high prevalence of maltreatment in this population, determining whether knowledge of this history can guide differential treatment strategies in migraine and comorbid conditions is an exciting new avenue of research.