Àííîòàöèÿ: Upon endocrynologic ways of diagnosting PTSD in the "victims" of CSA
THE PEDOPHILE'S GUIDE INTO DEVELOPMENTAL TRAUMATOLOGY, BY CYRIL E. GALABURDA
Filmmakers like Ramsey and Scorsese urge war veterans to brain "pedophiles" and save children from PTSD (post-traumatic stress disorder). In reality, "whereas single trauma exposure in children occasionally precipitates the classic PTSD reactions that the DSM-III (Diagnostic & Statistical Manual of Mental Disorders developed by the American Psychiatric Association) originally defined for combat veterans and burn victims, repeatedly traumatized children meet diagnostic criteria for many diagnoses (Ackerman et al., 1998; Culp et al., 1987), none of which capture their profound developmental disturbances or the traumatic origins of their particular clinical presentations. Symptoms of PTSD in chronically traumatized children are usually not prominent" (der Kolk, 2003; Tofoli et al., 2011).
F.i., such symptom as "persistent avoidance of stimuli associated with the trauma(s)" is not obligatory to diagnose PTSD because it is said that children "under conditions of uncontrollable shock do not learn escape behaviors" (de Bellis & Zisk, 2011). Also "in almost all cases the children" show "no understanding or recall of traumatic events in their early life" (Perry, 2006), that's why flashbacks cannot serve as an obligatory symptom of PTSD.
Hence, the Vietnam syndrome and "childhood sexual trauma" are totally different kinds of PTSD that cannot be compared! Despite of the fact that in one study "no cases met the DSM-IV algorithm for PTSD" among "sixty-two traumatized children" (Schneeringa et al., 2003), scientists are still preconceived to diagnose PTSD in any case of CSA (childhood sexual "abuse").
In order to declare as many children as possible to be victims the "more objective criteria" of PTSD are developed, and PTSD is "conceptualized as a dimensional process (rather) than a categorical all-or-none outcome" (de Bellis et al., 2011). What symptoms can be invented for the invisible forms of PTSD?
"The presence of elevated levels of glucocorticoids (hormons like cortisol produced by the adrenal glands) has so consistently been associated with stress that it has come to be considered an indicator that a stress reaction has taken place" (van Voochees & Scarpa, 2004). Indeed, "augmented mean morning serial plasma cortisol levels were found in sexually abused girls recruited within six months of disclosure compared with non-abused socio-demographically matched controls. This suggests morning hypersecretion of cortisol in sexually abused girls (Putnam et al., 1991"; de Bellis et al., 1994; Cicchetti & Rogosch, 2001; de Bellis, 2002; Favarelli et al., 2010).
Yes, the same elevated levels of cortisol and of hormons needed for cortisol secretion were found in male combat veterans with PTSD (Pittman & Orr, 1990; Bremner et al., 1997; Yehuda, 1998; Baker et al., 1999) so that CSA-related PTSD may be diagnosed even in the case when it does not meet the DSM criteria.
If only! "In clinically referred samples, the reported incidence rates of PTSD (satisfying the DSM criteria for PTSD and) resulting from sexual abuse range from 42% to 90% (Dubner & Motta, 1999; Lipschitz et al., 1999; McLeer et al., 1994)," and while some scientists tell us the rest of the "victims" of CSA have less cortisol in their urine (Lemieux & Coe, 1995, - contrary to de Bellis & Zisk, 2011), another scientists tell us they have more cortisol in their plasma (Bremner et al., 2003)!
It is impossible to diagnose PTSD by humoral levels that are different in the morning and in the afternoon (Kaufman, 1991; Hart et al., 1996), when psychologically, endocrinously "stimulated" or are abnormally "basal" (Francis et al., 1996; Heim et al., 2001), for cortisol and for another hormons involved into the HPA (hypothalamic-pituitary-adrenal) axis (de Bellis et al., 1994; Tarullo & Gunnar, 2006) like ACTH (adrenocorticotropic hormone provoking the adrenal glands into cortisol secretion) and CRH (corticotropin-releasing hormone provoking the pituitary gland into ACTH secretion).
No wonder, that while "one study of sexually abused girls showed a blunted ACTH response to CRH challenge but a normal cortisol response (De Bellis et al., 1994"; Bremner et al., 2003; de Bellis & Zisk, 2011), another showed "increased ACTH response (Kaufman et al., 1997)" or "lower basal cortisol levels" (Stein et al., 1997; Heim et al., 2001; der Kolk, 2003; Trickett et al., 2011).
Normal and even lower cortisol levels?! Now, they call it "a dysregulatory disorder of the HPA axis", and "interpret low cortisol as a biological marker for PTSD disease severity (e.g., based on the correlations between low cortisol and high symptom severity)" (Bremner et al., 2003) - and not only in the "victims" of CSA but also in war veterans (Mason et al., 1986; Yehuda et al., 1990; Pittman & Orr, 1990; Boscarino, 1996; Yehuda et al., 1996). According to one study, "combat veterans with PTSD suppressed cortisol to a greater extent than did combat veterans without PTSD and normal controls in response to both doses of dexamethasone" (Yehuda et al., 1995).
Though one meta-analysis has "found no systematic difference in basal cortisol levels between people with PTSD and controls" (Meewise et al., 2007)! When put together, all these scientific data make absolutely no sense. By no means PTSD can be diagnosed humorally.
The contradiction between attributing hypercortisolism and attributing hypocortisolism to the "victims" of CSA is tried to be explained as their steady or "catch-up growth, including remission of severe psychopathology and normalization of cognitive function (Koluchova, 1972; Koluchova, 1976; Money et al., 1983"; Gunnar & Vazquez, 2001; Rutter & O'Connor, 2004), and "a chronic compensatory adaptation of the HPA axis to persistently elevated levels of central CRH" (Yehuda et al., 1990; Chrousos & Gold, 1992; Susman, 2006; McEwen, 2007; Carpenter et al., 2007; Tyrka et al., 2008).
It is said, f.i., that "a longitudinal study of sexually abused girls has documented this transition from hypercortisolism to hypocortisolism, reporting elevated basal morning levels at around age 11 (de Bellis & Putnam, 1994) and low basal levels at around age 18 (Putnam, 2003)." (See also de Bellis et al., 1999, and Trickett et al., 2011.) Nevertheless, we know that "an increased cortisol response" after "both sexual and physical abuse" in childhood was observed even in adults (Heim et al., 2008; Lemieux & Coe, 1995; Heim et al., 2000; Heim et al., 2001; Rasmusson et al., 2001; Bremner et al., 2003; Lindley, Carlson & Benoit, 2004), that's why the "victim's" growing does not resolve the contradiction of attributing both elevated and low cortisol levels to the "victims" of CSA.
Neither do "the habituation phenomena" because contrary to adaptation "some authors have hypothesized... a biological "wound" that increases the individual's vulnerability to stressors later in life and, thus, predisposes an individual to develop mood or anxiety disorders that are known to manifest or worsen in relationship to acute or chronic life stress (Arborelius et al., 1999; Heim & Nemeroff, 2001; Safren et al., 2002; Nemeroff, 2004; Faravelli et al., 2010; Bandelow et al., 2004). In fact, once the HPA axis is over-activated during the developmental processes, it remains permanently unstable, overdriven, vulnerable or dysfunctional (Nemeroff, 2004; Tyrka et al., 2008; Joëls, Krugers & Karst, 2008),.. elevations in cortisol levels that persist across time could also tune HPA axis activity to a higher level and could result in damage of the hippocampal glucocorticoid receptors or even a loss of hippocampal neurons (Bremner et al., 2003), reducing the negative feedback of CRH secretion and resulting in higher CRH and cortisol concentrations (Greaves-Lord et al., 2007)."
Thus, scientists cannot agree upon whether the "victims" of CSA have elevated, normal or low levels of cortisol, and scientists cannot convince us that one "victim" can be both poisoned with and deprived of cortisol.
It means that hyper-/hypocortisolism cannot serve as a diagnostic criterium for PTSD. During the meta-analysis "among studies with the same time frame for years since trauma no differences were found for cortisol levels of people with PTSD and controls" (Meewise et al., 2007).
So when a "victim" of CSA cannot be diagnosed with PTSD we may provide two explanations:
• there is no PTSD;
• there is PTSD but it is concealed by the impaired HPA axis.
The latter explanation contradicts Occam razor and Popper falsifiability principles, but the first is quite credible.
We know that 85% of CSA cases are non-compulsory (Lanyon, 1986), in more than 64% children participate (Virkkunen, 1981), in more than 40% children are initiators (Mohr et al., 1964; Rossman, 1976; Bernard, 1982; Kilpatrick, 1992). More than a half (54%) of the 12-year-olds who reported sexual contacts with an adult described it as a positive experience (Lahtinen et al., 2014), "but less than half of the (15-years-olds reporting CSA) perceived these experiences as sexual abuse" (Helweg-Larsen & Larsen, 2006).
If sex is wanted by the child it is neither abusive, nor stressful, nor traumatic, and PTSD may be caused by non-sexual abuse, neglect, disclosure, compulsory treatment, and anti-sexual rearing. Yet the idea that willing sex causes PTSD is far from being proved - and before it is proved Richard Hackle's, Paul Cooper's, William Elliot's, Robert Berdick's, Bijan Ebrahimi's and another "pedophiles'" violent deaths remain unfair.
SOURCES
• Arborelius et al., 1999: "The role of corticotropin-releasing factor in depression and anxiety disorders", quoted from Faravelli et al., 2012.
• Ackerman et al., 1998: "Prevalence of post traumatic stress disorder and other psychiatric diagnoses in three groups of abused children (sexual, physical, and both)", quoted from der Kolk, 2003.
• Baker et al., 1999: "Serial CSF corticotropin-releasing hormone levels and adrenocortical activity in combat veterans with posttraumatic stress disorder", quoted from de Bellis, 2002.
• Bandelow et al., 2004: "Early traumatic life events, parental rearing styles, family history of mental disorders, and birth risk factors in patients with social anxiety disorder", quoted from Faravelli et al., 2012.
• Bartol, 2004: "Criminal Behavior: A Psychosocial Approach", the Russian translation.
• Bernard, 1982: "Kinderschänder? Paedophilie - von der Liebe mit Kindern", quoted from Norlik, 2013.
• Boscarino, 1996: "Posttraumatic stress disorder, exposure to combat, and lower plasma cortisol among Vietnam veterans: Findings and clinical implications", quoted from Carrion et al., 2002.
• Bremner et al., 1997: "Magnetic Resonance Imaging-Based Measurement of Hippocampal Volume in Posttraumatic Stress Disorder Related to Childhood Physical and Sexual Abuse."
• Bremner et al., 2003: "Assessment of the Hypothalamic-Pituitary-Adrenal Axis over a 24-Hour Diurnal Period and in Response to Neuroendocrine Challenges in Women with and without Childhood Sexual Abuse and Posttraumatic Stress Disorder."
• Brongersma, 1990: "Loving Boys", vol. 2.
• Carpenter et al., 2007: "Decreased adrenocorticotropic hormone and cortisol responses to stress in healthy adults reporting significant childhood maltreatment", quoted from Videlock et al., 2009.
• Carrion et al., 2002: "Diurnal Salivary Cortisol in Pediatric Posttraumatic Stress Disorder."
• Chrousos & Gold, 1992: " The concepts of stress and stress system disorders: overview of physical and behavioral homeostasis", quoted from de Bellis, 2002.
• Cicchetti & Rogosch, 2001, quoted.
• Culp et al., 1987: "Differential developmental progress of maltreated children in day treatment", quoted from der Kolk, 2003.
• De Bellis & Putnam, 1994: " The psychobiology of childhood maltreatment", quoted from Tarullo & Gunnar, 2006.
• De Bellis & Zisk, 2011: "The Biological Effects of Childhood Trauma."
• De Bellis et al., 1994: "Urinary catecholamine excretion in sexually abused girls", an abstract and quoted from Tarullo & Gunnar, 2006.
• De Bellis et al., 1999: "Developmental traumatology, part II: Brain development", quoted from van Voorchees & Scarpa, 2004.
• De Bellis et al., 2011: "Neurodevelopmental Biology Associated With Childhood Sexual Abuse."
• De Bellis, 2001: "Developmental traumatology: The psychobiological development of maltreated children and its implications for research, treatment, and policy."
• De Bellis, 2002: "Developmental traumatology: a contributory mechanism for alcohol and substance use disorders."
• Der Kolk, 2003: "The neurobiology of childhood trauma and abuse."
• Dubner & Motta, 1999: "Sexually and physically abused foster care children and posttraumatic stress disorder", quoted from de Bellis et al., 2011.
• Faravelli et al., 2010: "Childhood traumata, Dexamethasone Suppression Test and psychiatric stymptoms: a trans-diagnostic approach", quoted from Tofolli et al., 2011.
• Faravelli et al., 2012: "Childhood stressful events, HPA axis and anxiety disorders."
• Francis et al., 1996: "Early environmental regulation of forebrain glucocorticoid receptor gene expression."
• Goenjian et al., 1996: "Basal Cortisol, Dexamethasone Suppression of Cortisol, and MHPG in Adolescents after the 1988 Earthquake in Armenia."
• Greaves-Lord et al., 2007: "Higher cortisol awakening response in young adolescents with persistent anxiety problems", quoted from Faravelli et al., 2012.
• Gunnar & Vazquez, 2001: "Low cortisol and a flattening of expected daytime rhythm: potential indices of risk in human development", quoted from van der Vegt et al., 2008.
• Hart et al., 1996: "Altered neuroendocrine activity in maltreated children related to symptoms of depression", quoted from van Voorhcees & Scarpa, 2004.
• Heim & Nemeroff, 2001: "The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies", quoted from Tarullo & Gunnar, 2006.
• Heim et al., 2000: "Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood", quoted from Tarullo & Gunnar, 2006.
• Heim et al., 2001: "Altered Pituitary-Adrenal Axis Responses to Provocative Challenge Tests in Adult Survivors of Childhood Abuse."
• Heim et al., 2008: "The dexamethasone/corticotropin-releasing factor test in men with major depression: role of childhood trauma", quoted from Tofoli et al., 2011.
• Helweg-Larsen & Larsen, 2006: "The prevalence of unwanted and unlawful sexual experiences reported by Danish adolescents: Results from a national youth survey in 2002", quoted from O'Carroll, 2018.
• Joëls et al., 2008: "Stress-induced changes in hippocampal function", quoted from Faravelli et al., 2012.
• Kaufman, 1991: "Depressive disorders in maltreated children", quoted from Bremner et al., 2003; Tarullo & Gunnar, 2006; van Voorches & Scarpa, 2004.
• Kilpatrick, 1992: "Long-Range Effects of Child and Adolescent Sexual Experiences", quoted from Norlik, 2013.
• Koluchova, 1972: "Severe deprivation in twins: A case study", quoted from de Bellis, 2001.
• Koluchova, 1976: "The further development of twins after severe and prolonged deprivation: A second report", quoted from de Bellis, 2001.
• Lahtinen et al., 2014, quoted from O'Carroll, 2018.
• Lanyon, 1986: "Theory and treatment in child molestation" (?), quoted from Bartol, 2004, and Norlik, 2013.
• Lemieux & Coe, 1995: "Abuse-related posttraumatic stress disorder, evidence for chronic neuro-endocrine activation in women", quoted from de Bellis, 2002, and Faravelli et al., 2012.
• Lindley et al., 2004: "Basal and dexamethasone suppressed salivary cortisol concentrations in a community sample of patients with posttraumatic stress disorder", quoted from Faravelli et al., 2012.
• Lipschitz et al., 1999: "Posttraumatic stress disorder in hospitalized adolescents: psychiatric comorbidity and clinical correlates", quoted from de Bellis et al., 2011.
• Mason et al., 1986: "Urinary free cortisol levels in post-traumatic stress disorder patients", quoted from Bremner et al., 2003, and Goenjian et al., 1996.
• McEwen, 2007: "The neurobiology of stress: from serendipity to clinical relevance", quoted from de Bellis & Zisk, 2011.
• McLeer et al., 1994: "Psychiatric disorders in sexually abused children", quoted from de Bellis et al., 2011.
• Meewise et al., 2007: "Cortisol and post-traumatic stress disorder in adults."
• Mohr et al., 1964: "Pedophilia and Exhibitionism", quoted from Norlik, 2013.
• Money et al., 1983: "Abuse-dwarfism syndrome: After rescue, statural and intellectual catchup growth correlate", quoted from de Bellis, 2001.
• Nemeroff, 2004: "Early-Life Adversity, CRF Dysregulation, and Vulnerability to Mood and Anxiety Disorders", quoted from Faravelli et al., 2012.
• Norlik, 2013: "Tabuzone".
• O'Carroll, 2018: "Nothing like Nordic noir to cheer us up!", "Heretic TOC".
• Perry, 2006: "Neurobiological sequelae of childhood trauma: PTSD in children."
• Pittman & Orr, 1990: "Twenty-four hour cortisol and catecholamine excretion in combat-related posttraumatic stress disorder", quoted from de Bellis, 2002.
• Putnam et al., 1991: "Cortisol abnormalities in sexually abused girls", quoted from de Bellis, 2002.
• Putnam, 2003: Personal communication with Megan Gunnar, quoted from Tarullo & Gunnar, 2006.
• Rasmusson et al., 2001: "Increased pituitary and adrenal reactivity in premenopausal women with posttraumatic stress disorder", quoted from Faravelli et al., 2012.
• Rossman, 1976: "Sexual Experience between Men and Boys", quoted from Norlik, 2013.
• Rutter & O'Connor, 2004: "Are there biological programming effects for psychological development?", quoted from van der Vegt et al., 2008.
• Safren et al., 2002: "History of childhood abuse in panic disorder, social phobia, and generalized anxiety disorder", quoted from Faravelli et al., 2012.
• Schneeringa et al., 2003: "New findings on alternative criteria for PTSD in preschool children", an abstract.
• Stein et al., 1997: "Enhanced Dexamethasone Suppression of Plasma Cortisol in Adult Women Traumatized by Childhood Sexual Abuse", an abstract.
• Susman, 2006: "Psychobiology of persistent antisocial behavior: Stress, early vulnerabilities and the attenuation hypothesis", quoted from Trickett et al., 2011.
• Tarullo & Gunnar, 2006: "Child maltreatment and the developing HPA axis."
• Tofoli et al., 2011: "Early life stress, HPA axis, and depression."
• Trickett et al., 2011: "The impact of sexual abuse on female development: Lessons from a multigenerational, longitudinal research study."
• Tyrka et al., 2008: "Childhood parental loss and adult hypothalamic-pituitary-adrenal function", quoted from Faravelli et al., 2012.
• Van der Vegt et al., 2008: "Early neglect and abuse predict diurnal cortisol patterns in adults. A study of international adoptees."
• Van Voochees & Scarpa, 2004: "The Effects of Child Maltreatment on the Hypothalamic-Pituitary-Adrenal Axis."
• Videlock et al., 2009: "Childhood Trauma Is Associated With Hypothalamic-Pituitary-Adrenal Axis Responsiveness in Irritable Bowel Syndrome."
• Virkkunen, 1981: "The Child as Participating Victim", quoted from Brongersma, 1990, and Norlik, 2013.
• Yehuda et al., 1990: "Low urinary cortisol excretion in patients with post-traumatic stress disorder", quoted from Goenjian, 1996.
• Yehuda et al., 1995: "Dose-response changes in plasma cortisol and lymphocyte glucocorticoid receptors following dexamethasone administration in combat veterans with and without posttraumatic stress disorder", an abstract.
• Yehuda et al., 1996: "Increase pituitary activation following metyrapone administration in post-traumatic stress disorder", quoted from Carrion et al., 2002.
• Yehuda, 1998: "Psychoneuroendocrinology of post-traumatic stress disorder", quoted from van Voochees & Scarpa, 2004.