The Pedophile's Guide into Developmental Traumatology

Galaburda, Cyril; Mar 16 2020
Type of WorkEssay

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).


  • “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 [hormonal?] 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 [hormonally?].

The contradiction between attributing hyper-cortisolism and attributing hypo-cortisolism 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 hyper-cortisolism to hypo-cortisolism, 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.