The current paradigm of child abuse limits pre-childhood causal research

As an adult, what would be your primary concern if you suspected that your early life had something to do with current problems? Would you be interested in effective treatments of causes of your symptoms?

Such information wasn’t available in this 2016 Miami review of the effects of child abuse. The review laid out the current paradigm mentioned in Grokking an Adverse Childhood Experiences (ACE) score, one that limits research into pre-childhood causes for later-life symptoms.


The review’s goal was to describe:

“How numerous clinical and basic studies have contributed to establish the now widely accepted idea that adverse early life experiences can elicit profound effects on the development and function of the nervous system.”

The hidden assumption of almost all of the cited references was that these distant causes can no longer be addressed. Aren’t such assumptions testable here in 2016?

As an example, the Discussion section posed the top nine “most pressing unanswered questions related to the neurobiological effects of early life trauma.” In line with the current paradigm, the reviewer assigned “Are the biological consequences of ELS [early life stress] reversible?” into the sixth position.

If the current paradigm encouraged research into treatment of causes, there would probably already be plenty of evidence to demonstrate that directly reducing the source of the damage would also reverse the damaging effects. There would have been enough studies done so that the generalized question of reversibility wouldn’t be asked.

Aren’t people interested in human treatments of originating causes so that their various symptoms don’t keep bubbling up? Why wouldn’t research paradigms be aligned accordingly?


The review also demonstrated how the current paradigm of child abuse misrepresents items like telomere length and oxytocin. Researchers on the bandwagon tend to forget about the principle Einstein expressed as:

“No amount of experimentation can ever prove me right; a single experiment can prove me wrong.”

That single experiment for telomere length arrived in 2016 with Using an epigenetic clock to distinguish cellular aging from senescence. The seven references the review cited for telomere length that had “is associated with” or “is linked to” child abuse findings should now be viewed in a different light.

The same light shone on oxytocin with Testing the null hypothesis of oxytocin’s effects in humans and Oxytocin research null findings come out of the file drawer. See their references, and decide for yourself whether or not:

“Claimed research findings may often be simply accurate measures of the prevailing bias.”

http://www.cell.com/neuron/fulltext/S0896-6273%2816%2900020-9 “Paradise Lost: The Neurobiological and Clinical Consequences of Child Abuse and Neglect”

The effects of imposing helplessness

This 2016 New York rodent study found:

“By using unbiased and whole-brain imaging techniques, we uncover a number of cortical and subcortical brain structures that have lower activity in the animals showing helplessness than in those showing resilience following the LH [learned helplessness] procedure. We also identified the LC [locus coeruleus] as the sole subcortical area that had enhanced activity in helpless animals compared with resilient ones.

Some of the brain areas identified in this study – such as areas in the mPFC [medial prefrontal cortex], hippocampus, and amygdala – have been previously implicated in clinical depression or depression-like behavior in animal models. We also identified novel brain regions previously not associated with helplessness. For example, the OT [olfactory tubercle], an area involved in odor processing as well as high cognitive functions including reward processing, and the Edinger–Westphal nucleus containing centrally projecting neurons implicated in stress adaptation.

The brains of helpless animals are locked in a highly stereotypic pathological state.”

Concerning the study’s young adult male subjects:

“To achieve a subsequent detection of neuronal activity related to distinct behavioral responses, we used the c-fosGFP transgenic mice expressing c-FosGFP under the control of a c-fos promoter. The expression of the c-fosGFP transgene has been previously validated to faithfully represent endogenous c-fos expression.

Similar to wild-type mice, approximately 22% (32 of 144) of the c-fosGFP mice showed helplessness.”

The final sentence of the Introduction section:

“Our study..supports the view that defining neuronal circuits underlying stress-induced depression-like behavior in animal models can help identify new targets for the treatment of depression.”


Helplessness is both a learned behavior and a cumulative set of experiences during every human’s early life. Therapeutic approaches to detrimental effects of helplessness can be different with humans than with rodents in that we can address causes.

The researchers categorized activity in brain circuits as causal in the Discussion section:

“Future studies aimed at manipulating these identified neural changes are required for determining whether they are causally related to the expression of helplessness or resilience.”

Studying whether or not activity in brain circuits induces helplessness in rodents may not inform us about causes of helplessness in humans. Our experiences are often the ultimate causes of helplessness effects. Many of our experiential “neural changes” are only effects, as demonstrated by this and other studies’ induced phenotypes such as “Learned Helplessness” and “Prenatally Restraint Stressed.”

Weren’t the researchers satisfied that the study confirmed what was known and made new findings? Why attempt to extend animal models that only treat effects to humans, as implied in the Introduction above and in the final sentence of the Discussion section:

“Future studies aimed at elucidating the specific roles of these regions in the pathophysiology of depression as well as serve as neural circuit-based targets for the development of novel therapeutics.”

http://journal.frontiersin.org/article/10.3389/fncir.2016.00003/full “Whole-Brain Mapping of Neuronal Activity in the Learned Helplessness Model of Depression” (Thanks to A Paper a Day Keeps the Scientist Okay)

State-dependent brain functions and adrenaline

This 2015 German/Italian rodent study investigated:

“How a specific neuromodulatory input may influence the information content and the readout of cortical information representations of sensory stimuli.

The locus coeruleus (LC) is a brainstem neuromodulatory nucleus that likely plays a prominent role in shaping cortical states via a highly distributed noradrenaline release in the forebrain. In particular, the LC:

  • contributes to regulation of arousal and sleep;
  • it is involved in cognitive functions such as vigilance, attention, and selective sensory processing; and
  • it modulates cortical sensory responses and cortical excitability.

An important addition of our work to previous models of state dependence was the inclusion of the contribution of an important neuromodulator—the noradrenergic system. Our results support the hypothesis that the temporal structure of LC firing causally influences cortical dynamics.

Our work highlights the importance of timing of LC burst: suitably timed LC burst (for example, triggered by an alerting stimulus) can very rapidly trigger transitions into excitable cortical states, which in turn decrease the threshold for cortical responses and thus dynamically facilitate the processing of salient or attended events.

State dependence may either:

  • force neurons to transmit information only using codes that are robust to state fluctuations (e.g., relative firing rates), or may
  • force downstream neurons to gain information about the state of the networks sending the sensory messages and then to use the knowledge of state to properly interpret neural responses.

Our results suggest that the latter information transmission scheme is feasible, because detecting state by either monitoring the dynamics of cortical ongoing activity alone or by also monitoring the dynamics of noradrenergic modulation substantially increased the amount of information about sensory stimuli in the late response components relevant for behavior.”

The study added to the evidence that state dependencies can’t be overlooked in explanations of brain function and resultant physical and mental activity. Locus coeruleus neural activity “can very rapidly trigger transitions into excitable cortical states..and thus dynamically facilitate the processing of salient or attended events.”

Adrenaline from the locus coeruleus produced a state of arousal in multiple brain and body areas tied into the subjects’ sympathetic nervous systems. Such internal state changes may be accompanied by state-dependent memories, following the findings of What can cause memories that are accessible only when returning to the original brain state?

The study highlighted the capability of a lower brain structure to influence other brain areas. Its findings should inform researchers in attention and behavior studies, especially when investigating causes of certain attention and behavior difficulties.

http://www.pnas.org/content/112/41/12834.full “Modeling the effect of locus coeruleus firing on cortical state dynamics and single-trial sensory processing”

If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

This 2014 rodent research reliably induced many disorders common to humans. Here are some post-birth problems the researchers caused, primarily by applying different types of stress, as detailed in the study’s supplementary material:

  • Social defeat
  • Social avoidance behavior
  • Learned helplessness
  • Irritable bowel syndrome
  • Depression
  • Anxiety
  • Anhedonia

Yet the researchers’ goal was to identify a brain receptor for:

“Novel therapeutic targets for stress-related disorders.”

In other words, develop new drugs to treat the symptoms.


Where are the studies that have goals to prevent these common problems being caused in humans by humans?

Where is the research on treatments to reverse the enduring physiological responses to stress by treating the causes?


What do you think of this excerpt?

“Accumulating evidence suggests that traumatic events particularly during early life (e.g., parental loss or neglect) coupled with genetic factors are important risk factors for the development of depression and anxiety disorders.

Moreover, the brain is particularly vulnerable to the effects of stress during this period.

Maternal separation in rodents is a useful model of early-life stress that results in enduring physiological and behavioral changes that persist into adulthood, including increased hypothalamic–pituitary–adrenal (HPA)–axis sensitivity, increased anxiety, and visceral hypersensitivity.”

http://www.pnas.org/content/111/42/15232.full “GABAB(1) receptor subunit isoforms differentially regulate stress resilience”

The brainstem nucleus locus coeruleus is the primary source of norepinephrine

This 2014 rodent study provided further information on the locus coeruleus segment of the brainstem:

“The brainstem nucleus locus coeruleus is the primary source of norepinephrine to the mammalian neocortex.

Neurons in the locus coeruleus maintain segregated connections to brain regions with distinctly different functions. Specifically, cells that communicate with the prefrontal cortex, a region involved in cognition and executive function, are characterized by properties that allow for independent and asynchronous modulation of operations in this area, compared with those that project to the motor cortex and regulate movement generation.”

http://www.pnas.org/content/111/18/6816.full “Heterogeneous organization of the locus coeruleus projections to prefrontal and motor cortices”

Rebooting the brain with anesthesia: Implications for Primal Therapy and evolution

Here are some paragraphs from a 2013 summary article of 105 studies entitled Evolution of consciousness: Phylogeny, ontogeny, and emergence from general anesthesia:

“The emergence of consciousness (from anesthesia) (as judged by the return of a response to command) was correlated primarily with activity of the brainstem (locus coeruleus), hypothalamus, thalamus, and anterior cingulate (medial prefrontal area). Surprisingly, there was limited neocortical involvement that correlated with this primitive form of consciousness.

In the sleep study, midline arousal structures of the thalamus and brainstem also recovered function well before cortical connectivity resumed. Thus, the core of human consciousness appears to be associated primarily with phylogenetically ancient structures mediating arousal and activated by primitive emotions, in conjunction with limited connectivity patterns in frontal–parietal networks.

The emergence from general anesthesia may be of particular interest to evolutionary biology, as it is observed clinically to progress from primitive homeostatic functions (such as breathing) to evidence of arousal (such as responsiveness to pain or eye opening) to consciousness of the environment (as evidenced by the ability to follow a command) to higher cognitive function.

Regarding ontogeny of H. sapiens, peripheral sensory receptors are thought to be present from 20 wk of gestation in utero. The developmental anlage of the thalamus is present from around day 22 or 23 postconception, and thalamocortical connections are thought to be formed by 26 wk of gestation. Around the same time of gestation (25–29 wk), electrical activity from the cerebral hemispheres shifts from an isolated to a more continuous pattern, with sleep–wake distinctions appreciable from 30 wk of gestation.

Thus, both the structural and functional prerequisites for consciousness are in place by the third trimester, with implications for the experience of pain during in utero or neonatal surgery.


I recently came out of anesthesia after being anesthetized for three hours during rotator cuff surgery. I felt pain, and went into a primal reliving of a painful memory.

I interpret the event as a reliving of my birth experience because of the following:

  • The beginning point was complete anesthetization as it was at my birth. My mother was completely anesthetized, so I, weighing less than one twentieth of her, was also completely anesthetized.
  • I felt a great urge and impulse to “get out” as it was at my birth. The attending nurse told me the next day that she called over another person to help her restrain me in the post-op chair.
  • I had a great need for oxygen and started breathing rapidly as it could have been at my birth. The nurse told me the next day that she was already giving me oxygen, and per the monitors, I didn’t need more oxygen.
  • I had to frequently “spit up” as it could have been at my birth. There was nothing in my current situation to cause me to expectorate.
  • My lower brain and limbic system were in control, as I thrashed, cried and moaned. I probably used primarily the same brain areas as what were the developed parts of my brain at birth.

The attending nurse told me the next day when I called her that she followed the established protocol, which was to get me out of the experience. She intentionally distracted me away from my pain. I was instructed to sit still, to think of some place pleasant, and to calm down.

I heard her as though she was at the other end of a tunnel at first, and then started to comply as I regained cognitive awareness.


I understand how such a powerful event could present a danger to a patient. It didn’t occur to me to tell the nurse until the next day that I had relevant history, that I have had relivings while in therapy, and wasn’t in the same danger that her regular patients may have been.

Even if I had said something, however:

  • Neither the anesthesiologist nor the attending nurse had a method of understanding how an evolutionary-determined sequential process – such as rebooting a person’s brain after prolonged anesthesia – may have therapeutic benefits.
  • They had no training to recognize aspects of neurobiologic therapeutic value in what was going on inside of me during this event, as a therapist in Dr. Arthur Janov’s Primal Therapy has.
  • The default response per medical protocol would be to shut down a patient’s expressions of their feelings.

As a result, my experience of this event was pretty much the opposite of what happens in Primal Therapy. Although I didn’t feel harmed, my reliving wasn’t therapeutic, as previous relivings had been. Its progression through my levels of consciousness was purposely interrupted, and approached from a non-therapeutic direction.

Unlike my experience of coming out of anesthesia, Dr. Arthur Janov’s Primal Therapy isn’t something the patient is thrown into and potentially overwhelmed by their feelings. It’s a gradual process where the patient is in control.

This summary study showed that existing science is already in alignment with the background of Primal Therapy, that the core of human consciousness is in the limbic system and lower brain structures. My anesthesia experience showed that medical professionals are familiar with at least the outward signs of a primal reliving.

The challenge seems to be how to use this complementary knowledge for people’s benefit. What can be done so that people aren’t burdened with the continuing adverse effects of traumas?

How can scientists and medical professionals get the eyes to see what’s in front of them?