, Birth & Trauma
          The Biological Role of the
         Endogenous Hallucinogens
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Abstract and Prologue                                                                                         

Please note:  Shorter journal-ready versions of this monograph can be seen in

This monograph with its complete sections, including birth, trauma therapy and REM sleep, all involving the functions of endogenous hallucinogens was first entered into this website in 2008.


LSD, Birth, Trauma and REM Sleep:  The Biological Roles of Hallucinogens. 

 By Bruce McConnell, PhD 


It’s a bit late in the day to communicate a notion about the biological role of hallucinogens based on LSD experiences that happened some thirty years ago. Along with the demonization of hallucinogens by the media in the '60s, '70s and '80s, there was the lack of published research that would provide a convincing sense of depth and refinement for a hypothesis that might be hard to sell at the time.  Thanks to the Internet and to this last three decade’s progress in hallucinogen biology, a notion of the role of hallucinogens in birth, born three decades ago in an over-stimulated mind, can now be offered with attention to published results that would convey some gravitas to the effort.

It’s curious that others dedicated to clinical or laboratory studies have not considered hallucinogens in the context of human parturition, or so it seems.  In retrospect, there were clues.  Perhaps some hallucinogen workers did, but had no time to put aside demanding projects with their paucity of grant money, disappearing sources of legal hallucinogens and two decades of hysteria banning clinical studies on this most promising of drugs.   However there’s a much better reason why the notion would be missed by clinical and laboratory workers or by others.   It is unlikely in the extreme that they would have had the opportunity for such an exceptional initial LSD experience originating from an accident of birth involving an obstetric procedure abandoned in the 1960s, together with the manic curiosity of a trained biochemist.  

This curiosity brought about a sea change in my research during the last three years of my professorship, from the study of DNA proton lifetimes by NMR to that of brain receptors.   In a short time, I found Dr. Aghajanian’s 1968 paper showing that LSD shuts off the activity of raphe neurons and soon after, I learned the origin of my first LSD effects from Dr. Stanislav Grof as we talked after his lecture at my university.   For some weeks I resisted his assertion that it was a birth memory, because I was dourly resistant to both the idea and the practitioners in “rebirthing”, popular at the time.   Eventually, there seemed to be no choice but to accept the birth memory tale of Dr. Grof, who, after all, was famous for his Prague accounts of thousands of patients treated with LSD.   I could see (and hopefully you, the reader will) that the connection between my LSD sensations and those of an infant born by the Twilight sleep method was unmistakable.  I came to “feel it in my bones” that this first LSD session was not only retrieval of a Twilight birth memory, but originated somewhere within the brainstem/cerebellum in response to Aghajanian’s LSD raphe inhibition.   Simply put, a memory lodged in a secret crypt at birth was released 45 years later into my conscious awareness by the LSD inhibition of certain raphe nuclei, a process shown to dis-inhibit the reticular formation of the brainstem.  I was “sure” this was the process that unblocked the channels of impulse flow from the memory site into conscious awareness.  I was also aware of the delusory potential of this idea, enthralled as I was with the writings of Aubrey, Loren Eiseley and others on the mystique of biology, as well as the books on LSD kept under lock and key in the lower bowels of the university library.  Some of these profane readings warned against falling in love with any idea after LSD exposure.

Undaunted, like a mercifully uninformed graduate student, I threw myself into periods of 30 consecutive 12 to 16 hour days of testing the hallucinogen-birth possibility.  I restrained myself from applying for a NIH grant until I could publish something, because an earlier unsuccessful NIH grant attempt on another project was rewarded with a publication written verbatim by no less than one of my grant reviewers!   Scientists live in an unforgiving academic world of publications and I didn't pursue punishment.   Money from a grant application to a local obstetric hospital was not forthcoming (only MDs get money there), but I was given placenta to look for hallucinogen secretion at birth.   This was not the best approach, since the hallucinogens I did indeed find in placental extracts would not necessarily be secreted or be operative in the fetal brain. Placenta, already known to harbor a hallucinogen receptor, might be their only target.  Regardless, placenta is a good source of mother’s blood in labor and I chose this route as a quick publication for safety in grant applications.  The better choice might have been to measure the rise of the hallucinogen in maternal blood during labor from a statistically sound cohort of mothers (however, see 1.12 Testing Hypotheses).  This would take too long and would require loss of control to MD co-authors.   At this time the abrupt onset of chronic fatigue syndrome put a stop to my research and my faculty position.   I retired with my data unpublished and the placental hallucinogen unidentified.   Understandably, the  several hypotheses that emerged from an incomplete study might be suspect, were it not for the clarity and simplicity of the LSD experiences qualifying as unequivocal scientific results.

As to publication venues for this monograph, Machiavelli’s complaint comes to mind, “If you’re not ‘in’ with the rulers of Florence, not even the dogs will bark at you”.  Of course, publishing houses and psychedelic organizations must be wary of loose crackpots on a daily basis.  Also, this monograph would not pass peer review as a scientific paper, because 1) the author has no credentials in this area, 2) is no longer affiliated with a university, 3) it’s outside his previous field, 4) the experimental dosages are vague, 5) there’s no scientific confirmation that the drug was really LSD.  Nevertheless, real results form the basis of the interpretation. The authenticity of the street blotter LSD was verified by the very same effects produced by three other known hallucinogens, whose source and chemical verification were made.

The hallucinogen effects to be described here are exceptional, appearing in a small fraction of users born by the same bizarre birthing method that was popular between 1910 and 1970.  Called "dammerschlag" by its German inventors and "Twilight Sleep" in the USA, it involved injections of morphine and scopolamine to obliterate the mother's (cerebral) memory of the labor, doing the same for the fetus, who nevertheless, like the mother, did indeed store the memory in another part of the brain: The sub-cerebral realm below the hypothalamus, likely within a deep nucleus of the cerebellum.  It can be asserted with a certainty, despite Heisenberg, that all those born this way in this six decade period have no cerebral memory of their birth, but harbor a hidden subcortical memory that influences throughout life, can be erased and reveals that flashbacks are natural signs of autonomic attempts at healing these engrams each night during REM sleep.  It will be shown that long-term damage was inflicted on these Twilight newborns through an interruption of normal sequences of hormone secretion during birth.  The formal journal submissions for two papers are being installed and edited in the companion website,

LSD, Birth, Trauma and REM Sleep:  The Biological Roles of Hallucinogens.

 By Bruce McConnell, PhD

Abstract and Detailed Summary

The Holy Inquisition was correct in disallowing Galileo’s Copernican Heliocentric theory, as it was not a proof, but only an interpretation based on planetary position.

It is proposed that the biological roles of endogenous hallucinogens lay in the events of human parturition, in the control of trauma memory and in the role of REM sleep.   A neurobiological model is introduced to account for memory consolidation at birth and as a biological definition of trauma.  

These hypotheses are derived from two relatively rare LSD effects of completely different modalities on the same individual.  As discussed in Part 1 of the website above, the first modality was a conscious re-living of fetal sensations unique to a long-abandoned obstetric procedure called “Twilight Sleep”, in which scopolamine and morphine were employed to induce amnesia and semi-conscious anesthesia for the laboring mother.  This LSD recall of a birth memory was followed spontaneously by a series of exact encores or “flashbacks” that diminished with time until further recall was not forthcoming. The properties of these flashbacks suggest a natural ongoing process of removing noxious memories during REM sleep.

The second modality of LSD effect, occurring repeatedly in subsequent LSD trials, is presented in Part 2 of the website.  These took the form of effects in three phases during each entire session: 1) A short-lived “spike” of autonomic activation, measured as large simultaneous increases in heart rate, blood pressure and oral temperature, followed by, 2) Pleasurable urges to undertake repeating cycles of prodigiously strong and energetic movements into various body positions the fetus might take during the mother’s labor contractions and 3) a one to three day “recovery” period, remarkable for a drastic existential departure from the subject’s normal chronic, anhedonic depression.  This aftereffect appeared as a wholesome mental and physical integration with confident and pleasurable relaxation, increased awareness and much higher levels of athletic prowess.  As these three phases were reliably reproduced in many subsequent LSD sessions, it is concluded that LSD acted as a conventional pharmaceutical, in contrast to its present reputation as an unpredictable drug. LSD activated a pharmacological target that functions to initiate the normal sequence of hormone secretion, to activate the fetus and to mediate fetal memory consolidation. Thus, LSD was a surrogate to fetal endogenous hallucinogen(s) during normal birth.  For the subject, it is proposed that the full function of this pharmacological target had been interrupted by the use of scopolamine and remained incomplete as a developmental deficit.

These two distinct modalities of LSD effect, i.e., memory recall and fetal activation, are used as prima facie evidence for several hypotheses   amenable to testing in the laboratory and clinic.  They are as follows:

Hypothesis1, the Model.   A neuro-molecular model of specific functions within the brainstem accounts for the first result of LSD release of hidden memory and its flashbacks.  According to this model, binding of LSD to the brainstem 5-HT1a receptor inhibits the firing of serotonin neurons to suppress normal activity of raphe (Ra) nuclei.  This process removes normal inhibition of a proximal reticular nucleus (RN) to liberate impulse flow from cerebellar storage into the cerebral cortices that interpret these as re-lived pain.  Called the RaRN model, it is bi-directional:  RN activation opens a memory substrate that can both release or consolidate memory.

    Evidence: Intense skull sensations, free of psychological components and released from long-term memory by LSD, conformed in precise order to the pain and pressure a fetus would experience from the obstetrician’s efforts made according to the protocol of Twilight sleep.  The pristine physicality of these events suggests subcortical storage.

     Cited Evidence:  1) The well documented inverse relationship between the activities of raphe nuclei and the reticular formation, 2) The preference of indole hallucinogens for serotonin receptor subtypes, 3) Recent success in PTSD treatment with the use of MDMA, acting (hypothetically) as a 5-HT1a agonist and 4) the relative success of serotonin congeners as re-uptake inhibitors (SSRIs) in treating posttraumatic stress disorder (PTSD) .

      Argument: The RaRN model provides a biological definition of “trauma” in the requirement of raphe 5-HT neuron suppression for opening substrates that receive or liberate noxious memory.  Thus, the model clarifies many possible misconceptions in PTSD and hallucinogen therapy pertaining to the persistence of flashbacks, thus far considered to be negative symptoms of “injury”.  Here it is proposed that flashbacks are signs of the organism’s stepwise attempts to resolve or eliminate noxious memory (trauma).

Hypothesis 2, the Basic Idea.  It is proposed that adult re-living of a birth memory and consolidation of this memory at birth occur from the same RaRN brainstem condition, the former initiated by LSD and the latter involving fetal endogenous hallucinogens (EH). Both the mother and the fetus are under the influence of the endogenous hallucinogen, identified as N,N-dimethyltryptamine (DMT) and/or its congeners (DMT+).

Evidence:  It was an indole hallucinogen, LSD, that triggered a process of re-living a kind of memory that remained hidden for 45 years.  The proposed similarity of adult and fetal brainstem conditions and the inclusion of DMT+ are based on the continued spontaneous appearance of flashbacks as exact encores of the first recall.

     Cited evidence:   LSD and endogenous DMT+ are N,N-substituted indole amines that bind strongly as agonists to the inhibitory 5-HT1a and excitatory 5-HT2a (serotonin) receptors; the 2a receptor mediates the powerful hallucinogenic effects in the prefrontal cortex.

Hypothesis 3, the Pharmacological Target.   During normal parturition a pharmacological process is activated by DMT+ to: 1) stimulate fetal (and maternal) skeletal muscle in support of the mother’s contractions, 2) activate the hypothalamus for secretion of hormones stimulating the fetus, supporting newborn development and supporting the mother.  For the adult subject, LSD acted as a true pharmacological agent, producing these effects as a surrogate to fetal DMT+.

     Evidence: Subsequent trials with larger doses of LSD began quickly with the onset of autonomic activation, measured as short-lived simultaneous “spikes” in blood pressure, body temperature and heart rate.  After these measurements returned to normal, repeating sequences of (fetal)  body positions began, culminating with prodigious force and energy to dominate the rest of the session.  At the end of each session the “recovery” period was notable for the remarkable and wholesome physical and mental integration in the next two or three days.  Attempts to ignore the energetic urges in the muscular phase led to a "hangover" of mental and physical irritability with lowered stamina.

     Cited Evidence: 1)Early spikes of the same duration in fetal heart rate are used in contemporary obstetric practice as markers of fetal readiness.  2) Some of these effects mirror similar hormonal and physiological measurements of volunteers injected with DMT (Strassman and Qualis, 1994).  3) These effects, in addition to hallucinations, appear sporadically in cases of serotonin toxicity produced by large amounts of serotonin in the blood.

Hypothesis 4, Scopolamine.   Used in the subject’s birth, scopolamine accounts for the pristine physicality of memory re-living in the first trial, the repeated fetal activations in the second series and the freedom from PTSD in the decades following birth.  It is proposed that the adult subject as a fetus was seriously hindered in sensing or responding to critical developmental sensory information during his mother’s labor
Evidence:  Early LSD effects in of the first trial included the “stoned” feelings of anesthesia and catalepsy, both documented as symptoms of scopolamine potentiation.  The pharmacological effect in the second series of trials was notable for the continued repetition of fetal responses in each new LSD session, i.e., the lack of "resolution" of LSD-induced fetal activation.

     Cited Evidence:  1) Scopolamine is a powerful M3 anticholinergic agent that prevents consolidation of new information into memory by the hippocampus.  2) As an anticholinergic it interferes with relay function in the hypothalamus.  3) Scopolamine potentiates catalepsy induced by morphine and hallucinogens as well as morphine anesthesia.

Hypothesis 5, Fetal development.  At some critical time during the mother’s contractions, the fetus must receive and store the wholesome sensory feedback associated with its strong muscular efforts.  Born with a scopolamine protocol, the fetus is unable to provide this effort and lacks this supportive memory.  As a newborn, the subject was in some distress, having missed the “recovery” period following the expulsion phase.

     Evidence:  The “recovery “ period of each LSD session in the second trial series introduced the adult subject to a drastic existential departure from his ordinary life of chronic depression and anhedonic symptoms.  The new experience of relaxed self-confidence, increased overall pleasurable awareness and elevated athletic ability for the following two or three days was totally dependent upon participating fully in the intense muscular work during the entire session. 

Hypothesis 6, REM Sleep. REM sleep is a nightly process of healing noxious memory by opening memory substrates according to the same RaRN mechanism that operates to produce spontaneous flashbacks.   DMT+ secretion accompanies REM sleep.

     Evidence:  1) The appearance of flashbacks in the first trial during the time after awakening from a nights (REM) sleep and later at some specific times during the afternoon. 2) Their reflection of memory erasure as a natural spontaneous process.   

     Cited Evidence: 1) REM sleep exhibits certain key physiological characteristics that are earmarks of hallucinogen inebriation.  2) REM sleep deprivation results in decreases in cognitive ability, irritated behavior and sleep disturbances, which are reversed only by REM sleep "catch-up". 

    Supporting claims:  1) Resolution of the controversy over the role and origin of REM dreaming by introducing the special character of RaRN-controlled memory.  2) The Crick-Mitchison theory (1983) postulating the same healing role for REM sleep for removing memory traces, in agreement with the previous work of  Gaarder K. (1966) Arch. Gen. Psychiatry 14, 253 and Newman EA and Evans CR. (1965) Nature 206, 534.  3) The progression of dream issues reported in the work of Carl Jung and 4) The success of Francine Shapiro’s EMDR therapy.

Hypothesis 6a, REM depression. Some types of chronic depression are a form of PTSD.
    Argument:  Noxious memories remaining unresolved during REM sleep qualify as trauma according to the RaRN definition.

Next: This link to the Introduction page is recommended.

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