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The Hallucinogen in Birth

1.8 NORMAL” BIRTHS: THE MENTAL STATE OF THE MOTHER-TO-BE


At this point, a digression into the cacophony of obstetric practice is mentioned primarily as a situation inimical to a mother’s sub rosa needs as she faces the immediate future in the delivery room.  It is becoming increasingly apparent that obstetric care in the US is taking into consideration these basic biological needs of the mother and baby.  Quiet rooms within a hospital are provided for natural childbirth with a midwife, where a nurse checks in occasionally and can gain quick access to a doctor in case of the need for intervention.   This is a development made in response to the rather dismal statistics of hospital birth in the recent past.  According to a recent documentary film, “The Business of Being Born”, women in the US are probably the most misinformed about the birth process than anyone in the developed world (Epstein, 2007) .  This ignorance is not only one of the lack of information, but one of misinformation: In the US women fear birthing.   This can be traced back to negative 1920 AMA and insurance propaganda about home births and midwifery depicting midwives as slovenly and unclean street people.  As a result only 8% of American births occur at home with midwives.  Today, over 70% of births in Europe and Japan are managed with midwives.  In the US Caesarean births have increased almost 50% between 1996 and 2002 and today, one out of three or four births are C-section operations.    Women have been taught that their own bodies don’t have the necessary inner knowledge to handle the birth, that it has to be painful and that the doctor knows best how to “do” the delivery.  The outcome is that the US has the second highest infant mortality rate among all the developed countries and is first among seven of these countries in this dismal statistic.  Moreover, 20 to 40 percent of US mothers suffer from postpartum post-traumatic stress disorder, depending on the area of the survey (Czarrnocka & Slade, 2000).   In addidion,  studies have shown that elective caesarian is more dangerous than planned vaginal delivery (Liu et al, 2007; Kitzinger, 2001).

From the ‘20s into the ‘60s a woman’s fear of birth brought on the practice of Twilight Sleep and today it is the rush to scheduled Caesarean section to fit someone’s schedule.   To her, the act of birth is terrifying and, at the same time, trivialized in many hospitals, as if it was an assembly line appendix operation.  Time in the delivery room has to conform to Insurance and Hospital financial mandates requiring that it be as short as possible.    When her contractions begin she is given an epidural injection of an anesthetic, carted into the delivery room, and placed on her back, often with her legs in stirrups.  This position is known to interfere with the abdominal contractions she will use for pushing.   As the anesthetic slows down uterine contraction, the mother may be given a shot of Pitocin, a synthetic analog of her natural contractile agent, oxytocin. The undue pain and the length of Pitosin contractions have been discussed  previously.  Pain, unrelieved by natural opiates, produces a call for another epidural and the prolonged cycle of epidural/Pitosin often leads to a 20 minute Caesarean section to clear the delivery room.

It has been shown that the positive outcome of home/midwife delivery far exceeds that of the hospital and the likelihood of intervention.   This is not to say that the skill and training of the doctor  is not valuable, but this skill is really needed only when intervention is really necessary.  At home, the mother is not a helpless creature obeying every word of the obstetrician.  Now, she is in charge.  The birth belongs to her.  She is in a quiet atmosphere free of the delivery room distractions, as in movies with people coaching her to breathe and push, mostly at the wrong time. Her pushing and breathing are not to be forced, as they obey the natural timing of the birth process.

The question is whether the condition of the mother’s psyche is supported in a manner that correlates  with the profound physiological changes that are occurring as labor proceeds.  Clues can be gleaned from reading comments by midwives and mothers in natural childbirth.  It’s “a rite of passage”, a “transformative” experience, “life-changing”, a “trip to the moon”, “otherworldly”.   However fulfilling, these are not necessarily “pleasant” experiences and there’s often a point called the “wall”, where the mother had to do something she’s convinced is impossible.    “Between a rock and a hard place”, she has to push against pain that she feels is too great just before expulsion of the baby.  When she actually does it she learns on some deep level that she can take on anything.  This realization of empowerment is within a high, altered psychic state that brings on the spiritual nature of the comments.   She’s in love with the baby, owing to the natural oxytocin.  In a sense, she has been born, too, arriving into a different realm of perception about herself.   Then again, there are examples of natural births without any pain at all.


1.8.1 POSTULATE: THE PARTURIENT MOTHER IS UNDER THE INFLUENCE

The model of Figure 9c demands that, during labor, the mother’s (and the baby’s) brainstem reticular nuclei must be activated in order to account for the storage of M’s physical memory.   This could occur by raphe inhibition from EH, e.g., DMT circulating in the placental blood or directly from the fetus (in sheep, it is the fetus that inaugurates labor).  The effect of DMT on the 5-HT2a receptors in the higher cortical regions would coincide with that of the 5-HT1a to elicit the mother’s alert and positive state of anticipation.  This conclusion will be argued from hints derived from frequent observations on the psychic state of the parturient mother during labor, midwife documentation in the context of “natural” childbirth, historical use of birthing hallucinogens and the biology of parturition. Arguments that the fetus is in this LRN activated state will be presented in Part 2.

1.8.2 THE HIDDEN PROCESS

The mother’s putative altered mental state would be a reflection of hallucinogenic 5-HT2a/2c receptors in the thalamic and cerebral regions.   This would be a herald symptom for the parallel physiological (non-hallucinogenic) events mediated by the raphe 5-HT1a receptors.   Introducing the idea of a “birth hallucinogen” active in the mother implies that her perceptive priorities would be removed somewhat from the usual activity in the delivery room.   As with a hallucinogen, she would find herself immersed in a strange new world of alert energy and relatively fearless anticipation.  

The sine-qua-non for obtaining any real psycho-physiological value from taking a hallucinogen is that the imbiber be in a quiet place with attractive, comfortable and safe surroundings, confident that seasoned assistance is nearby.  This was the environment of M’s LSD experiences and, as will be discussed in Part 2, the results at issue were not experienced in more distracting situations.  One reason for this is that the hallucinogen evokes, for lack of a better phrase, one’s subtle and fragile inner domain, something eliciting profound physical awareness, a kind of knowing difficult to express in words.  Speculating on the mother’s mental state, the effect of the hallucinogen at this time would be an unfamiliar but proper sense, as if something “knowing” is taking over the body’s physiology and providing a psychic realm of alert anticipation relatively free of fear.  This inner environment would include the ordinary world within a larger sphere of awareness that shifts our priorities.  On moderate or “museum” doses (Shulgin and Shulgin, 1991), both this new and ordinary worlds are accessible.   If, say, the telephone rings while one is in the altered state, the return to the ordinary domain is effortless and the caller’s convoluted demands are handled easily.  After completing this chore, the subject can return to his or her inner domain.  With somewhat greater doses or higher personal sensitivity, the inebriant is aware, but uninterested in such ordinary trivia and doesn’t even answer the phone.  Something much too profound is happening within.  Nevertheless, cognitive abilities are still present and interruptions will be judged as to their urgency.   

Distractions can militate against accessing and maintaining this fragile state, especially in conventional obstetrics, where preparation and management of the mother’s labor involves the assembly line protocols mentioned above.  While the situation is improving, it is little wonder that doctors, nurses, even midwives and the mothers themselves are generally oblivious to the possibility that a profound holistic change, a transcendent conversion, would now be taking place to give her holy courage and render her anticipation of the contractions as a fulfilling sensual and psychological experience, a condition that evolved over eons to orchestrate parturition and promote survival.  Looking at this in an evolutionary sense, it conforms to the common definition of a miracle, i.e., as a process scarcely believable and directed by a powerful unseen fiat.  The speed and complexity of embryonic development alone is a fabulous process. as it proceeds through biological phyla, our ancient ancestors, a tail, and gills, onto a human with a brain that is forming billions of neurons and synapses with incomprehensible speed.  Ontogeny recapitulates phylogeny; a miracle profound and mysterious recapitulates, a memory from the labyrinths of the ancient, prehistoric past revisits our ancestral lines.    Then, the baby is guided through the birth canal by another fiat that trumps any known choreography in the order and synchronization of the dance.  And all of this takes place without a scintilla of rational thought.  That it is so common, we take it for granted and prefer our miracles to be the tears of blood from a holy statue.   Contemplation of the common miracle of birth is seldom, if ever, part of anyone’s preparation, and expectant mothers are generally afraid of what’s ahead.   But, the evidence exists, though rarely publicized, in regards to the requirements of the mother's inner domain.  Establishing this condition deliberately would require the mother’s freedom from the less important, but noisy hubub during the onset and immersion in the entire birthing process, including late pregnancy.  Today’s expecting mother is no longer in touch with the primordial knowing shared by primate mothers and by humans of the third world without access to a hospital.   The mandate for such conditioning is seldom expressed in books on birthing or midwifery.   A superb exception is the book, “Birthing from Within” (England and Horowitz 1998), which emphasizes that this “knowledge” can be accessed in quiet surroundings and can even emerge in dreams.   The issue of dreams is significant, since REM dreaming and M’s LSD experience may share similarities in terms of raphe activity.  Also, the hypnotic state, another fascinating researh direction for brainstem function, is used in birthing (Mongan 1998) and may involve similar modulations of the raphe nuclei.

1.8.2.1 There are numerous allusions to the altered mental state of the parturient mother by obstetric nurses and doulas (midwives), but they are hard to find in the literature.  The examples mentioned here were obtained from conversations with midwives and obstetric personnel.   Some midwives assess the stage of labor by asking some mundane question, e.g., “Do you want a glass of water?   At one stage, she will hear the question, but find it so “out of context” and trivial to the new influence within that she will not find the answer. This behavior is not a result of perceptual overload or her cognitive preoccupation with overwhelming events.  Rather, there is simply less importance attached to activity in the delivery room.  Her state is well outside anything pertaining immediately to this inner adventure.  Uncharacteristic behavior such as synesthesia and time distortion, are noted occasionally towards the end and after completion of delivery.  One of the symptoms most frequently seen is her loss of habituation, i.e., loss of the normal “tuning out” of common noise.   Now, ringing of a distant telephone and other noises are heard.   Small flying insects, never before noticed, are now seen at long distances, as are new details of her surroundings.  Brain hypoxia, another partner of dehabituation, can be created by hyperventilation at “rest” (as opposed to cardiovascular exercise) and can’t be excluded as a factor.  This could occur as the laboring mother breathes hard naturally, or in response to verbal cues.   However, dehabituation has long been a herald symptom of hallucinogenic inebriation (McGlothin and Arnold, 1971; Szara 1994, Julian 2001).   There are several references to the activation of the locus ceruleus and dopamine sites by hallucinogens that elicit the perception of “newness” and other impressions that would fall under the rubric of dehabituation (Nichols, 2004, p. 147).   It is sometimes seen in spite of the fear and pain levels combined with the bustle of activity in the labor room, but more often in more quiet “natural” situations after the end of labor.   It’s likely that dehabituation corresponds to Phase 3 of the somatic LSD effects presented in Part 2, a phase that would correspond to the time after delivery.

1.8.3 EARLIER HALLUCINOGEN USE IN BIRTHING.

The connection between hallucinogens and birth is not new.  More recent translations of ancient Greek manuscripts, free of the moral strictures of Victorian translators, have inspired commentaries on the presence of hallucinogens in venues such as Greek wine concoctions at private parties, the Kykeon of the Greater Mystery of Eleusis ( Wasson, et al 1998) and the Mystery’s influence on famous Greeks like Euripides and Sophocles.   From 400 to 5000 BC Greek midwives worshipped the Goddess of Birth, who had an interesting choice for a consort: not a man or animal, but a plant (Wasson et al 1986).   This “plant” was probably the fungus Claviceps purpuria, the source of ergot based hallucinogens that infected the rye and barley grown on the Rarian plain about fourteen miles from Athens.   Today this mythologized plain lies under a few feet of water as a wrecking lot for abandoned vehicles.  The present town of Eleusis is an environmentally destroyed port for oil tankers and its ornate Temple of Eleusis, the Telesterion, is a ruin, owing to the vandalism and attempted murder of the Hierophants (Leaders of the Eleusian Mystery) initiated by the Bishop of Milan in ca. 475 AD.   The ancient Greeks and their trading partners, the Egyptians, were well versed in the use of hallucinogenic sources, including the Egyptian red water lily and Grecian mushrooms.

More comfortable evidence for hallucinogenic application for the laboring mother has been found in medieval midwifery in the 16th century, which employed ergot preparations to quicken labor and staunch postpartum hemorrhage.  The crude ergot extract obtained from the fungus that infects rye and barley is a dangerous mixture that caused widespread sufferng at this time.  Purified components, e.g., ergotamine and ergometrine, ergonovine (Ergotrate) and methylergonovine (Methergine), produce uterine contraction, but they can cause gangrene as strong vasoconstrictors and are used mainly in the late stages of labor to control hemhhorage.   In fact, further modification of ergot’s active principle to enhance its “uterotonic” action led to the synthesis of LSD in 1938 and its discovery as the hallucinogen in 1943 by the distinguished Swiss chemist, Dr. Albert Hoffman.   A fascinating history is provided in Dr. Hoffman’s book, “LSD, My Problem Child” ( Hofmann 2005), which identifies Sandoz drugs (Methergide) developed from the ergot indole structure for stopping postpartum hemorrhage and Hydergide, an anti-dementia drug.  Neither of these is used in within the context of enhancing the mother’s mental state and or in quickening desultory progress in labor.  These commercial drugs are'nt notable for their halucinogenic properties.  Could a hallucinogen quicken a mother's labor without imposing the problem of vasoconstriction?

Midwives of today’s Mazatec people, highly skilled in the traditional use of psychoactive plants for millennia, use mushroom psilocybin to enliven the parturient mother’s mentality and restore her desultory contractions to timely effect (Harrison, 2007).    It is curious that the possibility for the existence of a natural endogenous hallucinogen functioning at birth seems to have been missed in view of all these historical and scientific hints. 

1.8.4 THE BIOLOGY OF PARTURITION

Ample evidence exists in the literature to show that there’s no apparent need for an endogenous hallucinogen in the hormonal and enzymatic processes involved in the initiation of human labor (Karim, 1971;  Fuchs et al, 1971).   However, all this work had been done without consideration of a role for hallucinogens.  The only view of the onset of labor is restricted to the roles of oxytocin and prostaglandins that produce uterine contraction.  Prostaglandins are inflammatory factors also involved in cervical ripening and changes in membrane structure in addition to its role in contraction of the myometrium (Gibb W, 1998).    Their concentrations increase abruptly at the onset and duration of labor.

A partial scenario can be gleaned from research on rat parturition. During late pregnancy, the secretion of endogenous opioids suppresses the activity of oxytocin neurons to protect the fetus from premature labor and the secretion of birth glucocorticoids (Russel and Brunton, 2006).    Just before the onset of labor, progesterone concentrations decrease abruptly and it’s enzymatic product, allopregnalone, promotes activation of the GABA(A) system within the supraoptic (vasopressin) nucleus of the hypothalamus and the Para ventricular nuclei (Fenelon and Herbison, 2000).   In addition, allopregnalone removes opioid suppression of oxytocin neurons. The resulting release of oxytocin switches the GABA(A) system off and uterine contraction begins with the additional secretion of inflammatory prostaglandins, now free from GABA(A) inhibition (Leng and Russell, 1999).   

The role of the fetus in the initiation of labor and support of the mother will be discussed (Part 2) In terms of autonomic activation and fetal movements.  An additional clue to fetal engagement is taken from ovine studies showing that initiation of the onset of labor in sheep originates from the fetus.  Results of work in other areas have revealed that prostaglandins are produced in the outer fetal membrane (chorion) and inner membrane (amnion) that surrounds the embryo.  Placental involvement arises from the decidua as well, i.e., the part of the placental lining contributed by the mother (Gibb, 1998). The release of oxytocin promotes the production of prostaglandins in the decidua as labor begins. Also, oxytocin secretion originating in the fetus is increased under conditions of hypoxia.   Other pivotal contributions of the fetus arise from its secretion of serotonin (Eiler & Fecteau,  2000).

Is there a role for EH at this level of parturition?  Normally, the hypothalamus is activated at the onset of labor for the pituitary secretion of oxytocin (uterine contraction), natural opiates (analgesia) and ACTH (cortisol secretion) along with other corticotrophins, e.g., growth hormone and gonadotrophin in timely support of the newborn.  Similar increases in hypothalamus/pituitary secretions follow DMT injection in humans (Strassman and Qualis, 1994).  In Part 2 it will be reported that “fetal” autonomic activation, i.e., spikes in heart rate, blood pressure and oral temperature, all sequalae of hypothalamus activation, are seen in this adult subject with ingestion of LSD.

As to the specific mechanism of EH involvement, reports from studies on rat parturition include involvement of both the inhibitory GABA(A) system and both the dorsal and medial raphe. Their serotonergic axons project into the mmagnocellular area of the hypothalamus, which mediates secretion of the pituitary hormones and vasopressin.  How these systems function isn’t clearly defined, owing to the indirect nature of c-Fos histology, which measures new RNA synthesis (gene opening) for the production of GABA(A) proteins.  Since this implies GABAergic "activation", it's difficult to see how activation of the inhibitory GABA(A) system leads to activation of the hypothalamus to secrete birth hormones.  On the other hand, the hypothalamic nucleus could be analogous to RN in the RaRN model, i.e., dis-inhibition by EH binding to a the 5-HT1a receptor. The dorsal and medial raphe nuclei project to the magnocellular area of the hypothalamus, presumably to inhibit chronically (Cabot et al, 1975). 

Regarding the question of 5-HT receptor identity, once again, the question arises as to how EH and and raphe nuclei interact within the context of GABA(A) involvement.  The dorsal raphe nucleus itself is a complex nucleus consisting of at least five separate systems, including inhibitory (GABA(A) and excitatory neuron systems.   However, only the 5-HT neurons within these nuclei are inhibited by EH/LSD binding and this has been shown to occur directly without intermediate mediation (Aghajanian et al, 1972).  The question remains as to the actual role of the raphe serotonergic neurons.

It has been shown in rat studies that it is the 5-HT2a (not raphe) receptor that mediates the secretion of hypothalamus-pituitary factors, ACTH (cortisol), plasma prolactin and adrenaline (Aulakh et al, 1944).   The possibility that the human 5-HT1a may be involved can only be speculated upon from species variability. As suggested above, with raphe inhibition, human hypothalamic nuclei would now be free to secrete the supportive hormones at the onset of labor in a manner similar to the proposed RaRN model.   EH and LSD, not the inhibitory GABAa system,  would be the factors releasing  hypothalamic corticotrophins for the pituitary secretion of oxytocin, endorphins and ACTH.   However, there is evidence that the dorsal/medial raphe nuclei are involved in combination with the GABAergic system for hypothalamic activity only during parturition, but not before or after (Lin SH, et al., 1995 Lin SH, et al, 1998).  Thus, the initiators of uterine contraction, analgesia, alert strength and paracrine management would emerge in support of the mother in response to both systems.

This involvement of raphe nuclei in promoting hypothalamic, and therefore pituitary, secretion brings up an interesting point related to species differences mentioned previously.  Discriminative cues for 2a in the rat may involve 1a in the primate.  Hypothalamic secretion to produce pituitary hormone release has been seen in the rat in response to the powerful 5HT2a agonist, DOM a phenethylamine hallucinogen (Aulakh, 1994; Nichols, 2004 p 141).  This 2a agonist is blocked in stimulus discrimination in the presence of strong 5HT2a antagonists (Nichols, 2004 p 141, Fiorella et al, 1995).  On the other hand, 2a antagonists do not block LSD stimulus discrimination in the monkey (Nichols, 2004 p141; Nielsen, 1985).  In this more closely related species, it is the 5-HT1a that is involved in antagonist blocking of LSD cue discrimination (Nichols, 2004; Winter et al, 2000).   Is it stretching this species extrapolation too far to suggest that the endogenous hallucinogen 5-HT1a in humans may mediate the same functional venues mediated by the 5-HT2a in the rat?  Might one of these venues be activation of the hypothalamus?   Probably not, since the involvement of raphe nuclei hasn’t been shown in this kind of study.  A trivial pursuit fact might be added: Serotonin re-uptake inhibitors induce birth and spawning in invertebrates (Fong and Warner, 2005; Fong et al, 2008, Cunha & Machado, 2001).

Summarizing, this hypothesis on the role of EH in parturition includes activation of the hypothalamus-pituitary-adrenal-gonadal axis, in addition to those LSD effects related to M’s experience of memory recall, i.e., the opening of memory substrates in the and fetus (and mother) and bolstering the mother’s mental state.  An additional role for EH is further implied from the results of Part 2, in which the use of LSD elicited strong fetal movements in the adult, quite similar to the mother’s abdominal contractions in “pushing”.  While EH is not directly involved in the onset of smooth muscle contraction to start the labor process, it would be involved in the secretion of oxytocin.   In addition, evidence will be presented in Part 2 for the possible role of EH in promoting the contractions of skeletal muscle related to the urge to “push” for the mother and movement for the fetus. 

1.9 WHAT IS THE ENDOGENOUS HALLUCINOGEN?

Referral to the birth agonist as the "endogenous hallucinogen" is somewhat misleading for the main purpose of this dissertation.  This label is made on the the basis that LSD mediates its famous hallucinogenic effects at the cortical 5-HT2a receptors, but the centerpiece of the proposed RaRN model is its non-hallucinogenic effect on the 5-HT1a receptor of the brainstem raphe nuclei.  The most attractive choice for identifying the endogenous agonist would be one having a similar indole structure as LSD and documented to be as potently hallucinogenic and having the same binding properties to these receptors.  Obvously, N,N-dimethyltryptamine and its congeners stand out (below).

As discussed above, the secretion of an endogenous hallucinogen with the onset of labor is a possibility encouraged  by anecdotal, historical and biological arguments for the mother’s (putative) state of raphe suppression.  More than the identification of a particular agonist, the important issue is the nature of the receptor, which, by virtue of M’s LSD effects, is taken to be serotonergic.  Accordingly, among the possibilities discussed below, serotonin itself (5-HT) can be considered as the birth factor along with the others.


As stated in the General Discussion of Part 2, 5-HT can elicit several “hallucinogen” effects that have been observed here and elsewhere, provided it is present at blood concentrations sufficient to produce “serotonin syndrome” or “serotonin toxicity”, i,e., 200 to 300% of normal.   5-HT would be expected to rise during the mother’s labor according to its well-known response to stress.  However, blood concentration means very little.   It is the local concentration among the brainstem areas of serotonergic function that is important, particularly the amount in the synaptic cleft and the raphe neuron dendrites.   One  clue to the possibility of the birth role for 5-HT is the finding that it could increase as much as 1500% in the region of the rat hippocampus under the condition of imposed stress in knockout rats (Linthorst et al, 2000).   The relevance of this fact to parturition is that this increase requires mock stimulation of the hypothalamus by the addition of corticosteroid releasing factor (CRH).   Since CRH secretion is crucial in parturition, [5-HT] could rise to a high local level appropriate for functional binding to the 5-HT1a and 2a receptors at some location close to the target nuclei well above it's toxic levels. Therefore, an argument can be made for 5-HT among the candidates for mediation of the roles of memory consolidation and fetal acivation in the adult.  Another consideration in favor of 5-HT in these birth aspects is the fact that serotonergic neurons are the sources of 5-HT that occupy the critical areas of raphe and limbic processes.  However, a more interesting possibility for the natural serotonergic agonist exists among a group of natural tryptamines that are powerfully hallucinogenic in amounts orders of magnitude lower than required for serotonin.


 The hallucinogens found in human tissue are:  N,N-dimethyltryptamine (DMT), 5-methoxy-N,N-DMT, bufotenin (N,N dimethylserotonin or 5-hydroxy DMT) and an oxidized form of epinephrine, adrenochrome.  The most attractive candidate is dimethyltryptamine (DMT), known for at least fifty years as a drug detectable in body tissues (Barker et al, 2001).  Interest in the late ‘60s was stimulated by the similarity between hallucinogenic effects and symptoms of schizophrenia, leading to the discovery of its synthetic enzyme, indoleamine methyl tranferase in human blood plasma, urine and lung tissue.  DMT is equal to LSD in potency and affinity for 5-HT2a and 5-HT1a receptors (Jacob and Shulgin,1994; Strassman et al, 1994; Glennon et al., 1986).  It is this similarity and the greater interest DMT provides for human studies (Strassman 1996) that favors its identification as the birth hallucinogen. The effective dose of 5-MeO-DMT as a hallucinogen is much smaller than that of DMT.  Moreover, the preferred receptor for 5-MeO-DMT (in primates) is the 5-HT1a (see Nichols 2004 p. 141).   Since the following comments on DMT would apply to 5-MeO-DMT and bufotenin, they will be referred to collectively as DMT+.


A likely source of DMT+ is the pineal gland, located just above the posterior midbrain and only millimeters away from the brainstem raphe.  Notably, it contains 5’-tryptophan hydroxylase (36), N,N-dimethyltransferase (37)  and O-methyl-transferase for 5-MeO-DMT (38) and all the tryptamine substrates needed for DMT+ synthesis .  The sleep molecule, melatonin, shares the tryptamine (indole) structure with DMT+ and the 5-methoxy with 5 methoxy DMT.  Melatonin promotes both REM and hallucinogenic states (when awake) at high doses taken as a supplement (Wikipedia-melatonin).  While the source of DMT is unknown, the pineal gland would be rounded out completely as the sleep organ, providing melatonin for deep sleep and, putatively, DMT+ for REM sleep.  Notably, melatonin is a powerful free radical scavenger that would confer stability for DMT+ during its travels to the raphe (38).  Further argument for the pineal is the presence of an inhibitor of methyltransferase for DMT’s N,N-dimethyl group (Narasimhachari et al, 1974) and bufotenin (5-hydroxy DMT) is found in pineal extracts (and uterine tissue) (van der Horst and Ebels 1980). This is a research direction yet to be explored (Sandrock Jr. et al 1980). 


 Sampling blood for DMT+ according to the time frames for parturition, PTSD or REM sleep is a doubtful approach.  The  determination of whether or not DMT+ is secreted would add further complexity to a complex mixture as syringes pre-loaded with harmaline or pargyline, both inhibitors of monoamine oxidase (MAO).   The amount of DMT is very small in all tissues and its half-life when injected is short (Kaplan et al, 1974), owing largely to its rapid oxidation by MAO-a.  For this reason, a test for hallucinogens has to be quite sensitive, requiring methods sensitive to picomole amounts, e.g., isotope dilution of N,N-deuteriomethyl tryptamines (Barker et al, 2001) or by gas chromatography/mass spectrometry (Forsström et al, 2001). 

 


Obviously (and ironically), the detection of DMT+ is the most important issue in this monograph, as it will test severely the validity of the RaRN model and, if this is possible, would form the basis for a broad area related to PTSD therapy, parturition, and REM sleep.  A key argument for the pineal gland is of special interest.  The secretions of the pineal are not sent directly into the bloodstream, but into the cerebral spinal fluid (CSF), entering the third ventricle from the pineal recess that penetrates into the pineal stalk (Tricoire et al, 2003).  This offers close proximity to brainstem raphe nuclei via the cerebral aqueduct, the fourth ventricle and the cisterns and apertures delivering CSF to the brainstem,  The total volume of these spaces is generally small (<5ml) and melatonin (and presumably, DMT+) so the concentrations in the third ventricle are quite high during synthesis (Wurtman et al, 1969).  The question of measuring DMT+ e.g., in saliva or after subdural CSF collection, is enhanced by the lack of monoamine oxidases, which quickly degrade monoamines in circulating blood.  This sequestered arrangement insures against systemic effects of drugs on DMT such as MAOa inhibitors (see [3.] 1.4.4 “REM Sleep Heals Trauma) and maintains homeostatic balance in the brain, which would be lost from systemic appearance of this powerful hallucinogen.

 

Thus, it is likely that a biological mechanism for liberating DMT synthesis and release may be found to link this hallucinogen to the pineal and to secretion during parturition. 

DMT has been found in lung tissue after hyperventilation at rest, the same kind of breathing that begins naturally for the mother in labor. DMTs strongly hallucinogenic effect, if administered without a MAO inhibitor, lasts less than two minutes (Strassman et al., 1996).   Much longer lasting influence requires MAO inhibitors such as those derived from plant preparations used as adjuncts to DMT in the ayahuaska ceremonies of South American shamans (Schultes RE et al., 2001 p 129).   Since externally administered MAO inhibitors (MAOIs) are reported as inhibitors of REM sleep, sharply contradicting  expectations from results on REM stimulation by 5-HT1a agonists ([3.] 1.4.4), consideration must be given to the sequestered nature of DMT in the brainstem.   The action of LSD described in Part 2 of this monograph is the first demonstration of this drug as a pharmaceutical in the conventional sense. This same conventional pharmacology is seen by the dose-response character of DMT’s autonomic effects (Strassman, et al., 1994). 

 


References  for  “What is the Endogenous Hallucinogen?”


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Schultes RE, Hofmann A and Ratsch, C. 2001 “Plants of the Gods” Healing Arts Press, Rochester VT ISBN 0-98281-979-0

Strassman, R. J. (1996). Human psychopharmacology of N,N-dimethyltryptamine. Behav Brain Res 73, 121 – 124.

Strassman, R. J., & Qualls, C. R. (1994). Dose-response study of N,N- dimethyltryptamine in humans: I. Neuroendocrine, autonomic, and car- diovascular effects. Arch Gen Psychiatry 51, 85 – 97.

Strassman, R. J., Qualls, C. R., Uhlenhuth, E. H., & Kellner, R. (1994). Dose-response study of N,N-dimethyltryptamine in humans: II. Subjective effects and preliminary results of a new rating scale. Arch Gen Psychiatry 51, 98 – 108.

Strassman, R. J., Qualls, C. R., & Berg, L. M. (1996). Differential tolerance to biological and subjective effects of four closely spaced doses of N,N- dimethyltryptamine in humans. Biol Psychiatry 39, 784 – 795.

Strassman RJ (2001)  DMT: The Spirit Molecule Rochester, VT: Park Street Press, 2001, 358 pp + xviii, $16.95 pb  Journal of Near-Death Studies

van der Horst CJ, Ebels I. (1980)  Extraction of pineal and uterine tissue at different pH values: a preliminary report on the occurrence of a few groups of compounds in both tissues.  Cytobios.;29(115-116):191-203.



Barker SA, Littlefield-Chabaud MA, David C. (2001)  Distribution of the hallucinogens N,N-imethyltryptamine and 5-methoxy-N,N-dimethyltryptamine in rat brain following intraperitoneal injection: application of a new solid-phase extraction LC-APcI-MS-MS-isotope dilution method. J Chromatogr B Biomed Sci Appl. 2 Feb 10;751(1):37-47.


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Glennon RA, Titler M, Young R. (1986) Structure-activity relationships and mechanism of action of hallucinogenic agents based on drug discrimination and radioligand binding studies. Psychopharmacol Bull. 22 953-8.


Jacob III P and Shulgin AT. (1994) www.nida.nih.gov/pdf/monographs/146.pdf


Narasimhachari N, Lin RL, Himwich HE. (1974)

Inhibitor of indolethylamine N-methyltransferase in pineal extract. Res Commun Chem Pathol Pharmacol. )1Oct;9(2):375-8.


Nichols DE (2004) Hallucinogens Pharmacology & Therapeutics 101 (2004) 131–181176


Sandrock Jr. AW, Leblanc GG, Wong DL, & Ciaranello RD (1980) Regulation of rat pineal hydroxyindole-O-methyltransferase: evidence of S-adenosylmethionine-mediated glucocorticoid control.

J Neurochem. 1980 Sep;35(3):536-43.


Schultes RE, Hofmann A and Ratsch, C. 2001 “Plants of the Gods” Healing Arts Press, Rochester VT ISBN 0-98281-979-0


Strassman, R. J. (1996). Human psychopharmacology of N,N-dimethyltryptamine. Behav Brain Res 73, 121 – 124.


Strassman, R. J., & Qualls, C. R. (1994). Dose-response study of N,N- dimethyltryptamine in humans: I. Neuroendocrine, autonomic, and car- diovascular effects. Arch Gen Psychiatry 51, 85 – 97.


Strassman, R. J., Qualls, C. R., Uhlenhuth, E. H., & Kellner, R. (1994). Dose-response study of N,N-dimethyltryptamine in humans: II. Subjective effects and preliminary results of a new rating scale. Arch Gen Psychiatry 51, 98 – 108.


Strassman, R. J., Qualls, C. R., & Berg, L. M. (1996). Differential tolerance to biological and subjective effects of four closely spaced doses of N,N- dimethyltryptamine in humans. Biol Psychiatry 39, 784 – 795.


Strassman RJ (2001)  DMT: The Spirit Molecule Rochester, VT: Park Street Press, 2001, 358 pp + xviii, $16.95 pb  Journal of Near-Death Studies


van der Horst CJ, Ebels I. (1980)  Extraction of pineal and uterine tissue at different pH values: a preliminary report on the occurrence of a few groups of compounds in both tissues.  Cytobios.;29(115-116):191-203.


 

 

1.11  PRECEDENT FOR A “TWO-STAGE” BIDIRECTIONAL NUCLEUS

The precedent is seen in results from research on Pavlov conditioning, which were undertaken exhaustively by Thompson and co-workers (Thompson, 2005).  As an analogy to the proposed RaRN model, the centerpiece of this work is a single nucleus deep within the cerebellum that responds to factors that either stimulate or inhibit its ability to allow impulse traffic.   

Ring a bell and a rabbit will blink, because the rabbit was conditioned to associate the bell ring with blinks of the nictitating membrane of the eye induced by simultaneous puffs of air.  Similar experiments led R.F. Thompson and colleagues to the conclusion that a neuron bundle deep within the cerebellum, the interpositus nucleus (IP), was involved.  The conditioned bell ring blink could be stopped in well-trained rabbits by inhibiting this nucleus with muscimole (a GABA agonist), or re-started by removing the inhibition (Krupa  and Thompson, 1993 ).  

Further research into bell/blink association revealed for the first time the physical picture of a simple memory.   A recent review of this work can be seen in Thompson’s article, “In search of memory traces” (Thompson, 2005) and in other reviews (Thompson an Krupa, 1994).   In training the rabbit, the air puff inducing the blink (the unconditioned stimulus, US, and the bell sound (the conditioned stimulus, CS, are carried by different kinds of fibers that meet as a bi-synaptic junction within the IP.   Of course, the physical picture of the memory is much more complex, involving the cerebral sensory-motor cortex and cerebellar cortex (blinking), the limbic memory in the cerebrum (bell ring), networks in the thalamus and brainstem and the cerebellar cortex.  However, all these can be removed without destruction of the memory association, as long as the interpostis nucleus (IP) remains intact.   Thus, the centerpiece of memory storage is a single (but complex) nucleus, whose stimulation or repression dictates memory implementation in the larger eye-blink association circuit.  

The processes within the cerebellum are well known and involve four kinds of fibers: The mossy, climbing, parallel and Purkinje fibers.   Their orthogonal 3-dimensional arrangement accounts for the high speed of cerebral-cerebellar feedback that is expressed in intricate motor skills (McGeer et al, 1985; Allen and Tsukahara, 1974).   The parallel fibers running along the cerebellum’s cortical region interact with the Purkinje, mossy (MO) and climbing fibers (CL).  MO, carrying and CL are input fibers that start from two brainstem nuclei, the red nucleus and the inferior olive, respectively.   The mossy fibers carry the conditioned stimulus CS into the cerebellar cortex via the granule cells, which synapse with the cortical parallel fibers.   The climbing fibers carry the unconditioned stimulus US (air puff) and are intertwined with the Purkinje fibers that descend from the cortex to carry out-going impulses that inhibit IP.  When the association is activated by CS, the strong influence of the climbing fibers inhibits Purkinje cells and the IP is dis-inhibited, allowing for the flow of relay impulses from IP to the extra-cerebellar circuits.  This was shown by electrically stimulating the mossy and climbing fibers simultaneously to measure Purkinje inhibition.  The motor response of eye-blink now follows the well-established servo-feedback between the pyramidal cells of the cerebral motor cortex and the cerebellum (Allen and Tsukahara, 1974;  McGeer et al, 1987; Kandel et al, 2001).   With IP activation, the sensory circuits in the brainstem now operate with respect to the conditioned stimulus, producing a conditioned response of the eye-blink at the mossy-climbing fiber bi-synapse within the IP.   
Thompson presents a fine description of hunting for the indispensible memory kernel, first, in the hippocampus and finally in the interpostis nucleus of the cerebellum.

This mechanism of normal Purkinje inhibition of IP and its dis-inhibition can be viewed as analogous to and a precedent for the “on-off” model proposed here.   While the memories in both eye blink/bell ring and M’s LSD recall are physically represented by circuits within the global brain, both would involve an indispensable nucleus that represents the site of persistent association, that is, “storage”.   In the Pavlov studies the memory kernel itself lies within a nucleus as an indispensable storage area, whose absorption or release of associated impulses depends on controlling agents (Purkinje output).   In the analogy, the Purkinje and raphe activity is inversely associated with the IP and a reticular nucleus, respectively.  Both the Purkinje inhibition by the climbing fibers and raphe inhibition by LSD or EH are analogous as agents of memory release.

Of course, this analogy suffers from gross over-simplification in view of the results now reported on experiments in synaptic plasticity.   It is increasingly accepted that eyeblink learning in the cerebellum isn’t exclusively located within a deep cerebellar nucleus.  Learning involves long-term depression of specific synapses, i.e., a weakening of neuronal synapses that lasts from hours to days and is associated with a decrease in receptor density in post-synaptic dendrites.  This LTD can result from strong stimulation of a neuron, or from repeated weak stimulation, as has been seen in the hippocampus, which may be important for the clearing of old memory.  Almost always, LTD follows the influx of excitatory calcium ion into the neuron, which depends on the frequency and timing of the stimulation (Dudek & Bear, 1992).  This Ca+ influx is associated with excitatory glutamate receptors, called mGluRs, i.e., Group 1 metabotropic receptors (increasing metabolic rates).  In the cerebellum it has been shown that co-activation of the climbing fiber synapse (providing the Purkinje neurons with the unconditioned stimulus, US) and parallel fiber arrays coding the conditioned stimulus (CS) leads to LTD of the parallel fiber-Purkinje synapses (Hansel & Linden, 2000, Hansel et al, 2001).  The location of bi-synaptic association can’t completely exclude the cortical region of the cerebellum.  Moreover, the reversal of LTD by long-term potentiation (LTP) provides an bi-directional mechanism for impulse flow (Dudek & Bear, 1993).   However, on the grosser level in citing this analogy to the RaRN model does not exclude synaptic plasticity. Impulse flow through a nucleus is determined by the activity of controlling neurons, either as Purkinje or raphe 5-HT neurons.


The question is now raised as to the identity and location of the skull memories recalled by M’s LSD session. Adhering to the likelihood that the memory is located within a nucleus, the cerebellum is one possibility and the blocking reticular nucleus (LRN) itself is another.  Also, within the broader scope of traumatic injuries already discussed, long-term limbic storage is a possibility.  However, in the Pavlov studies the hippocampus of the limbic system operates as a secondary memory source placed after consolidation of the association memory.  It is disposable and would be completely out of the picture in M’s skull memories because of the scopolamine.  The possibility that (LRN) carries the memory is lessened by its primary role suggested by its rich exchange of afferent and efferent fibers with the cerebellum (Nolte, 2001).  This pushes the choice to that of a deep cerebellar nucleus communicating with LRN to provide a satisfactory arrangement of communication between all brainstem and cerebral elements for the activation and recall of a stored “pain” memory, as shown previously in Figures 9a,b and c.   Furthermore, the primitive physical quality of M’s skull memory must be one of association between several components, i.e., anesthesia and catalepsy associated with all the different skull areas.   Several bi-synaptic connections of the kind shown in Thompson’s studies would be expected to reside within the same type of nucleus, the IP.   Also, their connections  could be imagined as sequential to account for the sequential appearance of sensations with LSD recall of the memory.

As to the cerebellum itself, the cerebellar cortex is not the storage place in the Pavlov association studies (Wada et al, 2007).   Although the post-synaptic dendrites of the Purkinje cells intertwine with the cortical parallel fibers, this cortex is not for “storage”.   Rather, the cerebellar cortex is involved in the timing and adaptation of the conditioned response (Cook et al, 2004), which involves learned-dependent timing responses set in place by long-term synaptic depression (Koekkoek et al, 2003; Linden, 2003).   Adhering to the notion that the memory kernel location is nuclear, not cortical, the storage site for M’s skull memory in the cerebellum would be most likely in the vestibular or deep (e.g., IP) nuclei of the cerebellum, e.g., the same interpostis nucleus. (Christian and Thompson, 2005: du Lac, et al, 1995: Klein et al, 2002; Thompson and Krupa, 1994).


1.12 TESTING THE HYPOTHESIS

The DMT Problem.

The telling gap in supporting the RaRN model is that the centerpiece of this monograph, DMT+, has never been measured in living tissue within any biological context and, so far, an assay doesn't exist for reliable measurement.  These hypotheses, though consistent with this LSD result, must remain as speculation until the critical experiment can be carried out i.e., detecting the appearance or secretion of DMT+ near its putative source within the time frames demanded by the hypotheses.  In view of the notorious instability of DMT+ in the circulatory system, it is a compelling, but elusive choice.  No attempts have been made to detect or measure it in this context and no  reports have appeared on the relationship between hallucinogens and birth, trauma or REM sleep.  How endogenous melatonin or DMT+ gets into the blood at all is puzzling (see below) and blood would be a poor source for assay.  If DMT+ was secreted in sufficient amounts, most would appear as the liver breakdown or oxidation products in the  bloodstream.  This would only partially be overcome with the addition of  powerful MAO inhibitors such as pargyline or harmaline. 

The obvious place to look for DMT+ would be the saliva, the routine source for measuring melatonin.  Saliva contains about 70% of the total secretion of melatonin and is a fair measure, as the remaining amount is loosely bound to plasma albumin (Kennaway & Voultsios, 1998).   Sampling saliva for DMT+ would be a convenient method for the timed protocol necessary for the hypotheses, e.g.,  DMT+ should track  with the rise and fall of REM sleep two or three times each night.  Most likely, saliva  gets melatonin or DMT+ from the total CSF.   In humans, the pineal secretes melatonin and presumably the other tryptamines into the cerebral spinal fluid (CSF) of the third ventricle (Tricoire et al 2002).  Melatonin enters the Cerebrospinal Fluid through the Pineal Recess (Tricoire and Locatelli, 2002) to bathe the brainstem raphe close-by via the cerebral aqueduct before it reaches the 4th ventricle.  The total average volume of the 3rd, aqueduct and 4th is only 2 ml.  Flow from the 4th ventricle returns to the total CSF with a total volume of 135 ml, a ~ 70-fold dilution.  This mixing would not allow sufficient time resolution.  For example, the increases and decreases in DMT+ with the two or three onsets of REM sleep would be smoothed out into a broad concentration vs time plot, as seen with melatonin (Kennaway and Voltsios, 1998).  Moreover, DMT+ tryptamines, so close structurally to melatonin, would be difficult to distinguish in a radio-immune assay requiring the development of a unique antibody.

Kennaway DJ  & Voltsios  A (1998) Circadian Rhythm of Free Melatonin in Human Plasma Journal of Clinical Endocrinology and Metabolism 83. 1013-15

Tricoire H, Locatelli A, Chemineau P and Malpaux B. (2002) Melatonin Enters the Cerebrospinal Fluid through the Pineal Recess Endocrinology Vol. 143, No. 1 84-90
 

One non-invasive approach, combining locality and detection would be to obtain a spectrum of the six methyl protons of DMT from a focused magnetic resonance image (MRS) within the area of the third ventricle and brainstem.  A similar experiment has been done for the small area of the optical chiasm to detect the brain metabolites, choline/phosphatidyl choline, creatine/creatine phosphate and N-acetylaspartic acid, but requires 3 to 14 mmolar concentration range for a singe proton. For DMT+ the requirement would be 1/3 or 1/6 this amount, depending on the rotational freedom of the methyl groups.  The question is whether the concentration of DMT+ can be estimated a-priori to fulfill this requirement.  A   starting point would be the dose needed for the putative hallucinogenic state for the parturient mother, PTSD sufferer or the REM sleeper.  A clue is obtained from
Strassman's estimation of 0.2mg/kg as the minimum DMT dose for intermuscular injection for his volunteers (Strassman, 2001). 

Taking Strassman's minimum injected dose, a 70kg subject would need 14mg or 14/188 = 0.072mmoles (188= DMT molecular weight). The amount surviving MAO and reaching the brain's blood volume of 200ml
is unknown. Injected DMT+ would reach cortical 5-HT2a hallucinogenic receptors from the internal carotid artery and the brainstem 5-HT1a receptors by the separate vertebral-brachial system.  Since the onset of the DMT effect in Strassman's experiments was quite rapid, well within a minute, a loss of 30% is assumed. The hallucinogenic amount would be 0.7 X .072 = 0.05mmol DMT.  First appearing in the 3rd ventricle (1ml), the concentration DMT+ .05 mmol/ml or 0.3mmol/ml for a single six proton resonance. This is insufficient for detection under the present state of MRS resolution.  

Thus, it appears unlikely that the centerpiece of this monograph, DMT+, can be measured at all in humans.  In animals, administration of radioactive serotonin would be an approach, but still plagued by discriminating melatonin from DMT+ tryptamines.  The tiny spaces of the third and fourth ventricles may reflect a design for such high exclusivity in delivering DMT+ to the raphe nuclei that any source for assay, i.e., blood, urine or CSF is not possible.

The ramifications of M’s LSD experiences lay well beyond the simple demonstration of DMT+ secretion in parturition, PTSD and REM sleep.  There are other claims to be tested.   At the phenomenological level a hidden memory was released, leading to a simple model that involved specific putative categories of brainstem components: the raphe nuclei, reticular nuclei and the cerebellum.  The obvious approach would be to use fMRI and/or PET scan approaches to get brain images demonstrating activity changes in these brainstem nuclei as well as the S I and SII regions in the cerebral cortex.   This approach is problematical, owing to restrictions on the resolution of the images, particularly with fMRI requiring statistical subtraction of controls.  Recent advances in PET technology appear to have overcome the 3mm limit imposed by the distance between the original radiation and the nuclear target that produces the detected radiation.  Recent PET studies can resolve the pineal-habenula region to determine their coupling with raphe nuclei within the brainstem (Morris et al, 1999)

Fortunately, established fMRI protocols now exist to determine brain areas activated by scripted cues that provoke an emotional state recalled by a traumatized subject during the fMRI experiment.  In one study, sub-cortical areas within the cingulate gyrus and tegmental areas above the brainstem were activated with recall of different emotions (Lanius et al, 2000).  Using the RaRN model as a paradigm, further activation within separated areas such as the deep cerebellum, brainstem, thus far unseen, may be activated with administration of the 5-HT1a agonist.

To test the proposed opening of a memory substrate by raphe suppression, an attractive experiment would be based on the recent demonstration of fMRI brainstem and cortical activity in response to pain (Iannetti et al, 2005).   In a control experiment the brainstem and cerebral elements “light up” as active areas when controlled pain is imposed on a subject pre-sensitized to a peripheral location (the leg).   These authors demonstrated that pain-related activities in the brainstem and cortical regions could be compared with those, in which a specific drug to alleviate pain was administered.  The images revealed which of the brain areas were affected by the pain relief drug.  In the same way, the control images for pain induction could be compared with those, in which the subject was given a 5H1a agonist such as lisuride, to show new activity in a cerebellar nucleus and in the SII cortex.   If the memory substrate were in the cerebellum, problems with image resolution within the brainstem would be evaded.  This experiment would either nail or refute the proposal that suppression of the raphe nucleus opens a subcortical memory substrate.   Further, the possibility that this substrate contains memory of the pain could be approached.  At sometime after the induction of pain, i.e., when raphe activity recovered, the administration of the 5-HT1a or 2a agonist once again would test the possibility of new memory traffic between cerebellar storage and thalamocortical regions.   In these experiments the observance of raphe activity per se is questionable, owing to the present state of fMRI instrument resolution. The possibility that these experiments would require the exclusive administration of an hallucinogenic agonist, e.g., LSD or DMT, might reveal the possibility for 5-HT2a involvement in memory consolidation as well and could be compared to those experiments using drugs more exclusive to 2a, the phenethylamines, DOI or DOM.

A test for the REM sleep hypothesis described in Part 1 seems  simple, but at first sight, would be considered not to work.  The anticipation that a 5-HT1a agonist would enhance the REM State would likely produce the reverse if agonists were injected systemically.  REM suppression occurs with the administration of SSRIs and 1a agonists.  However, as discussed in the REM Sleep page, agonist suppression of REM sleep by systemic administration would be misleading in view of repeated demonstrations that REM sleep is induced by direct application of the agonist to the dorsal raphe nucleus.  Moreover, if the requirement for modifying the time and latency of REM sleep can be related to the RaRN model, additional support may be seen in the success of 5-HT1a agonists in treating PTSD as discussed on the page, Raphe---Trauma Therapy

A key demonstration inadvertently suggesting the requirement for raphe inhibition in the treatment of PTSD has already been published (MAPS).  In regards to other tests on the RaRN model, there is no need to instruct the better-informed neurobiologists on the delicious armamentarium of drugs, enzyme inhibitors, antagonists, and agonists at their disposal.  Additional testing will be mentioned in Part 2.  

1.13 THE SMOKING GUN

She’s the kind that leaves her bed in the morning and starts the day without hesitation or even without thinking, especially about lingering a bit longer in that delicious envelope against the cold room.   As a young Vermont girl she had to arise and wash her face with ice water.  Now, at age 75 she goes to the refrigerator for the coffee beans and English muffins destined unknowingly for the toaster and the pleasure they will give with a little butter and Betty’s three-berry jam.  As she pulls the refrigerator handle, a spike of fear, a visceral shock and a dreadful tableau reaches her sunny consciousness.  She sees vividly the look of concentration on the little face of her four year-old daughter levitating silently and helplessly in a small estuary as it slowly filled with the incoming tide.   At a beach party 35 years previously, she had been assured that older daughters of the group would be watching her first born, but a few minutes out of sight was a bit too long and she went looking.  Was it the same reaching for her daughter’s salvation in a careless world as she reached for the refrigerator door that resurrected an unwanted  memory soon after awakening?



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