Cures Not Wars

Copyright © 1995-1996, Paul De Rienzo, Dana Beal
and Members of the Project

All Rights Reserved

CHAPTER 17: Cures Not Wars

In February, 1994, Robert Rygor died. He’d become a beneficiary of the free pot program, and as facilitator of ACT UP Coordinating Committee, which set the agenda for the Monday night meeting, helped make sure Ibogaine got a fair shake. His death was a direct loss. But more ominous was that during the entire hour-plus obituary at the next ACT UP meeting, facilitator Scott Sawyer (of the regular leadership) refused to call on Beal, pointedly denying him the legitimacy to thank Robert for so often negotiating behind the scenes for the bubble of tolerance that enabled Ibogaine work to go forward.

A few weeks later Dana was in Philadelphia, relating the remnants of the Problem to Kiyoshi Kuromiya. Kiyoshi was co-author of Buckminister Fuller’s last book Critical Path, and edits a journal of the same name, devoted to AIDS. Dana was explaining the implications of the re-discovery of Gnostic substances: mind over immune-system–

“Miraculous healing, true prophecy, liberation from destructive reflex (“sin”), victory over death–Ibogaine reliably, and harmaline if used correctly, provide a version of all of them. The NDE is the key to all four. By means of the dreamtime, we gain a different access to time itself.”

Then Kiyoshi recounted his own experiments with lucid dreaming, in which he wrote down the location of a shoe store 5 years before it was changed to a shoe store from a diner. “That’s the trouble,” Dana mused, “You may end up in a stretch of the future that’s totally boring–that tells you very little. The Essenes solved this problem by sending thousands of random observers to map things out–mass invasion of the future.

They foresaw the Fall of the Temple–and that there was no way to stop it. But in the process, they determined not only how to master additional techniques to replicate the NDE more precisely, but the exact circumstances in which, up ahead in the future, one might through this mastery intervene and reverse the outcome of History.

“We can now physically explain the crucifixion and resurrection,” said Dana, “but we are still left with the problem of time. He promised Torah would conquer the whole world, and that Israel would be re-established thereby. But that’s really an extremely long shot. How could they visualize, as early as 600 BC, outcomes 2, 600 years later, to be able to set up the Crucifixion?” Kiyoshi volunteered an article from The Scientific American, which proposed that transmission of information from the future, at least, might not contradict quantum physics. In it, writers David Deutsch and Michael Lockwood discuss the fashioning of quantum-level “worm-holes” into “Closed Timelike Curves” (CTCs):

“Does our universe now, or will it ever contain CTCs? We do not know, but there are various theoretical conjectures about how they might be formed. The mathematician Kurt Godel found a solution to Einstein’s equations that described CTCs. In that solution the whole universe rotates (according to current evidence, the actual universe does not). CTCs also appear in solutions of Einstein’s equations describing rotating black holes…

“A kind of shortcut through space-time, called a wormhole, has been mooted by Princeton University Physicist John A. Wheeler. Kip S. Thorne of the California Institute of Technology and others have shown how two ends of a wormhole could be moved so as to form a CTC. According to a recent calculation by J. Richard Gott of Princeton, a cosmic string (another theoretical construct that may or may not exist in nature) passing rapidly by another would generate CTCs… They may…become accessible to future civilizations…” (The Quantum Physics of Time Travel, Scientific American, March 1994, pg. 70)

From the standpoint of expenditure of energy, transmission of information backward in time presents the fewest problems, and apparently no fundamental contradiction on the quantum level, allowing our world to be shunted orthogonally, at key decision-points, onto another track of the Multiverse.

“Do you realize what this means?” asked Dana. “If science can duplicate the Resurrection, the fall of the Papacy will be bigger than the collapse of the Soviet Union. The Gnostics were only trying to keep the key to prophecy from the hated Empire. But after the fall of the Temple and exile of Israel, European Orthodoxy took over. The Trinity and the Virgin Birth.

The laws against psychedelic research represent the perpetuation, in secular law, of the original Eclessiastical cover-up of the true circumstances of the Resurrection! Not only couldn’t they allow anyone to know how it was done, they had to ban any investigation of plant substances that might lead to re-discovery of how it was done. That’s why under Church law, any attempt to foretell the future was punishable as witchcraft. And nothing’s changed! “Drugs” is the only taboo where government licenses militant religion–12 step groups–to convert heretics forceably. I don’t think ACT UP is ready for this.”

Kiyoshi asked what he meant.

Dana went on: “ACT UP got in enough trouble for breaking the host at St. Pat’s. For them to bring proofs that the wine and wafer are only standins for the real sacraments repeats the same action on a vastly higher conceptual level– one reason I always felt the original St. Pat’s action was like a strange attractor for Ibogaine.* Philip Dick has a scene in a Church where, as the priest dips the wafer in the consecrated wine saying, “The Blood of Our Lord Jesus Christ, which was shed for thee..,” the Son of Man calls out from the back pews–“The blood is not there nor the body either.” –and when the Priest looks up to see who it is is, Emmanual says– “You do not have the authority.”** The Christians are going to freak out! I wonder if we’ll get in as much trouble as Salmon Rushdie.

“In a way it’s unfair to involve ACT UP in this. They’ve already got their hands full finding a cure for AIDS.”

Confrontation with the Christians came soon enough, in the form of the Philly Convention of Sue Rusche’s PRIDE–Parent’s Resource Insitute for Drug Education. The Harm Reduction Working Group had set two spring actions– Philly March 3-5, New York May 7– hoping to derive some spin for the overall push against the Drug War. Gilbert Baker, in town to do a mile-long rainbow flag for Stonewall 25, popped in with new spring slogan: Cures not Wars.

New York ACT UP also fired off a letter to one of Rusche’s minions, the Drug Czar of Michigan, who’d circulated a letter characterizing ACT UP as part of the pot lobby. But the actual protest-date Philly ACT UP picked for the PRIDE zap was Feb 27. So it ended up as 40 AIDS activists picketing Philly’s Convention Center the weekend before the PRIDE Conference–when no one from PRIDE was even in town yet.

The harm reduction crew came back from Philly to find that Aldyn MacKean had died. In the obituary, on the floor, Andy Velez and several others recounted a vision Aldyn had had when he was very sick in the hospital, before he recovered enough to come back to his last few ACT UP meetings. Jon Greenberg, another treatment activist who’d died a year earlier, had appeared beside Aldyn’s bed, telling him that he would be his guide, and not to worry. Interesting kappa opiate phenomenon, thought Dana, but he lay awake thinking about it until late at night– “Now you have a companion who never sickens, or fails, or dies; you are bonded to the eternal, and will shine like the healing sun itself.”–

“As you go back into the world I will guide you from day to day. And when you die I will notice and come to pick you up. I will carry you back to your home, out of which you come and back to which you go.”

“You are strangers here, but you are hardly strangers to me; I have known you from the start. This has not been your world, but I will make it your world; I will change it for you. Fear not. What assails you will perish and you will thrive.” (VALIS , pps. 199-200)

Interaction with the actual PRIDE convention was limited to leafleting the kids with the most recent OMNI article on Debbie Mash’s work, together with a press conference denouncing PRIDE’s very public campaign to keep Drug Czar Lee Brown from meeting harm reduction advocates. The Inquirer printed ACT UP charges that meetings about Ibogaine research were on hold because of ACT UP’s vocal endorsement of medical marijuana. This prompted a support letter from ACT UP and a flurry of phonecalls to and from Lee Brown’s office. No meeting ensued.

According to Howard Lotsof, everytime the politicians in ONDCP ask their experts about Ibogaine, they get advice to develop longer-acting cocaine analogs instead. More “methadone-like.”

Right around April 1,* however, an independent panel chosen by the National Academy of Science published a preliminary report, “Development of Anti-Addiction Medication,” which endorsed virtually every ACT UP Harm Reduction demand, including accelerated approval, parallel track and physician-inititiated treatment INDs for new anti-addiction drugs, and tapping the Drug Forfeiture** fund to fully fund Medication Development up $95 million authorized–instead of the current $36 million.

In addition, the Committee identified DEA over-regulation as the principle source of unnecessary red tape. They recommend DEA review be folded into a one-step FDA/DEA approval; and that Clinton sign an order giving Medication Development Presidential priority. Best of all, in the first paragraph on strategies for discovery of a cocaine medication (p. 33), the committee wrote:

“A medication developed for the treatment of drug addiction ideally is effective when administered orally or is able to be implanted, is long-acting, clinically safe, causes few side effects, is acceptable to patients, is designed to reduce both reinforcing and toxic effects of the addictive drug, has little abuse liability and is useful for more than one class of abused dugs (because many substance-abusers use more than one drug.)”

This is impossible for any maintenance agonist, antagonist or mono-clonal enzyme currently under development to do, of course. Failure to come up with something that really works is the principle reason for “the absence [cited in the report] of a large, vocal advocacy group that would voice strong support and lobby for treatment funding and research”***–although criminalizing addicts certainly doesn’t encourage activism.

Back in New York, Dana’s working majority on the ACT UP floor was coming to an end. It started when the floor rejected, 12 to 11, adoption of Cures Not Wars as a new harm reduction slogan. Then, just before the end of March, John Spacely died of AIDS. In an obituary, Dana bitterly recounted how John Spacely had asked for Ibogaine treatment in 1981, before he was probably even infected, and told the floor he understood perfectly the frustration of not being able to get people drugs in time to save their lives. Later in the evening, Dana and Dennis Peron got a healthy majority of ACT UP to back the annual Stop the Drug Wars Parade, by sponsoring one of two feeder rallies May 7th.

Egged on by Dan Raymond, however, Donald Grove of the Lower East Side Needle Exchange flip-flopped and turned against May 7th after initially backing it. He attacked the whole idea of substituting non-injectable substances for heroin or cocaine, saying it wasn’t legitimate AIDS-prevention, because it diverted energy from needle exchange. And he charged the underlying premise of blanket de-crim of 6 plants–market separation of marijuana– stigmatized hard-drug users. Others passionately felt ACT UP should reject any moves to safeguard medical marijuana access by expanding existing New York State de-crim to 6 plants, because it would mainly benefit drug users who didn’t have AIDS.

This reaction blocked approval of all posters with ACT UP’s name until there was no time left, and the Harm Reduction Coalition reluctantly announced it was going ahead without it. The opponents of Ibogaine, miffed at being bypassed, pressed for a star chamber proceeding May 2nd facilitated by Amy Bauer, where Dana’s character was dissected without his being able to answer allegations against him.

Some one even charged that John Spacely didn’t die of AIDS–that Dana’d improperly taken up time under obituaries for a drug overdose death. Later in the evening it became clear that the AIDS Cure Project had enlisted the decisive votes with Donald Grove and the regular leadership in return for support for a full page ad in the New York Times. It was supposed to cost N.Y. ACT UP only $4,000– it ended up with the Treasurers refusing to pay theTimes the full $18,000, depriving ACT UP of any other ads in theTimes ever again. A written notice of cancellation of the ad hadn’t been sent in. Bad luck.

Dana, on the other hand, was busily working on preparations for the Cures not Wars Parade/Rally when an article on harmaline crossed his desk. It was from the “Abuse Folio” by David E. Smith of the Haight-Ashbury Free Clinic, and warned that high-dose harmaline, like Ibogaine, may indeed cause numbness, (presumably of hands and feet first).*

The rally, when it happened May 7th, was far more enormous than anything ACT UP expected. The picture and caption in the New York Times presented a balanced harm reduction message– not, as feared, just a marijuana protest.

But with negative groupthink dominating ACT UP, only a handful of harm reduction loyalists showed up and experienced the rally. The ACT UP floor didn’t want to acknowledge or deal with 8,000 young people who were not predominately gay or i.v. users. ACT UP’s youth group, YELL, didn’t even give out condoms.

Three days later Charlie Kaplan stopped into 9 Bleecker, on his way to Texas to do NIDA contract-work. He offered an interesting notion they’d come up with before he’d left Erasmus: that Ibogaine reset the angle of the endorphin receptors– the tilt of the receptor surfaces. He also reported Dutch authorities were tolerating harmaline use–but only as part of a quasi-religious ceremony–while some kind of challenge percolates up through the courts.

“It’s the original root religion,” Dana interjected, “Both of the 3 Monotheisms and Hinduism. I should really help them in their suit, by furnishing a pharmacologic explanation for the Resurrection. Flattery (p. 93) says it is taboo for Sikhs and Hindus today because the Brahmin priests long ago realized it infringed upon their magical monopoly on revelation. And all Catholics knew was that it was used by the followers of Ahriman to contact Hell. But the Shia still burn harmel seed as incense; and the story is that at the birth of Jesus three Magians showed up with incense. So if Persian Kings customarily took Soma to increase their perscipacity and grasp of righteousness (p. 98), how could the Prince of Peace not avail himself of the same insight for His immeasurably greater, more demanding Mission?”

Dana recommended that before going to Texas, Kaplan pick up the VALIS trilogy for $6 at Jim Druggas’ store at 34 Carmine street. Dana also urged him to attend the second design session for NIDA’s Phase I/II protocol May 16th, but that was the day Kaplan was starting work, so he couldn’t make it.

Since mid-April the harm reduction working group had been operating with the understanding that the ACT UP name would henceforth be used only in connection with the needle exchange. Medications development and AIDS-prevention for non-i.v. drug users would be the focus of a new group, CURES NOT WARS. But this was not finalized until May 30th. On May 16th Dana Beal, Johann Moore and David Goldstein, still representing ACT UP, attended the second Ibogaine Protocol design session. It was an exciting day.

Frank Vocci opened with an overview of what NIDA/MDD is planning. He reviewed history of Ibogaine research, especially Molliver and O’hearn’s findings of toxiticty in rats, which stopped human testing in September of ’92, as well as primate data that prompted FDA to approve resumed clinical research at very low doses last August. He summarized where we left off in October, when the first design session was unable to agree to proceed quickly.

NIDA pharmacologist Nora Chang presented what is known about Ibogaine pharmacokinetics. She stressed two points: discovery that Ibogaine bioavailability in rats and dogs is much greater in larger doses, and the discovery by Hearn of the Miami team of the major metabolite of Ibogaine called noribogaine.

Biochemist James O’Callahan next did a quick workshop on the state of the art in measuring neurotoxicity. He presented slides showing the neurotoxicity of a large number of psychoactive drugs in various species of animals, and provided cross-species comparative scales of neurotoxicity.

The “marker” he was using was the activation of astrocyte fibers of microglial cells — macrophages that consume damaged neuronal tissue whenever there’s toxicity. Ibogaine received a very low tox rating on this scale. He also presented data showing greater Ibogaine effect in female rats than in males.

Mark Molliver, leading researcher on Ibogaine neurotoxicity in the cerebellum, started by saying the cerebellum is the least known part of the brain– we know how it works, but we don’t know what it does. The effect in rats that set off alarms in ’92, however, was excito-toxic– the result of overstimulation of very well-shielded Purkinje cells subjected to rhythmic bursts from the inferior olive.

The reaction in primates was completely different. Molliver was astounded to find Ibogaine, when administered orally in doses up to 150 mg-per-kg, had none of the gross effects on his monkeys that he’d seen in rats. In order to maintain such effects (tremors, ataxia) longer than twelve hours, (because he suspected excito-toxicity in rats was due to length of tremor) he found it necessary to administer 50 mg/kg, interperitoneal Ibogaine in solution, every 2.5 hours.

Five out of seven animals had seizure activity with each injection. But to check for signs of Purkinje damage, Molliver and O’hearn needed to adapt immune markers from humans and tissue stains from rats. It became clear to Molliver and O’hearn that the stains designed for rats, trying to pick up markers derived from humans weren’tworking in primates. Findings of no toxicity merely meant their “tools” couldn’t detect it if it was there.

On the first 6 monkeys, nothing they had worked. Furthermore, control animals also showed irregular, “spotty” distribution of Purkinje cells in corresponding regions of the vermis– that’s normal in primates. So after 5 sharp assaults with Ibogaine, Molliver was able to find only the most equivocal evidence of damage in one monkey.

Dana Beal asked if the 5 sharp assaults, with seizures, were really comparable to the long rolling peak the human experiences with oral administration. He noted that Ibogaine injected, according to Hans-Georg Behr, also produces a shorter peak experience in humans, more similar to Molliver’s i.p. administration in the primate.

Next up was Deborah Mash, one of the University of Miami researchers with the IND from FDA to do Ibogaine safety-testing in humans. Her results earlier had conflicted with Molliver’s, in that her animal subjects did not experience ataxia. No neurological deficits were found in her human subjects or her primates. Her IND is continuing. She expected to study three more male humans at higher doses. She said her team would like to accelerate the dose regimen, but that this had not been approved.

She was followed by Juan Sanchez-Ramos, the movement-disorders specialist who is director of Miami laboratory and the initiator of the IND. He placed humans receiving the 1 mg/kg dose on a neurotest apparatus — the “wobble board.” This wobble board was designed to diagnose the presence and severity of Parkinson’s disease. It measures wholebody tremor at various frequencies, and can detect fine tremor invisible even to trained specialists. At the low, one kmg./kg. dose, two subjects reported feeling nothing, while a third actually became calmer.

Linda Weinhold presented NIDA/MDD Ibogaine Phase I/II Protocol Proposals, ie., the protocol that had been mailed in advance to participants. It involves a cohort of 60, or 15 at four centers, a nested double-blind dose run-up Phase I safety study, with a followup Phase II efficacy component to track interruption or diminishment of cocaine use.

Subjects must be using $150 of cocaine a week. Out of fifteen subjects at each center, three will receive placebo, three will receive 150 mg, three will receive 300 mg, three will receive 600 mg, and three will receive 900 mg. One-week inpatient status preceding administration of ibogaine, one-week out-patient, with anniversary check-ups at three months, six months, and one year.

She asked for questions, and it was half a minute before Beal broke the silence with a query following his earlier line of questions to Molliver: Since EEGs were being run before and after, how about doing an EEG as far into the treatment as the subject could tolerate? Subsequent discussion elicited views suggesting subjects would probably not object as much to this during the dreamlike phase as they would during the second, cognitive-evaluation phase starting about 6 hours into the procedure.

The panel also seemed to be growing more comfortable with the idea that Ibogaine activity might be replacing REM. Ed Friedrich stated that since sleep deficit is a significant part of addiction sequellae, a sleep specialist should be present during Ibogaine treatment.

Doblin suggested use of a PET scan on subjects. This suggest ion was rejected.

There was much discussion of an active placebo, since subjects know they’re getting Ibogaine. Since Ibogaine is a psychedelic, said Yensen, training given to each treatment team should include briefings on human behavior during psychedelic experiences. Rick Strassman further stressed importance of set and setting. An expert on DMT, he reiterated the need for sensitivity to psychedelic phenomena on the part of treatment teams.

For an active placebo, Yensen suggested LSD, prompting alot of comparisons with Ibogaine to the effect to that it’s more intense, but that the dreamlike quality makes it more benign, unlikely to trigger a schizophrenic break.

Beal suggested mitragynine, reportedly used to interrupt heroin addiction in New Zealand, derived from the Rubiaceaea kratom.* Both suggestions were rejected by Charles Grudzinskas, acting Deputy Director of NIDA, who said that even less is known about the latter than about Ibogaine. This prompted general laughter and a release of tension.

Things were running late, so Alan Trachtenberg of NIDA Basic Research launched into his presentation on 3 inclusion and 3 exclusion criteria while many panelists were still out of the room for a coffee break. The inclusion criteria are as follows: healthy male cocaine user (25-40 years old) with $150/week habit. Urine-tests will be used to determine that subjects are THC negative, methadone negative, and cocaine positive. HIV or t.b. positive subjects are excluded. Women are excluded until NIDA finds some clinical indication of efficacy in males, because of a greater sensitivity in the female to Ibogaine across a broad range of species, including human females.

Christine Ollo came next, with protocol questionnaires to measure psychological state of subjects both prior to and following the Ibogaine session. There was significant discussion of the amount and endpoint of testing. After Ollo’s presentation, discussion centered on need for treatment team to show sensitivity to mood of persons undergoing psychedelic experiences, specifically in accepting subjects’ possible refusal to answer questions.

The session wrap-up discussion had two facilitators. Paul Fudalla asked if anyone objected to proceding to a clinical trial; no one responded. Wright, FDA case officer for Ibogaine, at this point refined the question to inquire at what point the trial would be aborted. There was a heated discussion of the “Go/No go” decision points , i.e. the interpretation of behavioral manifestations in human subjects and the establishment of criteria for intervention, i.e., stopping.

O’hearn was asked to weigh in; she said the data from just one animal was too preliminary. Tractenberg said he agreed with earlier comments that giving the animal 50 mg./kg. i.p. jolts of Ibogaine was not equivalent to the oral dose in humans; especially if it’s really not much more long-lasting in humans, when injected, than in primates.

At this point Molliver came back into the room, passing Dana, who whispered that it looked like the panel was overreacting to the toxicity findings again. Mark immediately went to the microphone. After a minute or two he commented: “My feeling is that this is going to be a safe drug in humans.” With this remark there was a palpable shift in the sentiment of the room. He went on to say his results suggested that even in double-doses injected i.p. 5 times in 12 hours, Ibogaine damage was very hard to find in primates.

Juan Sanchez-Ramos volunteered that he was ready to stop the minute he had proof of even the slightest cell loss. But Curtis Wright surprised everyone by ruling that in dealing with addiction, a life-threatening disorder, a little braincell loss might be okay. Wright then specified that the Data Safety Committee ought to have clear evidence that “something is broken” before intervention. For example, persistent minor tremor should not be sufficient to interrupt the study. Finally, Wright of FDA said “It sounds to me like you folks have a Phase I clinical trial.”

Carlo Contoreggi now took over, asking for further suggestions as to how to proceed. It was agreed that nicotine and alcohol consumption be monitored as part of the followup.

Ed Friedrich also suggested there should be follow-up immune function studies. “Sleep medicine experts should be involved in Ibogaine research. If Ibogaine first releases REM, then allows catch-up Slow Wave Sleep as an after-effect, we have to beware of undesirable rapid healing effects of sleep restoration– latent antigens belatedly attacked by the revived immune mechanism, causing rheumatoid arthritis, etc.” Friedrichs urged extreme caution in administering Ibogaine to the aged.

MDD seemed amenable a suggestion about adding another echelon– 1200 mg,, or the lowest full dose– if all went well. That would bring the total cohort up to 75. The timeline was set, but no dates given.

At this point Beal asked when the trial would start. Wright turned the floor over to NIDA pharmacologist Belinda Hayes, who explained that ongoing preclinical work intended to determine the half-life of Ibogaine in the blood and to correlate blood levels with Ibogaine’s different phases would have to be completed first. Mash spoke up and said things were moving quickly– that the ACT UP side should be satisfied.

Johann Moore asked when the Ibogaine would get to junkies on the street.

Beal ended the session by remarking that narcotics agents in Staten Island had just strangled a man, Ernest Sayon, and that New York had a real possibility of exploding, Los Angeles-style: “As long as people have a hope of doing something about a problem, they’ll wait instead of lashing out– but we can only keep hope going for so long without actually delivering something.”

When Johann, Rommell and Dana went on the ACT UP floor the next week they told them the ball was now in ACT UP’s court so far as doing anything about exclusion of women; and that it was really up to the floor if they wanted anything to happen to make it available to junkies with HIV, the original target group, any time soon. What Harm Reduction recommended was to see if females tolerated mitragynine better, so that it also might be fast-tracked.

The next step was to make contact with New Zealand. A phonecall established that mitragynine had been given for methadone addiction detox. Kratom was smoked whenever withdrawals occured, with treatment extending over 6 weeks. Turned out there was also a visualization effect, but shifted into regular sleep, occuring at night as vivid, hypnagogic dreams. But some re-regulation of the sleep cycle, indicated by an “Ibogaine-like glow,”* seemed to persist as long as kratom is smoked.

A few weeks later Juan Sanchez-Ramos, upon reading an earlier, 15 Chapter version of this report, furnished a paper** on treating Parkinson’s disease with harmaline, an MAO-inhibitor, which was tried and abandoned around 1930. More selective monoamine-oxidase inhibitors discovered during the ’60’s are the current standard of care for Parkinson’s. And MAO-inhibitors inhibit oxidative stress, known to have a role in the progress of AIDS.*** So harmala can also impart a glow (and is used to improve skin complexion, according to Flattery, ¶xx). However, according to Lotsof, more up-to-date techniques have determined that Iboga alkaloids, at first found by Dhahir to be MAO inhibitors, are not.

Now Mark Molliver had also detected, although he barely mentioned it on the 16th, Ibogaine activity in the thalamus and locus coeruleus. The particular part of the thalamus activated by Ibogaine has an excitatory function, while the locus coeruleus is involved in concentration and dealing with novel situations. Both regions are implicated, like the cerebellum, in the generation of brain-waves–with the thalamus at 40 cycles-a-second synchronizing on every fourth beat and “binding” the slower 10 cycles-a-second rhythm of the olivo- cerebellum that governs body movement in a process known as “entrainment.” According to Dr. Rodolfo Llinas of N.Y.U., brainwave activity must “entrain” (synchronize), lest the brainwaves clash–so the thalamus has to “keep time” with Ibogaine activity in the olivo-cerebellum.

The thalamus handles sensory perception. Llinas has discovered that a doughnut-shaped group of cells in the thalamus called the intralaminar nucleus sends out a wave that scans all areas of the cerebral cortex every 12.5 thousandth of a second. This fires synchonized cells in the cerebral cortex that are currently recording sensory information, which instantly fire a coherent wave of messages back down to the thalamus. This synchronous firing, according to Sandra Blakeslee,***{***”How the Brain Might Work: A New Theory of Consciousness,” Tuesday, March 21, ’95 N.Y.Times, p. C1} is thought to be the basis of waking consciousness.

At night, on the other hand, the locus coeruleus is active in REM; while the thalamus generates both the the slow-wave of deep sleep (when the cerebral cortex is shut down), and then while we dream, cells in the thalamus and cerebral cortex oscillate together for brief periods, according to experiments conducted in Quebec, by Dr. Mircea Steriade. The brain, in essence, is an organ that generates images. Wakefulness “is a dream guided by the senses,” Llinas told Blakeslee.

In the standard model of addiction, as we saw in Chap. 7,** visualization in the striatum triggers craving in the nucleus accumbens, which sets up a dopaminergic cascade of further visualizations and cravings that finally trip the dopamine switch in the pre-frontal cortex, initiating drug-taking. Not all visualization is dopaminergic, however.

Glick showed Ibogaine weakly binds to the kappa receptor during the initial hours of a treatment. The kappa receptor, which is normally activated not by endorphins or enkephalins but a third class of endogenous opioids called dynorphins, may actually down-regulate or reverse the effect of endorphins on the mu or enkephalin stimulation of mu and delta receptors. Kappa opiate receptors have in fact been found (1986 Science, Vol. 233, pgs. 774-6, Pfeiffer, et al) to generate “dysphoric pseudo-hallucinations” as a part of an endogenous opiate system completely opposed to the normal euphoric analgesia of mu receptor agonists– a possible reason why the FDA now considers Ibogaine to have low potential for abuse. Geerte F., on the other hand, believes the only true junkies are the 3 per cent or so of the population whose heroin experience has significant kappa receptor qualities. They get an out-of-body experience on heroin.

Moreover, “…somesthetic changes and disturbances in the perception of space and time… de-personalization, de-realization and loss of self-control” induced by Pfeiffer et al. using the potent benzomorphan kappa agonist MR 2033 are consistent with the naturally-occuring NDE.

Now if the function of an active placebo is that neither subjects or clinicians be able to tell whether they’re getting Ibogaine, harmaline is a logical candidate. Fred Gotbetter, who’s taken both, says harmaline is very close-more euphoric than Ibogaine, but similar in peak and duration. It is tremorigenic and oneiric (similar “two world super-imposition” effect), and has a much more solid track record of reasonably safe use in humans than any substance recently discovered, including LSD. Lee Cummings, informed that harmaline was once so widely used in Indo-European cultures, asked if it could be used to treat addiction. As a matter of fact, ayahuasca preparations are used in traditional South American medicine to curb alcoholism, curse of tribal peoples.* But telepathine, the compound in ayahuasca consisting principally of harmaline, contains additional tryptamines–which would explain while no Old World materia medica, working with pure harmala preparations from the wild rue, mentions treatment of alcoholism.

Mitragynine, because its gradual mode of administration is not enough like Ibogaine, must actually be ruled out as an active placebo. But as far as any “efficacy component” of the current research is concerned, use of harmaline would allow fine comparisons with the weak binding to the kappa receptor which the additional architecture of the Ibogaine molecule seems to confer. Small doses of compounds that selectively bind to the kappa receptors could even be administered with harmaline, to see to what degree addiction interruption is dependent on such transient, or “weak” receptor activity. This may be the only way to determine whether, on Ibogaine, because of “sensitive dependence on initial conditions,” the weak kappa binding which makes the experience less euphoric than harmaline, also makes it effective against addiction.

The discovery of an endogenous nor-harman by E.M.Dzoljic**** should put to rest NIDA fears about harmaline toxicity. Turns out the active molecule in the little white flower by the side of the road is a naturally occuring neuro-transmitter.***** Dzoljic also found that activation of the opiate receptor types–mu, delta, and kappa–kicks up higher level of nor-harman. Lotsof believes increased leveals of this nurotransmitter represent the body’s endogenous response to opiate dependency–but that heroin by itself overwhelmes nor-harmans ability by itself to counter-act the addictive effect.

Recent findings on metabolization of Ibogaine in humans suggest the existence of a natural pathway in the liver (chi )that may also retard metabolization of nor-harman, so that it can be accumulated and released in a squirt during REM, in all probability as part of the digestive process, like TNF alpha.****** As an MAO-inhibiter, it modifies completely the effect of a significant simultaneous release during REM of the endogenous triptamine serotonin–making it “trippy.” One or more harmala alkaloids seem to be the brain’s own natural substance for generating long-term memory, dream content, eidetic visions, “peak experiences” (P.K. Dick’s “blinding pink beam of light”), and in an emergency, the NDE–via complex interaction with dynorphin-generated kappa activity designed to counteract mu analgesia and stave off respiratory collapse. When this happens, years flash past like a movie and folks find themselves floating autoscopically above the operating table.

NDE research gives us a window into a quantum state in which the personality is out-of-phase with space and time, where kappa and harmala receptors peek around the regular four dimensions through one of the seven that “collapsed” (but not quite completely) not long after the Big Bang, according to “superstring” theory.

The ancients, in the course of centuries of harmaline use, apparently discovered the genuine prophetic effect comes not with ephedra, but can be magnified by simultaneously flooding the system with endorphins. The ritual mortification of flesh is a fossil remnant of this in the practices of present day Christian and Islamic sects. The Native American Sundance ritual, involving use of peyote (mescaline) while hanging, crucified, skewered through the pectorals, is a living example.

Late in the summer, Dana talked to Carlo again, who felt a long-lasting metabolite, stored in the liver, might explain why some people get into distress hours after taking Ibogaine, when it should be wearing off: “Most people have the metabolic equivalent of a 4 lane tunnel to de-methylate the Ibogaine into nor-ibogaine, so that it can be metabolized. But sometimes 4 lanes of Ibogaine gets all jammed up trying to go through a one lane tunnel, an blood levels go way up. We think we can test for that susceptibility.”

Dana was doubtful: “Howard says Glick has a new paper out showing no Purkinje loss in the vermis of his rats at 40 mg-per-kg. I don’t think toxicity results are going to tell you what you want to know, because it’s another variation of the “guilty cell” approach.”

“What do you mean?,” Carlo asked.

“The original idea was that the Ibogaine effect was like psychosurgery–killing the cells where the addiction is. Another possibility, if brainwave actually ceases for a minute interval during the “splitting of the skull” is that in one in 6,000 people, it doesn’t restart perfectly. The autopsy of Nicola K. released at long last by Dutch authorities, showed ‘no determinable cause of death.’

“We may have to face the fact that if we run thousands and thousands of people through the NDE, every so often some one won’t come back. In Gabon about one in 6,000 die, usually a woman or a physically slight male. We always chalked that up to other cyto-toxic iboga compounds, uncertain release-rate from crude root bark scrapings, etc.; and thought it could be controlled in a hospital setting with full resucitation facilities. But perhaps, even though the NDE’s pharmaceutically-induced, you have an occasional ‘psycho-somatic death.’

“Uncertainty can be fatal. On the other hand, you have to balance it against 15 people dropping dead here last week from too-pure heroin,” and then he asked–

“Do you think the liver’s capacity to store long-lasting Ibogaine metabolite is related to the endogenous neuro-transmitter involved in the NDE?”

A week later Bob Sisko and Dana were walking up Third street, discussing the notion that the NDE is the key to access, on the quantum level– through Closed Timelike Curves– to Time–

“That harmaline book really turned out to be the key,” exulted Dana, “to understanding the ramifications of the Passover Plot. The Essenes scoured the dreamtime for the meaningful touches Christ incorporated into his Action. To access the far distant future, his own harmaline trip had to be wrapped around some event of fundamental symbolic import, whose strange attractor would stamp itself on everything for millenia to come, so it would resonate. One way to understand it is to remember that consciousness, as Molliver says, is a matter of widely distributed circuits oscillating in phase with each other.

“The resonance was undeniable. Remember, even after 1900 years the Grim King was so repelled by the example of the Suffering Just One that he scoffed at ‘Jew-clear’ physics! The Nazis taught that Aryan psychic powers had not been pharmacologic, but genetic– lost chiefly by interbreeding with Asians, Jews, etc. In the Theosophical swirl surrounding the appearance of Nazism, Himmler identified Eastern religions generally with the renunciation and self-abnegation of the Buddhism of Hermann Hesse– a chief competitor with Nazism in Germany during the 20’s. He was both fascinated and afraid, creating SS research bureaus to plumb “the secrets of Tibet.” Himmler was convinced Tibetan Buddhism was behind the Jews [!], who of course controlled Rome through the Buddha-nature of Jesus. [See next page. ]

“Did you know that, acording to Hans Georg Behr, a Legion was in fact stationed in Jerusalem during Jesus’ lifetime that was up to one third Buddhist? The 10th. They had been stationed in the East. After the Resurrection, some became Christians, and carried Christianity with them when they were transferred north of the Alps.”

Dana went on: “For the Nazis, Eastern religion existed to weaken the West. They brought back St. Michael as the personification of Germany: the German Michael (See next page ). So Himmler, who believed he was Baldur (the German Mithras)–and was the one who decided which nuclear physics were politically correct!–never caught on to the soma angle, or the relevance of certain Buddhist techniques which bring the apparent heartbeat down to zero. ”

“Hitler was such a loser,” said Sisko. “I never understood that until I read ‘How Hitler Lost the War’. * We used to think of Hitler as almost winning, but the author of this book shows how he made one wrong decision after another. I’ve thought a lot about this. And the only thing you can say is that through the Holocaust, the Nazis were diverted from their larger object, the destruction of humanity.”

“Victory went to followers of Christ,” said Dana, “Not Mithras. Remember, in the original Mithadic vision, the world ended in fire. Because Germany and Japan win and go on to annihilate each other,** whereas Marxism and Christianity shared an anti-racist premise that enabled the Soviets and the West to reconcile. The Dream of the Prophets– of Universal World Government– was realized. And Israel was re-established, armed with nukes.”

“So Jesus was a Jewish radical,” exclaimed Sisko. “The original Abbie Hoffman!”

“You’t gotta read Schonfield’s other book, Those Incredible Christians, ” said Dana. “He believes the Book of Revelations is actually the earlier document. Like the Book of John, it is associated with the Beloved Disciple. who is reputed to have lived more than a century, and seems to have been written by some one whose first language was Hebrew, unlike John, which is written in the Platonic manner, with dialogue, in Greek. That could make parts of Revelations the equivalent to the visions Wiraz dictated to the scribe when he arose from thestared state–the product of excursions forward of Jesus and others to next decision point.*** The interest of the Beloved Disciple was to debrief Jesus after his trip to the end of the Epoch initiated by his Crucifixion and Resurrection–

“Rev. 22: 1 ‘And he showed me a pure river of water of life, pure as crystal, proceeding out of the throne of God and the Lamb. “22: 2 In the midst of the street of it, and on either side of the river, was the Tree of Life, which bare twelve manner of fruits, and yielded her fruit every month; and the leaves of the Tree were for the Healing of the Nations’.”

“But also 22: 13 ‘I am the Alpha and Omega, the beginning and the end, the first and the last.’ and 22: 14 Blessed are they that do his commandments, that they may have right to the Tree of Life, and may enter through the gates into the City.'”

“What this implies is that only those who keep kosher, by regarding the host not as the literal blood of Jesus, but as the plant soma of the Tree of Life –i.e., the living blood of the Spirit which indwelt in Jesus when He was baptised by John the Baptist–get to enter the Village of the Dead!

“I told Charlier Kaplan,” Dana went on, “that the effect of millions of addicts taking Ibogaine might well be like the ‘scatter’ from city light messing up interstellar observatories –a sudden zone of translucence, which would be perceived as from a distance as the event-limit. And dig this! According to Flattery (p. 90-91), in Zoroastrian eschatology, at the end of Time a final yasna (sacrifice/communion) will be performed in which the bull Hadayus and its fat mixed with “white haoma.” This differs from ordinary haoma just as the Hadayus bull differs from ordinary cattle,**** (i.e, hadanaepata being the ancient Priestly usage for haoma that actually contained harmel). But the mixture is the draught of immortality to the resurrected dead. The Ancestors.”

“You know, I read a book called the Sign and the Seal that claims the Arc of the Covenent still exists. This guy Graham Hancock uses textual analysis, his own archeology, and the well-known fact that the falashas of Ethiopia practiced Old Temple rites not used in mainstream Judaism since the Babylonian exile to bolster the claim that the Kahanes actually spirited the Arc of the Covenant off to Egypt, to keep it from being defiled when Menasha tried to introduce idols into the Temple.***** Hancock found ruins of a replica of the first Temple on the Egyptian Island of Elephantine, near Aswan, from the end of the Persian Empire, when he says the Arc was removed to an island on Lake Tanith in the Abyssinian Highlands. There he found intact the stone altar for animal sacrifice, on the spot where the Arc was kept in a tent for 814 years. Then it wound up in a church in Axum during the mass conversion of Ethiopian Jews to Christianity around the time of Constantine the Great. Ethiopia was the only place where most Jews accepted Jesus as Moshioch” Dana mused. “Half the population were Jews. They were there for a long time–maybe before Solomon and Sheba.”

“The Ethiopians actually brought the Arc out in front of their army in 1898, when they met the Italians at Adowa. They say St. George came riding down on his dragon with a heavenly host, and the Italians were defeated–the largest European army ever to invade Africa up til that time. Emperor Menelik reproached his couriers, saying that it was not right that they rejoice at the deaths of so many Christians.

“In 1935, the Italians used poison gas. And in ’36, fascist blackshirts massacred the monks at Axum. But Mussolini, who thought he was Caesar, didn’t know or care about the Arc. He lost his armies in 1941–first, a quarter of a million men before the British in Libya, in February. Then the British brought Haile Selassie back from exile, to Khartoum, and as he ascended into Ethiopia, tens of thousands of Rastafarians came down from the hills, and the House of David re-entered Addis Ababa at the head of a mighty host. In all of East Africa, a second quarter million Italian troops were captured, almost without a shot being fired. After that, Italy was out of the war.

“Those who want to understand what comes next with Ibogaine ought to study that abject collapse–study its strange attractor: the re-match between Caesar and Christ, the return of the Negus. Remember, he was Jesus’ distant great grandnephew. The Arc is still at Axum. No one gets to see it but a single custodian, who always goes blind with cataracts after a couple years. Goes with the job. Once a year, at Kineret, they bring out a replica, covered with a blue robe emblazoned with the dove ot the Holy Spirit,” Dana concluded.

“That seems to be the story–Arc of the Covenant into Africa, Ibogaine out–’cause now, out of Africa, comes a New sacrament.

It restores the cultural importance of Dreamtime.

It obviates the need for mortification of flesh. From the Sundance to accupuncture. The improvement over harmaline is sufficiently dramatic to rehabilitate a lost form of medicine. Ibogaine heals ‘wounds that will not heal.’ Therefore, for addiction medicine, it’s like ‘the key that opens every door.’

“What dopaminergic visualization can do, kappa opiate visualization can undo, by going back in virtual time to undo it. And it is appropriate that emancipation from pathologic reflex is located in the dreamtime. All our concepts of a Spiritual Realm, a Platonic realm of Ideal analogs which generate everything in the real world, are cultural relics of a harmaline induced state. As Dick poetically put it about the previous possibilities of harmala alkaloids, “St. Sophia is going to be born again; she was not acceptable before.” (VALIS, p.100)

“A few pages earlier (p. 97) he also wrote–‘The Godhead is impaired; some primordial crisis occurred in it which we do not understand.’

“Ibogaine clears up the problem with primordial crisis, at least: It wasn’t the Godhead but the previous sacrament, harmaline, that was impaired. Incomplete. A perfect sacrament wouldn’t require additives.

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